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1
acromegaly due to pituitary adenoma 2005:2010[pubdate] *count=100
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Items 1 to 100 of about 170
1.
Ali O, Banerjee S, Kelly DF, Lee PD:
Management of type 2 diabetes mellitus associated with pituitary gigantism.
Pituitary
; 2007;10(4):359-64
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[Title]
Management of type 2 diabetes mellitus associated with
pituitary
gigantism.
Pituitary
gigantism, a condition of endogenous
growth hormone
(
GH
) hypersecretion prior to epiphyseal closure, is a rare condition.
In the adult condition
of GH
excess,
acromegaly
, the occurrence of type 2 diabetes mellitus (T2DM) and diabetic ketoacidosis (DKA) have been reported, with resolution following normalization
of GH
levels.
We report the case of a 16-year-old male with
pituitary
gigantism due to a large invasive suprasellar
adenoma
who presented with T2DM and DKA.
Despite surgical
de
-bulking, radiotherapy and medical treatment with cabergoline and pegvisomant,
GH
and insulin-like
growth
factor-I (IGF-I) levels remained elevated.
We review the pathophysiology of T2DM and DKA in
growth hormone
excess and available treatment options.
[MeSH-minor]
Adenoma
/ complications.
Adenoma
/ surgery.
Adenoma
/ therapy. Adolescent. Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Ergolines / therapeutic use. Human
Growth Hormone
/ analogs & derivatives. Human
Growth Hormone
/ therapeutic use. Humans. Hypoglycemic Agents / therapeutic use. Insulin / analogs & derivatives. Insulin / therapeutic use. Insulin Glargine. Insulin, Long-Acting. Male. Metformin / therapeutic use.
Pituitary
Neoplasms / complications.
Pituitary
Neoplasms / surgery.
Pituitary
Neoplasms / therapy. Radiotherapy
Genetic Alliance.
consumer health - Diabetes
.
Genetic Alliance.
consumer health - Diabetes, Type 2
.
Genetic Alliance.
consumer health - Gigantism
.
Genetic Alliance.
consumer health - Diabetes mellitus type 2
.
MedlinePlus Health Information.
consumer health - Diabetes Type 2
.
Hazardous Substances Data Bank.
METFORMIN HYDROCHLORIDE
.
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[Cites]
Postgrad Med J. 1996 Nov;72(853):682-3
[
8944212.001
]
[Cites]
Diabetes. 2000 Dec;49(12):2063-9
[
11118008.001
]
[Cites]
Metabolism. 2001 Dec;50(12):1457-61
[
11735093.001
]
[Cites]
Eur J Biochem. 1997 Jun 1;246(2):259-73
[
9208914.001
]
[Cites]
Clin Endocrinol (Oxf). 2003 Feb;58(2):132-5
[
12580925.001
]
[Cites]
Clin Endocrinol (Oxf). 2003 Feb;58(2):128-31
[
12580924.001
]
[Cites]
Int J Clin Pract. 1997 Oct;51(7):476-7
[
9536592.001
]
[Cites]
Acta Med Scand. 1988;223(4):327-35
[
3369313.001
]
[Cites]
J Indian Med Assoc. 1997 Oct;95(10):546-7
[
9567599.001
]
[Cites]
Horm Res. 1991;36 Suppl 1:32-5
[
1806481.001
]
[Cites]
Eur J Endocrinol. 1994 Jun;130(6):581-6
[
8205258.001
]
[Cites]
Trends Endocrinol Metab. 2001 Nov;12 (9):408-13
[
11595543.001
]
[Cites]
Growth Horm IGF Res. 2003 Aug;13 Suppl A:S18-21
[
12914720.001
]
[Cites]
Pituitary. 1999 Jun;2(1):29-41
[
11081170.001
]
[Cites]
Circ Res. 2007 Feb 16;100(3):328-41
[
17307971.001
]
[Cites]
Obes Res. 1998 Jan;6(1):47-53
[
9526970.001
]
[Cites]
J Clin Endocrinol Metab. 1967 Oct;27(10):1418-30
[
6057823.001
]
[Cites]
Arch Intern Med. 2004 Sep 27;164(17):1925-31
[
15451769.001
]
[Cites]
J Pediatr Endocrinol Metab. 1999 Nov-Dec;12(6):907-9
[
10614552.001
]
[Cites]
Pituitary. 2001 Sep;4(4):275-8
[
12501980.001
]
[Cites]
Diabet Med. 2003 Jan;20(1):3-15
[
12519314.001
]
[Cites]
Diabetes. 2000 Jun;49(6):896-903
[
10866040.001
]
[Cites]
J Clin Invest. 2001 Oct;108(8):1167-74
[
11602624.001
]
[Cites]
J Endocrinol Invest. 1993 Mar;16(3):181-7
[
8514973.001
]
[Cites]
Eur J Endocrinol. 2003 Dec;149(6):521-7
[
14640992.001
]
[Cites]
Biochem Pharmacol. 2000 Apr 1;59(7):887-90
[
10718348.001
]
[Cites]
Clin Endocrinol (Oxf). 1980 Jan;12(1):71-9
[
7379316.001
]
[Cites]
Clin Endocrinol (Oxf). 1999 May;50(5):561-7
[
10468920.001
]
[Cites]
Cancer Control. 2002 May-Jun;9(3):232-5
[
12090246.001
]
[Cites]
Medicine (Baltimore). 1994 Sep;73(5):233-40
[
7934807.001
]
[Cites]
Drugs. 1999;58 Suppl 1:31-9; discussion 75-82
[
10576523.001
]
[Cites]
Diabetes. 1994 Jul;43(7):920-8
[
8013758.001
]
[Cites]
Eur J Endocrinol. 2007 Jan;156(1):75-82
[
17218728.001
]
[Cites]
Endocrinol Jpn. 1983 Jun;30(3):329-34
[
6420141.001
]
[Cites]
Endocr Relat Cancer. 2001 Dec;8(4):287-305
[
11733226.001
]
[Cites]
Endocrine. 2003 Apr;20(3):271-8
[
12721507.001
]
[Cites]
J Neurosurg. 2003 Feb;98(2):350-8
[
12593622.001
]
[Cites]
Diabetes. 2002 Aug;51(8):2420-5
[
12145153.001
]
[Cites]
Diabetes. 2002 Feb;51 Suppl 1:S134-7
[
11815472.001
]
[Cites]
Clin Endocrinol (Oxf). 2003 Feb;58(2):136-7
[
12580926.001
]
[Cites]
Endocr Pract. 2000 Nov-Dec;6(6):450-2
[
11155217.001
]
[Cites]
J Pediatr Endocrinol Metab. 2003 Jan;16(1):5-22
[
12585335.001
]
[Cites]
N Engl J Med. 2000 Apr 20;342(16):1171-7
[
10770982.001
]
[Cites]
Diabetologia. 1999 Feb;42(2):128-38
[
10064091.001
]
(PMID = 17629784.001).
[ISSN]
1386-341X
[Journal-full-title]
Pituitary
[ISO-abbreviation]
Pituitary
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Ergolines; 0 / Hypoglycemic Agents; 0 / Insulin; 0 / Insulin, Long-Acting; 12629-01-5 / Human Growth Hormone; 2ZM8CX04RZ / Insulin Glargine; 9100L32L2N / Metformin; LL60K9J05T / cabergoline; N824AOU5XV / pegvisomant
2.
Minniti G, Jaffrain-Rea ML, Osti M, Esposito V, Santoro A, Solda F, Gargiulo P, Tamburrano G, Enrici RM:
The long-term efficacy of conventional radiotherapy in patients with GH-secreting pituitary adenomas.
Clin Endocrinol (Oxf)
; 2005 Feb;62(2):210-6
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[Title]
The long-term efficacy of conventional radiotherapy in patients with
GH
-
secreting
pituitary
adenomas
.
OBJECTIVE: To assess the long-term efficacy and safety of conventional radiotherapy (RT) in the control of
acromegaly
according to recent stringent criteria of cure.
PATIENTS AND METHODS: Forty-seven patients with active
acromegaly
were treated with conventional RT between 1982 and 1994.
All patients were first operated on and successively irradiated at a dose of 45-50 Gy in 25-28 fractions for persistent (n = 40) or recurrent (n = 7)
disease
.
MEASUREMENTS: Long-term
GH
/IGF-I secretion and local tumour control were evaluated regularly, and possible side-effects were searched for systematically, especially in terms of secondary endocrine dysfunction.
Biochemical cure of
acromegaly
was defined by glucose-suppressed plasma
GH
levels below 1 microg/l during an oral glucose tolerance test (OGTT) and normal age-corrected IGF-I values.
Suppression
of GH
during OGTT was seen in 9% of patients at 2 years, 29% at 5 years, 52% at 10 years, and 77% at 15 years.
Normalization
of GH
/IGF-I mainly depended on pre-RT levels.
CONCLUSION: Conventional RT is effective in the long-term control
of GH
-
secreting
pituitary
adenomas
, although with a high prevalence of progressive hypopituitarism.
[MeSH-major]
Acromegaly
/ radiotherapy.
Adenoma
/ radiotherapy.
Adenoma
/ secretion.
Growth Hormone
/ secretion.
Pituitary
Neoplasms / radiotherapy.
Pituitary
Neoplasms / secretion
[MeSH-minor]
Adult. Female. Follow-Up Studies. Glucose Tolerance Test. Humans. Insulin-Like
Growth
Factor I / analysis. Male. Middle Aged. Retrospective Studies. Survival Rate. Treatment Outcome
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
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(PMID = 15670198.001).
[ISSN]
0300-0664
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone
3.
Ferone D, de Herder WW, Pivonello R, Kros JM, van Koetsveld PM, de Jong T, Minuto F, Colao A, Lamberts SW, Hofland LJ:
Correlation of in vitro and in vivo somatotropic adenoma responsiveness to somatostatin analogs and dopamine agonists with immunohistochemical evaluation of somatostatin and dopamine receptors and electron microscopy.
J Clin Endocrinol Metab
; 2008 Apr;93(4):1412-7
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[Title]
Correlation of in vitro and in vivo somatotropic
adenoma
responsiveness to somatostatin analogs and dopamine agonists with immunohistochemical evaluation of somatostatin and dopamine receptors and electron microscopy.
OBJECTIVE AND PATIENTS: Twenty-four
pituitary
adenomas
from acromegalic patients (13 females, 11 males; age range 19-65 yr) were characterized for somatostatin receptor subtype 2A (sst(2A)), dopamine D(2) receptor (D(2)R),
GH
, and prolactin (PRL) expression by immunohistochemistry, and results correlated with the in vitro and in vivo
hormone
responses to octreotide and quinagolide.
In nine cases,
GH
and PRL content was further studied by immunoelectron microscopy.
Sst(2A) was scored as 2 in 13 cases, 1 in 10, and 0 in one; D(2)R was scored as 2 in 13 cases, 1 in nine, and 0 in 2;
GH
was 2 in 15 cases and 1 in nine; PRL was 2 in six cases, 1 in 13, and 0 in 5.
Sst(2A) was positively correlated with in vitro (P = 0.003) and in vivo (P = 0.006) percent
GH
suppression by octreotide and with the chronic suppression of IGF-I by somatostatin analogs (P =0.008).
D(2)R was positively correlated with in vitro percent
GH
(P =0.000) and PRL (P =0.005) suppression by quinagolide.
Electron microscopy revealed two pure
somatotroph adenomas
, five somatomammotrophs with a variable coexpression
of GH
and PRL in the same cells, and two tumors consisting of mixed
cell
types, which were less sensitive to quinagolide and octreotide.
CONCLUSION: Sst(2A) and D(2)R are frequently coexpressed in
adenomas
from acromegalic patients, and immunohistochemistry may be helpful in characterizing receptor expression in
pituitary
adenomas
to select patients responsive to different treatments.
[MeSH-major]
Adenoma
/ drug therapy. Aminoquinolines / therapeutic use. Dopamine Agonists / therapeutic use.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ drug therapy. Octreotide / therapeutic use. Receptors, Dopamine D2 / analysis. Receptors, Somatostatin / analysis
[MeSH-minor]
Adult. Female. Human
Growth Hormone
/ blood. Humans. Immunohistochemistry. Male. Microscopy, Electron. Middle Aged. Prolactin / blood
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(PMID = 18211974.001).
[ISSN]
0021-972X
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Aminoquinolines; 0 / Dopamine Agonists; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / somatostatin receptor sst2A; 12629-01-5 / Human Growth Hormone; 80Q9QWN15M / quinagolide; 9002-62-4 / Prolactin; RWM8CCW8GP / Octreotide
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4.
Schindler K, Christ ER, Mindermann T, Wieser HG:
Transient MR changes and symptomatic epilepsy following gamma knife treatment of a residual GH-secreting pituitary adenoma in the cavernous sinus.
Acta Neurochir (Wien)
; 2006 Aug;148(8):903-8; discussion 908
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[Title]
Transient MR changes and symptomatic epilepsy following gamma knife treatment of a residual
GH
-
secreting
pituitary adenoma
in the cavernous sinus.
OBJECTIVE: To report a rare side effect of gamma knife treatment of
pituitary
macroadenoma.
CASE REPORT: In a forty-one-year old female patient
acromegaly
was diagnosed due to a
growth hormone secreting
pituitary
macroadenoma.
Following transsphenoidal surgery the patient underwent gamma knife treatment for persistent uncontrolled
acromegaly
activity of residual tumor, infiltrating the left cavernous sinus.
CONCLUSION: Gamma knife surgery of a
pituitary adenoma
may cause radiation induced MR changes of the mesial temporal lobe mimicking glioma or radionecrosis and cause symptomatic epileptic seizures.
[MeSH-major]
Adenoma
/ surgery. Brain Injuries / etiology. Epilepsy / etiology.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ surgery. Radiation Injuries / etiology. Radiosurgery / adverse effects
[MeSH-minor]
Acromegaly
/ etiology.
Acromegaly
/ surgery. Adult. Cavernous Sinus / pathology. Cavernous Sinus / physiopathology. Cavernous Sinus / surgery. Female. Humans. Magnetic Resonance Imaging. Necrosis /
diagnosis
. Necrosis / etiology. Necrosis / physiopathology. Neoplasm Recurrence, Local / surgery.
Pituitary
Gland
/ pathology.
Pituitary
Gland
/ physiopathology.
Pituitary
Gland
/ surgery. Positron-Emission Tomography. Postoperative Complications /
diagnosis
. Postoperative Complications / etiology. Postoperative Complications / physiopathology. Temporal Lobe / pathology. Temporal Lobe / radiation effects. Temporal Lobe / radionuclide imaging
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(PMID = 16761113.001).
[ISSN]
0001-6268
[Journal-full-title]
Acta neurochirurgica
[ISO-abbreviation]
Acta Neurochir (Wien)
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Austria
5.
Ben Salem Hachmi L, Kammoun I, Bouzid C, Smida H, Nagi S, Turki Z, Ben Slama C:
[Management of acromegaly in pregnant woman].
Ann Endocrinol (Paris)
; 2010 Feb;71(1):60-3
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[Title]
[Management of
acromegaly
in pregnant woman].
[Transliterated title]
Prise en charge
de
l'acromégalie évolutive au cours
de
la grossesse.
On the other hand, pregnancy may cause an enlargement of the
adenoma
or an increase
of growth hormone
(
GH
) secretion.
We report the case of a 26-year-old woman with a
GH
-
secreting
pituitary
macroadenoma who was operated by transphenoidal approach.
After surgery, she had a persistent
acromegaly due
to an intrasellar tumour.
Lanreotide was stopped when
the diagnosis
of pregnancy was established.
The
pituitary adenoma
was not significantly enlarged during pregnancy.
Therefore, pregnancy doesn't influence
acromegaly
in young women well controlled by medical treatment.
[MeSH-major]
Acromegaly
/ surgery.
Adenoma
/ surgery.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ surgery. Pregnancy Complications / surgery
[MeSH-minor]
Adult. Anti-Inflammatory Agents / therapeutic use. Female. Human
Growth Hormone
/ blood. Humans. Insulin-Like
Growth
Factor I / metabolism. Magnetic Resonance Imaging. Peptides, Cyclic / therapeutic use. Pregnancy. Pregnancy Outcome. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use
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consumer health - Health Problems in Pregnancy
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[Copyright]
Copyright (c) 2009 Elsevier Masson SAS. All rights reserved.
(PMID = 19926070.001).
[ISSN]
0003-4266
[Journal-full-title]
Annales d'endocrinologie
[ISO-abbreviation]
Ann. Endocrinol. (Paris)
[Language]
fre
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
France
[Chemical-registry-number]
0 / Anti-Inflammatory Agents; 0 / Peptides, Cyclic; 118992-92-0 / lanreotide; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I
6.
Abbassioun K, Amirjamshidi M, Mehrazin A, Khalatbary I, Keynama M, Bokai H, Abdollahi M:
A prospective analysis of 151 cases of patients with acromegaly operated by one neurosurgeon: a follow-up of more than 23 years.
Surg Neurol
; 2006 Jul;66(1):26-31; discussion 31
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[Title]
A prospective analysis of 151 cases of patients with
acromegaly
operated by one neurosurgeon: a follow-up of more than 23 years.
BACKGROUND: Transsphenoidal adenomectomy has been the accepted surgical management for treatment
of growth hormone
(
GH
)-
secreting
pituitary
adenomas
.
Although the goal of treatment might be to keep
the GH
level in the reference range, the actual definition of success in control of
acromegaly
is not yet clear.
The preoperative hormonal studies documenting the high
GH
and/or insulin-like
growth
factor were available in all the cases.
RESULTS: There were 90 patients with pure
GH
-
secreting
adenoma
(59.6%) with the highest
GH
level of 235 mU/L.
A second group of 12 patients had normal
GH
level but elevated serum level of insulin-like
growth
factor 1 (8%).
The group with mixed secretion
of GH
and prolactin included 49 cases (32.4%).
Normal postoperative serum
GH
level could be achieved in 98 patients (94.2%) of 104 cases with full follow-up.
CONCLUSION: In the developing countries, early
diagnosis
and proper surgical extirpation of the
GH
-
secreting
adenoma
by an experienced and dedicated
pituitary
surgeon is mandatory to reduce the mortality and increase the chance of cure of this rather mortal endocrionopathy.
[MeSH-major]
Acromegaly
/ surgery.
Adenoma
/ surgery.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ surgery. Hypophysectomy / methods
[MeSH-minor]
Adolescent. Adult. Aged. Cerebrospinal Fluid Rhinorrhea / etiology. Cerebrospinal Fluid Rhinorrhea / physiopathology. Diabetes Insipidus / etiology. Diabetes Insipidus / physiopathology. Early
Diagnosis
. Female. Follow-Up Studies.
Growth Hormone
/ blood.
Growth Hormone
/ secretion. Humans. Hypopituitarism / etiology. Hypopituitarism / physiopathology. Insulin-Like
Growth
Factor I / metabolism. Insulin-Like
Growth
Factor I / secretion. Male. Middle Aged.
Pituitary
Gland
/ physiopathology.
Pituitary
Gland
/ secretion.
Pituitary
Gland
/ surgery. Postoperative Complications / etiology. Postoperative Complications / physiopathology. Prolactin / blood. Prolactin / secretion. Prospective Studies. Sella Turcica / anatomy & histology. Sella Turcica / pathology. Sella Turcica / surgery. Sphenoid Bone / anatomy & histology. Sphenoid Bone / pathology. Sphenoid Bone / surgery. Treatment Outcome
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(PMID = 16793431.001).
[ISSN]
0090-3019
[Journal-full-title]
Surgical neurology
[ISO-abbreviation]
Surg Neurol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
67763-96-6 / Insulin-Like Growth Factor I; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone
7.
Wang HF, Huang CC, Chen YF, Ho DM, Lin HD:
Pituitary apoplexy after thyrotropin-releasing hormone stimulation test in a patient with pituitary macroadenoma.
J Chin Med Assoc
; 2007 Sep;70(9):392-5
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[Title]
Pituitary
apoplexy after thyrotropin-releasing
hormone
stimulation test in a patient with
pituitary
macroadenoma.
Pituitary
apoplexy is a rare complication of
pituitary
tumors.
We report a case of a 41-year-old female with
acromegaly due
to a
pituitary
macroadenoma, who developed
pituitary
apoplexy after a thyrotropin-releasing
hormone
(TRH) 200 microgram intravenous injection stimulation test.
Two days later, the
pituitary
mass, removed by transsphenoidal approach, showed ischemic necrosis and acute hemorrhage.
The TRH test is generally safe for evaluating
pituitary
function, but
pituitary
apoplexy may occur after the procedure.
CT and MRI may miss
the diagnosis
of
pituitary
apoplexy, especially if performed immediately after the acute episode.
[MeSH-major]
Adenoma
/ complications.
Pituitary
Apoplexy / etiology.
Pituitary
Function Tests / adverse effects.
Pituitary
Neoplasms / complications. Thyrotropin-Releasing
Hormone
[MeSH-minor]
Adult. Female. Human
Growth Hormone
/ blood. Humans
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(PMID = 17908654.001).
[ISSN]
1726-4901
[Journal-full-title]
Journal of the Chinese Medical Association : JCMA
[ISO-abbreviation]
J Chin Med Assoc
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
China (Republic : 1949- )
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 5Y5F15120W / Thyrotropin-Releasing Hormone
8.
Flitsch J, Lüdecke DK, Saeger W, Veit JA, Metternich FU:
[Acromegaly-associated lesions of the nasal mucosa. Case report].
HNO
; 2009 Aug;57(8):845-50
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[Title]
[
Acromegaly
-associated lesions of the nasal mucosa. Case report].
Acromegaly
is a rare
disease
caused by a
growth
-
hormone
-
secreting
pituitary adenoma
.
Besides these "cosmetic" symptoms,
the disease
is associated with hypertension and diabetes mellitus, as well as with an increased risk for
adenomas
and carcinomas of the colon.
The average time span from first symptom to
diagnosis
is well over 6 years; a single determination of insulin-like
growth
factor 1 in serum can confirm
the disease
.
The treatment of choice remains surgical resection of the
adenoma
in suitable patients, whereas in extensive
disease
with invasion of surrounding tissue, drug therapy and/or radiotherapy may be necessary.
[MeSH-major]
Acromegaly
/ complications.
Acromegaly
/ surgery.
Adenoma
/ etiology.
Adenoma
/ surgery. Nasal Mucosa / surgery. Nose Neoplasms / etiology. Nose Neoplasms / surgery
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[Cites]
Clin Endocrinol (Oxf). 1994 Jul;41(1):95-102
[
8050136.001
]
[Cites]
Pathophysiology. 2001 Dec;8(2):69-75
[
11720801.001
]
[Cites]
Exp Clin Endocrinol Diabetes. 2000;108(7):480-5
[
11083069.001
]
[Cites]
Neuroendocrinology. 2006;83(3-4):230-9
[
17047388.001
]
[Cites]
Acta Neurochir (Wien). 1982;66(1-2):123-6
[
7180605.001
]
[Cites]
Eur J Endocrinol. 2001 Aug;145(2):137-45
[
11454508.001
]
[Cites]
Laryngoscope. 1981 Dec;91(12):2071-84
[
7321725.001
]
[Cites]
Eur J Endocrinol. 2008 Nov;159(5):541-5
[
18708434.001
]
(PMID = 19557321.001).
[ISSN]
1433-0458
[Journal-full-title]
HNO
[ISO-abbreviation]
HNO
[Language]
ger
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Germany
9.
Wasko R, Jaskuła M, Plewa R, Komarowska H, Poreba E, Goździcka-Józefiak A, Liebert W, Bednarek J, Sowiński J:
The evaluation of ghrelin mRNA expression in human somatotroph adenomas.
Neuro Endocrinol Lett
; 2006 Feb-Apr;27(1-2):169-73
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[Title]
The evaluation of ghrelin mRNA expression in human
somatotroph adenomas
.
Ghrelin is one of the peptides involved into
GH
-release, binding to specific GHS receptors on hypothalamus and
pituitary
.
The ghrelin peptide and ghrelin mRNA have been detected in several regions of hypothalamus, in normal
pituitary
, as well as in various types of
pituitary adenoma
, with different levels of expression in different tumour types.
We decided to determine the expression of ghrelin in
somatotroph adenomas
.
Human
pituitary
somatotroph
adenoma
tissues were obtained at the time of transsphenoidal surgery from 3 acromegalic patients and studied for ghrelin mRNA expression.
We wished to determine the number of copies of ghrelin gene within the single
cell
.
[MeSH-major]
Adenoma
/ metabolism. Human
Growth Hormone
/ metabolism. Peptide Hormones / biosynthesis.
Pituitary
Neoplasms / metabolism
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(PMID = 16648773.001).
[ISSN]
0172-780X
[Journal-full-title]
Neuro endocrinology letters
[ISO-abbreviation]
Neuro Endocrinol. Lett.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Sweden
[Chemical-registry-number]
0 / Actins; 0 / DNA, Complementary; 0 / Ghrelin; 0 / Peptide Hormones; 0 / RNA, Messenger; 12629-01-5 / Human Growth Hormone; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases
10.
Cordero RA, Barkan AL:
Current diagnosis of acromegaly.
Rev Endocr Metab Disord
; 2008 Mar;9(1):13-9
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[Title]
Current
diagnosis of
acromegaly
.
Acromegaly
is a rare and chronic condition that is characterized by sustained unregulated hypersecretion
of growth hormone
(
GH
).
More than 99% of the cases of
acromegaly
are due to a pathologic proliferation of
pituitary
somatotrophs presenting in the form of a
pituitary adenoma
.
The excessive amounts
of GH
and its target
hormone
, insulin like
growth
factor-1 (IGF-1) cause metabolic changes and tissue enlargement that, collectively, lead to significant morbidity and a two to threefold increase in mortality.
Thus, early
diagnosis
has proved to be crucial to improve survival and quality of life in this condition.
The development of radioimmunoassay (RIA) in the 1960s provided clinicians with a biochemical tool to diagnose
acromegaly
.
Many limitations were inherent to this methodology which necessitated the development of more sensitive tools, such as immunoradiometric (IRMA) or immunoluminometric (ILMA) assays for
GH
and IGF-1 measurements.
The reference ranges to describe normalcy of the somatotropic axis and the biochemical criteria of "cure" of
acromegaly
are areas of great debate.
Nevertheless, the current international consensus agrees that
the diagnosis
of
acromegaly
should be based on both clinical presentation and biochemical data.
[MeSH-major]
Acromegaly
/
diagnosis
.
Growth Hormone
/ blood. Insulin-Like
Growth
Factor I / metabolism
[MeSH-minor]
Adenoma
/ blood.
Adenoma
/ complications.
Adenoma
/ pathology. Humans.
Pituitary
Gland
/ metabolism.
Pituitary
Gland
/ pathology.
Pituitary
Neoplasms / blood.
Pituitary
Neoplasms / complications.
Pituitary
Neoplasms / pathology
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[Cites]
Eur J Endocrinol. 2005 Dec;153(6):737-40
[
16322377.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Oct;83(10):3419-26
[
9768641.001
]
[Cites]
Science. 1997 Oct 17;278(5337):419-24
[
9334293.001
]
[Cites]
Clin Endocrinol (Oxf). 1994 Jul;41(1):95-102
[
8050136.001
]
[Cites]
N Engl J Med. 1990 Apr 5;322(14):966-77
[
2179724.001
]
[Cites]
Horm Res. 1999;51 Suppl 1:20-6
[
10393487.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Feb;89(2):495-500
[
14764751.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Nov;83(11):3808-16
[
9814451.001
]
[Cites]
N Engl J Med. 1992 Jan 23;326(4):266-7
[
1727980.001
]
[Cites]
J Clin Endocrinol Metab. 1988 Jul;67(1):69-73
[
2897974.001
]
[Cites]
Endocr Rev. 1988 Aug;9(3):357-73
[
3145190.001
]
[Cites]
Acta Med Scand. 1988;223(4):327-35
[
3369313.001
]
[Cites]
Horm Res. 2004;62 Suppl 1:108-15
[
15761242.001
]
[Cites]
Neuroendocrinology. 2006;83(3-4):211-7
[
17047385.001
]
[Cites]
J Craniomaxillofac Surg. 1991 Nov;19(8):332-40
[
1795045.001
]
[Cites]
Clin Endocrinol (Oxf). 2007 Jul;67(1):65-70
[
17437512.001
]
[Cites]
Endokrynol Pol. 2006 Jan-Feb;57(1):32-6
[
16575760.001
]
[Cites]
Horm Res. 2003;60(2):53-60
[
12876414.001
]
[Cites]
J Clin Endocrinol Metab. 1996 Jul;81(7):2642-6
[
8675591.001
]
[Cites]
J Endocrinol Invest. 2007 May;30(5):421-7
[
17598976.001
]
[Cites]
Arthritis Rheum. 1988 Aug;31(8):1022-7
[
2900639.001
]
[Cites]
Clin Endocrinol (Oxf). 1999 Mar;50(3):285-93
[
10435052.001
]
[Cites]
Pituitary. 1999 Jun;2(1):29-41
[
11081170.001
]
[Cites]
Ann Endocrinol (Paris). 2005 Dec;66(6):540-4
[
16357817.001
]
[Cites]
J Clin Invest. 1996 Feb 1;97(3):699-705
[
8609225.001
]
[Cites]
J Neurosurg. 1993 Feb;78(2):205-15
[
8421204.001
]
[Cites]
Clin Endocrinol (Oxf). 1999 Nov;51(5):611-8
[
10594522.001
]
[Cites]
Clin Endocrinol (Oxf). 1997 Aug;47(2):123-35
[
9302383.001
]
[Cites]
J Clin Endocrinol Metab. 1994 Jun;78(6):1403-10
[
7911124.001
]
[Cites]
J Clin Endocrinol Metab. 1989 Dec;69(6):1225-33
[
2511221.001
]
[Cites]
Growth Horm IGF Res. 2003 Aug;13(4):185-92
[
12914751.001
]
[Cites]
Am J Physiol. 1986 Mar;250(3 Pt 1):E269-73
[
3513613.001
]
[Cites]
J Clin Endocrinol Metab. 1992 Sep;75(3):812-9
[
1517371.001
]
[Cites]
Nucl Med Biol. 1994 Apr;21(3):369-79
[
9234302.001
]
[Cites]
Nature. 1963 Aug 24;199:784-7
[
14071191.001
]
[Cites]
Clin Endocrinol (Oxf). 2003 Jan;58(1):86-91
[
12519417.001
]
[Cites]
Endocr Pathol. 2007 Spring;18(1):46-52
[
17652801.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Feb;89(2):658-61
[
14764777.001
]
[Cites]
J Endocrinol Invest. 1993 Mar;16(3):181-7
[
8514973.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Jul;87(7):3142-7
[
12107214.001
]
[Cites]
Clin Endocrinol (Oxf). 1998 Jul;49(1):101-6
[
9797853.001
]
[Cites]
Ann Endocrinol (Paris). 2003 Apr;64(2):170-7
[
12773957.001
]
[Cites]
Pituitary. 2003;6(3):135-40
[
14971738.001
]
[Cites]
Acta Paediatr Scand Suppl. 1990;370:63-70; discussion 71
[
2260460.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Feb;85(2):526-9
[
10690849.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Sep;83(9):3104-9
[
9745411.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Jul;86(7):2929-34
[
11443145.001
]
[Cites]
J Clin Endocrinol Metab. 1999 Jan;84(1):249-56
[
9920092.001
]
[Cites]
Endocr Rev. 2001 Oct;22(5):675-705
[
11588148.001
]
[Cites]
Pituitary. 2007;10(3):311-9
[
17373589.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Jul;83(7):2554-61
[
9661642.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Aug;87(8):3537-42
[
12161471.001
]
[Cites]
Endocr Rev. 2004 Feb;25(1):102-52
[
14769829.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Apr;87(4):1909; author reply 1909
[
11932345.001
]
[Cites]
Ann Intern Med. 1994 Oct 1;121(7):478-83
[
8067645.001
]
[Cites]
J Clin Endocrinol Metab. 1992 May;74(5):1012-9
[
1569148.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Jun;89(6):2789-96
[
15181059.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Mar;90(3):1377-82
[
15585548.001
]
[Cites]
J Clin Endocrinol Metab. 2006 Dec;91(12 ):4776-80
[
16968791.001
]
[Cites]
Eur J Endocrinol. 2004 Oct;151(4):439-46
[
15476442.001
]
[Cites]
Endocr Rev. 1994 Oct;15(5):555-73
[
7843068.001
]
[Cites]
Endocr Rev. 1987 May;8(2):115-31
[
3301316.001
]
[Cites]
Clin Endocrinol (Oxf). 2001 Feb;54(2):183-8
[
11207632.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Jan;85(1):179-82
[
10634384.001
]
[Cites]
Clin Endocrinol (Oxf). 1998 Feb;48(2):243-50
[
9579239.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Aug;83(8):2730-4
[
9709939.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Apr;86(4):1551-7
[
11297582.001
]
[Cites]
Q J Med. 1993 May;86(5):293-9
[
8327647.001
]
[Cites]
N Engl J Med. 1979 Nov 22;301(21):1138-42
[
492275.001
]
[Cites]
N Engl J Med. 2006 Dec 14;355(24):2558-73
[
17167139.001
]
[Cites]
Eur J Endocrinol. 1996 Mar;134(3):352-6
[
8616534.001
]
[Cites]
Eur J Nucl Med. 1993 Apr;20(4):283-92
[
8491220.001
]
(PMID = 18236162.001).
