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1. Chang JS, Santhanam R, Trotta R, Neviani P, Eiring AM, Briercheck E, Ronchetti M, Roy DC, Calabretta B, Caligiuri MA, Perrotti D: High levels of the BCR/ABL oncoprotein are required for the MAPK-hnRNP-E2 dependent suppression of C/EBPalpha-driven myeloid differentiation. Blood; 2007 Aug 1;110(3):994-1003
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  • [Title] High levels of the BCR/ABL oncoprotein are required for the MAPK-hnRNP-E2 dependent suppression of C/EBPalpha-driven myeloid differentiation.
  • The inability of myeloid chronic myelogenous leukemia blast crisis (CML-BC) progenitors to undergo neutrophil differentiation depends on suppression of C/EBPalpha expression through the translation inhibitory activity of the RNA-binding protein hnRNP-E2.
  • In fact, high levels of p210-BCR/ABL are required for enhanced hnRNP-E2 expression, which depends on phosphorylation of hnRNP-E2 serines 173, 189, and 272 and threonine 213 by the BCR/ABL-activated MAPK(ERK1/2).
  • Similarly, pharmacologic inhibition of MAPK(ERK1/2) activity decreases hnRNP-E2 binding to the 5'UTR of C/EBPalpha mRNA by impairing hnRNP-E2 phosphorylation and stability.
  • This, in turn, restores in vitro and/or in vivo C/EBPalpha expression and G-CSF-driven neutrophilic maturation of differentiation-arrested BCR/ABL(+) cell lines, primary CML-BC(CD34+) patient cells and lineage-negative mouse bone marrow cells expressing high levels of p210-BCR/ABL.
  • Thus, increased BCR/ABL oncogenic tyrosine kinase activity is essential for suppression of myeloid differentiation of CML-BC progenitors as it is required for sustained activation of the MAPK(ERK1/2)-hnRNP-E2-C/EBPalpha differentiation-inhibitory pathway.
  • Furthermore, these findings suggest the inclusion of clinically relevant MAPK inhibitors in the therapy of CML-BC.

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  • (PMID = 17475908.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 078890; United States / NCI NIH HHS / CA / P01 CA078890; United States / NCI NIH HHS / CA / CA 16058; United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / CA 095512; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / CA 9555111
  • [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] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Enzyme Inhibitors; 0 / Heterogeneous-Nuclear Ribonucleoproteins; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  • [Other-IDs] NLM/ PMC1924762
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2. Murata-Ohsawa M, Tohda S, Kogoshi H, Sakano S, Nara N: The Notch ligand, Delta-1, alters retinoic acid (RA)-induced neutrophilic differentiation into monocytic and reduces RA-induced apoptosis in NB4 cells. Leuk Res; 2005 Feb;29(2):197-203
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  • [Title] The Notch ligand, Delta-1, alters retinoic acid (RA)-induced neutrophilic differentiation into monocytic and reduces RA-induced apoptosis in NB4 cells.
  • Effects of Notch activation on retinoic acid (RA)-induced differentiation and apoptosis were investigated.
  • NB4, an acute promyelocytic leukemia (APL) cell line, undergoes neutrophilic differentiation and apoptosis by RA.
  • Notch activation induced by a recombinant Notch ligand, Delta-1, did not affect the growth by itself.
  • Treatment with RA plus Delta-1 made part of NB4 cells monocyte-like shaped and reduced the apoptosis.
  • Similar phenomenon was also observed in primary APL cells.
  • RA treatment induced cleavage of caspase-8 and PARP in NB4.
  • [MeSH-major] Apoptosis / drug effects. Cell Differentiation / drug effects. Membrane Proteins / metabolism. Membrane Proteins / pharmacology. Neutrophils / cytology. Tretinoin / antagonists & inhibitors
  • [MeSH-minor] Antigens, CD / metabolism. Caspase 8. Caspases / drug effects. Caspases / metabolism. Cell Line, Tumor. Cell Lineage / drug effects. Flow Cytometry. Humans. Intracellular Signaling Peptides and Proteins. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / metabolism. Ligands. Monocytes / physiology. Poly(ADP-ribose) Polymerases / drug effects. RNA, Messenger / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptor, Macrophage Colony-Stimulating Factor / genetics. Receptors, Notch

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  • [CommentIn] Leuk Res. 2005 Feb;29(2):127-9 [15607358.001]
  • (PMID = 15607369.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Intracellular Signaling Peptides and Proteins; 0 / Ligands; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / Receptors, Notch; 0 / delta protein; 5688UTC01R / Tretinoin; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases
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3. Jacobson S, Martin DB, Deng A, Cooper JZ: Pyoderma gangrenosum following tattoo placement in a patient with acute myelogenous leukemia. J Dermatolog Treat; 2008;19(1):58-60
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  • [Title] Pyoderma gangrenosum following tattoo placement in a patient with acute myelogenous leukemia.
  • A 37-year-old African American female with a diagnosis of acute myelogenous leukemia (AML) being treated with chemotherapy presented with a lesion on her lower back within the confines of a newly inked tattoo.
  • Five days after tattoo placement, she developed an oozing, indurated, necrotic plaque at the site.
  • Four days later, she developed chills, fever, and neutropenia.
  • A skin biopsy was performed and was consistent with pyoderma gangrenosum (PG) or neutrophilic dermatoses.
  • PG is an inflammatory skin disease associated with both cutaneous trauma and systemic disease, including hematologic malignancy.
  • PG after tattoo placement, in both healthy patients and those with hematologic malignancies, has, to our knowledge, not yet been described in the literature.
  • While further studies are necessary to investigate the link between PG and tattooing, oncologists may wish to counsel patients with leukemia to refrain from obtaining new tattoos.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Pyoderma Gangrenosum / etiology. Tattooing / adverse effects


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4. Stegmaier K, Corsello SM, Ross KN, Wong JS, Deangelo DJ, Golub TR: Gefitinib induces myeloid differentiation of acute myeloid leukemia. Blood; 2005 Oct 15;106(8):2841-8
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  • [Title] Gefitinib induces myeloid differentiation of acute myeloid leukemia.
  • Cure rates for patients with acute myeloid leukemia (AML) remain low despite ever-increasing dose intensity of cytotoxic therapy.
  • In an effort to identify novel approaches to AML therapy, we recently reported a new method of chemical screening based on the modulation of a gene expression signature of interest.
  • Among the compounds inducing neutrophilic differentiation was DAPH1 (4,5-dianilinophthalimide), previously reported to inhibit epidermal growth factor receptor (EGFR) kinase activity.
  • Here we report that the Food and Drug Administration (FDA)-approved EGFR inhibitor gefitinib similarly promotes the differentiation of AML cell lines and primary patient-derived AML blasts in vitro.
  • Gefitinib induced differentiation based on morphologic assessment, nitro-blue tetrazolium reduction, cell-surface markers, genome-wide patterns of gene expression, and inhibition of proliferation at clinically achievable doses.
  • Importantly, EGFR expression was not detected in AML cells, indicating that gefitinib functions through a previously unrecognized EGFR-independent mechanism.