[ISSN]
1389-9155
[Journal-full-title]
Reviews in endocrine & metabolic disorders
[ISO-abbreviation]
Rev Endocr Metab Disord
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Germany
[Chemical-registry-number]
67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone
[Number-of-references]
72
11.
Bhayana S, Booth GL, Asa SL, Kovacs K, Ezzat S:
The implication of somatotroph adenoma phenotype to somatostatin analog responsiveness in acromegaly.
J Clin Endocrinol Metab
; 2005 Nov;90(11):6290-5
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[Title]
The implication
of somatotroph
adenoma
phenotype to somatostatin analog responsiveness in
acromegaly
.
CONTEXT: Persistently elevated
GH
and IGF-I levels are associated with increased mortality.
OBJECTIVE: The objective of this study was to examine the significance
of somatotroph
adenoma
type on response to SSA.
PATIENTS: Forty patients with
acromegaly
were studied.
MAIN OUTCOME MEASURES: Normalization of IGF-I levels and
GH
responses were the main outcome measures.
RESULTS: Univariate analysis revealed that responders were more likely to have densely granulated
somatotroph adenomas
(80% vs. 43.8%; P = 0.024), to be older (51.3 vs. 38.2 yr; P < 0.003), to have smaller tumors (stage < or =3; 78.6% vs. 35.7%; P = 0.022), to have lower baseline IGF-I (453 vs. 716 microg/liter; P < 0.001) and
GH
levels (2.7 vs. 7.8 microg/liter; P < 0.05), and to require a lower maximum dose of SSA (24 vs. 31 mg every 4 wk; P = 0.013).
Multivariate analysis confirmed that a densely granulated
adenoma
was the strongest predictor of complete response [adjusted odds ratio (OR), 58.41; 95% confidence interval (CI), 1.24-1000.00; P = 0.04] compared with other covariates, including older age at time
of diagnosis
(OR, 1.15/yr; 95% CI, 1.01-1.31; P = 0.03), and tumor stage of 3 or less (OR, 29.77; 95% CI, 1.01-885.45; P < 0.05).
CONCLUSIONS:
Somatotroph
tumor type represents a strong clinical predictor of response to SSA treatment and will help to identify patients who warrant more vigilant management of their
disease
.
[MeSH-major]
Acromegaly
/ drug therapy.
Adenoma
/ drug therapy. Octreotide / therapeutic use.
Pituitary
Neoplasms / drug therapy
[MeSH-minor]
Adult. Aged. Female. Human
Growth Hormone
/ blood. Humans. Insulin-Like
Growth
Factor I / analysis. Male. Middle Aged. Multivariate Analysis. Phenotype. Retrospective Studies
Genetic Alliance.
consumer health - Acromegaly
.
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
COS Scholar Universe.
author profiles
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
SciCrunch.
KEGG: Data: Disease Annotation
.
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(PMID = 16118335.001).
[ISSN]
0021-972X
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; RWM8CCW8GP / Octreotide
12.
Noh SJ, Ahn JY, Lee KS, Kim SH:
Pituitary adenoma and concomitant Rathke's cleft cyst.
Acta Neurochir (Wien)
; 2007 Dec;149(12):1223-8
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[Title]
Pituitary adenoma
and concomitant Rathke's cleft cyst.
Although
pituitary
adenomas
and Rathke's cleft cysts have a shared ancestry, they rarely occur simultaneously.
Only 32 reports involving a
pituitary adenoma
and a concomitant Rathke's cleft cyst were identified upon review of the literature.
Next to
growth hormone
, Prolactin was the most commonly hypersecreted
pituitary
hormone
.
Here, we report a patient with a
growth hormone
-
secreting
pituitary adenoma
associated with a Rathke's cleft cyst.
When a non-enhancing cyst-like structure is demonstrated on imaging in a patient with a
pituitary adenoma
, the possibility of a coexisting Rathke's cleft cyst should be considered.
[MeSH-major]
Adenoma
/ surgery. Central Nervous System Cysts / surgery.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ surgery. Neoplasms, Multiple Primary / surgery.
Pituitary
Neoplasms / surgery
[MeSH-minor]
Diagnosis
, Differential. Female. Humans. Image Processing, Computer-Assisted. Magnetic Resonance Imaging. Middle Aged. Neuronavigation.
Pituitary
Gland
/ pathology
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(PMID = 17914599.001).
[ISSN]
0942-0940
[Journal-full-title]
Acta neurochirurgica
[ISO-abbreviation]
Acta Neurochir (Wien)
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Austria
[Number-of-references]
28
13.
Pegvisomant: new preparation. A last resort in acromegaly.
Prescrire Int
; 2005 Feb;14(75):10-3
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[Title]
Pegvisomant: new preparation. A last resort in
acromegaly
.
(1) The first-line treatment for
acromegaly
is transsphenoidal surgery.
As an adjunct to surgery, and for patients with inoperable tumours, the first-line drug therapy is a somatostatin analogue (octreotide or lanreotide). (2) Pegvisomant, a
growth hormone
(
GH
) receptor antagonist, is licensed for patients who have a poor response to surgery and/or radiation therapy and in whom somatostatin analogue therapy has failed. (3) There are no published comparative trials evaluating pegvisomant as alternative for patients who have already tried a somatostatin analogue.
It showed that pegvisomant, at a dose of 10 mg to 20 mg/day subcutaneously, normalised the level of insulin-like
growth
factor type 1 (IGF-1) and improved some symptoms.
This trial does not provide enough evidence to support the approved indication. (4) Pegvisomant lowers the IGF-1 level but also increases
the GH
level.
An increase in the size of the
pituitary adenoma
, due to the resulting hyperfunctioning, was observed in four of the 160 patients treated in clinical trials. (5) Evaluation data on pegvisomant does not resolve the question of possible hepatic toxicity. (6) In practice, pegvisomant therapy is justified for patients with serious complications of
acromegaly
and who have no other treatment options.
[MeSH-major]
Acromegaly
/ drug therapy. Human
Growth Hormone
/ therapeutic use
[MeSH-minor]
Adenoma
/ surgery. Drug Approval. Europe. Humans. Octreotide / administration & dosage. Octreotide / adverse effects. Octreotide / therapeutic use. Randomized Controlled Trials as Topic. Somatostatin / administration & dosage. Somatostatin / adverse effects. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use
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(PMID = 15751152.001).
[ISSN]
1167-7422
[Journal-full-title]
Prescrire international
[ISO-abbreviation]
Prescrire Int
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
France
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
14.
Andrioli M, Pecori Giraldi F, Losa M, Terreni M, Invitti C, Cavagnini F:
Cushing's disease due to double pituitary ACTH-secreting adenomas: the first case report.
Endocr J
; 2010;57(9):833-7
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[Title]
Cushing'
s disease
due to double
pituitary
ACTH-
secreting adenomas
: the first case report.
Double
pituitary
adenomas
are rare occurrences in autoptical, surgical and neuroradiological series and are mostly due to non-functioning
pituitary
adenomas
,
GH
-
secreting
and prolactin-
secreting adenomas
.
ACTH
secreting
tumours are more rare and, to our knowledge, two distinct ACTH-
producing adenomas
within the same
pituitary
have never been reported.
We herewith describe a 56 year old woman with Cushing'
s disease
due to two clearly distinct ACTH-
secreting
pituitary
adenomas
.
She presented with signs and symptoms of hypercortisolism and hormonal testing was indicative for
pituitary
-dependent Cushing' s syndrome.
Sellar MRI visualized an asymmetric
pituitary
gland
with suspect lesions in both the right and the left
pituitary
lobes.
Pathology confirmed the existence of two distinct
adenomas
located in different sites in
the gland
.
Our case indicates that double ACTH-
secreting
pituitary
adenomas
may occur in patients with Cushing'
s disease
.
[MeSH-major]
ACTH-
Secreting
Pituitary Adenoma
/ pathology.
Adenoma
/ pathology. Neoplasms, Multiple Primary / pathology.
Pituitary
ACTH Hypersecretion / etiology
[MeSH-minor]
Cushing Syndrome / etiology. Female. Humans. Middle Aged.
Pituitary
Neoplasms / pathology
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(PMID = 20595779.001).
[ISSN]
1348-4540
[Journal-full-title]
Endocrine journal
[ISO-abbreviation]
Endocr. J.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
15.
Isikay I, Berker M, Balci S, Cila A:
Somatotroph adenoma cells may populate paranasal sinus mucosa.
Acta Neurochir (Wien)
; 2010 Sep;152(9):1629-30; discussion 1630
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[Title]
Somatotroph
adenoma
cells may populate paranasal sinus mucosa.
[MeSH-major]
Growth Hormone
-
Secreting
Pituitary Adenoma
/ secondary. Nasal Mucosa / pathology. Neoplasm Invasiveness / pathology. Paranasal Sinus Neoplasms / secondary.
Pituitary
Neoplasms / pathology. Sphenoid Sinus / pathology
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(PMID = 20446098.001).
[ISSN]
0942-0940
[Journal-full-title]
Acta neurochirurgica
[ISO-abbreviation]
Acta Neurochir (Wien)
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
Austria
16.
Mercado M, Galeana M:
[Pharmacological treatment of acromegaly].
Gac Med Mex
; 2006 Jul-Aug;142(4):327-31
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[Title]
[Pharmacological treatment of
acromegaly
].
[Transliterated title]
Tratamiento farmacológico
de
la acromegalia.
Acromegaly
is an endocrine
disorder
usually due to a
growth hormone
(
GH
)-
secreting
pituitary adenoma
.
This deforming
disease
is associated with several metabolic abnormalities and results in an elevated cardiovascular mortality.
Pituitary
transsesphenoidal surgery has been considered the treatment of choice, however, even in the most experienced hands this procedure succeeds in curing only 50 to 60% of the patients.
Therefore, close to 50% of patients require an adjunctive form of treatment such as radiation therapy or the use of diverse medications that modulate
GH
secretion (somatostatin analogues) or action (
GH
receptor antagonists).
[MeSH-major]
Acromegaly
/ drug therapy
[MeSH-minor]
Humans. Receptors,
Somatotropin
/ antagonists & inhibitors. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use
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(PMID = 17022308.001).
[ISSN]
0016-3813
[Journal-full-title]
Gaceta médica de México
[ISO-abbreviation]
Gac Med Mex
[Language]
spa
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Mexico
[Chemical-registry-number]
0 / Receptors, Somatotropin; 51110-01-1 / Somatostatin
[Number-of-references]
66
17.
Fusco A, Zatelli MC, Bianchi A, Cimino V, Tilaro L, Veltri F, Angelini F, Lauriola L, Vellone V, Doglietto F, Ambrosio MR, Maira G, Giustina A, degli Uberti EC, Pontecorvi A, De Marinis L:
Prognostic significance of the Ki-67 labeling index in growth hormone-secreting pituitary adenomas.
J Clin Endocrinol Metab
; 2008 Jul;93(7):2746-50
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[Title]
Prognostic significance of the Ki-67 labeling index in
growth hormone
-
secreting
pituitary
adenomas
.
OBJECTIVE: The aim of the study was to evaluate the Ki-67 index prognostic relevance in a group of acromegalic patients who underwent transsphenoidal surgery for a
GH
-
secreting
pituitary adenoma
.
The Ki-67 index was determined by immunohistochemistry on tissue samples obtained from each
adenoma
after surgery.
Periodical
pituitary
magnetic resonance imaging and hormonal evaluation were performed during the follow-up.
Pituitary
magnetic resonance imaging showed residual/recurrent
disease
in 25 of 68 patients after 6 months.
No correlation was found between Ki-67 index and age, tumor size,
GH
, or IGF-I plasma levels.
We suggest routine Ki-67 evaluation in
GH
-
secreting
pituitary
adenomas
.
[MeSH-major]
Adenoma
/ pathology.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ pathology. Ki-67 Antigen / analysis
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
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(PMID = 18460561.001).
[ISSN]
0021-972X
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Ki-67 Antigen; 51110-01-1 / Somatostatin
18.
Jezková J, Marek J, Hána V, Krsek M, Weiss V, Vladyka V, Lisák R, Vymazal J, Pecen L:
Gamma knife radiosurgery for acromegaly--long-term experience.
Clin Endocrinol (Oxf)
; 2006 May;64(5):588-95
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[Title]
Gamma knife radiosurgery for
acromegaly
--long-term experience.
OBJECTIVE: The Leksell gamma knife (LGK) is one of the treatment options for
pituitary
adenomas
.
We report on our long-term experience treating
acromegaly
using LGK.
DESIGN: Since 1993 we have followed 96
acromegaly
patients through periods of from 12 to 120 months.
Thirteen patients were irradiated twice, due to persistent activity of the
adenoma
or its residue.
Pituitary
functions were tested at 6-month intervals, post-irradiation.
RESULTS: Fifty per cent of the patients achieved mean
GH
< 2.5 microg/l within 42 months, normalized their IGF-I within 54 months, and achieved
GH
suppression in the oral glucose tolerance test (oGTT) < 1 microg/l with normal IGF-I within 66 months.
LGK effectiveness was dependent on initial
adenoma
hormonal activity (
GH
and IGF-I serum levels), not on the size of the
adenoma
.
Irradiation arrested all
adenoma
growth
, causing tumour shrinkage in 62.3% of patients.
Twenty-six developed hypopituitarism when irradiated by 15 Gy (or more) on functional peritumoral
pituitary
tissue.
CONCLUSIONS: In
acromegaly
, LGK is a useful adjunct to primary neurosurgery when treating post-surgical residues because it can limit the duration of medical therapy.
[MeSH-major]
Acromegaly
/ surgery.
Adenoma
/ surgery.
Pituitary
Neoplasms / surgery. Radiosurgery / instrumentation
[MeSH-minor]
Adolescent. Adult. Aged. Blood Glucose / analysis. Combined Modality Therapy. Female. Follow-Up Studies.
Growth Hormone
/ blood. Humans. Insulin-Like
Growth
Factor I / analysis. Male. Middle Aged. Neurosurgical Procedures. Statistics, Nonparametric. Treatment Outcome
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(PMID = 16649981.001).
[ISSN]
0300-0664
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Blood Glucose; 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone
19.
Zada G, Sivakumar W, Fishback D, Singer PA, Weiss MH:
Significance of postoperative fluid diuresis in patients undergoing transsphenoidal surgery for growth hormone-secreting pituitary adenomas.
J Neurosurg
; 2010 Apr;112(4):744-9
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[Title]
Significance of postoperative fluid diuresis in patients undergoing transsphenoidal surgery for
growth hormone
-
secreting
pituitary
adenomas
.
OBJECT: Following successful transsphenoidal surgery in patients with
growth hormone
(
GH
)-
secreting
pituitary
adenomas
, a characteristic fluid diuresis has been described.
In this paper the authors aimed to further analyze the degree of fluid diuresis as it relates to postoperative
GH
levels.
METHODS: Between 2000 and 2008, 85 patients underwent transsphenoidal surgery for a
GH
-
secreting
adenoma
at the USC University Hospital.
Patients with negative fluid balances at 48 hours after surgery were more than twice as likely to have a
GH
level of < 1.5 ng/ml (55 vs 25%, p = 0.023).
At 48 hours after surgery, patients with a negative overall fluid balance had a significantly lower median
GH
level than those with a positive overall fluid balance (1.3 vs 2.4 ng/ml, p = 0.039).
By 48 hours following surgery, patients with postoperative Day 1
GH
levels < 1.5 ng/ml had, on average, experienced diuresis of fluid > 1.1 L (median 1.5 L) more than patients with
GH
levels > 1.5 ng/ml.
CONCLUSIONS: Successful resection
of GH
-
secreting adenomas
is associated with a more pronounced fluid diuresis and negative overall fluid balance within 48 hours following transsphenoidal surgery.
Patients with a negative fluid balance by postoperative Day 2 have a higher likelihood of having significantly reduced postoperative
GH
levels that may correlate with long-term surgical remission.
[MeSH-major]
Adenoma
/ surgery. Diuresis.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ surgery. Postoperative Complications /
diagnosis
. Water-Electrolyte Balance
[MeSH-minor]
Acromegaly
/ surgery. Adolescent. Adult. Aged. Female. Human
Growth Hormone
/ secretion. Humans. Male. Middle Aged. Plasma Volume. Retrospective Studies. Sphenoid Bone / surgery. Young Adult
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.
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(PMID = 19698049.001).
[ISSN]
1933-0693
[Journal-full-title]
Journal of neurosurgery
[ISO-abbreviation]
J. Neurosurg.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone
20.
Miyoshi T, Otsuka F, Kawabata T, Inagaki K, Mukai T, Kawashima M, Ogura T, Yamamura M, Sei T, Makino H:
Manifestation of rheumatoid arthritis after transsphenoidal surgery in a patient with acromegaly.
Endocr J
; 2006 Oct;53(5):621-5
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[Title]
Manifestation of rheumatoid arthritis after transsphenoidal surgery in a patient with
acromegaly
.
Acromegalic arthropathy is one of the most frequent manifestations occurring in
acromegaly
patients.
In contrast, rheumatoid arthritis (RA) is a rare clinical complication in
acromegaly
patients.
Here, we report a 70-year-old Japanese woman with
acromegaly
, who complained of bilateral finger stiffness and polyarthralgia two months after transsphenoidal surgery of a
growth hormone
(
GH
)-
secreting
pituitary adenoma
.
Postoperative levels of serum
GH
and insulin-like
growth
factor-1 (IGF-1) were markedly decreased without any secretory deficiency of other anterior
pituitary
hormones.
Regardless of the levels
of GH
and IGF-1,
acromegaly
patients frequently complain about joint-related symptoms even after remission.
Therefore, careful observation of bone erosive changes and immunological activity in
acromegaly
patients is required when joint-related symptoms persist.
[MeSH-major]
Acromegaly
/ complications. Arthritis, Rheumatoid / etiology. Sphenoid Bone / surgery
[MeSH-minor]
Adenoma
/ complications.
Adenoma
/ radiography.
Adenoma
/ surgery. Aged. Bone Marrow Diseases / complications. Bone Marrow Diseases / radiography. C-Reactive Protein / analysis. Female.
Growth Hormone
/ blood.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ complications.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ radiography.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ surgery. Hand / radiography. Humans. Synovitis / complications. Synovitis / radionuclide imaging
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(PMID = 16896264.001).
[ISSN]
0918-8959
[Journal-full-title]
Endocrine journal
[ISO-abbreviation]
Endocr. J.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
9002-72-6 / Growth Hormone; 9007-41-4 / C-Reactive Protein
21.
Fougner SL, Lekva T, Borota OC, Hald JK, Bollerslev J, Berg JP:
The expression of E-cadherin in somatotroph pituitary adenomas is related to tumor size, invasiveness, and somatostatin analog response.
J Clin Endocrinol Metab
; 2010 May;95(5):2334-42
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[Title]
The expression of E-cadherin in
somatotroph
pituitary
adenomas
is related to tumor size, invasiveness, and somatostatin analog response.
CONTEXT: Appropriate
cell
-to-
cell
adhesion is fundamental for the epithelial phenotype of
pituitary
cells.
In
somatotroph adenomas
, a variable and reduced expression of E-cadherin has been demonstrated.
In addition, nuclear translocation of E-cadherin was found to correlate with
pituitary
tumor invasion.
OBJECTIVE: The objective was to examine the protein expression of E-cadherin in
somatotroph
pituitary
adenomas
in relation
to adenoma
size, invasiveness, and somatostatin analog (SMS) efficacy.
Adenoma
E-cadherin protein expression was analyzed by Western blot (61 patients) and immunohistochemistry (IHC) (80 patients) with antibodies directed against both extracellular and intracellular domains (IHC).
RESULTS: Membranous E-cadherin was lost in several
adenomas
.
The E-cadherin level correlated positively to tumor reduction after SMS treatment, and
adenomas
with nuclear E-cadherin staining had lower IGF-I reduction and tumor shrinkage.
Preoperatively treated
adenomas
had reduced E-cadherin protein levels, but the IHC expression was unaltered.
CONCLUSION: Reduced E-cadherin expression may correlate to a dedifferentiated phenotype in
the somatotroph
pituitary
adenomas
.
[MeSH-major]
Cadherins / genetics. Peptide Fragments / therapeutic use.
Pituitary
Neoplasms / genetics. Somatostatin / therapeutic use
[MeSH-minor]
Acromegaly
/ complications.
Acromegaly
/ surgery. Adult. Female.
Growth Hormone
/ blood. Humans. Immunohistochemistry. Insulin-Like
Growth
Factor I / metabolism. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Invasiveness
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(PMID = 20335450.001).
[ISSN]
1945-7197
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / CTAP octapeptide; 0 / Cadherins; 0 / Peptide Fragments; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone
22.
Meij BP, Auriemma E, Grinwis G, Buijtels JJ, Kooistra HS:
Successful treatment of acromegaly in a diabetic cat with transsphenoidal hypophysectomy.
J Feline Med Surg
; 2010 May;12(5):406-10
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[Title]
Successful treatment of
acromegaly
in a diabetic cat with transsphenoidal hypophysectomy.
Plasma concentrations
of growth hormone
(
GH
) (51 microg/l, reference range 0.8-7.2 microg/l) and insulin-like
growth
factor 1 (IGF-1) (3871 microg/l, reference range 39-590 microg/l) were highly elevated, whereas those of alpha-melanocyte-stimulating
hormone
, adrenocorticotropic
hormone
and cortisol were normal.
Computed tomography revealed a thick palatum molle and an enlarged
pituitary
gland
, indicating a
pituitary
neoplasm.
Microsurgical transsphenoidal hypophysectomy was performed and microscopic examination of the surgical specimen revealed an acidophilic, infiltrative
pituitary adenoma
that showed positive immunostaining for
GH
.
One year after hypophysectomy the plasma concentrations
of GH
and IGF-1 were 2.4 microg/l and 113 microg/l, respectively.
PRACTICAL RELEVANCE: This is the first report detailing transsphenoidal hypophysectomy as a feasible and effective treatment for feline
acromegaly due
to a
pituitary
somatotroph
adenoma
.
The surgery is discussed in the context of human and other feline therapies for
acromegaly
.
[MeSH-major]
Acromegaly
/ veterinary. Adenocarcinoma / veterinary. Cat Diseases / surgery. Hypophysectomy / veterinary
[MeSH-minor]
Adrenocortical Hyperfunction / blood. Adrenocortical Hyperfunction / complications. Adrenocortical Hyperfunction / surgery. Adrenocortical Hyperfunction / veterinary. Animals. Blood Glucose / metabolism. Cats. Diabetes Mellitus / blood. Diabetes Mellitus / surgery. Diabetes Mellitus / veterinary.
Growth Hormone
/ blood. Insulin-Like
Growth
Factor I / metabolism. Male. Sphenoid Bone. Treatment Outcome
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[Copyright]
Copyright 2010 Elsevier Ltd. All rights reserved.
(PMID = 20417901.001).
[ISSN]
1532-2750
[Journal-full-title]
Journal of feline medicine and surgery
[ISO-abbreviation]
J. Feline Med. Surg.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Blood Glucose; 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone
23.
Xu T, Ye F, Wang B, Tian C, Wang S, Shu K, Guo D, Lei T:
Elevation of growth hormone secretagogue receptor type 1a mRNA expression in human growth hormone-secreting pituitary adenoma harboring G protein alpha subunit mutation.
Neuro Endocrinol Lett
; 2010;31(1):147-54
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[Title]
Elevation
of growth hormone
secretagogue receptor type 1a mRNA expression in human
growth hormone
-
secreting
pituitary adenoma
harboring G protein alpha subunit mutation.
OBJECTIVE: The purpose of this study was to investigate the relationship between the ghrelin or GHSR-1a mRNA levels and clinical characteristics and to confirm the effect of gsp mutations on ghrelin/GHSR-1a system in human
GH
-
secreting
pituitary
adenomas
.
The gsp mutations in 43 cases of human
GH
-
secreting
pituitary
adenomas
were detected using PCR-DNA direct sequencing analysis.
Clinical data were obtained from the medical records of 43 acromegalic patients who had
GH
and IGF-1 assays in the same laboratory.
The expression level of GHSR-1a mRNA was significantly higher in gsp positive
adenomas
than in negative
adenomas
(p<0.05).
Whereas, there was no significant difference in the expression of ghrelin mRNA between gsp mutation-positive and -negative
adenomas
(p>0.05).
Additionally there was a significant positve correlation between the ghrelin and GHSR-1a mRNA expression levels in gsp-positive (R=0.553, p=0.040) or -negative
adenomas
(R=0.489, p=0.007).
Gsp mutations may upregulate the expression of GHSR-1a mRNA and have no effect on ghrelin mRNA levels in human
GH
-
secreting
pituitary
adenomas
.
[MeSH-major]
Adenoma
/ genetics. GTP-Binding Protein alpha Subunits / genetics.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ genetics. Mutation. Receptors, Ghrelin / genetics
[MeSH-minor]
Acromegaly
/ etiology.
Acromegaly
/ genetics. Adult. Female. Ghrelin / genetics. Ghrelin / metabolism. Humans. Male. Middle Aged. RNA, Messenger / metabolism. Retrospective Studies. Tumor Burden. Up-Regulation. Young Adult
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(PMID = 20150876.001).
[ISSN]
0172-780X
[Journal-full-title]
Neuro endocrinology letters
[ISO-abbreviation]
Neuro Endocrinol. Lett.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Sweden
[Chemical-registry-number]
0 / GTP-Binding Protein alpha Subunits; 0 / Ghrelin; 0 / RNA, Messenger; 0 / Receptors, Ghrelin
24.
Benech F, Perez R, Fontanella MM, Morra B, Albera R, Ducati A:
Cystic versus solid vestibular schwannomas: a series of 80 grade III-IV patients.
Neurosurg Rev
; 2005 Jul;28(3):209-13
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[MeSH-major]
Acromegaly
/ etiology.
Acromegaly
/ therapy.
Adenoma
/ surgery. Human
Growth Hormone
/ metabolism. Neurosurgical Procedures / methods.
Pituitary
Neoplasms / surgery
[MeSH-minor]
Adult. Aged. Connective Tissue / pathology. Connective Tissue / surgery. Female. Humans. Immunohistochemistry. Male. Microsurgery. Middle Aged. Neoplasm Recurrence, Local.
Pituitary
Hormones / deficiency
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[Cites]
AJNR Am J Neuroradiol. 1993 Sep-Oct;14(5):1241-7
[
8237710.001
]
[Cites]
J Clin Neurosci. 2002 Jul;9(4):453-5
[
12217679.001
]
[Cites]
Acta Neurochir (Wien). 1991;110(3-4):120-3
[
1927602.001
]
[Cites]
Neurosurgery. 1997 Mar;40(3):469-81; discussion 481-2
[
9055285.001
]
[Cites]
Virchows Arch A Pathol Anat Histopathol. 1992;420(1):59-64
[
1539452.001
]
[Cites]
Stereotact Funct Neurosurg. 1996;66 Suppl 1:103-11
[
9032850.001
]
[Cites]
J Formos Med Assoc. 1995 Aug;94(8):487-93
[
7549578.001
]
[Cites]
Acta Neurochir (Wien). 1999;141(12):1281-5; discussion 1285-6
[
10672298.001
]
[Cites]
J Laryngol Otol. 2000 Dec;114(12):935-9
[
11177361.001
]
[Cites]
Arch Otolaryngol Head Neck Surg. 1994 Dec;120(12):1333-8
[
7980897.001
]
[Cites]
Acta Otolaryngol Suppl. 1997;530:1-27
[
9288227.001
]
[Cites]
Neurosurgery. 1997 Jan;40(1):11-21; discussion 21-3
[
8971819.001
]
[Cites]
Can Assoc Radiol J. 1993 Dec;44(6):453-9
[
8252428.001
]
[Cites]
Acta Neurochir (Wien). 1996;138(6):695-9
[
8836284.001
]
[Cites]
Laryngoscope. 1994 Nov;104(11 Pt 1):1348-52
[
7968163.001
]
[Cites]
Otolaryngol Head Neck Surg. 1985 Apr;93(2):146-7
[
3921901.001
]
[Cites]
J Laryngol Otol. 1994 May;108(5):375-9
[
8035113.001
]
[Cites]
Neuroradiology. 1986;28(3):208-14
[
3725009.001
]
[Cites]
Acta Otolaryngol. 1993 Jul;113(4):519-23
[
8379308.001
]
(PMID = 15739069.001).
[ISSN]
0344-5607
[Journal-full-title]
Neurosurgical review
[ISO-abbreviation]
Neurosurg Rev
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Pituitary Hormones; 12629-01-5 / Human Growth Hormone
25.
Isidro ML, Castro JA, Penín M, Armenta J, Cordido F:
The choice of therapy in acromegaly: results of treatment at a tertiary care hospital.
Neuro Endocrinol Lett
; 2008 Dec;29(6):1038-44
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[Title]
The choice of therapy in
acromegaly
: results of treatment at a tertiary care hospital.
Demographic, hormonal, visual and imaging data at
diagnosis
and during follow-up were recorded, as well as the treatments applied.
RESULTS: In 73.0% of the patients,
acromegaly
was due to a
pituitary
macroadenoma.
Considering normal age and sex-matched concentrations of IGF-I as a control criteria, surgery resulted in
disease
control in 10% of the patients who had surgery, while medical treatment controlled
the disease
in 76.9% (P <0.05).
CONCLUSIONS: Not all centres obtain the results reported in the literature in terms
of disease
control and morbidity after surgical treatment
of growth hormone
-
secreting
tumours.
[MeSH-major]
Acromegaly
/ therapy.
Adenoma
/ complications. Insulin-Like
Growth
Factor I / analysis.
Pituitary
Neoplasms / complications. Somatostatin / therapeutic use
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(PMID = 19112390.001).
[ISSN]
0172-780X
[Journal-full-title]
Neuro endocrinology letters
[ISO-abbreviation]
Neuro Endocrinol. Lett.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Sweden
[Chemical-registry-number]
51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I
26.
Mondok A, Aranyi Z, Kovacs GG, Czirjak S, Pusztai P, Varga I, Racz K:
Rapid progression of amyotrophic lateral sclerosis in an acromegalic patient after surgical resection of a growth hormone-producing pituitary adenoma.
Neurologist
; 2010 Sep;16(5):315-8
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[Title]
Rapid progression of amyotrophic lateral sclerosis in an acromegalic patient after surgical resection of a
growth hormone
-
producing
pituitary adenoma
.
INTRODUCTION: Insulin-like
growth
factor-1 (IGF-1) promotes the survival of neurons, mediates neuritic
growth
, and in 1 clinical trial human recombinant IGF-1 delayed the progression of functional impairment and decline of health-related quality of life in patients with amyotrophic lateral sclerosis (ALS).
CASE REPORT: We describe a case of a 65-year-old woman with a 2-year history of symptoms and signs of
acromegaly
because of a
pituitary
microadenoma.
The patient posed a challenging diagnostic dilemma because of the presence of dysarthria, which was initially considered as the consequence of
acromegaly
.
After octreotide long-acting release (LAR) treatment, the patient underwent uneventful
pituitary
surgery.
Although postoperative evaluation indicated a cure of
acromegaly
, progressive bulbar symptoms developed, which were followed by upper limb weakness and muscle atrophy.
Neurologic investigations confirmed
the diagnosis
of ALS and riluzole therapy was given.
One year after surgery
growth
-
hormone
deficiency was diagnosed, but a trial with human recombinant
growth hormone
failed to produce any significant improvement.
Histopathologic examination of the brain and spinal cord confirmed
the diagnosis
of ALS.
CONCLUSIONS: This is the first report showing a rapid progression of ALS after a surgical cure of coexisting
acromegaly
presumably because of cessation of high endogenous IGF-I levels.
[MeSH-major]
Acromegaly
. Amyotrophic Lateral Sclerosis.
Disease
Progression.
Growth Hormone
-
Secreting
Pituitary Adenoma
.
Pituitary
Neoplasms
[MeSH-minor]
Aged. Antineoplastic Agents, Hormonal / therapeutic use. Fatal Outcome. Female. Human
Growth Hormone
/ deficiency. Human
Growth Hormone
/ therapeutic use. Humans. Insulin-Like
Growth
Factor I / metabolism. Octreotide / therapeutic use
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(PMID = 20827122.001).
[ISSN]
2331-2637
[Journal-full-title]
The neurologist
[ISO-abbreviation]
Neurologist
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; RWM8CCW8GP / Octreotide
27.
Seda Jr L, Cukiert A, Nogueira KC, Huayllas MK, Liberman B:
Intrasellar internal carotid aneurysm coexisting with GH-secreting pituitary adenoma in an acromegalic patient.
Arq Neuropsiquiatr
; 2008 Mar;66(1):99-100
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[Title]
Intrasellar internal carotid aneurysm coexisting with
GH
-
secreting
pituitary adenoma
in an acromegalic patient.
[MeSH-major]
Acromegaly
/ complications. Carotid Artery Diseases / complications.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ complications. Intracranial Aneurysm / complications
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(PMID = 18392428.001).
[ISSN]
0004-282X
[Journal-full-title]
Arquivos de neuro-psiquiatria
[ISO-abbreviation]
Arq Neuropsiquiatr
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Brazil
28.
Damjanovic SS, Neskovic AN, Petakov MS, Popovic V, Macut D, Vukojevic P, Joksimovic MM:
Clinical indicators of biochemical remission in acromegaly: does incomplete disease control always mean therapeutic failure?
Clin Endocrinol (Oxf)
; 2005 Apr;62(4):410-7
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[Title]
Clinical indicators of biochemical remission in
acromegaly
: does incomplete
disease
control always mean therapeutic failure?
OBJECTIVE: Correction
of GH
and IGF-I levels are associated with improvements in insulin secretion, cardiac performance and body composition in patients with
acromegaly
, but whether these parallel post-treatment levels
of GH
-IGF-I axis activity is undefined.
We investigate whether various biochemical outcomes after transsphenoidal
pituitary
surgery (TSS) in these patients are associated with clinically relevant differences in cardiac performance, insulin resistance and body composition.
DESIGN: Cross-sectional study of consecutive patients with
acromegaly
admitted to the hospital between 2001 and 2002.
PATIENTS AND METHODS: Forty-one patients after TSS for
somatotroph
pituitary adenoma
and 23 patients with naive
acromegaly
serving as positive controls were enrolled in the study.
Mean daily
GH
levels (mGH), IGF-I, leptin and lipid levels, glucose, insulin and
GH
concentrations during oral glucose tolerance test (oGTT) were measured in all study participants.
RESULTS: We found no difference in cardiac indices, insulin resistance, body composition and leptin levels between patients with complete biochemical remission and those with inadequately controlled
disease
(P > 0.05 for all) after TSS.
A similar decrease in LVM(i) was observed in controlled (108.4 +/- 30.0 g/m(2); P = 0.015) and inadequately controlled
disease
(108.8 +/- 30.7 g/m(2); P = 0.03) in comparison with naive
disease
(160.3 +/- 80.6 g/m(2)).
In controlled and inadequately controlled
disease
, R(HOMA) index was lower (2.2 +/- 1.4; P = 0.001 and 3.1 +/- 2.0; P = 0.05 vs. 5.1 +/- 3.1) while leptin concentration was higher (14.9 +/- 8.7 microg/l, P = 0.004 and 12.8 +/- 7.8 microg/l, P = 0.05 vs. 7.4 +/- 3.8 microg/l) than in naive
disease
.
Similar results were obtained if the definition of cure included both normal IGF-I levels and the ability to achieve
GH
nadir < 1 microg/l during oGTT.
CONCLUSION: This study shows that cardiac indices, insulin resistance and body composition were not different between patients with complete biochemical remission and those with discordant
GH
and IGF-I levels.
It appears that even incomplete
disease
control after TSS can result in improvement of these clinical markers.
[MeSH-major]
Acromegaly
/ surgery
[MeSH-minor]
Absorptiometry, Photon.
Adenoma
/ blood.
Adenoma
/ complications.
Adenoma
/ surgery. Adult. Aged. Area Under Curve. Biomarkers / blood. Blood Glucose / analysis. Body Composition. Echocardiography. Female.
Growth Hormone
/ blood. Humans. Insulin / blood. Insulin-Like
Growth
Factor I / analysis. Leptin / blood. Lipids / blood. Logistic Models. Male. Middle Aged.
Pituitary
Neoplasms / blood.
Pituitary
Neoplasms / complications.
Pituitary
Neoplasms / surgery. Remission Induction. Treatment Failure
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(PMID = 15807870.001).
[ISSN]
0300-0664
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers; 0 / Blood Glucose; 0 / Insulin; 0 / Leptin; 0 / Lipids; 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone
29.
DiGiovanni R, Serra S, Ezzat S, Asa SL:
AIP Mutations are not identified in patients with sporadic pituitary adenomas.
Endocr Pathol
; 2007;18(2):76-8
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[Title]
AIP Mutations are not identified in patients with sporadic
pituitary
adenomas
.
The pathogenesis of
pituitary
adenomas
remains a subject of interest.
Recently, mutations in the aryl hydrocarbon receptor-interacting protein (AIP) were identified as germline events leading
to pituitary
tumor predisposition in Finnish and Italian families with familial
growth hormone
-
secreting
pituitary
adenomas
and
acromegaly
.
We examined the frequency of AIP mutations in
pituitary
tumors and blood of Canadian patients with sporadic
pituitary
somatotroph adenomas
and sporadic
pituitary
adenomas of
other types.
Genomic DNA was extracted from
pituitary
tumors and white blood cells obtained from peripheral blood.
AIP mutations were not detected as germline events in blood or as somatic alterations in tumors of 66 patients with
pituitary
adenomas
.
These included 50 acromegalics and 16 patients with other types of
pituitary
tumor.
Our results indicate that mutations in AIP are not identified in sporadic
pituitary
adenomas of
Canadian patients.
This rare mechanism of
pituitary
tumorigenesis appears to be unique to the initial Finnish and Italian families described.
[MeSH-major]
Adenoma
/ metabolism.
Pituitary
Neoplasms / metabolism. Proteins / metabolism
[MeSH-minor]
Acromegaly
/ etiology. Canada / epidemiology. Cohort Studies. DNA / biosynthesis. DNA / genetics. DNA, Neoplasm / genetics. Exons / genetics. Gene Frequency. Germ-Line Mutation. Humans. Intracellular Signaling Peptides and Proteins
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[Cites]
Nat Genet. 2000 Sep;26(1):89-92
[
10973256.001
]
[Cites]
J Biol Chem. 2006 Jan 13;281(2):1215-23
[
16257957.001
]
[Cites]
J Biochem Mol Toxicol. 2002;16(6):317-25
[
12481307.001
]
[Cites]
Nucleic Acids Res. 1996 Dec 1;24(23):4741-50
[
8972861.001
]
[Cites]
Science. 1997 Apr 18;276(5311):404-7
[
9103196.001
]
[Cites]
Cancer. 2004 Aug 1;101(3):613-9
[
15274075.001
]
[Cites]
Clin Endocrinol (Oxf). 2003 Apr;58(4):464-70
[
12641630.001
]
[Cites]
Science. 2006 May 26;312(5777):1228-30
[
16728643.001
]
[Cites]
Nat Clin Pract Endocrinol Metab. 2006 Apr;2(4):220-30
[
16932287.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Feb;85(2):707-14
[
10690880.001
]
[Cites]
Nat Rev Cancer. 2002 Nov;2(11):836-49
[
12415254.001
]
[Cites]
J Clin Endocrinol Metab. 2006 Dec;91(12):5126-9
[
17018653.001
]
[Cites]
Nature. 1987 Dec 10-16;330(6148):566-8
[
2825031.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Sep;83(9):3210-2
[
9745428.001
]
[Cites]
Clin Endocrinol (Oxf). 2002 Oct;57(4):443-8
[
12354125.001
]
(PMID = 17916996.001).
[ISSN]
1046-3976
[Journal-full-title]
Endocrine pathology
[ISO-abbreviation]
Endocr. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Neoplasm; 0 / Intracellular Signaling Peptides and Proteins; 0 / Proteins; 0 / aryl hydrocarbon receptor-interacting protein; 9007-49-2 / DNA
30.
Pertuit M, Barlier A, Enjalbert A, Gérard C:
Signalling pathway alterations in pituitary adenomas: involvement of Gsalpha, cAMP and mitogen-activated protein kinases.
J Neuroendocrinol
; 2009 Nov;21(11):869-77
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[Title]
Signalling pathway alterations in
pituitary
adenomas
: involvement of Gsalpha, cAMP and mitogen-activated protein kinases.
Despite extensive research on sporadic
pituitary
adenomas
, it is not yet possible to assign one protein alteration to one specific type of
pituitary
adenomas
.
Nevertheless, alterations of the cAMP pathway appear to be molecular hallmarks of most
growth hormone
(
GH
)-
secreting adenomas
.
In this review, we summarise the literature regarding signalling alterations observed in
GH
-
secreting adenomas
.
In the light of results obtained on human
somatotroph
adenoma
cells in primary culture and on models of murine
somatotroph cell
lines, we postulate a crucial role for ERK1/2 in
GH
-
secreting adenomas
downstream of cAMP pathway alterations that might impact the tumoural phenotype.
[MeSH-major]
Adenoma
/ metabolism. Cyclic AMP / metabolism. GTP-Binding Protein alpha Subunits, Gs / metabolism. Mitogen-Activated Protein Kinases / metabolism.
Pituitary
Neoplasms / metabolism. Signal Transduction
[MeSH-minor]
Growth Hormone
/ secretion. Humans
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.
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(PMID = 19732293.001).
[ISSN]
1365-2826
[Journal-full-title]
Journal of neuroendocrinology
[ISO-abbreviation]
J. Neuroendocrinol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
9002-72-6 / Growth Hormone; E0399OZS9N / Cyclic AMP; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
[Number-of-references]
95
31.
Bush ZM, Vance ML:
Management of acromegaly: is there a role for primary medical therapy?
Rev Endocr Metab Disord
; 2008 Mar;9(1):83-94
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[Title]
Management of
acromegaly
: is there a role for primary medical therapy?
Acromegaly
is a chronic, debilitating
disease
caused by chronic
growth hormone
(
GH
) hypersecretion which results in chronic medical comorbidities, poor quality of life and high mortality rates.
Over 95% of
acromegaly
is caused by a
somatotroph
adenoma
of the
pituitary
, and the first-line treatment is generally transsphenoidal surgery, which can be curative in 50-60% of patients.
Nonetheless, high rates of persistent
acromegaly
following surgery and the limited efficacy of radiation therapy necessitate chronic medical treatment for many patients.
Cabergoline, a dopamine agonist, offers a lower-cost option and may be effective in patients with a
pituitary
tumor that co-secretes
GH
and prolactin.
Pegvisomant is a
GH
receptor antagonist that produces exceptional biochemical response rates but lacks any direct effects on the tumor, which may limit its effectiveness as life-long monotherapy.
While medical treatment options for
acromegaly
have significantly improved over the last 30 years, limitations remain, and a multi-specialty team approach is necessary for the effective long-term management of patients with
acromegaly
.
[MeSH-major]
Acromegaly
/ drug therapy
[MeSH-minor]
Combined Modality Therapy. Dopamine Agonists / therapeutic use. Humans. Neurosurgical Procedures / methods. Radiotherapy / methods. Receptors,
Somatotropin
/ antagonists & inhibitors. Somatostatin / analogs & derivatives
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[Cites]
Ital J Gastroenterol Hepatol. 1999 Oct;31 Suppl 2:S216-8
[
10604134.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Oct;83(10):3419-26
[
9768641.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Mar;90(3):1856-63
[
15613435.001
]
[Cites]
N Engl J Med. 1990 Apr 5;322(14):966-77
[
2179724.001
]
[Cites]
J Clin Endocrinol Metab. 2000 May;85(5):2068-71
[
10843197.001
]
[Cites]
Am J Physiol Endocrinol Metab. 2001 Dec;281(6):E1326-32
[
11701449.001
]
[Cites]
Drugs. 1989 Nov;38(5):658-702
[
2689136.001
]
[Cites]
J Clin Endocrinol Metab. 1979 May;48(5):784-9
[
372207.001
]
[Cites]
N Engl J Med. 1996 Jan 25;334(4):246-54
[
8532003.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Sep;86(9):4072-7
[
11549628.001
]
[Cites]
Digestion. 2002;65(4):200-6
[
12239460.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Jun;86(6):2779-86
[
11397887.001
]
[Cites]
Growth Horm IGF Res. 2003 Apr-Jun;13(2-3):55-74
[
12735927.001
]
[Cites]
Acta Endocrinol (Copenh). 1991 Sep;125(3):268-72
[
1835235.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Aug;90(8):4465-73
[
15886238.001
]
[Cites]
J Neurosurg. 1998 Jun;88(6):1002-8
[
9609294.001
]
[Cites]
Pituitary. 2001 Sep;4(4):239-49
[
12501974.001
]
[Cites]
Clin Endocrinol (Oxf). 2002 Jan;56(1):65-71
[
11849248.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Jul;85(7):2476-82
[
10902796.001
]
[Cites]
J Clin Endocrinol Metab. 1997 Oct;82(10):3187-91
[
9329336.001
]
[Cites]
J Clin Endocrinol Metab. 1995 Dec;80(12):3395-402
[
8530571.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Oct;83(10):3411-8
[
9768640.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Feb;89(2):667-74
[
14764779.001
]
[Cites]
J Endocrinol Invest. 1993 Mar;16(3):181-7
[
8514973.001
]
[Cites]
Proc Natl Acad Sci U S A. 1995 Feb 28;92(5):1580-4
[
7878022.001
]
[Cites]
Clin Endocrinol (Oxf). 1980 Jan;12(1):71-9
[
7379316.001
]
[Cites]
J Clin Endocrinol Metab. 1997 Apr;82(4):1047-53
[
9100571.001
]
[Cites]
Endocr Rev. 1996 Oct;17(5):423-80
[
8897021.001
]
[Cites]
Hosp Med. 2002 Mar;63(3):162-5
[
11933820.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Oct;88(10):4709-19
[
14557445.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Jul;86(7):2929-34
[
11443145.001
]
[Cites]
J Physiol Paris. 2000 May-Aug;94(3-4):205-10
[
11087998.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Aug;90(8):4483-8
[
15899958.001
]
[Cites]
Eur J Endocrinol. 2002 May;146(5):707-16
[
11980628.001
]
[Cites]
Endocr Rev. 2004 Feb;25(1):102-52
[
14769829.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Sep;83(9):3034-40
[
9745397.001
]
[Cites]
Eur J Endocrinol. 2005 Mar;152(3):379-87
[
15757854.001
]
[Cites]
J Clin Endocrinol Metab. 1999 Jul;84(7):2458-67
[
10404821.001
]
[Cites]
Nat Clin Pract Endocrinol Metab. 2006 Feb;2(2):109-17; quiz following 117
[
16932265.001
]
[Cites]
Endocrinol Metab Clin North Am. 1992 Sep;21(3):669-92
[
1521518.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Aug;83(8):2730-4
[
9709939.001
]
[Cites]
Metabolism. 1996 Aug;45(8 Suppl 1):67-71
[
8769387.001
]
[Cites]
Q J Med. 1993 May;86(5):293-9
[
8327647.001
]
[Cites]
Neurology. 1992 Jul;42(7 Suppl 6):75-81; discussion 82
[
1630643.001
]
[Cites]
Clin Endocrinol (Oxf). 2004 Aug;61(2):209-15
[
15272916.001
]
[Cites]
Clin Endocrinol (Oxf). 2001 Feb;54(2):137-54
[
11207626.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Aug 19;94(17):9343-8
[
9256484.001
]
[Cites]
Clin Endocrinol (Oxf). 1999 May;50(5):557-9
[
10468919.001
]
(PMID = 18163213.001).
[ISSN]
1389-9155
[Journal-full-title]
Reviews in endocrine & metabolic disorders
[ISO-abbreviation]
Rev Endocr Metab Disord
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / T32 DK007646
[Publication-type]
Journal Article; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / Dopamine Agonists; 0 / Receptors, Somatotropin; 51110-01-1 / Somatostatin
[Number-of-references]
88
32.
Manavela MP, Juri A, Danilowicz K, Bruno OD:
[Therapeutic management in 154 acromegalic patients].
Medicina (B Aires)
; 2010;70(4):328-32
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Acromegaly
is a chronic, invalidating
disease
due in over 95% of cases to a
growth hormone
(
GH
)
secreting
pituitary adenoma
.
Its clinical manifestations are associated to local complications related to the tumor
growth
and/or to the metabolic consequences
of GH
excess.
In only 14.0% of acromegalics drug therapy with dopaminergic agents was effective in controlling
the disease
.
In summary, multimodal therapy of
acromegaly
can lead to a global safe control of the
disease
in 55.2% of the cases.
[MeSH-major]
Acromegaly
/ therapy
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over. Female. Human
Growth Hormone
/ metabolism. Humans. Male. Middle Aged. Retrospective Studies. Young Adult
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(PMID = 20679052.001).
[ISSN]
0025-7680
[Journal-full-title]
Medicina
[ISO-abbreviation]
Medicina (B Aires)
[Language]
spa
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Argentina
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone
33.
Krzentowska A, Gołkowski F, Bałdys-Waligórska A, Hubalewska-Dydejczyk A:
[Gastrointestinal tract polyps in acromegaly patients].
Przegl Lek
; 2010;67(12):1266-9
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[Title]
[Gastrointestinal tract polyps in
acromegaly
patients].
Acromegaly
is a rare, chronic
disease
due to hypersecretion
of growth hormone
(
GH
) by
pituitary adenoma
arising from somatotrophs.
The course of the
disease
is related to long-term organ and systemic complications and malignancies.
Colon polyps seem to constitute the most frequent tumours in
acromegaly
apart from thyroid nodules.
The aim of this study was to evaluate the prevalence of colon polyps in patients with
acromegaly
.
Thirty one
acromegaly
patients, 22 females and 9 males (mean age 46.3 +/- 11.9 yrs), were enrolled to the study.
Polyps were histopatologically verified as tubular
adenoma
with low-grade dysplasia (10 patients, 76.9%) and hyperplastic polyps (3 patients, 23.1%).
The prevalence of colon polyps was significantly related to the duration of uncontrolled
acromegaly
(p < 0.01).
Median duration of uncontrolled
acromegaly
in patients with and without colon polyps were 10.0 (IQR = 2.0) yrs and 6.5 (IQR = 5.0) yrs, respectively.
IGF-1,
GH
basic and in 120 min of OGTT serum concentrations on
diagnosis
were not significantly related to the prevalence of colon polyps.
Our study indicates that duration of uncontrolled
acromegaly
, contrary to IGF-1,
GH
basic and in OGTT serum concentrations at
diagnosis
are essential for the colon polyps development.
Colonoscopy is considered to be routine in patients with
acromegaly
.
[MeSH-major]
Acromegaly
/ epidemiology. Colonic Polyps / epidemiology
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.
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.
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(PMID = 21591351.001).
[ISSN]
0033-2240
[Journal-full-title]
Przegla̧d lekarski
[ISO-abbreviation]
Prz. Lek.
[Language]
pol
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Poland
34.
Sakai N, Kim K, Sanno N, Yoshida D, Teramoto A, Shibasaki T:
Elevation of growth hormone-releasing hormone receptor messenger ribonucleic acid expression in growth hormone-secreting pituitary adenoma with Gsalpha protein mutation.
Neurol Med Chir (Tokyo)
; 2008;48(11):481-7; discussion 487-8
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[Title]
Elevation
of growth hormone
-releasing
hormone
receptor messenger ribonucleic acid expression in
growth hormone
-
secreting
pituitary adenoma
with Gsalpha protein mutation.
Growth hormone
-releasing
hormone
(GHRH) stimulates not only the synthesis and secretion
of GH
but also the proliferation of normal somatotrophs.
The expression of GHRH receptor (GHRHR) is regulated by GHRH, both of which are known to be expressed in human
GH
-
secreting
pituitary adenoma
cells.
Somatic mutations in the subunit of Gsalpha protein (gsp), lead to the constitutive activation of adenylyl cyclase in
pituitary
adenomas
that secrete
GH
.
It has not been examined how gsp mutations influence GHRHR expression in
GH
-
secreting adenomas
.
We therefore analyzed the expression levels of GHRHR messenger ribonucleic acid (mRNA) in
GH
-
secreting
pituitary
adenomas
focusing on a gsp mutation.
Furthermore, we investigated the effect of GHRH on the expression of GHRHR mRNA in primary cultures
of GH
-
secreting
pituitary adenoma
cells.
GHRHR mRNA expression levels were significantly elevated in gsp mutation-positive
GH
-
secreting adenomas
compared with those in gsp mutation-negative ones.
In primary-cultured
GH
-
secreting
adenoma
cells, the increase
of GH
secretion in response to GHRH was shown in both gsp mutation-positive and -negative
adenoma
cells with a significantly higher response in the latter
adenoma
cells.
GHRH increased GHRHR mRNA expression level in gsp mutation-negative
adenoma
cells while it was not influenced by GHRH in gsp mutation-positive
adenoma
cells.
These results suggest that gsp mutations up-regulate GHRHR mRNA expression in
GH
-
secreting
pituitary adenoma
cells, and that gsp mutations desensitize the
adenoma
cells to GHRH in terms of their GHRHR mRNA expression probably because of their saturation of GHRH signaling.
[MeSH-major]
Adenoma
/ genetics. GTP-Binding Protein alpha Subunits, Gs / genetics.
Growth Hormone
-Releasing
Hormone
/ secretion. Mutation, Missense. Neoplasm Proteins / genetics. Nerve Tissue Proteins / genetics.
Pituitary
Neoplasms / genetics. Point Mutation. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. Receptors, Neuropeptide / genetics. Receptors,
Pituitary
Hormone
-Regulating
Hormone
/ genetics
[MeSH-minor]
Acromegaly
/ etiology.
Acromegaly
/ surgery. Adult. Amino Acid Substitution.
Cell
Line, Tumor / drug effects.
Cell
Line, Tumor / metabolism.
Cell
Line, Tumor / secretion. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged
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.
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.
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(PMID = 19029774.001).
[ISSN]
1349-8029
[Journal-full-title]
Neurologia medico-chirurgica
[ISO-abbreviation]
Neurol. Med. Chir. (Tokyo)
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Neuropeptide; 0 / Receptors, Pituitary Hormone-Regulating Hormone; 0 / somatotropin releasing hormone receptor; 9034-39-3 / Growth Hormone-Releasing Hormone; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
35.
Mohammed S, Syro L, Abad V, Salehi F, Horvath E, Scheithauer BW, Kovacs K, Cusimano M:
Silent somatotroph adenoma of the pituitary in an adolescent.
Can J Neurol Sci
; 2009 Jan;36(1):123-5
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[Title]
Silent
somatotroph
adenoma
of the
pituitary
in an adolescent.
[MeSH-major]
Adenoma
/ pathology.
Growth Hormone
/ metabolism.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ pathology.
Pituitary
Neoplasms / pathology
[MeSH-minor]
Adolescent. Humans. Magnetic Resonance Imaging / methods. Male. Microscopy, Electron, Transmission / methods.
Pituitary
Gland
/ metabolism.
Pituitary
Gland
/ pathology.
Pituitary
Gland
/ ultrastructure
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consumer health - Pituitary Tumors
.
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(PMID = 19294904.001).
[ISSN]
0317-1671
[Journal-full-title]
The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques
[ISO-abbreviation]
Can J Neurol Sci
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Canada
[Chemical-registry-number]
9002-72-6 / Growth Hormone
36.
Ebisawa T, Tojo K, Tajima N, Kamio M, Oki Y, Ono K, Sasano H:
Immunohistochemical analysis of 11-beta-hydroxysteroid dehydrogenase type 2 and glucocorticoid receptor in subclinical Cushing's disease due to pituitary macroadenoma.
Endocr Pathol
; 2008;19(4):252-60
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[Title]
Immunohistochemical analysis of 11-beta-hydroxysteroid dehydrogenase type 2 and glucocorticoid receptor in subclinical Cushing'
s disease
due to
pituitary
macroadenoma.
Subclinical Cushing'
s disease
(SCD) is characterized by lack of clinically evident Cushingoid features, despite abnormal hypersecretion of ACTH.
Impaired glucocorticoid (GC) action may be correlated with the proliferation and development of
pituitary
macroadenomas causing SCD.
In this study, immunohistochemical analysis of the resected tumors were performed to evaluate the expression of 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) and glucocorticoid receptor (GR) in
pituitary
tissues obtained from two SCD (macroadenomas), eight Cushing'
s disease
(CD) (microadenomas), nine
acromegaly
, and nine normal
pituitary
(NP).
[MeSH-major]
11-beta-Hydroxysteroid Dehydrogenase Type 2 / metabolism. ACTH-
Secreting
Pituitary Adenoma
/ metabolism.
Adenoma
/ metabolism.
Pituitary
ACTH Hypersecretion / metabolism. Receptors, Glucocorticoid / metabolism
[MeSH-minor]
Acromegaly
/ metabolism.
Acromegaly
/ pathology. Adolescent. Adrenocorticotropic
Hormone
/ metabolism. Adult. Aged. Female. Humans. Immunohistochemistry / methods. Male. Middle Aged.
Pituitary
Gland
/ metabolism.
Pituitary
Gland
/ pathology. Young Adult
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[Cites]
J Clin Endocrinol Metab. 1994 Apr;78(4):835-41
[
8157708.001
]
[Cites]
Mol Endocrinol. 2005 Apr;19(4):885-97
[
15591535.001
]
[Cites]
Endocr Rev. 1999 Apr;20(2):136-55
[
10204115.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Mar;83(3):917-21
[
9506748.001
]
[Cites]
J Clin Endocrinol Metab. 2007 Jan;92(1):172-9
[
17062771.001
]
[Cites]
J Clin Endocrinol Metab. 1996 Jan;81(1):124-9
[
8550738.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Nov;83(11):4022-5
[
9814486.001
]
[Cites]
Domest Anim Endocrinol. 2002 Jun;22(4):201-10
[
12044610.001
]
[Cites]
Endocr J. 2003 Jun;50(3):325-31
[
12940462.001
]
[Cites]
Endocrinology. 1992 Dec;131(6):2873-80
[
1332850.001
]
[Cites]
J Endocrinol. 2005 Aug;186(2):251-71
[
16079253.001
]
[Cites]
Intern Med. 2002 Jul;41(7):566-70
[
12132526.001
]
[Cites]
Eur J Endocrinol. 2003 Sep;149(3):195-200
[
12943521.001
]
[Cites]
Clin Genet. 2007 Sep;72(3):175-82
[
17718852.001
]
[Cites]
Clin Endocrinol (Oxf). 1998 Sep;49(3):301-6
[
9861319.001
]
[Cites]
J Clin Endocrinol Metab. 1996 Feb;81(2):497-502
[
8636257.001
]
[Cites]
Arch Intern Med. 2001 Mar 26;161(6):892-3
[
11268235.001
]
[Cites]
J Clin Endocrinol Metab. 1998 May;83(5):1619-23
[
9589666.001
]
[Cites]
Mol Cell Endocrinol. 2002 Nov 29;197(1-2):69-72
[
12431798.001
]
[Cites]
J Cell Biochem. 1987 Dec;35(4):293-304
[
3326882.001
]
[Cites]
J Clin Endocrinol Metab. 1995 Jul;80(7):2203-9
[
7608280.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Jun;86(6):2728-33
[
11397878.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Aug;90(8):4963-9
[
15886242.001
]
[Cites]
J Endocrinol. 1998 Jan;156(1):169-75
[
9496246.001
]
[Cites]
Endocrinology. 2006 Feb;147(2):769-72
[
16254034.001
]
[Cites]
Proc Assoc Am Physicians. 1996 Jul;108(4):296-307
[
8863343.001
]
[Cites]
Oncogene. 2003 Mar 20;22(11):1663-7
[
12642869.001
]
[Cites]
J Endocrinol. 1997 Mar;152(3):387-94
[
9071959.001
]
[Cites]
Clin Endocrinol (Oxf). 2001 Sep;55(3):363-71
[
11589680.001
]
(PMID = 19048413.001).
[ISSN]
1046-3976
[Journal-full-title]
Endocrine pathology
[ISO-abbreviation]
Endocr. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Receptors, Glucocorticoid; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenase Type 2
37.
Popovic V:
Are there alternative tests for diagnosis of acromegaly?
J Endocrinol Invest
; 2005;28(11 Suppl International):73-4
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[Title]
Are there alternative tests for
diagnosis of
acromegaly
?
In
acromegaly
, clinical features are of the utmost importance, and biochemical confirmation is rarely difficult.
However, some clinically manifest acromegalics have subtle abnormalities in
GH
secretion resulting in post-glucose
GH
nadir in the designated "normal" range with high IGF-I levels.
Clinical decision may be based on the probability of the
disease
and elevated IGF-I levels.
The TRH test or the frequent
GH
sampling test may help confirm
acromegaly
but on their own have no diagnostic advantage.
A TRH-
GH
response is not specific
to acromegaly
, while frequent sampling is not practical.
Post-treatment assessment of the
disease
activity and definition of
acromegaly
cure, by measuring
GH
secretion, remain problematic.
IGF-I levels seem to differentiate normality less clearly and discordance
of GH
and IGF-I results is frequent.
Post-treatment probability for residual
disease
activity should include more clinical parameters such as insulin sensitivity, leptin and echocardiography.
Furthermore, with efforts to achieve tight biochemical control of the
disease
it is foreseeable that a proportion of patients may be rendered
GH
deficient, requiring stimulatory testing.
Acromegaly
is a disfiguring and disabling illness, in which by definition,
the disorder
is caused by a
pituitary
GH
-
secreting
adenoma
resulting in high circulating levels
of GH
and IGF-I.
The clinical features of
acromegaly
include those
of GH
and IGF-I on tissues and the effects of the
pituitary
tumor itself.
There is no single cut-off value for
GH
with perfect discrimination between
acromegaly
and normality.
The recommended post-glucose
GH
nadir value of 1 microg/l is now considered to be inappropriately high, and measurement of IGF-I levels although extremely valuable has its limitations.
Furthermore, some acromegalics may have subtle abnormalities in
GH
secretion, resulting in post-glucose
GH
nadir in the designated "normal" range with elevated IGF-I levels.
[MeSH-major]
Acromegaly
/
diagnosis
[MeSH-minor]
Glucose Tolerance Test. Human
Growth Hormone
/ blood. Human
Growth Hormone
/ secretion. Humans. Insulin-Like
Growth
Factor I / analysis.
Pituitary
Neoplasms. Thyrotropin-Releasing
Hormone
Genetic Alliance.
consumer health - Acromegaly
.
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(PMID = 16625850.001).
[ISSN]
0391-4097
[Journal-full-title]
Journal of endocrinological investigation
[ISO-abbreviation]
J. Endocrinol. Invest.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Italy
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 5Y5F15120W / Thyrotropin-Releasing Hormone; 67763-96-6 / Insulin-Like Growth Factor I
[Number-of-references]
11
38.
Feelders RA, Hofland LJ, van Aken MO, Neggers SJ, Lamberts SW, de Herder WW, van der Lely AJ:
Medical therapy of acromegaly: efficacy and safety of somatostatin analogues.
Drugs
; 2009 Nov 12;69(16):2207-26
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[Title]
Medical therapy of
acromegaly
: efficacy and safety of somatostatin analogues.
Acromegaly
is a chronic
disease
with signs and symptoms due to
growth hormone
(
GH
) excess.
The most frequent cause of
acromegaly
is a
GH
-
producing
pituitary adenoma
.
Chronic
GH
excess is accompanied by long-term complications of the locomotor (arthrosis) and cardiovascular (atherosclerosis, cardiomyopathy) systems and is, when untreated, associated with an increased mortality.
The aim of treatment of
acromegaly
is to improve symptoms, to achieve local tumour mass control, and to decrease morbidity and mortality.
Primary medical therapy has been increasingly applied in recent years, especially when a priori chances of surgical cure are low (because of
adenoma
size and localization) and in patients with advanced age and/or serious co-morbidity.
In addition, preoperative primary medical therapy may result in tumour shrinkage, facilitating tumour resection, and may reduce perioperative complications due to
GH
excess.
Treatment with somatostatin analogues results in
GH
control in approximately 60% of patients.
The currently available somatostatin analogues, octreotide and lanreotide, seem to be equally effective; however, this should still be evaluated in prospective, randomized trials evaluating efficacy with respect to
GH
control and tumour shrinkage.
In patients with an insufficient clinical and biochemical response to somatostatin analogues, combination therapy with dopamine receptor agonists or
the GH
receptor antagonist pegvisomant usually leads to
disease
control.
New developments in the medical therapy of
acromegaly
include the universal somatostatin receptor agonist pasireotide, which has a broader affinity for all somatostatin receptor (sst) subtypes compared with the currently available somatostatin analogues with preferential affinity for the sst2 receptor, and chimeric compounds that interact with both somatostatin and dopamine receptors with synergizing effects on
GH
secretion.
[MeSH-major]
Acromegaly
/ drug therapy. Receptors, Somatostatin / drug effects. Somatostatin / analogs & derivatives
[MeSH-minor]
Adenoma
/ complications. Antineoplastic Agents / adverse effects. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Female.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ complications. Human
Growth Hormone
/ metabolism. Human
Growth Hormone
/ secretion. Humans. Male. Octreotide / adverse effects. Octreotide / pharmacology. Octreotide / therapeutic use. Peptides, Cyclic / adverse effects. Peptides, Cyclic / pharmacology. Peptides, Cyclic / therapeutic use
Genetic Alliance.
consumer health - Acromegaly
.