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  • (PMID = 15998836.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5K08 CA098444-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ PMC1895296
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5. Srivastava M, Scharf S, Meehan SA, Polsky D: Neutrophilic eccrine hidradenitis masquerading as facial cellulitis. J Am Acad Dermatol; 2007 Apr;56(4):693-6
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  • [Title] Neutrophilic eccrine hidradenitis masquerading as facial cellulitis.
  • Neutrophilic eccrine hidradenitis typically manifests as erythematous plaques on the face, trunk, or extremities.
  • This eruption has been associated with numerous factors, but most commonly is seen with chemotherapy, particularly cytarabine.
  • We report a 73-year-old woman with acute myelogenous leukemia who developed rapidly expansive neutrophilic eccrine hidradenitis mimicking facial cellulitis only after a course of cytarabine was followed by granulocyte-colony stimulating factor.
  • Prompt diagnosis is imperative to prevent prolonged antimicrobial therapy.
  • [MeSH-major] Cellulitis / pathology. Cytarabine / adverse effects. Facial Dermatoses / pathology. Hidradenitis / chemically induced. Hidradenitis / pathology. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Biopsy, Needle. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Idarubicin / adverse effects. Idarubicin / therapeutic use. Immunohistochemistry. Risk Assessment

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  • (PMID = 17109994.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
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6. Piliotis E, Kutas G, Lipton JH: Allogeneic bone marrow transplantation in the management of chronic neutrophilic leukemia. Leuk Lymphoma; 2002 Oct;43(10):2051-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic bone marrow transplantation in the management of chronic neutrophilic leukemia.
  • Chronic neutrophilic leukemia (CNL) is a rare myeloproliferative disorder characterized by a clonal proliferation of mainly mature neutrophils, which is often difficult to differentiate from reactive leukocytosis or other myeloproliferative disorders.
  • Treatment to date has focused on disease control rather than cure.
  • Once the disease has progressed to a more aggressive leukemia there is typically little chance of obtaining a long lasting remission due to the older age of most patients as well as the acquisition of multiple poor prognostic cytogenetic abnormalities.
  • In this case report we describe a successful sibling allogeneic bone marrow transplant in a 60-year-old man with CNL performed while he was still in the stable phase of his disease.
  • We propose that even in older patients this curative approach may be considered in selected patients at an early stage of their disease, similar to the approach taken with chronic myelogenous leukemia.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia, Neutrophilic, Chronic / therapy
  • [MeSH-minor] Disease Management. Disease-Free Survival. Graft Survival. Graft vs Host Disease / drug therapy. Humans. Male. Middle Aged. Transplantation, Homologous


7. Rodríguez Bujaldon A, Vázquez C, Jiménez-Puya R, Galán M, Vélez A, Moreno JC, Rojas R, Arqueros V: [Neutrophilic eccrine hidradenitis secondary to thioguanine in a neutropenic patient]. Actas Dermosifiliogr; 2005 Nov;96(9):583-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Neutrophilic eccrine hidradenitis secondary to thioguanine in a neutropenic patient].
  • [Transliterated title] Hidradenitis ecrina neutrofílica secundaria a tioguanina en paciente neutropénico.
  • Neutrophilic eccrine hidradenitis (NEH) is an infrequent, self-limited inflammatory dermatosis characterized by a neutrophilic infiltrate around the eccrine glands.
  • Clinically, it presents with different types of lesions.
  • NEH occurs most frequently in patients who have undergone chemotherapy for hematologic neoplasms.
  • We present a case of NEH in a 70-year-old neutropenic male who received thioguanine for acute myeloid leukemia.
  • [MeSH-minor] Aged. Humans. Male

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  • (PMID = 16476301.001).
  • [ISSN] 0001-7310
  • [Journal-full-title] Actas dermo-sifiliográficas
  • [ISO-abbreviation] Actas Dermosifiliogr
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; FTK8U1GZNX / Thioguanine
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8. Chiang M, Fleming M: The pseudo-Pelger-Huët anomaly in pyoderma gangrenosum associated with myelodysplastic syndrome. Am J Dermatopathol; 2007 Jun;29(3):293-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The pseudo-Pelger-Huët anomaly in pyoderma gangrenosum associated with myelodysplastic syndrome.
  • We report a case of pyoderma gangrenosum in which most of the neutrophils exhibited the pseudo-Pelger-Huët (pPH) anomaly, a cytologic abnormality affecting the neutrophil nucleus.
  • The pPH anomaly is important because it is found mostly in patients with myelodysplastic syndromes or myeloid leukemias.
  • These patients are also at risk for developing neutrophilic dermatosis as well as leukemia cutis, the main differential diagnosis.
  • In our case, the proper diagnosis was made with the help of immunohistochemistry.
  • [MeSH-minor] Administration, Oral. Administration, Topical. Aged, 80 and over. Fatal Outcome. Glucocorticoids / therapeutic use. Humans. Leg Ulcer / drug therapy. Leg Ulcer / etiology. Leg Ulcer / pathology. Male. Prednisone / therapeutic use