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[Cites]
Drugs. 1997 Apr;53(4):681-99
[
9098666.001
]
[Cites]
J Clin Invest. 1997 Nov 1;100(9):2386-92
[
9410919.001
]
[Cites]
Eur J Endocrinol. 2005 Dec;153(6):737-40
[
16322377.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Oct;83(10):3419-26
[
9768641.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Mar;90(3):1856-63
[
15613435.001
]
[Cites]
Pituitary. 2001 Aug;4(3):163-71
[
12138989.001
]
[Cites]
Neuroendocrinology. 2004 Mar;79(3):142-8
[
15103227.001
]
[Cites]
Surg Neurol. 2006 Jul;66(1):26-31; discussion 31
[
16793431.001
]
[Cites]
Lancet. 2001 Nov 24;358(9295):1754-9
[
11734231.001
]
[Cites]
Clin Endocrinol (Oxf). 2003 Mar;58(3):288-95
[
12608933.001
]
[Cites]
Clin Endocrinol (Oxf). 2002 Oct;57(4):425-41
[
12354124.001
]
[Cites]
Eur J Endocrinol. 2006 Aug;155(2):371-9
[
16868153.001
]
[Cites]
Clin Endocrinol (Oxf). 2006 Sep;65(3):320-6
[
16918950.001
]
[Cites]
Eur J Endocrinol. 2004 Sep;151(3):317-24
[
15362960.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Jul;90(7):4405-10
[
15827109.001
]
[Cites]
Clin Endocrinol (Oxf). 2008 Mar;68(3):458-65
[
17941904.001
]
[Cites]
Clin Endocrinol (Oxf). 2000 Nov;53(5):577-86
[
11106918.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Jan;86(1):140-5
[
11231991.001
]
[Cites]
J Clin Endocrinol Metab. 1994 Sep;79(3):724-9
[
7521350.001
]
[Cites]
Eur J Endocrinol. 2005 Jul;153(1):67-71
[
15994747.001
]
[Cites]
J Clin Endocrinol Metab. 2006 Jan;91(1):85-92
[
16263832.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Sep;86(9):4072-7
[
11549628.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Jun;86(6):2779-86
[
11397887.001
]
[Cites]
J Biol Chem. 1987 Apr 15;262(11):4987-93
[
2881926.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Oct;90(10 ):5627-31
[
16046586.001
]
[Cites]
J Clin Endocrinol Metab. 1989 Apr;68(4):844-50
[
2537844.001
]
[Cites]
Endocrinology. 2002 Oct;143(10):4123-30
[
12239124.001
]
[Cites]
Pituitary. 2006;9(1):27-34
[
16703406.001
]
[Cites]
J Neurosurg. 2006 Jun;104(6):899-906
[
16776333.001
]
[Cites]
J Clin Neurosci. 2003 Jul;10 (4):444-8
[
12852883.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Aug;85(8):2958-61
[
10946911.001
]
[Cites]
Clin Endocrinol (Oxf). 2007 Aug;67(2):282-9
[
17524029.001
]
[Cites]
Drugs. 2003;63(22):2473-99
[
14609359.001
]
[Cites]
J Clin Endocrinol Metab. 2008 Oct;93(10 ):3853-9
[
18647806.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Jun;88(6):2797-802
[
12788890.001
]
[Cites]
Eur J Endocrinol. 2004 Apr;150(4):473-80
[
15080776.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Aug;90(8):4465-73
[
15886238.001
]
[Cites]
Eur J Endocrinol. 2008 Nov;159(5):525-32
[
18755874.001
]
[Cites]
Growth Horm IGF Res. 2003 Aug;13(4):171-84
[
12914750.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Feb;86(2):478-81
[
11157994.001
]
[Cites]
Mol Endocrinol. 2009 Mar;23(3):337-48
[
19131507.001
]
[Cites]
Anesth Analg. 2005 Oct;101(4):1170-81
[
16192540.001
]
[Cites]
Neuroendocrinology. 2006;83(3-4):230-9
[
17047388.001
]
[Cites]
Clin Endocrinol (Oxf). 2006 Feb;64(2):209-14
[
16430722.001
]
[Cites]
Clin Cancer Res. 1997 Feb;3(2):265-72
[
9815682.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8
[
12107192.001
]
[Cites]
Clin Endocrinol (Oxf). 2007 Aug;67(2):310-5
[
17555503.001
]
[Cites]
Mol Cell Endocrinol. 2008 May 14;286(1-2):69-74
[
17977644.001
]
[Cites]
Acta Neurochir (Wien). 2005 May;147(5):485-93; discussion 493
[
15806331.001
]
[Cites]
J Clin Endocrinol Metab. 2007 May;92(5):1592-9
[
17311860.001
]
[Cites]
Eur J Endocrinol. 2005 Jul;153(1):135-41
[
15994755.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Oct;83(10):3411-8
[
9768640.001
]
[Cites]
J Clin Endocrinol Metab. 1994 Jul;79(1):145-51
[
8027218.001
]
[Cites]
Eur J Endocrinol. 2007 Jan;156(1):65-74
[
17218727.001
]
[Cites]
Front Horm Res. 2006;34:236-55
[
16474223.001
]
[Cites]
Exp Clin Endocrinol Diabetes. 2005 Mar;113(3):139-44
[
15789272.001
]
[Cites]
Clin Endocrinol (Oxf). 2005 Mar;62(3):282-8
[
15730408.001
]
[Cites]
J Clin Pharmacol. 2005 Jul;45(7):836-44
[
15951474.001
]
[Cites]
Eur J Endocrinol. 2006 Jul;155(1):73-8
[
16793952.001
]
[Cites]
J Endocrinol Invest. 2003 Jul;26(7):599-603
[
14594107.001
]
[Cites]
Eur J Endocrinol. 2005 Aug;153(2):203-5
[
16061824.001
]
[Cites]
Rev Endocr Metab Disord. 2005 Jan;6(1):29-37
[
15711912.001
]
[Cites]
J Neurosurg. 1998 Sep;89(3):353-8
[
9724106.001
]
[Cites]
J Endocrinol Invest. 2003 Dec;26(12):1242-7
[
15055479.001
]
[Cites]
J Endocrinol Invest. 2005;28(11 Suppl International):43-7
[
16625844.001
]
[Cites]
Lancet. 2005 May 7-13;365(9471):1644-6
[
15885297.001
]
[Cites]
Clin Endocrinol (Oxf). 1980 Jan;12(1):71-9
[
7379316.001
]
[Cites]
J Clin Endocrinol Metab. 2008 Aug;93(8):2957-68
[
18477663.001
]
[Cites]
Clin Endocrinol (Oxf). 2003 Apr;58(4):471-81
[
12641631.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Dec;85(12):4712-20
[
11134133.001
]
[Cites]
J Endocrinol Invest. 2005;28(11 Suppl International):21-7
[
16625841.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Nov;86(11):5194-200
[
11701676.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Oct;88(10 ):4759-67
[
14557452.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Feb;85(2):781-92
[
10690891.001
]
[Cites]
Eur J Endocrinol. 2005 Jan;152(1):61-6
[
15762188.001
]
[Cites]
Cancer Res. 1990 Oct 1;50(19):6238-42
[
2169342.001
]
[Cites]
J Clin Endocrinol Metab. 2006 Apr;91(4):1397-403
[
16449332.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Dec;87(12):5545-52
[
12466351.001
]
[Cites]
J Clin Endocrinol Metab. 1994 Aug;79(2):461-5
[
8045964.001
]
[Cites]
J Clin Endocrinol Metab. 1995 Nov;80(11):3267-72
[
7593436.001
]
[Cites]
Mayo Clin Proc. 1997 Oct;72(10):893-900
[
9379690.001
]
[Cites]
J Clin Endocrinol Metab. 1985 Jul;61(1):98-103
[
2860120.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Jan;87(1):99-104
[
11788630.001
]
[Cites]
Clin Endocrinol (Oxf). 2003 Jul;59(1):115-28
[
12807513.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Feb;85(2):526-9
[
10690849.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Apr;88(4):1913-4
[
12679495.001
]
[Cites]
Growth Horm IGF Res. 2003 Aug;13 Suppl A:S144-51
[
12914744.001
]
[Cites]
Eur J Endocrinol. 2001 Aug;145(2):137-45
[
11454508.001
]
[Cites]
Eur J Endocrinol. 2000 Nov;143(5):577-84
[
11078980.001
]
[Cites]
J Clin Pathol. 2006 Mar;59(3):274-9
[
16505278.001
]
[Cites]
J Clin Endocrinol Metab. 1984 Dec;59(6):1148-51
[
6092412.001
]
[Cites]
Clin Endocrinol (Oxf). 2008 Jun;68(6):970-5
[
18031313.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Sep;87(9):4054-8
[
12213843.001
]
[Cites]
Clin Endocrinol (Oxf). 2008 Mar;68(3):473-80
[
17941902.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Apr;89(4):1577-85
[
15070915.001
]
[Cites]
Ann Intern Med. 1992 Nov 1;117(9):711-8
[
1416572.001
]
[Cites]
J Clin Endocrinol Metab. 2008 Aug;93(8):2984-90
[
18492760.001
]
[Cites]
Endocr Relat Cancer. 2006 Sep;13(3):955-62
[
16954443.001
]
[Cites]
J Clin Endocrinol Metab. 2006 Jun;91(6):2112-8
[
16537687.001
]
[Cites]
Science. 2000 Apr 7;288(5463):154-7
[
10753124.001
]
[Cites]
Front Neuroendocrinol. 1999 Jul;20(3):157-98
[
10433861.001
]
[Cites]
Metabolism. 1996 Aug;45(8 Suppl 1):27-30
[
8769375.001
]
[Cites]
Growth Horm IGF Res. 2004 Oct;14(5):382-7
[
15336231.001
]
[Cites]
Acta Endocrinol (Copenh). 1993 Jul;129 Suppl 1:18-20
[
8372606.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Aug;87(8):3537-42
[
12161471.001
]
[Cites]
J Clin Endocrinol Metab. 1995 Apr;80(4):1386-92
[
7714115.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Aug;87(8):3783-90
[
12161511.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Sep;83(9):3034-40
[
9745397.001
]
[Cites]
Clin Endocrinol (Oxf). 2004 Mar;60(3):375-81
[
15009004.001
]
[Cites]
Clin Endocrinol (Oxf). 2004 Aug;61(2):224-31
[
15272918.001
]
[Cites]
Clin Pharmacokinet. 1990 Oct;19(4):319-32
[
2208899.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Oct;87(10):4554-63
[
12364434.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Sep;88(9):4239-45
[
12970293.001
]
[Cites]
Clin Endocrinol (Oxf). 2006 Mar;64(3):342-51
[
16487447.001
]
[Cites]
Metabolism. 2002 Mar;51(3):387-93
[
11887179.001
]
[Cites]
Life Sci. 1995;56(5):333-42
[
7530798.001
]
[Cites]
Clin Endocrinol (Oxf). 2003 Oct;59(4):492-9
[
14510913.001
]
[Cites]
Science. 1973 Jan 5;179(4068):77-9
[
4682131.001
]
[Cites]
Clin Endocrinol (Oxf). 2001 Sep;55(3):411-5
[
11589686.001
]
[Cites]
N Engl J Med. 2000 Apr 20;342(16):1171-7
[
10770982.001
]
[Cites]
Eur J Endocrinol. 2004 Apr;150(4):489-95
[
15080778.001
]
[Cites]
Clin Pharmacokinet. 2006;45(10 ):1003-11
[
16984213.001
]
[Cites]
J Clin Invest. 1997 Feb 15;99(4):789-98
[
9045884.001
]
[Cites]
Pituitary. 2006;9(3):221-9
[
17036195.001
]
[Cites]
Endocrinology. 1997 Oct;138(10):4473-6
[
9322965.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Jul;88(7):3090-8
[
12843148.001
]
[Cites]
Clin Endocrinol (Oxf). 2007 Jun;66(6):859-68
[
17465997.001
]
[Cites]
N Engl J Med. 2006 Dec 14;355(24):2558-73
[
17167139.001
]
[Cites]
Clin Endocrinol (Oxf). 2007 Oct;67(4):512-9
[
17555511.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Feb;89(2):638-45
[
14764775.001
]
(PMID = 19852525.001).
[ISSN]
1179-1950
[Journal-full-title]
Drugs
[ISO-abbreviation]
Drugs
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
New Zealand
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Peptides, Cyclic; 0 / Receptors, Somatostatin; 0G3DE8943Y / lanreotide; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
[Number-of-references]
130
39.
Mendoza V, Sosa E, Espinosa-de-Los-Monteros AL, Salcedo M, Guinto G, Cheng S, Sandoval C, Mercado M:
GSPalpha mutations in Mexican patients with acromegaly: potential impact on long term prognosis.
Growth Horm IGF Res
; 2005 Feb;15(1):28-32
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[Title]
GSPalpha mutations in Mexican patients with
acromegaly
: potential impact on long term prognosis.
OBJECTIVE: The frequency of activating mutations of the GSPalpha gene as the etiology
of GH
-
secreting
pituitary
adenomas
has been the subject of important ethnogenetic variability.
Whereas up to 40% of Caucasian patients with
acromegaly
have tumors which harbor these somatic mutations, their prevalence among Asian populations is much lower.
In the present study, we investigated the prevalence of GSPalpha mutations in
GH
-
secreting
tumors obtained from a genetically homogenous population of Mexican patients with
acromegaly
.
We also sought to establish whether or not the presence of these mutations correlates in any way with the clinical or biochemical characteristics of the
disease
.
STUDY DESIGN AND METHODS: Fifty eight
GH
-
secreting
pituitary
adenomas
were examined for the presence of point mutations in either codon 201 or 227 of the GSPalpha gene, using PCR and direct sequencing of DNA extracted from either fresh or paraffin-embedded tissues.
Patients were prospectively followed clinically and biochemically for up to nine years after
pituitary
surgery.
The frequency and severity of the different clinical features of
acromegaly
did not differ between patients with and without GSPalpha mutations.
Patients with and without mutations had pre-operative
GH
and IGF-I elevations of similar magnitude, and although microadenomas appeared to be more frequent among patients with GSPalpha mutations, this did not reach statistical significance.
Upon short-term follow-up, biochemical cure (normal age- and gender-adjusted IGF-I and post-glucose
GH
below 1 ng/mL) was similarly achieved in both groups.
After 3-9 years of post-operative follow up however, a significantly greater proportion of patients with the mutation achieved a "safe" basal
GH
value (100% vs 33%, p=0.001) as well a lower nadir post-glucose
GH
(0.53+/-0.5 vs 2.9+/-6.2 ng/mL, p=0.04) although the rate of IGF-1 normalization did not differ between the 2 groups.
CONCLUSIONS: Our results show that the prevalence of GSPalpha mutations in Mexican patients with
acromegaly
is intermediate between that found in Asian and Caucasian populations.
In this well-defined genetic population the presence of codon 201 mutations appeared to be associated with a greater probability of achieving a "safe"
GH
value upon long-term follow-up.
[MeSH-major]
Acromegaly
/ genetics.
Adenoma
/ genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. GTP-Binding Protein alpha Subunits, Gs / physiology. Mutation.
Pituitary
Neoplasms / genetics
[MeSH-minor]
Adult. Codon. DNA Primers / chemistry. Exons. Female.
Growth Hormone
/ metabolism. Heterozygote. Humans. Male. Mexico. Middle Aged. Point Mutation. Sex Factors. Time Factors. Treatment Outcome
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(PMID = 15701569.001).
[ISSN]
1096-6374
[Journal-full-title]
Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society
[ISO-abbreviation]
Growth Horm. IGF Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Scotland
[Chemical-registry-number]
0 / Codon; 0 / DNA Primers; 9002-72-6 / Growth Hormone; EC 3.6.1.- / GNAS protein, human; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
40.
Nakashima M, Takano K, Matsuno A:
Analyses of factors influencing the acute effect of octreotide in growth hormone-secreting adenomas.
Endocr J
; 2009;56(2):295-304
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[Title]
Analyses of factors influencing the acute effect of octreotide in
growth hormone
-
secreting adenomas
.
Somatostatin analogues such as octreotide are used to treat active acromegalic patients by reducing serum
growth hormone
(
GH
) levels.
However, the acute effect of octreotide on
GH
secretion differs among patients.
To elucidate factors influencing the acute effect of octreotide, we collected data from 56 patients with
somatotroph
adenoma
from two institutions.
Monovariate analysis revealed a statistically significant inverse relation of Ki-67 SI with the reduction
of GH
by octreotide.
Post-test revealed that the plasma membrane-dominant staining pattern of SSTR 2A was significantly related to the reduction
of GH
by octreotide.
[MeSH-major]
Growth Hormone
-
Secreting
Pituitary Adenoma
/ secretion. Human
Growth Hormone
/ secretion. Octreotide / therapeutic use.
Pituitary
Neoplasms / secretion
[MeSH-minor]
Adult. Aged.
Cell
Membrane / metabolism. Female. Humans. Ki-67 Antigen / metabolism. Male. Middle Aged. Receptors, Somatostatin / metabolism. Regression Analysis
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(PMID = 19164866.001).
[ISSN]
1348-4540
[Journal-full-title]
Endocrine journal
[ISO-abbreviation]
Endocr. J.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Ki-67 Antigen; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 12629-01-5 / Human Growth Hormone; RWM8CCW8GP / Octreotide
41.
Yin J, Su CB, Xu ZQ, Yang Y, Ma WB, Tao W, Yang Z, Xia XW:
Effect of preoperative use of long-acting octreotide on growth hormone secreting pituitary adenoma and transsphenoidal surgery.
Chin Med Sci J
; 2005 Mar;20(1):23-6
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[Title]
Effect of preoperative use of long-acting octreotide on
growth hormone secreting
pituitary adenoma
and transsphenoidal surgery.
OBJECTIVE: To investigate whether somatostatin analog octreotide long acting release (LAR) shrinks
growth hormone
(
GH
)
secreting adenomas
, and improves the results of subsequent transsphenoidal surgery.
METHODS: Seventeen previously untreated active acromegalic patients with
pituitary
adenomas
were treated with LAR (30 mg intramuscular injection every 28 days) for 3 months prior to transsphenoidal surgery.
Clinical reaction, mean
GH
secretion, and tumor volume were measured under basal conditions and after LAR treatment.
RESULTS: Presurgical treatment improved
acromegaly
symptoms and induced a significant reduction
of GH
under the 5 ng/mL limit in microadenoma (P < 0.05), while only 18.2% (2/11) in macroadenoma.
During operation,
adenoma
was soft in 15 cases, with the exception of 2 cases in which the soft tumor was divided by fibrous septa, but all tumor removal was smooth.
CONCLUSIONS: A short term administration of preoperative LAR may induce a significant decrease in
GH
-secretion level and
adenoma
volume.
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(PMID = 15844307.001).
[ISSN]
1001-9294
[Journal-full-title]
Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih
[ISO-abbreviation]
Chin. Med. Sci. J.
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / Delayed-Action Preparations; 12629-01-5 / Human Growth Hormone; RWM8CCW8GP / Octreotide
42.
Ghostine S, Ghostine MS, Johnson WD:
Radiation therapy in the treatment of pituitary tumors.
Neurosurg Focus
; 2008;24(5):E8
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[Title]
Radiation therapy in the treatment of
pituitary
tumors.
The treatment of
pituitary
tumors has progressed into a multidisciplinary approach that involves neurosurgeons, radiation oncologists, and endocrinologists.
This has allowed improved outcomes in treatment of
pituitary
tumors due to a combination of surgical, medical, and radiation therapies.
In this study, the authors review the role of radiation therapy in the treatment of
pituitary
adenomas
.
[MeSH-major]
Adenoma
/ radiotherapy. Cranial Irradiation.
Pituitary
Neoplasms / radiotherapy
[MeSH-minor]
Acromegaly
/ drug therapy.
Acromegaly
/ etiology.
Acromegaly
/ radiotherapy.
Acromegaly
/ surgery. Brain / radiation effects. Combined Modality Therapy. Cushing Syndrome / etiology. Cushing Syndrome / radiotherapy. Cushing Syndrome / surgery. Humans. Hypophysectomy / methods. Hypopituitarism / etiology. Nelson Syndrome / radiotherapy. Nelson Syndrome / surgery. Postoperative Complications / etiology. Radiation Injuries / etiology. Radiation Injuries / prevention & control. Radiosurgery / adverse effects. Radiotherapy, Adjuvant / adverse effects. Radiotherapy, Computer-Assisted / methods. Treatment Outcome
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(PMID = 18447747.001).
[ISSN]
1092-0684
[Journal-full-title]
Neurosurgical focus
[ISO-abbreviation]
Neurosurg Focus
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
54
43.
Herrmann BL, Severing M, Schmermund A, Berg C, Budde T, Erbel R, Mann K:
Impact of disease duration on coronary calcification in patients with acromegaly.
Exp Clin Endocrinol Diabetes
; 2009 Sep;117(8):417-22
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[Title]
Impact
of disease
duration on coronary calcification in patients with
acromegaly
.
It is well established, that the increased mortality in patients with
acromegaly
is due to cardiac diseases.
Cardiomyopathy is the predominant cardiac alteration in patients with
acromegaly
.
There are less data about coronary heart
disease
or coronary calcifications.
The prospective study included 30 patients with
acromegaly
(mean age 53+/-14 year; 16 females, 14 males; BMI 28.1+/-3.6 kg/m (2); mean+/-SD), 12 patients had active
disease
(IGF-1 751+/-338 microg/L;
GH
25.6+/-36.4 microg/L), 9 were well-controlled (IGF-1 157+/-58 microg/L;
GH
1.8+/-1.1 microg/L) under somatostatin analogue octreotide (n=5), dopamine agonists (n=2), and
the GH
receptor antagonist pegvisomant (n=2;
GH
levels were not determined in this subgroup) and 9 were cured IGF-1 (148+/-57 microg/L;
GH
0.5+/-0.2 microg/L).
FRS was related to the CAC score (p=0.008, r (2)=0.22) and
the disease
duration (p=0.002, r (2)=0.29).
The CAC score correlated with LVMI (p=0.02, r (2)=0.17),
the disease
duration of
acromegaly
(p=0.004, r (2)=0.36), and the FRS (p=0.008, r (2)=0.22).
Patients with a high CAC score had a longer
disease
duration of 9.6+/-4.7 versus 5.4+/-2.8 years with CAC<75 (th) percentile (p=0.02).
In summary,
the disease
duration and consequently the accompanying metabolic disorders appear to influence the degree of CAC in patients with
acromegaly
.
The observations underline the importance of early and sufficient treatment of
acromegaly
in high risk patients.
[MeSH-major]
Acromegaly
/ complications. Calcinosis / complications. Cardiomyopathies / complications. Coronary
Disease
/ etiology
[MeSH-minor]
Adenoma
/ radiography.
Adenoma
/ surgery. Adult. Aged. Female. Human
Growth Hormone
/ blood. Humans. Insulin-Like
Growth
Factor I / metabolism. Luminescent Measurements. Male. Middle Aged.
Pituitary
Neoplasms / radiography.
Pituitary
Neoplasms / surgery. Prospective Studies. Radiosurgery. Risk Factors. Time Factors
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[Copyright]
J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart.New York.
(PMID = 19373755.001).
[ISSN]
1439-3646
[Journal-full-title]
Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
[ISO-abbreviation]
Exp. Clin. Endocrinol. Diabetes
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
44.
Almeida JP, Albuquerque LA, Ferraz CL, Mota I, Gondim J, Ferraz TM:
McCune-Albright syndrome and acromegaly: hormonal control with use of cabergoline and long-acting somatostatin--case report.
Arq Bras Endocrinol Metabol
; 2009 Feb;53(1):102-6
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[Title]
McCune-Albright syndrome and
acromegaly
: hormonal control with use of cabergoline and long-acting somatostatin--case report.
OBJECTIVES: The use of drug therapy based on cabergoline, octreotide and long-acting release (LAR) octreotide has presented varying results in the treatment
of GH
excessive production in patients with McCune-Albright Syndrome.
METHODS: We report the case of a 29 year-old female patient presenting McCune-Albright Syndrome and complaint of excessive bone
growth
.
RESULTS: The patient presented a
pituitary adenoma
involving the right internal carotid artery and excessive secretion
of growth hormone
(no
GH
suppression was observed after the oral glucose tolerance test).
At the one year follow-up,
GH
and IGF-1 levels were normal and no adverse effects were present.
CONCLUSION: The use of drug therapy based on the association of cabergoline and octreotide is safe and able to achieve complete hormonal control in the treatment of
acromegaly
for McCune-Albright patients.
[MeSH-major]
Acromegaly
/ drug therapy. Ergolines / therapeutic use. Facial Bones / drug effects. Fibrous Dysplasia, Polyostotic / drug therapy. Octreotide / therapeutic use
[MeSH-minor]
Adenoma
/ complications. Adult. Antineoplastic Agents, Hormonal / therapeutic use. Female. Human
Growth Hormone
/ analysis. Human
Growth Hormone
/ secretion. Humans. Insulin-Like
Growth
Factor I / analysis.
Pituitary
Neoplasms / complications. Skull / drug effects
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(PMID = 19347192.001).
[ISSN]
1677-9487
[Journal-full-title]
Arquivos brasileiros de endocrinologia e metabologia
[ISO-abbreviation]
Arq Bras Endocrinol Metabol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Brazil
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / Ergolines; 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide
45.
Yamazaki M, Sato A, Nishio S, Takeda T, Miyamoto T, Katai M, Hashizume K:
Acromegaly accompanied by Turner syndrome with 47,XXX/45,X/46,XX mosaicism.
Intern Med
; 2009;48(6):447-53
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[Title]
Acromegaly
accompanied by Turner syndrome with 47,XXX/45,X/46,XX mosaicism.
A
pituitary adenoma
with elevated serum levels
of growth hormone
(
GH
) and insulin-like
growth
factor-I (IGF-I) was detected, indicating
acromegaly
caused by
GH
-
secreting
pituitary adenoma
.
Transsphenoidal resection of the tumor decreased serum
GH
and IGF-I levels, but the edema was not improved.
This case may indicate the important relationships between
GH
/IGF-I and Turner syndrome.
[MeSH-major]
Acromegaly
/ genetics. Chromosomes, Human, X / genetics. Mosaicism. Turner Syndrome / genetics
[MeSH-minor]
Adenoma
/ blood.
Adenoma
/ complications.
Adenoma
/
diagnosis
. Adult.
Diagnosis
, Differential. Female.
Growth Hormone
/ blood. Humans. In Situ Hybridization, Fluorescence. Magnetic Resonance Imaging.
Pituitary
Neoplasms / blood.
Pituitary
Neoplasms / complications.
Pituitary
Neoplasms /
diagnosis
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(PMID = 19293545.001).
[ISSN]
1349-7235
[Journal-full-title]
Internal medicine (Tokyo, Japan)
[ISO-abbreviation]
Intern. Med.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
9002-72-6 / Growth Hormone
46.
Theodoropoulou M, Labeur M, Paez Pereda M, Haedo M, Perone MJ, Renner U, Arzt E, Stalla GK:
Novel medical therapies for pituitary tumors.
Front Horm Res
; 2010;38:158-64
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[Title]
Novel medical therapies for
pituitary
tumors.
Despite considerable progress, there is still no medical treatment available for some kinds of
pituitary
tumors, in particular
hormone
inactive
adenomas
and corticotroph
pituitary
tumors.
Moreover, treatment resistance is present in a considerable proportion of patients bearing
pituitary
tumors, for which medical treatment regimens are already available (prolactinomas,
somatotroph adenomas
).
Here, we summarize preclinical and clinical findings about
the hormone
and
growth
-suppressive action of various drugs, which will probably lead to novel future medical treatment concepts for
pituitary
tumors.
[MeSH-major]
Pituitary
Neoplasms / drug therapy
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.
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DOPAMINE
.
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[Copyright]
Copyright (c) 2010 S. Karger AG, Basel.
(PMID = 20616507.001).
[ISSN]
0301-3073
[Journal-full-title]
Frontiers of hormone research
[ISO-abbreviation]
Front Horm Res
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / BIM 23A760; 0 / Dopamine Agonists; 51110-01-1 / Somatostatin; 5688UTC01R / Tretinoin; 82115-62-6 / Interferon-gamma; 98H1T17066 / pasireotide; VTD58H1Z2X / Dopamine
[Number-of-references]
32
47.
Drutel A, Caron P, Archambeaud F:
[New medical treatments in pituitary adenomas].
Ann Endocrinol (Paris)
; 2008 Sep;69 Suppl 1:S16-28
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[Title]
[New medical treatments in
pituitary
adenomas
].
Currently, the role of dopaminergic and somatostatinergic agonists in the treatment of
pituitary
adenomas
is quite well established.
Nevertheless, a clearer understanding of the expression of dopaminergic and somatostatinergic receptors at the cellular level of
pituitary
adenomas
as well as the development of newer analogues compounds may drastically change current therapeutic modalities.
In the midst
of GH
-
secreting
pituitary
adenomas
, a positive correlation exists between the expression of Sst2 mRNA and the inhibition
of GH
release by somatostatin analogues.
The involvement of Sst5 subtype in
adenomas
resistant to preferential Sst2 agonists has recently been proved.
SOM-230 could therefore allow for much more effective methods in treating patients suffering from
acromegaly
.
Besides, the use of a chimeric molecule presenting a binding affinity to both Sst2 and D2 subtypes (BIM-23A287) inhibits the secretion
of GH
in ways similar to the Sst2 or D2 agonists used alone or concurrently but however in a concentration 50 times lower than that of the latter.
The discovery of Sst5 and D2 subtypes at the level of corticotropic
adenomas
reveals newer therapeutic perspectives with promising preliminary results with the use of SOM-230 ; these
finding
lead to a rise in interest in cabergoline.
In the midst of non-functioning
pituitary
adenomas
, the expression of Sst2, Sst3 and D2 receptors will perhaps allow the use of combined therapies associating the new somatostatin analogues to the dopaminergic agonists or even use dopastatin (BIM-23A760, chimeric molecule Sst2-Sst5-D2).
Nevertheless, it seems that
adenomas
resistant to dopaminergic agonist due to a lack of expression of D2 receptor fail to express Sst5 receptors as well.
On the other hand, dopastatin appears to be more efficient than cabergoline in the management of this type
of adenomas
.
Therefore, the growing awareness concerning the mechanisms involved in the control of
pituitary
secretions as well as cellular proliferation will perhaps allow physicians to treat the pathology of
pituitary
adenomas
, macroadenomas in particular, using solely pharmacological means instead of invasive surgical procedures and/or radiotherapy.
[MeSH-major]
Adenoma
/ drug therapy.
Pituitary
Neoplasms / drug therapy
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(PMID = 18954854.001).
[ISSN]
0003-4266
[Journal-full-title]
Annales d'endocrinologie
[ISO-abbreviation]
Ann. Endocrinol. (Paris)
[Language]
fre
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
France
[Chemical-registry-number]
0 / Dopamine Agonists; 0 / Peptides, Cyclic; 0 / Receptors, Dopamine; 0 / Receptors, Somatostatin; 118992-92-0 / lanreotide; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
[Number-of-references]
49
48.
Pisarek H, Pawlikowski M, Kunert-Radek J, Winczyk K:
Does the response of GH-secreting pituitary adenomas to octreotide depend on the cellular localization of the somatostatin receptor subtypes SSTR2 and SSTR5?
Endokrynol Pol
; 2010 Mar-Apr;61(2):178-81
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[Title]
Does the response
of GH
-
secreting
pituitary
adenomas
to octreotide depend on the cellular localization of the somatostatin receptor subtypes SSTR2 and SSTR5?
INTRODUCTION: The immunohistochemical examination of somatostatin receptor (SSTR) subtypes expression in different endocrine tumours, including
pituitary
adenomas
, revealed membranous or cytoplasmic distribution of SSTR1-5.
In an earlier study a positive correlation between the summarized score of SSTR2A + SSTR2B expressions and
growth hormone
(
GH
) response to octreotide administration was found, independently of receptor distribution within
the cell
.
In this study we searched for the relationship between
the GH
inhibitory response to acute octreotide administration and SSTR2A, SSTR2B, and SSTR5 cellular localization.
The drop in
GH
was defined as the percentage of the basal value.
The
pituitary
adenomas
from these patients were immunostained to determine the hormonal phenotype and expression of SSTR subtypes.
The drop in
GH
after octreotide administration varied between 57.1-96.7% (mean 82.1%).
Among the patients with the cytoplasmic localization of SSTR5, the decrease in
GH
was significantly higher (92.0 +/- 7.0%).
CONCLUSIONS: It seems that cytoplasmic localization of SSTR5, SSTR2A, and SSTR2B is connected with enhanced
GH
inhibition after octreotide administration.
As a consequence, the SSTR-immunopositivity in
cell
cytoplasm is increased.
[MeSH-major]
Adenoma
/ drug therapy.
Adenoma
/ pathology. Octreotide / pharmacology.
Pituitary
Neoplasms / drug therapy.
Pituitary
Neoplasms / pathology. Receptors, Somatostatin / analysis
[MeSH-minor]
Adult. Aged. Antineoplastic Agents, Hormonal / pharmacology. Chemotherapy, Adjuvant. Cytoplasm / pathology. Female.
Growth Hormone
/ secretion. Humans. Immunohistochemistry. Male. Middle Aged. Tissue Distribution
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(PMID = 20464704.001).
[ISSN]
0423-104X
[Journal-full-title]
Endokrynologia Polska
[ISO-abbreviation]
Endokrynol Pol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Poland
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 9002-72-6 / Growth Hormone; RWM8CCW8GP / Octreotide
49.
Petersenn S, Buchfelder M, Reincke M, Strasburger CM, Franz H, Lohmann R, Quabbe HJ, Plöckinger U, Participants of the German Acromegaly Register:
Results of surgical and somatostatin analog therapies and their combination in acromegaly: a retrospective analysis of the German Acromegaly Register.
Eur J Endocrinol
; 2008 Nov;159(5):525-32
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[Title]
Results of surgical and somatostatin analog therapies and their combination in
acromegaly
: a retrospective analysis of the German
Acromegaly
Register.
BACKGROUND: Data on surgical and medical treatment outcomes in
acromegaly
mostly originate from specialized centers.
We retrospectively analyzed the data on surgery, primary somatostatin analog (SSA) therapy, surgery preceded by SSA, and SSA preceded by surgery in 1485 patients from the German
Acromegaly
Register.
GH
and IGF1 normalized in 54.3 and 67.2%.
Partial or total
pituitary
insufficiency occurred in 28.6% initially and 41.2% post-surgery.
GH
and IGF1 normalized in 36.3 and 30.5%, increasing to 40.8 and 41.5% with longer SSA (>or=360 days) in 54 patients.
Pituitary
function did not change.
Post-surgery
GH
and IGF1 was normalized in 62.9 and 68.4%.
GH
improvement was slightly, but significantly better after SSA pretreatment.
GH
and IGF1 normalized during SSA in 24.1 and 45.5%.
Relative
GH
decrease was significantly larger compared with primary SSA.
CONCLUSIONS:
Pituitary
surgery was more effective to lower
GH
and IGF1 concentrations than primary SSA.
Debulking surgery may result in better final outcome in patients with a high
GH
concentration and a large tumor.
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(PMID = 18755874.001).
[ISSN]
1479-683X
[Journal-full-title]
European journal of endocrinology
[ISO-abbreviation]
Eur. J. Endocrinol.
[Language]
ENG
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; RWM8CCW8GP / Octreotide
[Investigator]
Allolio B; Badenhoop K; Bender G; Biering H; Blossey HC; Blum H; Bogner U; Brabant G; Buchfelder M; Caspar-Bell G; Demtröder F; Diederich S; Droste M; Engelbach M; Faust M; Finke R; Fölsch UR; Gain T; Gräf KJ; Gerbert B; Grussendorf M; Hampel R; Happ J; Heckmann C; Hehrmann R; Heike M; Herrmann BL; Höffken K; Hüfner M; Jacobeit J; Jaursch-Hancke C; Jockenhövel F; Knippert A; Koch C; Kornely E; Krone W; Lehnert H; Levasseur S; Lössner C; Mann K; Matern S; Meuser J; Meyer A; Minnemann T; Mönig Hl; Müller OA; Paschke R; Petersenn S; Pfeiffer A; Plöckinger U; Raue F; Reincke M; Reschke K; Rudorff KH; Rühle H; Santen R; Schöfl C; Schopohl J; Schories M; Schröder F; Schröder HE; Schröder U; Schulte HM; Stamm B; Steinmetz M; Strasburger CJ; Sturmvoll M; Tharandt L; Tuschy U; von Werder K; Weber MM; Wiedenmann B; Wiesner TD; Würl K; Zeuzem S
50.
Taslipinar A, Bolu E, Kebapcilar L, Sahin M, Uckaya G, Kutlu M:
Insulin-like growth factor-1 is essential to the increased mortality caused by excess growth hormone: a case of thyroid cancer and non-Hodgkin's lymphoma in a patient with pituitary acromegaly.
Med Oncol
; 2009;26(1):62-6
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[Title]
Insulin-like
growth
factor-1 is essential to the increased mortality caused by excess
growth hormone
: a case of thyroid cancer and non-Hodgkin's lymphoma in a patient with
pituitary acromegaly
.
The effects
of growth hormone
are mediated in part by stimulating the production of insulin-like
growth
factor-1.
Insulin-like
growth
factor-1 has significant effects on
cell
proliferation and differentiation, it is a potent mitogen, and it is a powerful inhibitor of programmed
cell
death (apoptosis).
Insulin-like
growth
factor-1 also has a well-established role in the transformation of normal cells to malignant cells.
Case reports on a possible association between elevated
growth hormone
and cancer risk in a variety of patient groups have been published.
Here, we describe clinical and laboratory findings for a patient with
acromegaly
who first developed thyroid cancer, and then, in the follow up period, probably due to poorly controlled insulin-like
growth
factor-1 levels, developed a large
cell
non-Hodgkin's lymphoma.
[MeSH-major]
Acromegaly
.
Adenoma
/ metabolism. Insulin-Like
Growth
Factor I / metabolism. Lymphoma, Non-Hodgkin / metabolism. Neoplasms, Multiple Primary. Thyroid Neoplasms / metabolism
[MeSH-minor]
Aged. Antineoplastic Agents, Hormonal / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Ergolines / therapeutic use. Human
Growth Hormone
/ analogs & derivatives. Human
Growth Hormone
/ secretion. Human
Growth Hormone
/ therapeutic use. Humans. Male. Octreotide / therapeutic use. Prednisone / therapeutic use. Thyroidectomy. Thyroxine / therapeutic use. Vincristine / therapeutic use
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[Cites]
Cancer Res. 1996 Feb 1;56(3):523-6
[
8564965.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Oct;83(10):3419-26
[
9768641.001
]
[Cites]
J Endocrinol Invest. 2007 Sep;30(8):693-9
[
17923803.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Sep;85(9):3218-21
[
10999811.001
]
[Cites]
Clin Endocrinol (Oxf). 1994 Jul;41(1):95-102
[
8050136.001
]
[Cites]
Endocr Pract. 2004 May-Jun;10(3):213-25
[
15382339.001
]
[Cites]
Endocr Pract. 1998 Sep-Oct;4(5):279-81
[
15251725.001
]
[Cites]
Yale J Biol Med. 2006 Dec;79(3-4):105-14
[
17940620.001
]
[Cites]
Thyroid. 1999 Aug;9(8):791-6
[
10482372.001
]
[Cites]
Arch Intern Med. 1991 Aug;151(8):1629-32
[
1678593.001
]
[Cites]
Baillieres Clin Endocrinol Metab. 1995 Apr;9(2):271-314
[
7625986.001
]
[Cites]
Endocr Res. 2005;31(1):51-8
[
16238191.001
]
[Cites]
Acta Med Scand. 1988;223(4):327-35
[
3369313.001
]
[Cites]
Horm Metab Res. 1999 Feb-Mar;31(2-3):80-9
[
10226786.001
]
[Cites]
Mol Cell Endocrinol. 2005 Jun 30;238(1-2):1-7
[
15939533.001
]
[Cites]
J Clin Endocrinol Metab. 1991 Feb;72(2):245-9
[
1991795.001
]
[Cites]
J Clin Endocrinol Metab. 1989 Mar;68(3):621-6
[
2537339.001
]
[Cites]
Lancet. 2004 Apr 24;363(9418):1336-7
[
15110485.001
]
[Cites]
Horm Metab Res. 2000 May;32(5):190-5
[
10871160.001
]
[Cites]
Eur J Cancer. 1992;28A(11):1904-9
[
1382501.001
]
[Cites]
Clin Endocrinol (Oxf). 2003 Jan;58(1):86-91
[
12519417.001
]
[Cites]
Rev Endocr Metab Disord. 2008 Mar;9(1):41-58
[
18157698.001
]
[Cites]
Endocr J. 2008 Mar;55(1):67-71
[
18202526.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Feb;89(2):667-74
[
14764779.001
]
[Cites]
J Endocrinol Invest. 1993 Mar;16(3):181-7
[
8514973.001
]
[Cites]
Nature. 1987 Dec 10-16;330(6148):537-43
[
2825030.001
]
[Cites]
J Endocrinol Invest. 2002 Mar;25(3):240-5
[
11936466.001
]
[Cites]
J Clin Endocrinol Metab. 1988 Jun;66(6):1158-65
[
2836470.001
]
[Cites]
Int J Impot Res. 2003 Aug;15 Suppl 4:S3-8
[
12934044.001
]
[Cites]
Clin Endocrinol (Oxf). 2005 Aug;63(2):161-7
[
16060909.001
]
[Cites]
Q J Med. 1970 Jan;39(153):1-16
[
5427331.001
]
[Cites]
Eur J Endocrinol. 2005 Apr;152(4):569-74
[
15817912.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Jul;86(7):2935-41
[
11443146.001
]
[Cites]
Pituitary. 1999;1(2):115-20
[
11081189.001
]
[Cites]
J Clin Endocrinol Metab. 1996 Mar;81(3):1278-82
[
8772612.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Aug;83(8):2730-4
[
9709939.001
]
[Cites]
Rev Endocr Metab Disord. 2008 Mar;9(1):13-9
[
18236162.001
]
(PMID = 18663612.001).
[ISSN]
1357-0560
[Journal-full-title]
Medical oncology (Northwood, London, England)
[ISO-abbreviation]
Med. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / Ergolines; 12629-01-5 / Human Growth Hormone; 5J49Q6B70F / Vincristine; 67763-96-6 / Insulin-Like Growth Factor I; 8N3DW7272P / Cyclophosphamide; LL60K9J05T / cabergoline; N824AOU5XV / pegvisomant; Q51BO43MG4 / Thyroxine; RWM8CCW8GP / Octreotide; VB0R961HZT / Prednisone; COP protocol 2
51.
Zatelli MC, Piccin D, Tagliati F, Bottoni A, Ambrosio MR, Margutti A, Scanarini M, Bondanelli M, Culler MD, degli Uberti EC:
Dopamine receptor subtype 2 and somatostatin receptor subtype 5 expression influences somatostatin analogs effects on human somatotroph pituitary adenomas in vitro.
J Mol Endocrinol
; 2005 Oct;35(2):333-41
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[Title]
Dopamine receptor subtype 2 and somatostatin receptor subtype 5 expression influences somatostatin analogs effects on human
somatotroph
pituitary
adenomas
in vitro.
Dopamine (DA) and somatostatin (SRIF) receptor agonists inhibit
growth hormone
(
GH
) secretion by
pituitary
adenomas
.
We investigated DA subtype 2 receptor (DR2) and SRIF receptor (sst) subtypes 2 and 5 expression in 25
GH
-
secreting
pituitary
adenomas
and tested in primary culture the effects on
GH
and prolactin (PRL) secretion of sst agonists selectively interacting with sst2 (BIM-23120), sst5 (BIM-23206), and sst2 and sst5 (BIM-23244).
All
adenomas
expressed sst2; eight
adenomas
expressed both sst5 and DR2, eight sst5 but not DR2, and eight DR2 but not sst5.
GH
secretion was inhibited by BIM-23120 in all samples, while it was reduced by BIM-23206 only in
adenomas
not expressing DR2.
BIM-23120's inhibitory effects correlated with sst2 and DR2 expression, whereas DR2 expression correlated inversely with BIM-23206 inhibitory effects on
GH
secretion.
In seven mixed
GH
-/PRL-
secreting
pituitary
adenomas
, PRL secretion was inhibited in sst5-expressing tumors by BIM-23206, but not by BIM-23120.
BIM-23244 reduced PRL secretion only in
adenomas
expressing sst2, sst5 and DR2. sst5 and DR2 expression correlated directly with BIM23206 inhibitory effects on PRL secretion.
Our results suggest that
adenomas
expressing DR2 are less likely to respond to clinically available SRIF analogs in terms
of GH
secretion inhibition.
Therefore, drugs interacting also with DR2 might better control secretion of
pituitary
adenomas
.
[MeSH-major]
Growth Hormone
-
Secreting
Pituitary Adenoma
/ metabolism. Protein Isoforms / metabolism. Receptors, Dopamine / metabolism. Receptors, Somatostatin / metabolism. Somatostatin / analogs & derivatives
[MeSH-minor]
Acromegaly
/ metabolism. Adult. Aged, 80 and over. Dopamine Agonists. Female. Human
Growth Hormone
/ secretion. Humans. Male. Middle Aged. Prolactin / secretion. RNA, Messenger / metabolism
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(PMID = 16216913.001).
[ISSN]
0952-5041
[Journal-full-title]
Journal of molecular endocrinology
[ISO-abbreviation]
J. Mol. Endocrinol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Dopamine Agonists; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Dopamine; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 9002-62-4 / Prolactin
52.
Mai PL, Korde L, Kramer J, Peters J, Mueller CM, Pfeiffer S, Stratakis CA, Pinto PA, Bratslavsky G, Merino M, Choyke P, Linehan WM, Greene MH:
A possible new syndrome with growth-hormone secreting pituitary adenoma, colonic polyposis, lipomatosis, lentigines and renal carcinoma in association with familial testicular germ cell malignancy: A case report.
J Med Case Rep
; 2007 Mar 28;1:9
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[Title]
A possible new syndrome with
growth
-
hormone secreting
pituitary adenoma
, colonic polyposis, lipomatosis, lentigines and renal carcinoma in association with familial testicular germ
cell
malignancy: A case report.
BACKGROUND: Germ-
cell
testicular cancer has not been definitively linked to any known hereditary cancer susceptibility
disorder
.
His evaluation as part of an etiologic study of familial testicular cancer revealed multiple colon polyps (adenomatous, hyperplastic, and hamartomatous) first found in his 50 s, multiple lipomas, multiple hyperpigmented skin lesions, left kidney cancer diagnosed at age 64, and a
growth
-
hormone producing
pituitary adenoma
with associated
acromegaly
diagnosed at age 64.
Alternatively, this family's phenotype might represent a novel neoplasm susceptibility
disorder
.
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[Cites]
Br J Neurosurg. 2004 Dec;18(6):629-31
[
15799199.001
]
[Cites]
Horm Res. 2004;62 Suppl 1:108-15
[
15761242.001
]
[Cites]
Am J Gastroenterol. 2005 Feb;100(2):476-90
[
15667510.001
]
[Cites]
Dig Dis Sci. 2004 Apr;49(4):662-6
[
15185875.001
]
[Cites]
Lancet Oncol. 2004 Jun;5(6):363-71
[
15172357.001
]
[Cites]
Cancer. 2003 Feb 15;97(4):984-92
[
12569597.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Dec;86(12):5658-71
[
11739416.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Sep;86(9):4041-6
[
11549623.001
]
[Cites]
J Neurosurg. 2000 Mar;92(3):413-8
[
10701527.001
]
[Cites]
J Natl Cancer Inst. 2005 Sep 21;97(18):1354-65
[
16174857.001
]
[Cites]
Science. 2006 May 26;312(5777):1228-30
[
16728643.001
]
[Cites]
Hum Mol Genet. 2006 Feb 1;15(3):443-51
[
16407372.001
]
(PMID = 17411461.001).
[Journal-full-title]
Journal of medical case reports
[ISO-abbreviation]
J Med Case Rep
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CP / N02CP11019
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC1847830
53.
Korbonits M, Carlsen E:
Recent clinical and pathophysiological advances in non-functioning pituitary adenomas.
Horm Res
; 2009 Apr;71 Suppl 2:123-30
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[Title]
Recent clinical and pathophysiological advances in non-functioning
pituitary
adenomas
.
Pituitary
adenomas
are being recognized and diagnosed with increasing frequency.
One of the most common forms of
pituitary
lesion is the clinically non-functioning
pituitary adenoma
(NFPA), which is often diagnosed incidentally.
The vast majority of
pituitary
adenomas
are sporadic, but familial
adenomas
can occur in the multiple
pituitary adenoma
type 1 syndrome, in Carney complex or in familial isolated
pituitary adenoma
.
NFPA often show
hormone
synthesis on tissue immunostaining without causing clinical symptoms.
Most often these are silent gonadotroph
adenomas
, with silent corticotroph or
somatotroph adenomas
occurring less frequently.
It is unclear why these silent
adenomas do
not release hormones at a clinically recognizable level, although it is probable that there is a continuum between fully functional and completely silent
adenomas
.
Temozolomide has been successfully used for the treatment of a few aggressive
pituitary
adenomas
, and the response to this drug could be influenced by the expression of the DNA repair enzyme O-6-methylguanine DNA methyltransferase.
The early
diagnosis
, prediction of long-term outcome and treatment of NFPAs remain a challenge for endocrinologists.
[MeSH-major]
Growth Hormone
-
Secreting
Pituitary Adenoma
. Prolactinoma
[MeSH-minor]
ACTH-
Secreting
Pituitary Adenoma
/
diagnosis
. ACTH-
Secreting
Pituitary Adenoma
/ metabolism. ACTH-
Secreting
Pituitary Adenoma
/ pathology. ACTH-
Secreting
Pituitary Adenoma
/ therapy. Female. Humans. Male
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[Copyright]
Copyright 2009 S. Karger AG, Basel.
(PMID = 19407508.001).
[ISSN]
1423-0046
[Journal-full-title]
Hormone research
[ISO-abbreviation]
Horm. Res.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Switzerland
[Number-of-references]
58
54.
Hofstetter CP, Mannaa RH, Mubita L, Anand VK, Kennedy JW, Dehdashti AR, Schwartz TH:
Endoscopic endonasal transsphenoidal surgery for growth hormone-secreting pituitary adenomas.
Neurosurg Focus
; 2010 Oct;29(4):E6
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[Title]
Endoscopic endonasal transsphenoidal surgery for
growth hormone
-
secreting
pituitary
adenomas
.
OBJECT: The aim of this study was to determine the preoperative predictors of the extent of resection and endocrinological remission following endonasal endoscopic removal
of growth hormone
(
GH
)-
secreting
pituitary
adenomas
.
Endocrinological remission was defined as normal insulin-like
growth
factor I (IGFI) serum levels and either a nadir
GH
level of < 0.4 ng/ml after an oral glucose load or a basal
GH
serum level < 1 ng/ml.
A smaller tumor volume and a postoperative reduction in
GH
serum levels were associated with a higher rate of biochemical cure (p < 0.05).
During a 23-month follow-up period 5 patients (21%) underwent Gamma Knife treatment of any residual
disease
to further reduce excess
GH
production.
CONCLUSIONS: A purely endoscopic endonasal transsphenoidal
adenoma
resection leads to a high rate of gross-total tumor resection and endocrinological remission in acromegalic patients, even those harboring macroadenomas with wide suprasellar extension.
[MeSH-major]
Acromegaly
/ surgery.
Adenoma
/ surgery.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ surgery. Human
Growth Hormone
/ secretion. Neurosurgical Procedures / methods.
Pituitary
Neoplasms / surgery
[MeSH-minor]
Adult. Aged. Endoscopy. Female. Humans. Insulin-Like
Growth
Factor I / analysis. Male. Middle Aged. Minimally Invasive Surgical Procedures / methods. Postoperative Period. Preoperative Period. Remission Induction. Sphenoid Bone. Treatment Outcome. Tumor Burden
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(PMID = 20887131.001).
[ISSN]
1092-0684
[Journal-full-title]
Neurosurgical focus
[ISO-abbreviation]
Neurosurg Focus
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
55.
Ronchi CL, Ferrante E, Rizzo E, Giavoli C, Verrua E, Bergamaschi S, Lania AG, Beck-Peccoz P, Spada A:
Long-term basal and dynamic evaluation of hypothalamic-pituitary-adrenal (HPA) axis in acromegalic patients.
Clin Endocrinol (Oxf)
; 2008 Oct;69(4):608-12
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[Title]
Long-term basal and dynamic evaluation of hypothalamic-
pituitary
-adrenal (HPA) axis in acromegalic patients.
OBJECTIVE: Long-term effects of trans-naso-sphenoidal surgery (TNS) or long-acting somatostatin analogs (SSA) on the function of hypothalamic-
pituitary
-adrenal (HPA) axis have been poorly investigated.
Aim of this study was to evaluate HPA axis integrity during the follow-up in patients with
GH
-
secreting
pituitary
adenomas
and preserved HPA function post-TNS or prior SSA.
No significant correlations between HPA axis deterioration and follow-up duration, serum
GH
/IGF-I levels, occurrence of other
pituitary
deficiencies, presence of secondary empty sella, changes in tumour or residual volume were observed.
[MeSH-major]
Acromegaly
/ physiopathology. Hypothalamo-Hypophyseal System / physiology.
Pituitary
-Adrenal System / physiology
[MeSH-minor]
Adenoma
/ drug therapy.
Adenoma
/ metabolism.
Adenoma
/ physiopathology. Adrenocorticotropic
Hormone
/ blood. Adrenocorticotropic
Hormone
/ metabolism. Adult. Aged. Basal Metabolism / physiology. Delayed-Action Preparations.
Disease
Progression. Female. Follow-Up Studies. Humans. Hydrocortisone / blood. Hydrocortisone / metabolism. Male. Middle Aged.
Pituitary
Neoplasms / drug therapy.
Pituitary
Neoplasms / metabolism.
Pituitary
Neoplasms / physiopathology. Retrospective Studies. Somatostatin / administration & dosage. Somatostatin / analogs & derivatives. Time Factors
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(PMID = 18410544.001).
[ISSN]
1365-2265
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Delayed-Action Preparations; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
56.
Müssig K, Gallwitz B, Honegger J, Strasburger CJ, Bidlingmaier M, Machicao F, Bornemann A, Ranke MB, Häring HU, Petersenn S:
Pegvisomant treatment in gigantism caused by a growth hormone-secreting giant pituitary adenoma.
Exp Clin Endocrinol Diabetes
; 2007 Mar;115(3):198-202
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[Title]
Pegvisomant treatment in gigantism caused by a
growth hormone
-
secreting
giant
pituitary adenoma
.
BACKGROUND: Gigantism is rare with the majority of cases caused by a
growth hormone
(
GH
)-
secreting
pituitary adenoma
.
Treatment options for
GH
-
secreting
pituitary
adenomas
have been widened with the availability of long-acting dopamine agonists, depot preparations of somatostatin analogues, and recently
the GH
receptor antagonist pegvisomant.
CASE REPORT: A 23-year-old male patient presented with continuous increase in height during the past 6 years due to a
GH
-
secreting
giant
pituitary adenoma
.
At immunohistochemistry, the tumour showed a marked expression
of GH
and a sparsely focal expression of prolactin.
Conversion from somatostatin analogue to pegvisomant normalized insulin-like-
growth
-factor-I (IGF-I) levels and markedly improved glucose tolerance.
CONCLUSION: Pegvisomant is a potent treatment option in patients with
pituitary
gigantism.
[MeSH-major]
Adenoma
/ secretion.
Adenoma
/ surgery. Gigantism / drug therapy. Gigantism / etiology. Human
Growth Hormone
/ analogs & derivatives. Human
Growth Hormone
/ secretion.
Pituitary
Neoplasms / secretion.
Pituitary
Neoplasms / surgery
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(PMID = 17427111.001).
[ISSN]
0947-7349
[Journal-full-title]
Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
[ISO-abbreviation]
Exp. Clin. Endocrinol. Diabetes
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / pegvisomant; 12629-01-5 / Human Growth Hormone
57.
Kajiwara K, Saito K, Yoshikawa K, Kato S, Akimura T, Nomura S, Ishihara H, Suzuki M:
Image-guided stereotactic radiosurgery with the CyberKnife for pituitary adenomas.
Minim Invasive Neurosurg
; 2005 Apr;48(2):91-6
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[Title]
Image-guided stereotactic radiosurgery with the CyberKnife for
pituitary
adenomas
.
Twenty-one patients with
pituitary
adenomas
received image-guided stereotactic radiosurgery with the CyberKnife, and were followed up for more than 18 months.
The patients consisted of 14 with non-functioning
adenomas
, 3 with prolactinomas, 2 with
acromegaly
, and 2 with ACTH-
producing
tumors.
The mean volumes of the non-functioning and functioning
adenomas
were 13.3 cm (3) and 7.5 cm (3), respectively.
The marginal irradiation dose ranged from 6.4 Gy to 27.7 Gy (mean: non-functioning
adenomas
12.6 Gy, functioning
adenomas
17.5 Gy), as a dose of a single fraction.
Hormonal function improved in all of the 7 functioning
adenomas
.
The hormone
level normalized in 1 prolactinoma, and decreased to less than normal in 1 ACTH-
producing
adenoma
.
Image-guided stereotactic radiosurgery with the CyberKnife is effective and safe against relatively large
pituitary
adenomas
.
[MeSH-major]
Adenoma
/ surgery.
Pituitary
Neoplasms / surgery. Radiosurgery / instrumentation. Surgery, Computer-Assisted / instrumentation
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(PMID = 15906203.001).
[ISSN]
0946-7211
[Journal-full-title]
Minimally invasive neurosurgery : MIN
[ISO-abbreviation]
Minim Invasive Neurosurg
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
58.
Losa M, Gioia L, Picozzi P, Franzin A, Valle M, Giovanelli M, Mortini P:
The role of stereotactic radiotherapy in patients with growth hormone-secreting pituitary adenoma.
J Clin Endocrinol Metab
; 2008 Jul;93(7):2546-52
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[Title]
The role of stereotactic radiotherapy in patients with
growth hormone
-
secreting
pituitary adenoma
.
CONTEXT: Single-session stereotactic radiotherapy (SR) may be a potential adjuvant treatment in
acromegaly
.
INTERVENTION: The patients were treated with SR for residual or recurrent
GH
-
secreting
adenoma
.
MAIN OUTCOME MEASURE: Normalization of age- and sex-adjusted IGF-I levels together with a basal
GH
level below 2.5 microg/liter without concomitant
GH
-suppressive drugs was the goal of therapy.
Multivariate analysis showed that low basal
GH
and IGF-I levels were associated with a favorable outcome.
This may lead to reconsider the role of SR in the therapeutic algorithm of
acromegaly
.
[MeSH-major]
Adenoma
/ surgery.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ surgery. Radiosurgery
[MeSH-minor]
Adult. Female. Human
Growth Hormone
/ blood. Humans. Insulin-Like
Growth
Factor I / analysis. Male. Retrospective Studies
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[CommentIn]
Nat Clin Pract Endocrinol Metab. 2008 Nov;4(11):592-3
[
18762791.001
]
(PMID = 18413424.001).
[ISSN]
0021-972X
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
59.
Kontogeorgos G, Mourouti G, Kyrodimou E, Liapi-Avgeri G, Parasi E:
Ganglion cell containing pituitary adenomas: signs of neuronal differentiation in adenoma cells.
Acta Neuropathol
; 2006 Jul;112(1):21-8
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[Title]
Ganglion
cell
containing
pituitary
adenomas
: signs of neuronal differentiation in
adenoma
cells.
Ganglion
cell
containing
pituitary
adenomas
are rare.
Recently accumulated information suggests a common origin for their neuronal and
pituitary
constituents.
The objective of this study was to report the clinical and morphologic findings of
pituitary
gangliocytomas and study their immunoprofile using neuronal markers.
Seven cases of
pituitary
gangliocytomas retrieved from 1,322 sellar lesions were studied.
All tumors were removed from patients with mild
acromegaly
.
Histologically they were biphasic composed of
pituitary adenoma
and clusters of ganglion cells embedded in a variably dense neuropil substrate.
All
adenomas
belonged to the category of sparsely granulated
somatotroph
adenoma
and were positive for
growth hormone
, whereas in five tumors, a few
adenoma
cells were also positive for prolactin.
Interestingly, all tumors contained varying numbers of
adenoma
cells with NFP-positive, dot-like areas of cytoplasmic reactivity, mostly tiny paranuclear, a
finding
not previously reported in human
pituitary
gangliocytomas.
The presence of NFP in
pituitary
adenomas
indicates neuronal differentiation in
adenoma
cells, suggesting a common origin for neuronal and
pituitary adenoma
cell
elements in gangliocytomas.
[MeSH-major]
Adenoma
/ classification.
Adenoma
/ pathology. Ganglioneuroma / classification. Ganglioneuroma / pathology.
Pituitary
Neoplasms / classification.
Pituitary
Neoplasms / pathology
[MeSH-minor]
Acromegaly
/ etiology. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neurofilament Proteins / metabolism. Sella Turcica / pathology
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(PMID = 16699777.001).
[ISSN]
0001-6322
[Journal-full-title]
Acta neuropathologica
[ISO-abbreviation]
Acta Neuropathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Neurofilament Proteins
60.
Swords FM, Monson JP, Besser GM, Chew SL, Drake WM, Grossman AB, Plowman PN:
Gamma knife radiosurgery: a safe and effective salvage treatment for pituitary tumours not controlled despite conventional radiotherapy.
Eur J Endocrinol
; 2009 Dec;161(6):819-28
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[Title]
Gamma knife radiosurgery: a safe and effective salvage treatment for
pituitary
tumours not controlled despite conventional radiotherapy.
OBJECTIVE: We report the use of 'gamma knife' (GK) radiosurgery in 25 patients with
pituitary
adenomas
not cured despite conventional therapy, including external beam radiotherapy.
PATIENTS AND METHODS: All patients had previously received conventional radiotherapy for a mean of 11.8 years prior to receiving GK; 23 out of 25 had also undergone
pituitary
surgery on at least one occasion.
Seventeen had hyperfunctioning
adenomas
that still required medical therapy without an adequate biochemical control--ten
somatotroph adenomas
, six corticotroph
adenomas
and one prolactinoma, while eight patients had non-functioning
pituitary
adenomas
(NFPAs).
RESULTS: Following GK, mean
GH
fell by 49% at 1 year in patients with
somatotroph
tumours.
To date, 80% of the patients with
acromegaly
have achieved normalisation of IGF1, and 30% have also achieved a mean
GH
level of <1.8 ng/ml correlating with normalised mortality.
A total of 75% NFPAs showed
disease
stabilisation or shrinkage post GK.
The results in corticotroph
adenomas
were variable.
Prior to GK, 72% of the patients were panhypopituitary, and 42% of the remainder have developed new anterior
pituitary
hormone
deficiencies to date.
CONCLUSIONS: These data indicate that GK is a safe and effective adjunctive treatment for patients with NFPAs and
acromegaly
not satisfactorily controlled with surgery and radiotherapy.
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(PMID = 19773368.001).
[ISSN]
1479-683X
[Journal-full-title]
European journal of endocrinology
[ISO-abbreviation]
Eur. J. Endocrinol.
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
61.
Buchfelder M, Schlaffer S, Droste M, Mann K, Saller B, Brübach K, Stalla GK, Strasburger CJ, German Pegvisomant Observational Study:
The German ACROSTUDY: past and present.
Eur J Endocrinol
; 2009 Nov;161 Suppl 1:S3-S10
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Pivotal studies have demonstrated that pharmacotherapy with pegvisomant (Somavert) is a highly effective treatment for
acromegaly
.
Treatment efficacy was monitored by IGF1 levels and the patients symptoms were evaluated by completion of a questionnaire (patient-assessed
acromegaly
symptom questionnaire).
In 71.3% of patients with previously not sufficiently treatable
acromegaly
, IGF1 levels were normalized by pegvisomant therapy.
It did not exceed the expected rate in patients with
acromegaly
not treated with pegvisomant.
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(PMID = 19684061.001).
[ISSN]
1479-683X
[Journal-full-title]
European journal of endocrinology
[ISO-abbreviation]
Eur. J. Endocrinol.
[Language]
ENG
[Publication-type]
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers; 0 / Blood Glucose; 0 / Hemoglobin A, Glycosylated; 0 / Hormone Antagonists; 0 / Receptors, Somatotropin; 0 / pegvisomant; 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase
[Investigator]
Droste M; Stalla GK; Allolio B; Faust M; Brendel M; Finke R; Tuchelt H; Bidlingmaier M; Engelbach M; Santen R; Hampel R; Mann K; Kann PH; Boehm B; Kasperk C; Helios CK; Wallaschofski H; Moenig H; Stumvoll M; Schopohl J; Völz B; Würl K; Ittner J; Reschke K; Jacobeit J; Ramadori G; Schindler A; Zeuzem S; Badenhoop K; Beil FU; Pfeiffer AF; Vogel C; Hofbauer LC; Strasburger CJ; Tuschy U; Plöckinger U; Seidlitz B; Demtröder F; Schmiegel; Gellner R; Gräf KJ; Schröder U; Ball P; Ventzke K; Hensen J; Lux H; Etzrodt H; Alexopoulos A; Spitzweg C; Schnabel D; Dost A; Weber MM; Wiemer K; Omran W; Keuser R; Salzgeber K; Gutekunst R; Terkamp C; Gaissmaier S; Eversmann T; Seufert J; Jaursch-Hancke C; Ritter M; Undeutsch C; Jochum E; Mutterhaus der Borromäerinnen S; Schleiffer T; Karges W; Meuser J; Wildbrett J; Krug J; Buchfelder M; Klingmüller D; Schmitz U; Perras B; Zick R; Leicht E; Manfras B; Schuppert F; Müller OA; Stahmer E; Kajdan U; Gallwitz; Rochlitz H; Heckmann C; Haak E; Weber R; Herrmann BL; Schneider S; Scherbaum WA; Deuss U; Jacobs B; Gerbert B; Wolf M; West T; Lippe J; Biering H
62.
Saveanu A, Gunz G, Guillen S, Dufour H, Culler MD, Jaquet P:
Somatostatin and dopamine-somatostatin multiple ligands directed towards somatostatin and dopamine receptors in pituitary adenomas.
Neuroendocrinology
; 2006;83(3-4):258-63
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[Title]
Somatostatin and dopamine-somatostatin multiple ligands directed towards somatostatin and dopamine receptors in
pituitary
adenomas
.
AIM: We report the comparative efficacy of octreotide, cabergoline and multiple ligands directed towards the different somatostatin subtypes (ssts), such as BIM-23A779 and SOM-230, and of chimeric analogs which bind both somatostatin and the dopamine D2 receptors (D2R), such as BIM-23A760 and BIM-23A781, in
cell
cultures from human
growth hormone
(
GH
)-
secreting
pituitary
adenomas
.
PROCEDURES: RT-PCR analysis of the quantitative expression of the different ssts and D2R mRNAs was performed on tumor fragments of 22
GH
-
secreting adenomas
collected after surgery.
Pharmacological studies, using the different ligands, were performed on
cell
cultures of such tumors.
The levels of expression of sst2 and D2R mRNAs were significantly correlated with the maximal
GH
suppression by either octreotide or cabergoline (p < 0.001).
In each tumor tested, 3 patterns of response, in terms
of GH
suppression, were observed.
GH
secretion was preferentially inhibited by the sst2 preferential compound octreotide in 61% of the tumors.
In 19% of the tumors, the maximal inhibition
of GH
release was achieved with the sst5 preferential compound BIM-23268.
The dopamine analog cabergoline was the most effective inhibitor
of GH
secretion in 21% of cases.
Among the compounds tested, the most potent inhibitors
of GH
secretion were the sst2, sst5, D2R chimeric compound BIM-23A760, followed by the sst universal ligand SOM-230.
CONCLUSIONS: The variable patterns of response to sst2, sst5 and dopamine D2 analogs may explain the greater efficacy of drugs which bind to the 3 receptors in suppressing
GH
secretion.
The biological potency (EC50) and efficacy of the chimeric compound BIM-23A760 on
GH
secretion can be partly explained by its high affinity for sst2.
The effect of multiple receptor activation on the functions of other
pituitary
tumor types, such as prolactinomas and corticotropinomas, is not presently analyzed, and the efficacy of multireceptor ligands remains to be elucidated.
[MeSH-major]
Adenoma
/ drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Dopamine / analogs & derivatives.
Pituitary
Neoplasms / drug therapy. Somatostatin / analogs & derivatives
[MeSH-minor]
Adult. Drug Screening Assays, Antitumor. Ergolines / therapeutic use. Female. Human
Growth Hormone
/ drug effects. Human
Growth Hormone
/ metabolism. Humans. Ligands. Male. Octreotide / therapeutic use. RNA, Messenger / analysis. Receptors, Dopamine D2 / drug effects. Receptors, Dopamine D2 / genetics. Receptors, Dopamine D2 / metabolism. Receptors, Somatostatin / classification. Receptors, Somatostatin / drug effects. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism. Recombinant Fusion Proteins / therapeutic use. Tumor Cells, Cultured
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DOPAMINE
.
The Lens.
Cited by Patents in
.
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(PMID = 17047391.001).
[ISSN]
0028-3835
[Journal-full-title]
Neuroendocrinology
[ISO-abbreviation]
Neuroendocrinology
[Language]
eng
[Publication-type]
Clinical Trial; Comparative Study; Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / BIM 23268; 0 / Ergolines; 0 / Ligands; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / Recombinant Fusion Proteins; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide; VTD58H1Z2X / Dopamine
63.
Adamo MA, Drazin D, Popp AJ:
Short-lasting, unilateral neuralgiform headache attacks with conjunctival injection and tearing syndrome treated successfully with transsphenoidal resection of a growth hormone-secreting pituitary adenoma.
J Neurosurg
; 2008 Jul;109(1):123-5
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[Title]
Short-lasting, unilateral neuralgiform headache attacks with conjunctival injection and tearing syndrome treated successfully with transsphenoidal resection of a
growth hormone
-
secreting
pituitary adenoma
.
In this paper the authors present a patient with a
growth hormone
-
secreting
pituitary adenoma
who experienced resolution of SUNCT syndrome after transsphenoidal tumor resection.
[MeSH-major]
Adenoma
/ surgery.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ surgery. SUNCT Syndrome / surgery
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(PMID = 18590441.001).
[ISSN]
0022-3085
[Journal-full-title]
Journal of neurosurgery
[ISO-abbreviation]
J. Neurosurg.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
64.
Acunzo J, Thirion S, Roche C, Saveanu A, Gunz G, Germanetti AL, Couderc B, Cohen R, Figarella-Branger D, Dufour H, Brue T, Enjalbert A, Barlier A:
Somatostatin receptor sst2 decreases cell viability and hormonal hypersecretion and reverses octreotide resistance of human pituitary adenomas.
Cancer Res
; 2008 Dec 15;68(24):10163-70
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[Title]
Somatostatin receptor sst2 decreases
cell
viability and hormonal hypersecretion and reverses octreotide resistance of human
pituitary
adenomas
.
In human
somatotroph adenomas
,
growth hormone
(
GH
) hypersecretion can be inhibited by somatostatin analogues such as octreotide.
Unfortunately, serum
GH
levels reach normal values in only 60% of treated patients.
In this present study, the sst2 gene was transferred by an adenoviral vector (
Ad
-sst2) in human
somatotroph
(n = 7) and lactotroph (n = 2)
adenomas
in vitro.
Ten days after infection at 20 multiplicity of infection (MOI), sst2 gene transfer decreased
cell
viability from 19% to 90% by caspase-dependent apoptosis.
At low viral doses (5 MOI),
Ad
-sst2 decreased
GH
or prolactin (PRL) basal secretion and mRNA expression.
Somatotroph
tumors were classified in three groups according to their octreotide sensitivity.
Four days after infection by 5 MOI
Ad
-sst2, the maximal
GH
suppression by octreotide increased from 31% to 57% in the octreotide partially resistant group and from 0% to 27% in the resistant ones.
In the octreotide-sensitive group, EC(50) values significantly decreased from 1.3 x 10(-11) to 6.6 x 10(-13) mol/L without improving maximal
GH
suppression.
[MeSH-major]
Antineoplastic Agents, Hormonal / pharmacology.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ drug therapy. Human
Growth Hormone
/ secretion. Octreotide / pharmacology.
Pituitary
Neoplasms / drug therapy. Prolactin / secretion. Prolactinoma / drug therapy
[MeSH-minor]
Adenoviridae / genetics.
Cell
Survival / physiology. Drug Resistance, Neoplasm. Humans. Immunohistochemistry. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptors, Somatostatin / biosynthesis. Receptors, Somatostatin / genetics. Transduction, Genetic. Transgenes
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.
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(PMID = 19074883.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin; RWM8CCW8GP / Octreotide
65.
Manahan MA, Dackiw AP, Ball DW, Zeiger MA:
Unusual case of metastatic neuroendocrine tumor.
Endocr Pract
; 2007 Jan-Feb;13(1):72-6
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OBJECTIVE: To report a rare case of metastatic
growth hormone
(
GH
)-
secreting
pituitary
carcinoma causing
acromegaly
.
RESULTS: A 68-year-old woman presented with persistent
acromegaly
after treatment for a
GH
-
secreting
pituitary adenoma
.
After operative treatment including total thyroidectomy, subtotal parathyroidectomy, partial thymectomy, and right modified radical neck dissection, the patient's symptoms diminished, and her
GH
levels approached the normal range.
Surgical pathology findings were consistent with a
GH
-
secreting
pituitary
carcinoma metastatic to the cervical lymph nodes, multinodular thyroid hyperplasia with a focus of papillary microcarcinoma, and parathyroid hyperplasia.
CONCLUSION: Overall,
pituitary
carcinomas are extremely rare.
To date, about 100 cases have been reported in the world's literature, and of these, only 19 cases originated from
GH
-
secreting
cells.
Our examination of the symptoms, signs,
diagnosis
, and treatment of our patient, in comparison with the previously reported cases, should enhance awareness of this unusual
disease
process.
[MeSH-major]
Adenoma
/ pathology.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ pathology. Parathyroid Neoplasms / secondary. Thymus Neoplasms / secondary. Thyroid Neoplasms / secondary
[MeSH-minor]
Acromegaly
/ etiology. Aged. Female. Humans. Lymphatic Metastasis
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(PMID = 17360306.001).
[ISSN]
1934-2403
[Journal-full-title]
Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
[ISO-abbreviation]
Endocr Pract
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
[Number-of-references]
29
66.
Ebner FH, Kürschner V, Dietz K, Bültmann E, Nägele T, Honegger J:
Craniometric changes in patients with acromegaly from a surgical perspective.
Neurosurg Focus
; 2010 Oct;29(4):E3
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[Title]
Craniometric changes in patients with
acromegaly
from a surgical perspective.
OBJECT: The objective of this study was to evaluate and analyze morphometric and volumetric changes of the skull due to
acromegaly
in areas relevant for neurosurgical practice, focusing on the surgical implications.
METHODS: On preoperatively acquired CT scans, cephalometric and volumetric measurements were performed on 45 patients with
acromegaly
(Group A) and 45 control patients (Group B).
The morphometric and volumetric CT data of the patients with
acromegaly
were compared with the data of a control group and correlated with clinical parameters.
A correlation of the vault thickness with preoperative human
growth hormone
, insulin-like
growth
factor-I levels, and duration of clinical history in
acromegaly
could not be established.
The outer anterior-posterior skull diameter of Group A (18.47 ± 0.94 cm) differed significantly (p = 0.0146) from Group B (17.98 ± 0.93 cm) and correlated significantly with preoperative human
growth hormone
(r = 0.3277; p = 0.0299) and insulin-like
growth
factor-–I serum levels (r = 0.3756; p = 0.0120).
Measurements of the anterior-posterior diameter of the sphenoidal sinus differed significantly (p = 0.0074) between patients with
acromegaly
and controls.
Volumetric analysis of the frontal sinus resulted in a statistically significant difference (p = 0.0382) between patients with
acromegaly
(14.89 ± 10.85 cm3) and controls (10.06 ± 6.93 cm3).
CONCLUSIONS: Significant craniometric changes and volumetric remodelling of the paranasal sinus occur in
acromegaly
.
Detailed preoperative diagnostic examination and planning as well as selection of appropriate instruments are mandatory for safe and successful
pituitary adenoma
removal in patients with
acromegaly
.
[MeSH-major]
Acromegaly
/ pathology.
Acromegaly
/ surgery. Cephalometry / statistics & numerical data. Skull / pathology. Skull / surgery
[MeSH-minor]
Adenoma
/ pathology.
Adenoma
/ surgery. Cone-Beam Computed Tomography / statistics & numerical data. Human
Growth Hormone
/ blood. Humans. Insulin-Like
Growth
Factor I / analysis. Maxillary Sinus / pathology. Neurosurgical Procedures / methods.
Pituitary
Neoplasms / blood.
Pituitary
Neoplasms / pathology.
Pituitary
Neoplasms / surgery. Preoperative Care. Sphenoid Sinus / pathology. Tomography, X-Ray Computed
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(PMID = 20887128.001).
[ISSN]
1092-0684
[Journal-full-title]
Neurosurgical focus
[ISO-abbreviation]
Neurosurg Focus
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
67.
Campbell PG, Kenning E, Andrews DW, Yadla S, Rosen M, Evans JJ:
Outcomes after a purely endoscopic transsphenoidal resection of growth hormone-secreting pituitary adenomas.
Neurosurg Focus
; 2010 Oct;29(4):E5
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[Title]
Outcomes after a purely endoscopic transsphenoidal resection
of growth hormone
-
secreting
pituitary
adenomas
.
OBJECT: Using strict biochemical remission criteria, the authors assessed surgical outcomes after endoscopic transsphenoidal resection
of growth hormone
(
GH
)-
secreting
pituitary
adenomas
and identified preoperative factors that significantly influence the rate of remission.
The authors reviewed cases in which an endoscopic resection
of GH
-
secreting
pituitary
adenomas
was performed.
The thresholds of an age-appropriate, normalized insulin-like
growth
factor-I concentration, a nadir
GH
level after oral glucose load of less than 1.0 μg/l, and a random
GH
value of less than 2.5 μg/l were required to establish biochemical cure postoperatively.
RESULTS: Overall, in 57.7% of patients undergoing a purely endoscopic transsphenoidal
pituitary
adenectomy for
acromegaly
, an endocrinological cure was achieved.
CONCLUSIONS: A purely endoscopic transsphenoidal approach to
GH
-
secreting
pituitary
adenomas
leads to similar outcome for noninvasive macroadenomas compared with traditional microsurgical techniques.
Furthermore, this approach may often provide maximal visualization of the tumor, the
pituitary
gland
, and the surrounding neurovascular structures.
[MeSH-major]
Acromegaly
/ surgery. Endoscopy / methods.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ surgery. Human
Growth Hormone
/ secretion
[MeSH-minor]
Adenoma
/ surgery. Adult. Aged. Female. Humans. Insulin-Like
Growth
Factor I / analysis. Longitudinal Studies. Male. Microsurgery / methods. Middle Aged. Neoplasm Invasiveness. Neurosurgical Procedures / methods.
Pituitary
Neoplasms / surgery. Remission Induction. Sphenoid Bone. Treatment Outcome
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(PMID = 20887130.001).
[ISSN]
1092-0684
[Journal-full-title]
Neurosurgical focus
[ISO-abbreviation]
Neurosurg Focus
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
68.
Melmed S, Sternberg R, Cook D, Klibanski A, Chanson P, Bonert V, Vance ML, Rhew D, Kleinberg D, Barkan A:
A critical analysis of pituitary tumor shrinkage during primary medical therapy in acromegaly.
J Clin Endocrinol Metab
; 2005 Jul;90(7):4405-10
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[Title]
A critical analysis of
pituitary
tumor shrinkage during primary medical therapy in
acromegaly
.
CONTEXT: Somatostatin analogs have been successfully used to treat patients with
GH
-
secreting
pituitary
adenomas
because they are safe, effective, and usually well tolerated.
The results of studies evaluating
acromegaly
treatment with the somatostatin receptor ligands (SRLs), octreotide and lanreotide, have supported the use of these agents for primary medical therapy before or as an alternative to traditional interventions of surgery and radiotherapy in selected cases.
EVIDENCE ACQUISITION: We therefore undertook a systematic literature overview to characterize the results of studies involving primary therapy with somatostatin analogs and their effects on
pituitary
tumor size.
Because most studies in which
pituitary
tumor shrinkage has been assessed involve uncontrolled, open-label, prospective trials or retrospective case series, the lack of a control arm does not permit pooling of data in a metaanalytic fashion to determine tumor size reduction.
EVIDENCE SYNTHESIS: Overall, for patients who experience significant shrinkage, an approximately 50% decrease in
pituitary
mass is achieved when a somatostatin analog is used exclusively or before surgery or radiotherapy.
Fourteen studies (n = 424) provided a definition of significant tumor shrinkage, and the results showed that 36.6% (weighted mean percentage) of patients receiving primary SRL therapy for
acromegaly
experienced a significant reduction in tumor size.
[MeSH-major]
Acromegaly
/ drug therapy.
Pituitary
Neoplasms / drug therapy. Somatostatin / therapeutic use
[MeSH-minor]
Clinical Trials as Topic. Dopamine Agonists / therapeutic use. Humans. Insulin-Like
Growth
Factor I / analysis
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(PMID = 15827109.001).
[ISSN]
0021-972X
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Dopamine Agonists; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I
69.
Okinaga H, Takano K, Hayashi S, Yasufuku-Takano J, Teramoto A, Fujita T:
Mechanisms of TRH-induced GH release (paradoxical response) in human somatotroph adenoma cells.
Endocr J
; 2005 Dec;52(6):763-7
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[Title]
Mechanisms of TRH-induced
GH
release (paradoxical response) in human
somatotroph
adenoma
cells.
The mechanisms of paradoxical TRH response in human
somatotroph
adenoma
cells were investigated using intracellular calcium measurement and static incubation assay.
These calcium responses, especially the second phase, was responsible for the TRH-induced
GH
release.
[MeSH-major]
Adenoma
/ secretion.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ secretion. Human
Growth Hormone
/ secretion. Thyrotropin-Releasing
Hormone
/ pharmacology
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CALCIUM, ELEMENTAL
.
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(PMID = 16410670.001).
[ISSN]
0918-8959
[Journal-full-title]
Endocrine journal
[ISO-abbreviation]
Endocr. J.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Calcium Channels; 12629-01-5 / Human Growth Hormone; 5Y5F15120W / Thyrotropin-Releasing Hormone; EC 2.7.11.13 / Protein Kinase C; SY7Q814VUP / Calcium
70.
Wasko R, Jankowska A, Waligorska-Stachura J, Andrusiewicz M, Jaskula M, Sowinski J:
Survivin expression in pituitary adenomas.
Neuro Endocrinol Lett
; 2005 Jun;26(3):209-12
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[Title]
Survivin expression in
pituitary
adenomas
.
Survivin expression has been described to be
cell
cycle-dependent and restricted to the G2-M checkpoint, where it inhibits apoptosis in proliferating cells.
OBJECTIVES: The aim of our study was to determine the survivin expression in different types of
pituitary
adenomas
.
METHODS: Tissue samples were obtained during surgical removal of the tumour from 12 patients with diagnosed:
acromegaly
in seven cases, non-functioning
pituitary
tumours in four cases and prolactinoma in one case.
Six patients with
acromegaly
received long-acting somatostatin analogues before tumour resection.
RESULTS: In agreement with the current view that survivin is a tumor-associated antigen, highly expressed in various tumours, we found the presence of survivin expression as a characteristic feature of human
pituitary
adenomas
.
The findings of our study demonstrated the presence of an active survivin gene in all twelve analysed
pituitary
tumours.
CONCLUSIONS: Based on these findings, we conclude that the estimation of survivin expression in human
pituitary
tumours may help predict tumour
growth
and prognosis.
[MeSH-major]
Adenoma
/ physiopathology. Biomarkers, Tumor / genetics. Gene Expression Regulation, Neoplastic. Microtubule-Associated Proteins / genetics. Neoplasm Proteins / genetics.
Pituitary
Neoplasms / physiopathology
[MeSH-minor]
Acromegaly
/ genetics.
Acromegaly
/ physiopathology. Adult. Aged. Female. HeLa Cells. Humans. Inhibitor of Apoptosis Proteins. Male. Middle Aged. Predictive Value of Tests. Prognosis. Prolactinoma / genetics. Prolactinoma / physiopathology. RNA, Messenger / analysis
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(PMID = 15990723.001).
[ISSN]
0172-780X
[Journal-full-title]
Neuro endocrinology letters
[ISO-abbreviation]
Neuro Endocrinol. Lett.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Sweden
[Chemical-registry-number]
0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
71.
Gradiser M, Matovinovic M, Vrkljan M:
Decrease in growth hormone and insulin-like growth factor (IGF)-1 release and amelioration of acromegaly features after rosiglitazone treatment of type 2 diabetes mellitus a patient with acromegaly.
Croat Med J
; 2007 Feb;48(1):87-91
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[Title]
Decrease in
growth hormone
and insulin-like
growth
factor (IGF)-1 release and amelioration of
acromegaly
features after rosiglitazone treatment of type 2 diabetes mellitus a patient with
acromegaly
.
A 28-year-old woman with clinical features of
acromegaly
and diabetes mellitus was admitted to our Reference Center for Clinical Neuroendocrinology and
Pituitary
Diseases at Sisters of Mercy University Hospital, Zagreb, Croatia.
Magnetic resonance scan of the brain showed
pituitary
macroadenoma.
After transsphenoidal resection, histological analysis confirmed it was a
growth hormone
(
GH
)-
secreting
pituitary adenoma
.
A month after the surgery, octreotide was introduced because of a further increase in
GH
and insulin-like
growth
factor-I (IGF-I), but discontinued after a week due to intolerance.
The concentration
of GH
and IGF-I in the week before rosiglitazone was introduced was 5.96 ng/mL and 990 ng/mL, respectively, and decreased to 2.92 ng/mL and 180.0 ng/mL, respectively, after 90 days of treatment.
It is possible that rosiglitazone induced the decrease in
GH
and IGF-I concentrations and its role in the long-term medical therapy of patients with
pituitary
tumors should be further investigated.
[MeSH-major]
Acromegaly
/ etiology. Diabetes Mellitus, Type 2 / drug therapy.
Growth Hormone
/ drug effects. Insulin-Like
Growth
Factor I / drug effects. Thiazolidinediones / therapeutic use
[MeSH-minor]
Adenoma
/ complications.
Adenoma
/ surgery. Adult. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ complications.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ surgery. Humans
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.
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ROSIGLITAZONE
.
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[Cites]
Clin Endocrinol (Oxf). 2005 Feb;62(2):259-61
[
15670207.001
]
[Cites]
J Biol Chem. 1999 Mar 26;274(13):9116-21
[
10085162.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Feb;85(2):526-9
[
10690849.001
]
[Cites]
Eur J Endocrinol. 2000 Nov;143(5):615-21
[
11078985.001
]
[Cites]
Clin Endocrinol (Oxf). 2001 Feb;54(2):183-8
[
11207632.001
]
[Cites]
J Clin Invest. 2003 May;111(9):1381-8
[
12727930.001
]
[Cites]
Pituitary. 2003;6(3):153-9
[
14971739.001
]
[Cites]
Diabet Med. 2004 May;21(5):415-22
[
15089784.001
]
[Cites]
Eur J Endocrinol. 2004 Jun;150(6):863-75
[
15191358.001
]
[Cites]
Endocr Rev. 1995 Feb;16(1):3-34
[
7758431.001
]
[Cites]
J Clin Endocrinol Metab. 1996 Feb;81(2):443-5
[
8636245.001
]
[Cites]
Diabetes. 1996 Dec;45(12):1661-9
[
8922349.001
]
[Cites]
Nature. 1998 Jan 1;391(6662):82-6
[
9422509.001
]
[Cites]
Diabetes. 1998 Apr;47(4):507-14
[
9568680.001
]
[Cites]
Growth Horm IGF Res. 2005 Jul;15 Suppl A:S31-5
[
16023876.001
]
(PMID = 17309144.001).
[ISSN]
1332-8166
[Journal-full-title]
Croatian medical journal
[ISO-abbreviation]
Croat. Med. J.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Croatia
[Chemical-registry-number]
0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone
[Other-IDs]
NLM/ PMC2080491
72.
Erturk E, Tuncel E, Kiyici S, Ersoy C, Duran C, Imamoglu S:
Outcome of surgery for acromegaly performed by different surgeons: importance of surgical experience.
Pituitary
; 2005;8(2):93-7
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[Title]
Outcome of surgery for
acromegaly
performed by different surgeons: importance of surgical experience.
Basal or nadir postglucose
growth hormone
levels of less than 2 ng/ml were accepted as cure criteria.
[MeSH-major]
Acromegaly
/ surgery
[MeSH-minor]
Adenoma
/ drug therapy.
Adenoma
/ surgery. Adult. Clinical Competence. Female. Human
Growth Hormone
/ blood. Humans. Male. Middle Aged. Octreotide / therapeutic use.
Pituitary
Neoplasms / drug therapy.
Pituitary
Neoplasms / surgery. Reoperation. Retrospective Studies. Treatment Outcome
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[Cites]
J Clin Endocrinol Metab. 1998 Oct;83(10):3419-26
[
9768641.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Oct;85(10):3779-85
[
11061538.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Aug;83(8):2646-52
[
9709926.001
]
[Cites]
QJM. 1999 Dec;92(12):741-5
[
10581337.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Jul;88(7):3105-12
[
12843150.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Jun;86(6):2779-86
[
11397887.001
]
[Cites]
J Endocrinol. 1997 Oct;155 Suppl 1:S53-5
[
9389996.001
]
[Cites]
J Neurosurg. 1993 Jul;79(1):70-5
[
8315471.001
]
[Cites]
Clin Endocrinol (Oxf). 2000 Sep;53(3):321-7
[
10971449.001
]
[Cites]
Neurosurgery. 2001 Jun;48(6):1239-43; discussion 1244-5
[
11383725.001
]
[Cites]
Pituitary. 1999 Jun;2(1):29-41
[
11081170.001
]
[Cites]
Growth Horm IGF Res. 2003 Aug;13(4):185-92
[
12914751.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Oct;83(10):3411-8
[
9768640.001
]
[Cites]
Neurosurgery. 1998 May;42(5):1013-21; discussion 1021-2
[
9588545.001
]
[Cites]
Clin Endocrinol (Oxf). 1999 May;50(5):561-7
[
10468920.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Dec;85(12):4596-602
[
11134114.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Sep;83(9):3034-40
[
9745397.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Oct;87(10):4554-63
[
12364434.001
]
[Cites]
J Neurosurg. 1996 Aug;85(2):239-47
[
8755752.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Aug;83(8):2730-4
[
9709939.001
]
[Cites]
Clin Endocrinol (Oxf). 1998 Nov;49(5):653-7
[
10197082.001
]
[Cites]
Q J Med. 1993 May;86(5):293-9
[
8327647.001
]
[Cites]
Clin Endocrinol (Oxf). 1996 Oct;45(4):407-13
[
8959078.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Jul;88(7):3090-8
[
12843148.001
]
[Cites]
Clin Endocrinol (Oxf). 1999 May;50(5):557-9
[
10468919.001
]
(PMID = 16195777.001).
[ISSN]
1386-341X
[Journal-full-title]
Pituitary
[ISO-abbreviation]
Pituitary
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; RWM8CCW8GP / Octreotide
73.
Toledo RA, Mendonca BB, Fragoso MC, Soares IC, Almeida MQ, Moraes MB, Lourenço DM Jr, Alves VA, Bronstein MD, Toledo SP:
Isolated familial somatotropinoma: 11q13-loh and gene/protein expression analysis suggests a possible involvement of aip also in non-pituitary tumorigenesis.
Clinics (Sao Paulo)
; 2010 Apr;65(4):407-15
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[Title]
Isolated familial somatotropinoma: 11q13-loh and gene/protein expression analysis suggests a possible involvement of aip also in non-
pituitary
tumorigenesis.
OBJECTIVE: Non-
pituitary
tumors have been reported in a subset of patients harboring germline mutations in the aryl hydrocarbon receptor-interacting protein (AIP) gene.
However, no detailed investigations of non-
pituitary
tumors of AIP-mutated patients have been reported so far.
PATIENTS: We examined a MEN1- and p53-negative mother-daughter pair with
acromegaly due
to somatotropinoma.
Subsequently, the mother developed a large virilizing adrenocortical carcinoma and a grade II B-
cell
non-Hodgkin's lymphoma.
No evidence of LOH was observed in the DNA sample from the mother's B-
cell
lymphoma, and this tumor displayed normal AIP immunostaining.
CONCLUSIONS: Our study presents the first molecular analysis of non-
pituitary
tumors in AIP-mutated patients.
The finding
of AIP inactivation in the adrenocortical tumor suggests that further investigation of the potential role of this recently identified tumor suppressor gene in non-
pituitary
tumors, mainly in those tumors in which the cAMP and the 11q13 locus are implicated, is likely to be worthwhile.
[MeSH-major]
Acromegaly
/ genetics.
Adenoma
/ genetics. Adrenocortical Carcinoma / genetics.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ genetics. Intracellular Signaling Peptides and Proteins / genetics.
Pituitary
Neoplasms / genetics
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[Cites]
Eur J Endocrinol. 2008 Sep;159(3):259-74
[
18524795.001
]
[Cites]
J Clin Endocrinol Metab. 2010 Mar;95(3):1318-27
[
20080836.001
]
[Cites]
Nat Genet. 2000 Sep;26(1):89-92
[
10973256.001
]
[Cites]
Cell Stress Chaperones. 2000 Jul;5(3):243-54
[
11005382.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Feb;86(2):542-4
[
11158006.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Oct;86(10):4970-3
[
11600572.001
]
[Cites]
Methods. 2001 Dec;25(4):402-8
[
11846609.001
]
[Cites]
Nature. 2002 Jun 27;417(6892):949-54
[
12068308.001
]
[Cites]
Am J Hum Genet. 2002 Dec;71(6):1433-42
[
12424709.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Dec;87(12):5658-61
[
12466368.001
]
[Cites]
J Biol Chem. 2003 Aug 29;278(35):33351-63
[
12810716.001
]
[Cites]
Eur J Endocrinol. 2004 May;150(5):643-8
[
15132719.001
]
[Cites]
Nature. 1989 Aug 31;340(6236):692-6
[
2549426.001
]
[Cites]
J Clin Endocrinol Metab. 1999 Jan;84(1):216-9
[
9920087.001
]
[Cites]
J Clin Endocrinol Metab. 1999 Feb;84(2):730-5
[
10022445.001
]
[Cites]
Pituitary. 2004;7(2):95-101
[
15761658.001
]
[Cites]
Clinics (Sao Paulo). 2006 Feb;61(1):59-70
[
16532227.001
]
[Cites]
Arq Bras Endocrinol Metabol. 2006 Feb;50(1):7-16
[
16628270.001
]
[Cites]
Science. 2006 May 26;312(5777):1228-30
[
16728643.001
]
[Cites]
Nat Genet. 2006 Jul;38(7):794-800
[
16767104.001
]
[Cites]
N Engl J Med. 2006 Dec 14;355(24):2558-73
[
17167139.001
]
[Cites]
Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4101-5
[
17360484.001
]
[Cites]
Clin Endocrinol (Oxf). 2007 Apr;66(4):499-502
[
17371465.001
]
[Cites]
J Biol Chem. 2007 May 4;282(18):13656-63
[
17329248.001
]
[Cites]
J Clin Endocrinol Metab. 2007 May;92(5):1891-6
[
17244780.001
]
[Cites]
J Clin Endocrinol Metab. 2007 May;92(5):1952-5
[
17299063.001
]
[Cites]
J Clin Endocrinol Metab. 2007 May;92(5):1934-7
[
17341560.001
]
[Cites]
Eur J Endocrinol. 2007 Jul;157(1):1-8
[
17609395.001
]
[Cites]
Clin Endocrinol (Oxf). 2007 Sep;67(3):377-84
[
17555499.001
]
[Cites]
Clinics (Sao Paulo). 2007 Aug;62(4):465-76
[
17823710.001
]
[Cites]
N Engl J Med. 2008 Feb 14;358(7):750-2
[
18272904.001
]
[Cites]
J Clin Endocrinol Metab. 2008 Jun;93(6):2390-401
[
18381572.001
]
[Cites]
Clin Endocrinol (Oxf). 2009 Feb;70(2):259-64
[
18710468.001
]
[Cites]
Horm Res. 2009 Apr;71 Suppl 2:116-22
[
19407507.001
]
[Cites]
Cancer. 2000 Feb 15;88(4):711-36
[
10679640.001
]
(PMID = 20454499.001).
[ISSN]
1980-5322
[Journal-full-title]
Clinics (São Paulo, Brazil)
[ISO-abbreviation]
Clinics (Sao Paulo)
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Brazil
[Chemical-registry-number]
0 / Intracellular Signaling Peptides and Proteins; 0 / aryl hydrocarbon receptor-interacting protein
[Other-IDs]
NLM/ PMC2862671
[Keywords]
NOTNLM ; AIP / Acromegaly / Adrenocortical tumor / FIPA / pituitary tumor
74.
Alons K, Bergé SJ, Rieu PN, Meijer GJ:
[Treatment of macroglossia due to acromegaly].
Ned Tijdschr Tandheelkd
; 2010 Jun;117(6):321-4
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[Title]
[Treatment of macroglossia due to
acromegaly
].
A 61-years-old woman had macroglossia due to
acromegaly
with complaints of dyspneu at a lying sleeping position and complaints of speech and dysphagia.
At the age of 55 years she was diagnosed with
acromegaly
induced by a
adenoma
of the
pituitary
gland
, which had been removed surgically.
Clinically,
acromegaly
is diagnosed on clinical signs, such as the morphology and the protrusion of the tongue.
Often, macroglossia is a secondary symptom of a systemic
disease
, needing causal treatment.
[MeSH-major]
Acromegaly
/ complications. Macroglossia / etiology. Macroglossia / surgery
Genetic Alliance.
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.
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consumer health - Macroglossia
.
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(PMID = 20614796.001).
[ISSN]
0028-2200
[Journal-full-title]
Nederlands tijdschrift voor tandheelkunde
[ISO-abbreviation]
Ned Tijdschr Tandheelkd
[Language]
dut
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Netherlands
75.
Zieliński G, Hendzel P, Szałański P, Gołowicz J, Gryszko L, Podgórski JK:
[Severe cardiovascular complications due to the pituitary adenoma with acromegaly. An interdisciplinary approach to the treatment. A case report].
Neurol Neurochir Pol
; 2006 Jul-Aug;40(4):354-60
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[Title]
[Severe cardiovascular complications due to the
pituitary adenoma
with
acromegaly
. An interdisciplinary approach to the treatment. A case report].
[Transliterated title]
Ciezkie powikłania sercowo-naczyniowe w przebiegu guza
przysadki
powodujacego akromegalie. Propozycja równoczesnego wielospecjalistycznego leczenia. Opis przypadku.
Acromegaly
reduces life expectancy and leads to 3-5-fold increase in mortality.
Successful therapy ought to normalize
GH
, IGF-I secretion, remove the
adenoma
mass and its local pressure effects and preserve
pituitary
functions intact to improve systemic morbidity and normalize mortality.
The primary therapy for most patients with
acromegaly
is still transsphenoidal adenomectomy.
The authors present a 64-year-old woman with diagnosed
GH
-
secreting
pituitary
macroadenoma suffering from severe coronary heart
disease
and diabetes mellitus.
[MeSH-major]
Acromegaly
/ surgery.
Adenoma
/ surgery. Coronary Artery
Disease
/ surgery.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ surgery.
Pituitary
Neoplasms / surgery
Genetic Alliance.
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.
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consumer health - Coronary Artery Disease
.
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.
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(PMID = 16967359.001).
[ISSN]
0028-3843
[Journal-full-title]
Neurologia i neurochirurgia polska
[ISO-abbreviation]
Neurol. Neurochir. Pol.
[Language]
pol
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Poland
76.
D'Amore M, Minenna G, D'Amore S, Scagliusi P, Caprio S:
[The strange case of a patient affected by acromegaly with osteoporomalacia without hypogonadism].
Reumatismo
; 2005 Dec;57(4):291-4
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[Title]
[The strange case of a patient affected by
acromegaly
with osteoporomalacia without hypogonadism].
Acromegaly
is a rare
disease
that, in the majority of cases, is due to the presence of a benign
growth hormone
(
GH
)-
producing
tumor of the
pituitary
.
Growth hormone
has profound effects on linear bone
growth
, bone metabolism, and bone mass.
In
acromegaly
, the skeletal effects of chronic
GH
excess have been mainly addressed by evaluating bone mineral density (BMD).
Most data were obtained in patients with active
acromegaly
, and apparently high or normal BMD was observed in the absence of hypogonadism.
The Autors describe a case of patient affected by
acromegaly
without hypogonadism with serious osteoporosis and biological signs of osteomalacia.
[MeSH-major]
Acromegaly
/
diagnosis
.
Adenoma
, Chromophobe /
diagnosis
. Osteomalacia /
diagnosis
. Osteoporosis /
diagnosis
.
Pituitary
Neoplasms /
diagnosis
[MeSH-minor]
Adult. Androgens / therapeutic use. Bone Density. Human
Growth Hormone
/ blood. Humans. Hypogonadism /
diagnosis
. Male. Reoperation. Testosterone / therapeutic use. Treatment Outcome
Genetic Alliance.
consumer health - Acromegaly
.
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consumer health - Osteoporosis
.
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
Hazardous Substances Data Bank.
TESTOSTERONE
.
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(PMID = 16380758.001).
[ISSN]
0048-7449
[Journal-full-title]
Reumatismo
[ISO-abbreviation]
Reumatismo
[Language]
ita
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Italy
[Chemical-registry-number]
0 / Androgens; 12629-01-5 / Human Growth Hormone; 3XMK78S47O / Testosterone
77.
Guerrero CA, Krayenbühl N, Husain M, Krisht AF:
Ectopic suprasellar growth hormone-secreting pituitary adenoma: case report.
Neurosurgery
; 2007 Oct;61(4):E879; discussion E879
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[Title]
Ectopic suprasellar
growth hormone
-
secreting
pituitary adenoma
: case report.
OBJECTIVE: Ectopic
pituitary
adenomas
are rare.
We present an unusual case of an ectopic
growth hormone
-
secreting
pituitary adenoma
in the suprasellar space.
CLINICAL PRESENTATION: A 31-year-old man presented with a history of chronic headache and typical clinical signs of
acromegaly
.
Magnetic resonance imaging scans revealed a suprasellar mass not arising from the normal looking
pituitary
gland
.
Histological examination showed a
growth hormone
-
secreting
pituitary adenoma
CONCLUSION: Although uncommon,
growth hormone
-
secreting
pituitary
adenomas
are encountered in the suprasellar region.
They should be added to the differential
diagnosis of
tumors in this location.
[MeSH-major]
Adenoma
/ radiography. Choristoma.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ radiography
Genetic Alliance.
consumer health - Pituitary adenoma, growth hormone-secreting
.
The Weizmann Institute of Science GeneCards and MalaCards databases.
gene/protein/disease-specific - MalaCards for growth hormone secreting pituitary adenoma
.
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NCI CPTAC Assay Portal
.
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(PMID = 17986925.001).
[ISSN]
1524-4040
[Journal-full-title]
Neurosurgery
[ISO-abbreviation]
Neurosurgery
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
[Number-of-references]
23
78.
Petersenn S, Schopohl J, Barkan A, Mohideen P, Colao A, Abs R, Buchelt A, Ho YY, Hu K, Farrall AJ, Melmed S, Biller BM, Pasireotide Acromegaly Study Group:
Pasireotide (SOM230) demonstrates efficacy and safety in patients with acromegaly: a randomized, multicenter, phase II trial.
J Clin Endocrinol Metab
; 2010 Jun;95(6):2781-9
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[Title]
Pasireotide (SOM230) demonstrates efficacy and safety in patients with
acromegaly
: a randomized, multicenter, phase II trial.
Because most
GH
-
secreting
pituitary
adenomas
express sst(2) and sst(5), pasireotide has the potential to be more effective than the sst(2)-preferential somatostatin analogs octreotide and lanreotide.
OBJECTIVE: Our objective was to evaluate the efficacy and safety of three different doses of pasireotide in patients with
acromegaly
.
PATIENTS: Sixty patients with
acromegaly
, defined by a 2-h five-point mean
GH
level higher than 5 microg/liter, lack of suppression
of GH
to less than 1 microg/liter after oral glucose tolerance test, and elevated IGF-I for age- and sex-matched controls.
MAIN OUTCOME MEASURE: A biochemical response was defined as a reduction in
GH
to no more than 2.5 microg/liter and normalization of IGF-I to age- and sex-matched controls.
After 4 wk of pasireotide 200-600 microg s.c. bid, 19% of patients achieved a biochemical response, which increased to 27% after 3 months of pasireotide; 39% of patients had a more than 20% reduction in
pituitary
tumor volume.
CONCLUSIONS: Pasireotide is a promising treatment for
acromegaly
.
Larger studies of longer duration evaluating the efficacy and safety of pasireotide in patients with
acromegaly
are ongoing.
[MeSH-major]
Acromegaly
/ drug therapy. Somatostatin / analogs & derivatives
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over. Blood Glucose / metabolism. Cross-Over Studies. Dose-Response Relationship, Drug. Double-Blind Method. Endpoint Determination. Female. Human
Growth Hormone
/ blood. Humans. Insulin-Like
Growth
Factor I / metabolism. Magnetic Resonance Imaging. Male. Middle Aged. Octreotide / adverse effects. Octreotide / therapeutic use.
Pituitary
Neoplasms / pathology. Young Adult
Genetic Alliance.
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.
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.
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
The Lens.
Cited by Patents in
.
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[CommentIn]
Nat Rev Endocrinol. 2010 Aug;6(8):417
[
20681073.001
]
(PMID = 20410233.001).
[ISSN]
1945-7197
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00088582
[Publication-type]
Clinical Trial, Phase II; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Blood Glucose; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I; 98H1T17066 / pasireotide; RWM8CCW8GP / Octreotide
[Investigator]
Brue T; Caron P; Chanson P; Cuneo R; Díaz A; Ghigo E; Gaillard R; Halperin I; Kleinberg D; Rohmer V; Romijn JA; Schlienger JL; Stewart P; Tabarin A; Trainer PJ; van der Lely AJ; Vance ML
79.
Daly AF, Beckers A:
Update on the treatment of pituitary adenomas: familial and genetic considerations.
Acta Clin Belg
; 2008 Nov-Dec;63(6):418-24
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[Title]
Update on the treatment of
pituitary
adenomas
: familial and genetic considerations.
Clinically-relevant
pituitary
adenomas
occur with a prevalence of approximately 1 per 1000 population in Belgium.
Pituitary
adenomas
that occur in families are likely to have an important genetic pathophysiological basis.
Currently about 5% of all
pituitary adenoma
cases have a family history of
pituitary
adenomas
, classically due to multiple endocrine neoplasia type 1 (MEN1) and Carney complex (CNC).
Over the last decade we have described non-MEN1/CNC familial
pituitary
tumours that include all tumour phenotypes, a condition named 'familial isolated
pituitary adenoma
' (FIPA).
Clinical features of FIPA differ from those of sporadic
pituitary
adenomas
in that patients with FIPA are often younger and have larger tumours at
diagnosis
.
In this review we examine new findings on the epidemiology of
pituitary
adenomas
and we review familial causes of
pituitary
adenomas
with a particular emphasis on modern clinical testing.
In addition, the clinical and genetic features of FIPA are described as FIPA represents a useful framework to study the features of
pituitary
adenomas
that occur in a familial setting.
[MeSH-major]
Adenoma
/ therapy.
Pituitary
Neoplasms / drug therapy.
Pituitary
Neoplasms / genetics
[MeSH-minor]
Acromegaly
. Animals. Humans. Intracellular Signaling Peptides and Proteins / genetics. Loss of Heterozygosity. Multiple Endocrine Neoplasia Type 1 / complications. Multiple Endocrine Neoplasia Type 1 / genetics. Mutation. Prolactinoma / drug therapy. Prolactinoma / genetics
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
ORBi (University of Liege).
Free full Text at ORBi
.
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(PMID = 19170361.001).
[ISSN]
1784-3286
[Journal-full-title]
Acta clinica Belgica
[ISO-abbreviation]
Acta Clin Belg
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Belgium
[Chemical-registry-number]
0 / Intracellular Signaling Peptides and Proteins; 0 / aryl hydrocarbon receptor-interacting protein
[Number-of-references]
54
80.
Dimaraki EV, Chandler WF, Brown MB, Jaffe CA, Kim SY, Taussig R, Padmanabhan V, Barkan AL:
The role of endogenous growth hormone-releasing hormone in acromegaly.
J Clin Endocrinol Metab
; 2006 Jun;91(6):2185-90
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[Title]
The role of endogenous
growth hormone
-releasing
hormone
in
acromegaly
.
CONTEXT: Some indirect evidence suggests hypothalamic control
of GH
secretion in
acromegaly
.
OBJECTIVE: The objective of the study is to examine whether
GH
secretion in
acromegaly
is dependent on endogenous GHRH.
PATIENTS AND STUDY DESIGN: We studied eight patients with untreated
acromegaly due
to a
GH
-
producing
pituitary
tumor.
GH
was measured every 10 min for 24 h during the normal saline infusion and on the last day of the GHRH-ant infusion.
A group of nine different patients with untreated
acromegaly
served as the control group and underwent blood sampling for
GH
every 10 min for two 24-h periods to assess the day-to-day variability
of GH
secretion.
MAIN OUTCOME MEASURE: Twenty-four-hour mean
GH
was the main outcome measured.
RESULTS: In six of eight subjects treated with GHRH-ant, 24-h mean
GH
decreased by 5.8-30.0% during iv GHRH-ant and, in three subjects, the change in the 24-h mean
GH
was greater than the upper limit of the 95% confidence interval of the spontaneous day-to-day variability of the mean
GH
in patients with
acromegaly
.
CONCLUSION: In some patients with
acromegaly due
to a
pituitary adenoma
,
GH
secretion is under partial control by endogenous GHRH.
[MeSH-major]
Acromegaly
/ metabolism.
Adenoma
/ secretion.
Growth Hormone
-Releasing
Hormone
/ physiology. Human
Growth Hormone
/ secretion.
Pituitary
Neoplasms / secretion
[MeSH-minor]
Adult. Female. GTP-Binding Protein alpha Subunits, Gs / genetics. Glucose Tolerance Test. Humans. Insulin-Like
Growth
Factor I / analysis. Male. Middle Aged. Mutation
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.
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.
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.
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(PMID = 16537684.001).
[ISSN]
0021-972X
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / 5P60 DK20572; United States / NCRR NIH HHS / RR / M01-RR00042; United States / NIDDK NIH HHS / DK / R0-1-DK38449
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; 9034-39-3 / Growth Hormone-Releasing Hormone; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
81.
Takano K, Yasufuku-Takano J, Morita K, Mori S, Takei M, Osamura RY, Teramoto A, Fujita T:
Evidence that PKA activity is constitutively activated in human GH-secreting adenoma cells in a patient with Carney complex harbouring a PRKAR1A mutation.
Clin Endocrinol (Oxf)
; 2009 May;70(5):769-75
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[Title]
Evidence that PKA activity is constitutively activated in human
GH
-
secreting
adenoma
cells in a patient with Carney complex harbouring a PRKAR1A mutation.
CONTEXT: The GHRH-protein kinase A (PKA) signalling pathway is essential for
cell
proliferation and
GH
synthesis/secretion in somatotrophs.
The basal PKA activity
of somatotroph
adenoma
cells from CNC has not been evaluated because of a limited amount of available tissue.
Primary cultured
adenoma
cells were subjected to electrophysiological experiments to evaluate PKA signalling in individual cells.
RESULTS: GHRH did not increase the nonselective cation current or the voltage-gated calcium current in these
adenoma
cells, in contrast to nonadenomatous
somatotroph
cells in which these currents increase through the PKA pathway.
Application of a PKA inhibitor inhibited the basal currents in these
adenoma
cells, results that were not observed in nonadenomatous somatotrophs.
CONCLUSIONS: The results demonstrate that PKA is activated at the basal state in these
adenoma
cells.
The data also show that both the nonselective cation current and the voltage-gated calcium current, vital regulators
of GH
secretion downstream of PKA, are maximally increased in these cells.
These maximally increased currents probably account for the excessive
GH
secretion.
[MeSH-major]
Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / genetics. Cyclic AMP-Dependent Protein Kinases / metabolism.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ enzymology.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ genetics. Lentigo / enzymology. Lentigo / genetics. Multiple Endocrine Neoplasia / enzymology. Multiple Endocrine Neoplasia / genetics. Mutation
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.
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(PMID = 19178533.001).
[ISSN]
1365-2265
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Calcium Channels; 0 / Codon, Nonsense; 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / DNA, Neoplasm; 0 / PRKAR1A protein, human; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
82.
Sasaki A, Horikawa Y, Suwa T, Enya M, Kawachi S, Takeda J:
Case report of familial Carney complex due to novel frameshift mutation c.597del C (p.Phe200LeufsX6) in PRKAR1A.
Mol Genet Metab
; 2008 Nov;95(3):182-7
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Carney complex is an autosomal dominantly inherited
disease
characterized by skin pigmentation, myxoma, primary pigmented nodular adrenocortical
disease
(PPNAD), and
acromegaly
.
However, only a few incidences of PPNAD combined with
acromegaly
are observed in patients.
Here, we report a female patient diagnosed with Cushing's syndrome and a
GH
-
producing
pituitary adenoma
without otherwise evident
acromegaly
that could be diagnosed only by specialized endocrinological tests.
Based on family history of
acromegaly
(mother and sister) and the fact that the combination of both diseases is very rare, genetic
diagnosis
involving Carney complex was considered to be appropriate.
Even family members with the same mutation can show distinct phenotypes, suggesting that Carney complex is a multifactorial
disorder
comprising various genetic and environmental factors.
Genetic
diagnosis
makes it possible to prepare more effective therapeutic strategies for patients and gene carriers and to avoid unnecessary tests for non-carriers in the family of the patient.
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(PMID = 18760947.001).
[ISSN]
1096-7206
[Journal-full-title]
Molecular genetics and metabolism
[ISO-abbreviation]
Mol. Genet. Metab.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human
83.
Melmed S:
Acromegaly pathogenesis and treatment.
J Clin Invest
; 2009 Nov;119(11):3189-202
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[Title]
Acromegaly
pathogenesis and treatment.
Dysregulated
growth hormone
(
GH
) hypersecretion is usually caused by a
GH
-
secreting
pituitary adenoma
and leads
to acromegaly
- a
disorder of
disproportionate skeletal, tissue, and organ
growth
.
High
GH
and IGF1 levels lead to comorbidities including arthritis, facial changes, prognathism, and glucose intolerance.
This Review discusses
acromegaly
pathogenesis and management options.
Somatostatin receptor (SSTR) ligands inhibit
GH
release, control tumor
growth
, and attenuate peripheral
GH
action, while
GH
receptor antagonists block
GH
action and effectively lower IGF1 levels.
Effective control
of GH
and IGF1 hypersecretion and ablation or stabilization of the
pituitary
tumor mass lead to improved comorbidities and lowering of mortality rates for this hormonal
disorder
.
Genetic Alliance.
consumer health - Acromegaly
.
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clinical trials - ClinicalTrials.gov
.
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.
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[Cites]
J Clin Endocrinol Metab. 2009 Apr;94(4):1255-63
[
19158203.001
]
[Cites]
Annu Rev Pathol. 2009;4:97-126
[
19400692.001
]
[Cites]
J Clin Endocrinol Metab. 2009 May;94(5):1500-8
[
19208728.001
]
[Cites]
J Clin Endocrinol Metab. 2009 May;94(5):1509-17
[
19208732.001
]
[Cites]
J Biol Chem. 2009 Jul 24;284(30):19937-44
[
19460757.001
]
[Cites]
Science. 2000 Apr 7;288(5463):154-7
[
10753124.001
]
[Cites]
N Engl J Med. 2000 Apr 20;342(16):1171-7
[
10770982.001
]
[Cites]
Recent Prog Horm Res. 2000;55:237-66; discussion 266-7
[
11036940.001
]
[Cites]
Dev Biol. 2001 Jan 1;229(1):141-62
[
11133160.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Jan;86(1):140-5
[
11231991.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Apr;86(4):1716-23
[
11297608.001
]
[Cites]
Neurosurgery. 2001 Jun;48(6):1239-43; discussion 1244-5
[
11383725.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Sep;86(9):4072-7
[
11549628.001
]
[Cites]
Endocr Rev. 2001 Dec;22(6):800-17
[
11739334.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Mar;87(3):1262-7
[
11889197.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8
[
12107192.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Sep;87(9):4142-6
[
12213862.001
]
[Cites]
Nat Genet. 2002 Oct;32(2):306-11
[
12355087.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Oct;87(10):4554-63
[
12364434.001
]
[Cites]
Endocrinology. 2003 Mar;144(3):967-74
[
12586774.001
]
[Cites]
Horm Res. 2003;60(2):53-60
[
12876414.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Sep;88(9):4239-45
[
12970293.001
]
[Cites]
N Engl J Med. 2003 Sep 18;349(12):1139-47
[
13679528.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Nov;88(11):5414-21
[
14602782.001
]
[Cites]
Nat Rev Drug Discov. 2003 Dec;2(12):999-1017
[
14654798.001
]
[Cites]
J Clin Invest. 2003 Dec;112(11):1603-18
[
14660734.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Feb;89(2):638-45
[
14764775.001
]
[Cites]
Endocr Rev. 2004 Feb;25(1):102-52
[
14769829.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Apr;89(4):1613-7
[
15070920.001
]
[Cites]
Nat Genet. 2004 Jul;36(7):720-4
[
15208626.001
]
[Cites]
J Clin Invest. 2004 Aug;114(3):349-56
[
15286801.001
]
[Cites]
N Engl J Med. 1979 Nov 22;301(21):1138-42
[
492275.001
]
[Cites]
J Clin Endocrinol Metab. 2006 Apr;91(4):1239-45
[
16403824.001
]
[Cites]
J Clin Endocrinol Metab. 2006 Apr;91(4):1397-403
[
16449332.001
]
[Cites]
Cancer Cell. 2006 Jun;9(6):459-71
[
16766265.001
]
[Cites]
Clin Chim Acta. 2006 Nov;373(1-2):176-9
[
16815351.001
]
[Cites]
Endocr Relat Cancer. 2006 Sep;13(3):707-16
[
16954426.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Oct 17;103(42):15558-63
[
17030811.001
]
[Cites]
Curr Opin Oncol. 2007 Jan;19(1):24-9
[
17133108.001
]
[Cites]
N Engl J Med. 2006 Dec 14;355(24):2558-73
[
17167139.001
]
[Cites]
Eur J Endocrinol. 2007 Jan;156(1):75-82
[
17218728.001
]
[Cites]
Mol Cell Biol. 2007 Feb;27(4):1495-504
[
17145768.001
]
[Cites]
Nat Clin Pract Endocrinol Metab. 2007 Mar;3(3):302-10
[
17315038.001
]
[Cites]
Rev Endocr Metab Disord. 2006 Dec;7(4):225-35
[
17308965.001
]
[Cites]
Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4101-5
[
17360484.001
]
[Cites]
Carcinogenesis. 2007 Mar;28(3):749-59
[
17071631.001
]
[Cites]
Endocr Rev. 2007 Apr;28(2):165-86
[
17325339.001
]
[Cites]
Pituitary. 2007;10(2):165-72
[
17458702.001
]
[Cites]
Clin Endocrinol (Oxf). 2007 Jun;66(6):859-68
[
17465997.001
]
[Cites]
Clin Endocrinol (Oxf). 2007 Jul;67(1):65-70
[
17437512.001
]
[Cites]
Clin Endocrinol (Oxf). 2007 Aug;67(2):282-9
[
17524029.001
]
[Cites]
Clin Endocrinol (Oxf). 2007 Aug;67(2):310-5
[
17555503.001
]
[Cites]
Eur J Endocrinol. 2007 Oct;157(4):371-82
[
17893250.001
]
[Cites]
IDrugs. 2007 Dec;10(12):885-95
[
18041687.001
]
[Cites]
Cell Death Differ. 2008 Jan;15(1):202-12
[
17962814.001
]
[Cites]
J Clin Endocrinol Metab. 2008 Jan;93(1):61-7
[
17971431.001
]
[Cites]
Rev Endocr Metab Disord. 2008 Mar;9(1):33-9
[
18075787.001
]
[Cites]
Clin Cancer Res. 2008 Apr 1;14(7):1984-96
[
18381936.001
]
[Cites]
J Clin Endocrinol Metab. 2008 Apr;93(4):1412-7
[
18211974.001
]
[Cites]
Nat Med. 1999 Nov;5(11):1317-21
[
10546001.001
]
[Cites]
Recent Prog Horm Res. 1999;54:397-438; discussion 438-9
[
10548885.001
]
[Cites]
Nature. 1999 Dec 9;402(6762):656-60
[
10604470.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Feb;85(2):707-14
[
10690880.001
]
[Cites]
J Clin Invest. 1982 Nov;70(5):965-77
[
6290540.001
]
[Cites]
Endocrinology. 1983 Apr;112(4):1553-5
[
6131812.001
]
[Cites]
Endocr Rev. 1983 Spring;4(2):97-130
[
6345149.001
]
[Cites]
Endocrinology. 1984 Nov;115(5):1952-7
[
6149116.001
]
[Cites]
Nature. 1987 Dec 10-16;330(6148):566-8
[
2825031.001
]
[Cites]
J Clin Invest. 1988 Apr;81(4):968-75
[
3127426.001
]
[Cites]
Proc Natl Acad Sci U S A. 1990 Jul;87(13):5061-5
[
2367524.001
]
[Cites]
Endocrinology. 1990 Sep;127(3):1033-40
[
2387246.001
]
[Cites]
Ann Intern Med. 1990 Dec 15;113(12):921-5
[
2240917.001
]
[Cites]
Endocrinology. 1990 Dec;127(6):3187-95
[
2123448.001
]
[Cites]
N Engl J Med. 1991 Dec 12;325(24):1688-95
[
1944469.001
]
[Cites]
J Clin Endocrinol Metab. 1992 Apr;74(4):914-9
[
1312542.001
]
[Cites]
Mol Endocrinol. 1992 Apr;6(4):598-606
[
1584223.001
]
[Cites]
Endocrinol Metab Clin North Am. 1992 Sep;21(3):597-614
[
1521514.001
]
[Cites]
Proc Natl Acad Sci U S A. 1992 Oct 15;89(20):9826-30
[
1409707.001
]
[Cites]
J Clin Endocrinol Metab. 1994 Sep;79(3):724-9
[
7521350.001
]
[Cites]
Mol Endocrinol. 1995 Jul;9(7):777-83
[
7476961.001
]
[Cites]
Recent Prog Horm Res. 1996;51:189-215; discussion 215-6
[
8701079.001
]
[Cites]
J Clin Invest. 1997 Feb 15;99(4):789-98
[
9045884.001
]
[Cites]
Mol Endocrinol. 1997 Apr;11(4):433-41
[
9092795.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7239-44
[
9207075.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Oct 14;94(21):11381-6
[
9326618.001
]
[Cites]
J Clin Invest. 1997 Nov 1;100(9):2386-92
[
9410919.001
]
[Cites]
Nat Genet. 1998 Apr;18(4):360-4
[
9537419.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Nov;83(11):3808-16
[
9814451.001
]
[Cites]
J Clin Endocrinol Metab. 1999 May;84(5):1518-23
[
10323372.001
]
[Cites]
Science. 1999 Jul 16;285(5426):418-22
[
10411507.001
]
[Cites]
Clin Endocrinol (Oxf). 1999 May;50(5):561-7
[
10468920.001
]
[Cites]
J Biol Chem. 2004 Dec 3;279(49):51100-6
[
15456744.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Feb;90(2):800-4
[
15562021.001
]
[Cites]
Endocrinology. 2005 Apr;146(4):1772-9
[
15618350.001
]
[Cites]
Mol Endocrinol. 2005 May;19(5):1383-91
[
15677710.001
]
[Cites]
Curr Opin Genet Dev. 2005 Jun;15(3):332-40
[
15917210.001
]
[Cites]
J Biol Chem. 2005 Jun 24;280(25):24011-21
[
15857828.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Jul;90(7):4405-10
[
15827109.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Aug;90(8):4483-8
[
15899958.001
]
[Cites]
Nat Struct Mol Biol. 2005 Sep;12(9):814-21
[
16116438.001
]
[Cites]
Clin Endocrinol (Oxf). 2008 Jun;68(6):970-5
[
18031313.001
]
[Cites]
J Clin Endocrinol Metab. 2008 Jun;93(6):2390-401
[
18381572.001
]
[Cites]
J Clin Endocrinol Metab. 2008 Jun;93(6):2035-41
[
18381584.001
]
[Cites]
Cell. 2008 Jun 13;133(6):1019-31
[
18555778.001
]
[Cites]
Endocrinology. 2008 Jul;149(7):3294-305
[
18388193.001
]
[Cites]
Int J Biochem Cell Biol. 2008;40(10):1984-9
[
17888716.001
]
[Cites]
Clin Chem. 2008 Aug;54(8):1268-76
[
18567697.001
]
[Cites]
Eur J Endocrinol. 2008 Aug;159(2):89-95
[
18524797.001
]
[Cites]
J Clin Endocrinol Metab. 2008 Aug;93(8):2957-68
[
18477663.001
]
[Cites]
J Clin Endocrinol Metab. 2008 Aug;93(8):2984-90
[
18492760.001
]
[Cites]
Mol Endocrinol. 2008 Sep;22(9):2190-202
[
18635665.001
]
[Cites]
J Clin Endocrinol Metab. 2008 Sep;93(9):3411-5
[
18611972.001
]
[Cites]
Mol Endocrinol. 2008 Oct;22(10):2278-92
[
18653781.001
]
[Cites]
J Clin Endocrinol Metab. 2008 Oct;93(10):4119-25
[
18628527.001
]
[Cites]
Proc Natl Acad Sci U S A. 2008 Nov 11;105(45):17498-503
[
18981426.001
]
[Cites]
Cancer Res. 2008 Dec 15;68(24):10163-70
[
19074883.001
]
[Cites]
Proc Natl Acad Sci U S A. 2008 Dec 23;105(51):20452-7
[
19088192.001
]
[Cites]
J Clin Endocrinol Metab. 2009 Jan;94(1):218-22
[
18957501.001
]
[Cites]
J Clin Endocrinol Metab. 2009 Feb;94(2):523-7
[
19033371.001
]
[Cites]
Mol Endocrinol. 2009 Mar;23(3):337-48
[
19131507.001
]
[Cites]
Cancer Res. 2009 Mar 1;69(5):1844-50
[
19223528.001
]
[Cites]
Eur J Endocrinol. 2009 Apr;160(4):543-8
[
19141605.001
]
[Cites]
Clin Endocrinol (Oxf). 2009 May;70(5):757-68
[
19178516.001
]
(PMID = 19884662.001).
[ISSN]
1558-8238
[Journal-full-title]
The Journal of clinical investigation
[ISO-abbreviation]
J. Clin. Invest.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA075979; United States / NCI NIH HHS / CA / CA 075979
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Review
[Publication-country]
United States
[Chemical-registry-number]
67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone
[Number-of-references]
125
[Other-IDs]
NLM/ PMC2769196
84.
Saeger W:
[Effects of irradiation therapy and inhibiting drugs on the pituitary and its adenomas].
Pathologe
; 2006 Feb;27(1):57-60
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[Title]
[Effects of irradiation therapy and inhibiting drugs on the
pituitary
and its
adenomas
].
Radiation therapies of
pituitary
adenomas
induce an increase in fibroses and nuclear pleomorphism.
Most
growth hormone
(
GH
)
secreting
pituitary
adenomas
react to somatostatin analogues by a distinct decrease
of GH
secretion.
Some cases show a shrinkage
of adenomas
that correlates with fibrosis of the tumor.
With these drugs, thyroid stimulating
hormone secreting adenomas
can also be treated.
Prolactin
secreting adenomas
are mostly treated primarily with dopamine agonists.
Up to 90% of cases show a strong decrease in
hormone
secretion and a distinct shrinkage of the
adenomas
based on strong decrease in
adenoma
cell
volume.
Long-term medication with high doses of glucocorticoids induces Crooke's cells in the anterior
pituitary
.
[MeSH-major]
Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use.
Pituitary
Gland
/ pathology.
Pituitary
Neoplasms / drug therapy.
Pituitary
Neoplasms / radiotherapy. Radiotherapy / adverse effects
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
MedlinePlus Health Information.
consumer health - Radiation Therapy
.
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[Cites]
Endocrine. 2004 Nov;25(2):141-5
[
15711028.001
]
[Cites]
Endocr Pathol. 2000 Winter;11(4):341-352
[
12114758.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8
[
12107192.001
]
[Cites]
Pathol Res Pract. 1986 Jun;181(3):280-90
[
3748874.001
]
[Cites]
Histol Histopathol. 1987 Apr;2(2):135-42
[
2980713.001
]
[Cites]
Ultrastruct Pathol. 2005 May-Aug;29(3-4):163-7
[
16036872.001
]
[Cites]
Endocrine. 2001 Apr;14(3):329-36
[
11444429.001
]
[Cites]
Pathol Res Pract. 1993 Nov;189(9):1044-51
[
8302723.001
]
[Cites]
Exp Clin Endocrinol. 1992;100(3):106-11
[
1305059.001
]
[Cites]
Acta Endocrinol (Copenh). 1991 Apr;124(4):487-91
[
2031445.001
]
[Cites]
Mayo Clin Proc. 1997 Oct;72(10):893-900
[
9379690.001
]
[Cites]
J Neurooncol. 2001 Sep;54(2):151-66
[
11761432.001
]
[Cites]
Microsc Res Tech. 1992 Jan 15;20(2):162-76
[
1547357.001
]
[Cites]
Exp Clin Endocrinol. 1988 Sep;92(1):59-68
[
2906615.001
]
(PMID = 16362259.001).
[ISSN]
0172-8113
[Journal-full-title]
Der Pathologe
[ISO-abbreviation]
Pathologe
[Language]
ger
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Dopamine Agonists; 0 / Glucocorticoids
85.
Tunici P, Yu JS:
Pituitary adenoma stem cells.
Methods Mol Biol
; 2009;568:195-201
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[Title]
Pituitary adenoma
stem cells.
The identification of a subpopulation of brain tumor cells with potent tumorigenic capacity strengthens the cancer stem
cell
hypothesis of the origin of the tumors that has recently attracted the attention of many researchers.
These cells express stem
cell
markers, and when differentiated they express glial and neuronal markers.
More recently we have isolated tumor stem-like cells also from benign tumors like
pituitary
adenomas
.
Cells derived from
pituitary
adenomas
are able to grow as floating aggregates resembling the neurospheres (typical of normal stem cells) in a medium supplemented by
growth
factors (EGF and bFGF).
The immunocytochemical analysis revealed that
pituitary
tumor stem-like cells are positives for nestin and, when grown for ten days in differentiation medium they express GFAP, BIII tubulin, and S-100.
In vitro tumor stem-like cells derived from a patient with a
somatotroph
adenoma
showed high production
of growth hormone
and prolactin, while cells derived from the same patient but grown in presence of fetal bovine serum showed no production of hormones.
[MeSH-major]
Cell
Culture Techniques / methods. Neoplastic Stem Cells / pathology.
Pituitary
Neoplasms / pathology
[MeSH-minor]
Human
Growth Hormone
/ metabolism. Humans. Immunohistochemistry. Prolactin / metabolism
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.
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(PMID = 19582428.001).
[ISSN]
1064-3745
[Journal-full-title]
Methods in molecular biology (Clifton, N.J.)
[ISO-abbreviation]
Methods Mol. Biol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin
86.
Lonser RR, Kindzelski BA, Mehta GU, Jane JA Jr, Oldfield EH:
Acromegaly without imaging evidence of pituitary adenoma.
J Clin Endocrinol Metab
; 2010 Sep;95(9):4192-6
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[Title]
Acromegaly
without imaging evidence of
pituitary adenoma
.
CONTEXT:
GH
-
secreting
pituitary
adenomas
are nearly always visible on conventional magnetic resonance (MR) imaging.
However, management and outcome of acromegalic patients lacking imaging evidence
of GH
-
secreting
pituitary
adenomas
are undefined.
OBJECTIVE: The aim was to evaluate surgical exploration for MR-invisible
GH
-
secreting
pituitary
adenomas
.
PATIENTS OR OTHER PARTICIPANTS: Consecutive acromegalic patients without imaging evidence of a
pituitary adenoma
on pre- and postcontrast, spin echo T1-weighted MR imaging and who lacked evidence of an ectopic (nonpituitary) source causing
GH
excess were included.
INTERVENTIONS: Surgical exploration with identification and resection of a
pituitary adenoma
was performed.
MAIN OUTCOME MEASURES: Laboratory values (
GH
, IGF-I), surgical findings, and clinical outcome were analyzed.
RESULTS: Six patients (three males, three females; 3% of all patients) with suspected
GH
-
secreting adenomas
did not demonstrate imaging evidence of
pituitary adenoma
on conventional MR imaging.
Three patients underwent a postcontrast, volumetric interpolated breath-hold examination MR-imaging sequence (1.2-mm slice thickness), which revealed a 4-mm
pituitary adenoma
not seen on the spin echo T1-weighted MR imaging in one patient.
A
pituitary adenoma
was identified and removed in all patients (mean diameter, 5.6 mm; range, 5 to 6.7 mm).
Histological analysis confirmed that the lesions were
GH
-
secreting adenomas
.
CONCLUSION:
Acromegaly
can be caused by
GH
-
secreting
pituitary
adenomas
that are not evident on conventional MR imaging.
Adenomas
in some of these patients become evident using volumetric interpolated breath-hold examination MR imaging.
Surgical exploration of the
pituitary
gland
in acromegalic patients with endocrine findings consistent with a
GH
-
secreting
adenoma
but negative MR imaging can lead to identification and removal of an
adenoma
.
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[Cites]
Pituitary. 1999 Jun;2(1):29-41
[
11081170.001
]
[Cites]
Pituitary. 2011 Dec;14(4):414-7
[
19904612.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Apr;88(4):1565-9
[
12679440.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Feb;89(2):667-74
[
14764779.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Jul;89(7):3099-102
[
15240576.001
]
[Cites]
AJR Am J Roentgenol. 1990 May;154(5):1075-7
[
2108545.001
]
[Cites]
AJR Am J Roentgenol. 2005 Jan;184(1):313-9
[
15615994.001
]
[Cites]
Eur Radiol. 2005 Mar;15(3):543-8
[
15627195.001
]
[Cites]
Eur J Endocrinol. 2005 Mar;152(3):379-87
[
15757854.001
]
[Cites]
J Neurosurg. 2006 Jan;104(1):7-19
[
16509142.001
]
[Cites]
N Engl J Med. 2006 Dec 14;355(24):2558-73
[
17167139.001
]
[Cites]
J Clin Endocrinol Metab. 2008 Jun;93(6):2035-41
[
18381584.001
]
[Cites]
Orphanet J Rare Dis. 2008;3:17
[
18578866.001
]
[Cites]
Endocr Pract. 2008 Sep;14(6):757-63
[
18996799.001
]
[Cites]
J Clin Endocrinol Metab. 2009 May;94(5):1509-17
[
19208732.001
]
[Cites]
AJNR Am J Neuroradiol. 2002 Jun-Jul;23(6):995-1002
[
12063232.001
]
(PMID = 20610592.001).
[ISSN]
1945-7197
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
ENG
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Case Reports; Journal Article; Multicenter Study; Research Support, N.I.H., Intramural
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2936064
87.
Bondanelli M, Bonadonna S, Ambrosio MR, Doga M, Gola M, Onofri A, Zatelli MC, Giustina A, degli Uberti EC:
Cardiac and metabolic effects of chronic growth hormone and insulin-like growth factor I excess in young adults with pituitary gigantism.
Metabolism
; 2005 Sep;54(9):1174-80
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[Title]
Cardiac and metabolic effects of chronic
growth hormone
and insulin-like
growth
factor I excess in young adults with
pituitary
gigantism.
Chronic
growth hormone
(
GH
)/insulin-like
growth
factor I (IGF-I) excess is associated with considerable mortality in
acromegaly
, but no data are available in
pituitary
gigantism.
The aim of the study was to evaluate the long-term effects of early exposure to
GH
and IGF-I excess on cardiovascular and metabolic parameters in adult patients with
pituitary
gigantism.
Six adult male patients with newly diagnosed gigantism due to
GH secreting
pituitary adenoma
were studied and compared with 6 age- and sex-matched patients with
acromegaly
and 10 healthy subjects.
Disease
duration was significantly longer (P<.05) in patients with gigantism than in patients with
acromegaly
, whereas
GH
and IGF-I concentrations were comparable.
Left ventricular mass was increased both in patients with gigantism and in patients with
acromegaly
, as compared with controls.
Left ventricular hypertrophy was detected in 2 of 6 of both patients with gigantism and patients with
acromegaly
, and isolated intraventricular septum thickening in 1 patient with gigantism.
Inadequate diastolic filling (ratio between early and late transmitral flow velocity<1) was detected in 2 of 6 patients with gigantism and 1 of 6 patients with
acromegaly
.
Impaired glucose metabolism occurrence was higher in patients with
acromegaly
(66%) compared with patients with gigantism (16%).
In conclusion, our data suggest that
GH
/IGF-I excess in young adult patients is associated with morphologic and functional cardiac abnormalities that are similar in patients with gigantism and in patients with
acromegaly
, whereas occurrence of impaired glucose metabolism appears to be higher in patients with
acromegaly
, although patients with gigantism are exposed to
GH
excess for a longer period.
[MeSH-major]
Gigantism / complications. Gigantism / metabolism. Human
Growth Hormone
/ blood. Hypertrophy, Left Ventricular / etiology. Hypertrophy, Left Ventricular / metabolism. Insulin-Like
Growth
Factor I / metabolism
[MeSH-minor]
Acromegaly
/ complications.
Acromegaly
/ metabolism. Adult. Blood Pressure. Echocardiography, Doppler. Electrocardiography. Glucose / metabolism. Glucose Intolerance / etiology. Glucose Intolerance / metabolism. Humans. Male. Ventricular Dysfunction, Left / etiology. Ventricular Dysfunction, Left / metabolism. Ventricular Dysfunction, Left / ultrasonography
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(PMID = 16125529.001).
[ISSN]
0026-0495
[Journal-full-title]
Metabolism: clinical and experimental
[ISO-abbreviation]
Metab. Clin. Exp.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; IY9XDZ35W2 / Glucose
88.
Morita K, Takano K, Yasufuku-Takano J, Yamada S, Teramoto A, Takei M, Osamura RY, Sano T, Fujita T:
Expression of pituitary tumour-derived, N-terminally truncated isoform of fibroblast growth factor receptor 4 (ptd-FGFR4) correlates with tumour invasiveness but not with G-protein alpha subunit (gsp) mutation in human GH-secreting pituitary adenomas.
Clin Endocrinol (Oxf)
; 2008 Mar;68(3):435-41
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[Title]
Expression of
pituitary
tumour-derived, N-terminally truncated isoform of fibroblast
growth
factor receptor 4 (ptd-FGFR4) correlates with tumour invasiveness but not with G-protein alpha subunit (gsp) mutation in human
GH
-
secreting
pituitary
adenomas
.
OBJECTIVE: Apart from the constitutively activating mutation of the G-protein alpha subunit (Gsalpha) (gsp mutation), factors involved in tumorigenesis or those in tumour behaviour remain elusive in sporadic
GH
-
secreting
pituitary
adenomas
.
Recently, the N-terminally truncated form of fibroblast
growth
factor receptor-4 (ptd-FGFR4) was identified in
pituitary
adenomas
.
This aberrant receptor has transforming activity, and causes
pituitary
adenomas
in transgenic mice.
MATERIALS AND METHODS: mRNA was extracted from excised
adenomas of
45 Japanese acromegalic patients. ptd-FGFR4 expression and gsp mutations were determined by reverse transcription polymerase chain reaction (RT-PCR) and direct sequencing.
Preoperative clinical data were collected by reviewing medical charts and
pituitary
magnetic resonance imaging (MRI) scans.
The presence of ptd-FGFR4 did not correlate with age at operation, sex, preoperative serum
GH
or IGF-1 levels.
CONCLUSIONS: We found that ptd-FGFR4 expression and gsp mutations occur independently of each other, and that ptd-FGFR4 expression is associated with more invasive tumours in patients with
GH
-
secreting
pituitary
adenomas
.
[MeSH-major]
GTP-Binding Protein alpha Subunits / genetics. Gene Expression.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ genetics. Mutation. Neoplasm Invasiveness.
Pituitary
Neoplasms / genetics. Receptor, Fibroblast
Growth
Factor, Type 4 / genetics
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(PMID = 18070145.001).
[ISSN]
1365-2265
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / GTP-Binding Protein alpha Subunits; 0 / Protein Isoforms; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 4
89.
Colao A, Cappabianca P, Caron P, De Menis E, Farrall AJ, Gadelha MR, Hmissi A, Rees A, Reincke M, Safari M, T'Sjoen G, Bouterfa H, Cuneo RC:
Octreotide LAR vs. surgery in newly diagnosed patients with acromegaly: a randomized, open-label, multicentre study.
Clin Endocrinol (Oxf)
; 2009 May;70(5):757-68
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[Title]
Octreotide LAR vs. surgery in newly diagnosed patients with
acromegaly
: a randomized, open-label, multicentre study.
Efficacy was assessed by changes in mean
GH
and IGF-I serum concentrations, at weeks 12, 24 and 48.
Patients uncontrolled after surgery received octreotide LAR 20 mg, increased to 30 mg if
acromegaly
was still uncontrolled.
CONCLUSION: This first randomized study in unselected patients indicates that the 48-week treatment outcome of octreotide LAR as first-line treatment of
acromegaly
does not significantly differ from surgery.
As a complete response to surgery in
GH
-
secreting
macro-
adenomas
can be difficult, first-line therapy with octreotide LAR can be considered as a viable alternative for most patients with
acromegaly
, due to its low complication rate.
[MeSH-major]
Acromegaly
/ drug therapy.
Acromegaly
/ surgery. Octreotide / therapeutic use
[MeSH-minor]
Adult. Aged. Female.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ blood.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ complications.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ drug therapy.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ surgery. Human
Growth Hormone
/ blood. Humans. Insulin-Like
Growth
Factor I / metabolism. Magnetic Resonance Imaging. Male. Middle Aged. Treatment Outcome. Young Adult
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[CommentIn]
Clin Endocrinol (Oxf). 2010 Jul;73(1):134; author reply 135-6
[
20039884.001
]
(PMID = 19178516.001).
[ISSN]
1365-2265
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; RWM8CCW8GP / Octreotide
90.
Zatelli MC, Minoia M, Filieri C, Tagliati F, Buratto M, Ambrosio MR, Lapparelli M, Scanarini M, Degli Uberti EC:
Effect of everolimus on cell viability in nonfunctioning pituitary adenomas.
J Clin Endocrinol Metab
; 2010 Feb;95(2):968-76
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[Title]
Effect of everolimus on
cell
viability in nonfunctioning
pituitary
adenomas
.
CONTEXT:
Pituitary
adenomas
can cause specific syndromes due to
hormone
excess and/or determine sellar mass symptoms.
Pituitary
cell growth
can sometimes be influenced by medical therapy, such as for
somatotroph adenomas
treated with somatostatin analogs or prolactinomas treated with dopaminergic drugs.
However, nonfunctioning
pituitary
adenomas
(NFAs) are still orphans of medical therapy.
Cell
viability and apoptosis were evaluated after 48 h, and vascular endothelial
growth
factor (VEGF) secretion was assessed after an 8-h incubation.
RESULTS: In 28 cultures (70%), Everolimus significantly reduced
cell
viability (by approximately 40%; P < 0.05 vs. control), promoted apoptosis (+30%; P < 0.05 vs. control), inhibited p70S6K activity (-20%), and blocked IGF-I proliferative and antiapoptotic effects.
CONCLUSIONS: Everolimus reduced NFA
cell
viability by inducing apoptosis, with a mechanism likely involving IGF-I signaling but not VEGF secretion, suggesting that it might represent a possible medical treatment of invasive/recurrent NFAs.
[MeSH-major]
Adenoma
/ drug therapy. Immunosuppressive Agents / pharmacology.
Pituitary
Neoplasms / drug therapy. Sirolimus / analogs & derivatives
[MeSH-minor]
Aged. Apoptosis / drug effects.
Cell
Line, Tumor.
Cell
Survival / drug effects. Ergolines / pharmacology. Everolimus. Female. Humans. Male. Middle Aged. Receptors, Somatostatin / physiology. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Somatostatin / analogs & derivatives. Somatostatin / pharmacology. Vascular Endothelial
Growth
Factor A / secretion
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.
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(PMID = 19965918.001).
[ISSN]
1945-7197
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Ergolines; 0 / Immunosuppressive Agents; 0 / Receptors, Somatostatin; 0 / Vascular Endothelial Growth Factor A; 0 / somatostatin receptor 2; 51110-01-1 / Somatostatin; 98H1T17066 / pasireotide; 9HW64Q8G6G / Everolimus; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; LL60K9J05T / cabergoline; W36ZG6FT64 / Sirolimus
91.
Mao ZG, He DS, Zhou J, Yao B, Xiao WW, Chen CH, Zhu YH, Wang HJ:
Differential expression of microRNAs in GH-secreting pituitary adenomas.
Diagn Pathol
; 2010 Dec 07;5:79
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[Title]
Differential expression of microRNAs in
GH
-
secreting
pituitary
adenomas
.
BACKGROUND: The purpose of this study was to (1) identify specific miRNAs in
growth
hormones (
GH
)-
secreting
pituitary
adenomas
;.
METHODS: Fifteen
GH
-
secreting adenomas
patients were treated with lanreotide for 4 months before surgery.
Patients with 50% reduction
of GH
secretion by lanreotide were considered as SSA responders, while patients with less than 50%
of GH
reduction were considered as SSA nonresponders.
We analyzed the miRNAs in 21
GH
-
secreting
pituitary
adenomas
and 6 normal pituitaries by miRCURY™ LNA array and some differentially expressed miRNAs were validated by quantitative real-time PCR.
RESULTS: Fifty-two miRNAs were differentially expressed between
GH
-
secreting
pituitary
adenomas
and normal pituitaries.
Differential expression of 9 miRNAs was observed between micro- and macro-
adenomas
.
Seven miRNAs were differentially expressed between SSA responders or
GH
nonresponders.
Several identified miRNAs may be involved in
cell
proliferation, apoptosis, cancer development and progression.
CONCLUSIONS: Our results indicate that altered miRNAs expression is involved in
GH
-
secreting
pituitary
adenomas
transformation, which will shed light on the mechanisms for the treatment of
acromegaly
by SSA.
Identification and characterization of the targets of altered miRNAs genes may elucidate molecular mechanisms involved in the pathogenesis of
pituitary adenoma
.
[MeSH-major]
Adenoma
/ genetics. Gene Expression Profiling.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ genetics. MicroRNAs / analysis
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
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[Cites]
Endocr Relat Cancer. 2008 Sep;15(3):721-43
[
18753362.001
]
[Cites]
RNA. 2008 Jul;14(7):1433-42
[
18492795.001
]
[Cites]
EMBO J. 2008 Oct 8;27(19):2616-27
[
18756266.001
]
[Cites]
Proc Natl Acad Sci U S A. 2008 Dec 9;105(49):19300-5
[
19033458.001
]
[Cites]
J Clin Endocrinol Metab. 2009 Jan;94(1):320-3
[
18840638.001
]
[Cites]
Eur J Endocrinol. 2010 Apr;162(4):661-6
[
20061334.001
]
[Cites]
Nature. 2000 Feb 24;403(6772):901-6
[
10706289.001
]
[Cites]
Nature. 2000 Nov 2;408(6808):86-9
[
11081512.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Jan;86(1):140-5
[
11231991.001
]
[Cites]
Neurosurgery. 2001 Jun;48(6):1239-43; discussion 1244-5
[
11383725.001
]
[Cites]
Nucleic Acids Res. 2001 May 1;29(9):e45
[
11328886.001
]
[Cites]
Biochim Biophys Acta. 2003 Sep 22;1616(1):1-84
[
14507421.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Apr;89(4):1577-85
[
15070915.001
]
[Cites]
J Cell Physiol. 2005 Jul;204(1):280-5
[
15648093.001
]
[Cites]
Cancer Res. 2005 Aug 15;65(16):7065-70
[
16103053.001
]
[Cites]
Nat Rev Cancer. 2006 Apr;6(4):259-69
[
16557279.001
]
[Cites]
Cancer Res. 2006 Aug 1;66(15):7390-4
[
16885332.001
]
[Cites]
Dev Cell. 2006 Oct;11(4):441-50
[
17011485.001
]
[Cites]
J Cell Physiol. 2007 Feb;210(2):370-7
[
17111382.001
]
[Cites]
N Engl J Med. 2006 Dec 14;355(24):2558-73
[
17167139.001
]
[Cites]
Eur J Endocrinol. 2007 Jan;156(1):65-74
[
17218727.001
]
[Cites]
Genes Dev. 2007 Apr 1;21(7):744-9
[
17403776.001
]
[Cites]
Trends Genet. 2007 May;23(5):243-9
[
17368621.001
]
[Cites]
Cell. 2007 Jun 29;129(7):1401-14
[
17604727.001
]
[Cites]
Clin Endocrinol (Oxf). 2007 Aug;67(2):282-9
[
17524029.001
]
[Cites]
Cancer Res. 2007 Aug 15;67(16):7713-22
[
17699775.001
]
[Cites]
Endocr Relat Cancer. 2007 Sep;14(3):791-8
[
17914108.001
]
[Cites]
J Biol Chem. 2007 Nov 9;282(45):32582-90
[
17827156.001
]
[Cites]
Nat Rev Mol Cell Biol. 2008 Mar;9(3):219-30
[
18270516.001
]
[Cites]
Semin Cancer Biol. 2008 Apr;18(2):103-10
[
18295504.001
]
[Cites]
J Clin Endocrinol Metab. 2008 Apr;93(4):1203-10
[
18198230.001
]
[Cites]
J Clin Endocrinol Metab. 2008 May;93(5):1616-24
[
18303074.001
]
[Cites]
Genes Chromosomes Cancer. 2008 Nov;47(11):939-46
[
18663744.001
]
(PMID = 21138567.001).
[ISSN]
1746-1596
[Journal-full-title]
Diagnostic pathology
[ISO-abbreviation]
Diagn Pathol
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00993356
[Publication-type]
Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / MicroRNAs; 0 / Peptides, Cyclic; 0G3DE8943Y / lanreotide; 51110-01-1 / Somatostatin
[Other-IDs]
NLM/ PMC3017030
92.
Lee YH, Noh TW, Lee MK, Jameson JL, Lee EJ:
Absence of activating mutations of CXCR4 in pituitary tumours.
Clin Endocrinol (Oxf)
; 2010 Feb;72(2):209-13
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[Title]
Absence of activating mutations of CXCR4 in
pituitary
tumours.
OBJECTIVE: Mutations of the gsp oncogene are responsible for 30-40%
of GH
-
producing
pituitary
adenomas
and 10% of nonfunctioning
pituitary
adenomas
(NFPAs).
However, the pathogenetic mechanism of the remaining
pituitary
tumours still remains to be identified.
Recently, the interaction between the chemokine stromal
cell
-derived factor 1 and its receptor CXCR4 was found to play an important role in
GH
production and
cell
proliferation in various
pituitary adenoma
cell
lines.
As CXCR4 is a Gi-coupled chemokine receptor, its constitutive activating mutations may be involved in
pituitary
tumour formation by cyclic adenosine monophosphate (cAMP)-independent, ERK-related pathways.
PATIENTS AND METHODS: We investigated whether somatic activating-mutations of CXCR4 might be a possible tumourigenic mechanism for gsp-negative
GH
-
secreting
pituitary
adenomas
and NFPAs.
Direct sequencing of polymerase chain reaction-amplified products for coding exons of CXCR4 were performed using genomic deoxyribonucleic acid samples from 37
GH
-
producing
pituitary
tumour tissues that were negative for the gsp mutation and 14 CXCR4 expressing NFPAs.
RESULTS: Immunohistochemical analyses and double immunofluorescent staining of sectioned paraffin-embedded
pituitary
tissues revealed that CXCR4 is highly expressed in
GH
-
producing
pituitary
adenomas
and NFPAs.
Direct sequencing showed that two synonymous mutations in exon 2 (87 C > T and 414 C > T) were detected in 4 out of 51
pituitary
tumours.
CONCLUSION: Our results indicate that an activating mutation of the CXCR4 may not be a common pathogenetic mechanism in
GH
-
producing
pituitary
tumours and NFPAs.
[MeSH-major]
Pituitary
Neoplasms / genetics.
Pituitary
Neoplasms / metabolism. Receptors, CXCR4 / genetics. Receptors, CXCR4 / metabolism
[MeSH-minor]
Growth Hormone
-
Secreting
Pituitary Adenoma
/ genetics.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ metabolism. Humans. Immunohistochemistry. Mutation. Polymerase Chain Reaction
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(PMID = 19473177.001).
[ISSN]
1365-2265
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Receptors, CXCR4
93.
Scacchi M, Cavagnini F:
Acromegaly.
Pituitary
; 2006;9(4):297-303
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[Title]
Acromegaly
.
Acromegaly
is a slowly progressive
disease
characterized by 30% increase of mortality rate for cardiovascular
disease
, respiratory complications and malignancies.
The estimated prevalence of the
disease
is 40 cases/1000000 population with 3-4 new cases/1000000 population per year.
The biochemical
diagnosis
is based upon the demonstration of high circulating levels
of GH
and IGF-I.
A random
GH
level lower than 0.4 microg/l and an IGF-I value in the age- and sex-matched normal range makes
the diagnosis
of
acromegaly
unlikely.
In doubtful cases, the lack
of GH
suppressibility below 1 microg/l (0.3 microg/l according to recent reports) after an oral glucose load will confirm
the diagnosis
.
A
pituitary adenoma
is demonstrated in most cases by CT scan or MRI.
A negative X-ray
finding
or the presence of empty sella do not exclude
the diagnosis
.
At the moment
of diagnosis
all patients should undergo colonscopy.
Surgery, radiotherapy and medical treatment represent the therapeutic options for
acromegaly
.
The outcome of transsphenoidal surgery is far better for microadenomas (80-90%) than for macroadenomas (less than 50%), which unluckily represent more than 70% of all
GH
-
secreting
pituitary
tumours.
Therefore,
pituitary
surgery is the first line treatment for microadenomas.
Medical therapy is based on
GH
-lowering drugs (somatostatin receptor agonists and, in some cases, dopaminergic agents) and
GH
receptor antagonists (pegvisomant).
However,
GH
-lowering drugs are also used as primary therapy when surgery is contraindicated or in the case of large
GH
-
secreting
macroadenomas which are not likely to be completely removed by surgery.
For the moment pegvisomant is indicated for patients resistant to
the GH
-lowering drugs and there is no evidence for drug-induced enlargement of the
pituitary
tumour.
In order to avoid this possibility, however, a combination of pegvisomant and
GH
-lowering compound can also be conceived.
It is indicated after unsuccessful surgical and/or medical treatment and allows the control of hormonal secretion and tumour
growth
in approx.
Acromegaly
is defined as controlled when, in the absence of clinical activity, IGF-I levels are in the age- and sex-matched normal range and
GH
is normally suppressible by the oral glucose load.
[MeSH-major]
Acromegaly
/ etiology.
Adenoma
/ complications.
Growth Hormone
-
Secreting
Pituitary Adenoma
/ complications
[MeSH-minor]
Algorithms. Biomarkers / blood. Cardiovascular Diseases / etiology. Combined Modality Therapy. Dopamine Agonists / therapeutic use. Glucose Tolerance Test.
Hormone
Antagonists / therapeutic use. Human
Growth Hormone
/ blood. Humans. Hypophysectomy. Insulin-Like
Growth
Factor I / analysis. Radiotherapy, Adjuvant. Respiration Disorders / etiology. Sleep Apnea Syndromes / etiology. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use. Treatment Outcome. Up-Regulation
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[Cites]
J Clin Endocrinol Metab. 2003 Mar;88(3):963-8
[
12629068.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Feb;89(2):495-500
[
14764751.001
]
[Cites]
Lancet. 2001 Nov 24;358(9295):1754-9
[
11734231.001
]
[Cites]
Endocr Rev. 2002 Oct;23 (5):623-46
[
12372843.001
]
[Cites]
Clin Endocrinol (Oxf). 2003 Feb;58(2):132-5
[
12580925.001
]
[Cites]
Clin Endocrinol (Oxf). 2003 Feb;58(2):128-31
[
12580924.001
]
[Cites]
Eur J Endocrinol. 2004 Apr;150(4):465-71
[
15080775.001
]
[Cites]
Ann Endocrinol (Paris). 2003 Dec;64(6):434-41
[
15067248.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Jun;86(6):2779-86
[
11397887.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8
[
12107192.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Aug;87(8):3534-6
[
12161470.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Mar;85(3):1287-9
[
10720077.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Feb;89(2):658-61
[
14764777.001
]
[Cites]
J Clin Endocrinol Metab. 2004 Feb;89(2):492-4
[
14764750.001
]
[Cites]
J Endocrinol Invest. 2003 Dec;26(12):1242-7
[
15055479.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Oct;88(10 ):4759-67
[
14557452.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Feb;85(2):526-9
[
10690849.001
]
[Cites]
J Clin Endocrinol Metab. 2002 Sep;87(9):4054-8
[
12213843.001
]
[Cites]
Endocr Rev. 2004 Feb;25(1):102-52
[
14769829.001
]
[Cites]
J Clin Endocrinol Metab. 1998 Sep;83(9):3034-40
[
9745397.001
]
[Cites]
J Clin Endocrinol Metab. 2003 Nov;88(11):5334-40
[
14602770.001
]
[Cites]
Clin Endocrinol (Oxf). 2003 Feb;58(2):136-7
[
12580926.001
]
[Cites]
Clin Endocrinol (Oxf). 2003 Apr;58(4):387-99
[
12641619.001
]
(PMID = 17077948.001).
[ISSN]
1573-7403
[Journal-full-title]
Pituitary
[ISO-abbreviation]
Pituitary
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers; 0 / Dopamine Agonists; 0 / Hormone Antagonists; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I
[Number-of-references]
23
94.
Jaquet P, Gunz G, Saveanu A, Barlier A, Dufour H, Taylor J, Dong J, Kim S, Moreau JP, Culler MD:
BIM-23A760, a chimeric molecule directed towards somatostatin and dopamine receptors, vs universal somatostatin receptors ligands in GH-secreting pituitary adenomas partial responders to octreotide.
J Endocrinol Invest
; 2005;28(11 Suppl International):21-7
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[Title]
BIM-23A760, a chimeric molecule directed towards somatostatin and dopamine receptors, vs universal somatostatin receptors ligands in
GH
-
secreting
pituitary
adenomas
partial responders to octreotide.
We report the comparative efficacy of a somatostatin receptor 1 and 5 subtypes (SSTR2 and SSTR5), and dopamine D2 (DAD2) compound, BIM-23A760, in suppressing
GH
secretion, in
cell
culture from human
GH
-
secreting
tumors, from patients partially responsive to long-term treatments with octreotide or lanreotide.
The SSTR2-selective analog, BIM-23197, the SSTR5-selective analog, BIM-23268, and the dopamine (DA) analog, BIM-53097, produced a mean maximal suppression
of GH
secretion (24 +/- 3, 20 +/- 3, and 20 +/- 3%, respectively) that was similar to that obtained with octreotide (23 +/- 3%).
Among a series of new chimeric compounds that bind the SSTR2, SSTR5, and DAD2 receptors with variable affinities, BIM-23A760 produced greater maximal suppression
of GH
secretion than octreotide (38 +/- 2 vs 24 +/- 2%; p<0.03).
In the presence of sulpride, the dose response inhibition
of GH
secretion by the trihybrid molecule, BIM-23A760, was partially reversed.
When SSTRs pan inhibitors such as BIM-23A779 (binding affinity for SSTR1, SSTR2, SSTR3, SSTR5, respectively: 2.5, 0.3, 0.6, 0.6 nmol/l) or SOM230 were tested for their suppressive effects on
GH
secretion, they were less potent than the previous dopastatin hybrid molecule.
After a brief exposure to a SSTR2-selective analog, BIM-23197, or to a DA analog, BIM-53097, the maximal
GH
suppression was achieved during 12 h.
Under exposure to BIM-23A760, in the same conditions, maximal suppression
of GH
secretion lasted for 24 h.
As compared to the dopastatin compound, the lower efficacy of the universal somatostatin ligands in the inhibition
of GH
secretion
of GH
-
secreting
tumors argues for the use of drugs targeted, according to specific receptors expression and functionality which may vary among the various classes of tumors.
[MeSH-major]
Human
Growth Hormone
/ secretion. Octreotide / therapeutic use.
Pituitary
Neoplasms / drug therapy.
Pituitary
Neoplasms / secretion. Receptors, Dopamine / metabolism. Receptors, Somatostatin / metabolism
[MeSH-minor]
Acromegaly
/ drug therapy. Adult. Female. Gene Expression. Humans. Male. Oligopeptides / pharmacology. Piperazines / pharmacology. Prolactin / secretion. RNA, Messenger / analysis. Receptors, Dopamine D2 / genetics
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.
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(PMID = 16625841.001).
[ISSN]
0391-4097
[Journal-full-title]
Journal of endocrinological investigation
[ISO-abbreviation]
J. Endocrinol. Invest.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Italy
[Chemical-registry-number]
0 / BIM 23197; 0 / Oligopeptides; 0 / Piperazines; 0 / RNA, Messenger; 0 / Receptors, Dopamine; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin; RWM8CCW8GP / Octreotide
95.
Chanson P:
[Acromegaly].
Presse Med
; 2009 Jan;38(1):92-102
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[Title]
[
Acromegaly
].
Acromegaly
is a rare
disease
usually caused by
growth hormone
(
GH
) hypersecretion, due to a
pituitary adenoma
; in very rare cases,
acromegaly
is due to ectopic secretion of GHRH, responsible for
pituitary
hyperplasia.
Owing to its insidious onset,
acromegaly
is often diagnosed late (4 to > 10 years after onset), at an average age of about 40 years, in front of an acquired, slowly progressing disfigurement mainly involving the face and extremities.
Acromegaly
has also rheumatologic, cardiovascular, respiratory and metabolic consequences which determine its prognosis.
The diagnosis
is based on an increased serum
GH
concentration unsuppressed following an oral glucose load (oral glucose tolerance test -OGTT-) and an increased insulin-like
growth
factor-I (IGF-I); according to a 2000 Consensus statement, if the basal serum
GH
is above 0,4microg/L (1.2mIU/L) and/or if the IGF-I is elevated, an OGTT must be performed.
If the lowest
GH
value (nadir) during OGTT remains above 1microg/L (3mIU/L),
acromegaly
is confirmed.
Treatment is aimed at correcting (or preventing) tumor compression by excising the culprit lesion, and at reducing
GH
and IGF-I levels to normal values (or at least to a "safe"
GH
level of < 2microg/L or < 6mIU/L).
A stepwise therapeutic strategy is used: transsphenoidal surgery is often the first-line treatment; when surgery fails to correct
GH
/IGF-I hypersecretion, medical treatment with somatostatin analogs and/or radiotherapy can be used, somatostatin analogs being generally preferred;
the GH
antagonist (pegvisomant) is used in patients that are resistant or intolerant to somatostatin analogs.
Prognosis of
acromegaly
has improved in the recent years: adequate hormonal
disease
control is achieved in most cases, allowing life expectancy similar to that of the general population.
[MeSH-major]
Acromegaly
/ etiology
[MeSH-minor]
Adenoma
/ complications.
Adenoma
/ surgery. Age Factors. Glucose Tolerance Test. Human
Growth Hormone
/ antagonists & inhibitors. Human
Growth Hormone
/ blood. Human
Growth Hormone
/ secretion. Humans. Insulin-Like
Growth
Factor I / analysis.
Pituitary
Neoplasms / complications.
Pituitary
Neoplasms / surgery. Prognosis. Risk Factors
Genetic Alliance.
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(PMID = 19004612.001).
[ISSN]
2213-0276
[Journal-full-title]
Presse medicale (Paris, France : 1983)
[ISO-abbreviation]
Presse Med
[Language]
fre
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
France
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
[Number-of-references]
34
96.
Pollock BE:
Radiosurgery for pituitary adenomas.
Prog Neurol Surg
; 2007;20:164-71
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[Title]
Radiosurgery for
pituitary
adenomas
.
Stereotactic radiosurgery has been used to manage patients with
pituitary
adenomas
for over 30 years.
Numerous studies have documented that more than 95% of
pituitary adenoma
patients have either tumor shrinkage or stabilization after radiosurgery.
Biochemical remission is possible in approximately 80% of properly selected patients with
hormone
-
producing
pituitary
adenomas
.
Factors associated with endocrine cure include the absence of
pituitary
suppressive medications at the time of radiosurgery and higher radiation doses.
Delayed anterior
pituitary
deficits occur in 20-50% of patients depending on the length and quality of the endocrine follow-up.
Since the effects of radiosurgery are gradual compared to surgical removal of
pituitary
adenomas
, surgical resection remains the primary therapy for the majority of patients with large tumors causing visual loss or for patients with symptomatic
acromegaly
or Cushing'
s disease
.
However, radiosurgery is effective for
pituitary adenoma
patients with persistent or recurrent tumors after prior surgery, or for patients considered high risk for open surgical procedures due to coexisting medical conditions.
[MeSH-major]
Adenoma
/ surgery.
Pituitary
Neoplasms / surgery. Radiosurgery / methods
[MeSH-minor]
Human
Growth Hormone
/ blood. Humans. Insulin-Like
Growth
Factor I / metabolism. Magnetic Resonance Imaging. Radiotherapy Dosage. Retrospective Studies. Survivors. Treatment Outcome
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(PMID = 17317984.001).
[ISSN]
0079-6492
[Journal-full-title]
Progress in neurological surgery
[ISO-abbreviation]
Prog Neurol Surg
[Language]
eng
[Publicati