9. Thuillier D, Lenglet A, Chaby G, Royer R, Vaida I, Viseux V, Dadban A, Billet A, Christophe O, Chatelain D, Marolleau JP, Lok C, Damaj G: [Bortezomib-induced eruption: Sweet syndrome? Two case reports]. Ann Dermatol Venereol; 2009 May;136(5):427-30
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  • [Title] [Bortezomib-induced eruption: Sweet syndrome? Two case reports].
  • [Transliterated title] Toxidermie au bortézomib : syndrome de Sweet? Deux cas.
  • BACKGROUND: Bortezomib (Velcade) is a proteasome inhibitor used in the treatment of myeloma and other blood dyscrasias.
  • We report the cases of two patients who developed a peculiar toxic rash suggestive of Sweet's syndrome while receiving bortezomib; one patient also presented giant mucous membrane ulcerations.
  • PATIENTS AND METHODS: Case 1: bortezomib treatment was started in a 62-year-old man for mantle cell lymphoma.
  • Ten days after the first treatment cycle, giant, painful oral ulcerations were noted but they resolved spontaneously.
  • One week after the second cycle, further oral ulceration appeared, this time with a papulonodular skin rash.
  • Histology showed neutrophilic dermal infiltrates in the skin with predominantly lymphocytic inflammation of the oral mucosa.
  • Bortezomib was stopped and all lesions resolved with colchicine treatment.
  • Case 2: a 46-year-old woman was receiving bortezomib treatment for plasma cell leukemia.
  • A febrile skin rash appeared two days after the first treatment cycle but resolved spontaneously.
  • DISCUSSION: Bortezomib-induced skin lesions are common and usually do not justify treatment withdrawal.
  • In our cases, these could be related to bortezomib-induced neutrophilic dermatosis.
  • [MeSH-minor] Biopsy. Bortezomib. Colchicine / therapeutic use. Dexamethasone / therapeutic use. Female. Humans. Leukemia, Plasma Cell / etiology. Lymphoma, Mantle-Cell / drug therapy. Male. Middle Aged. Skin Ulcer / chemically induced. Skin Ulcer / pathology. Treatment Outcome

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  • (PMID = 19442799.001).
  • [ISSN] 0151-9638
  • [Journal-full-title] Annales de dermatologie et de vénéréologie
  • [ISO-abbreviation] Ann Dermatol Venereol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Pyrazines; 69G8BD63PP / Bortezomib; 7S5I7G3JQL / Dexamethasone; SML2Y3J35T / Colchicine
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10. Jardin F, Vasse M, Debled M, Dominique S, Courville P, Callonnec F, Buchonnet G, Thiberville L, Tilly H: Intense paraneoplastic neutrophilic leukemoid reaction related to a G-CSF-secreting lung sarcoma. Am J Hematol; 2005 Nov;80(3):243-5
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  • [Title] Intense paraneoplastic neutrophilic leukemoid reaction related to a G-CSF-secreting lung sarcoma.
  • A white blood cell count more than 50 x 10(9)/l, not related to bone marrow involvement, is termed leukemoid reaction.
  • We report on the first case of an undifferentiated sarcoma of the lung associated with an intense paraneoplastic neutrophilic leukemoid reaction related to the production of granulocyte colony-stimulating factor (G-CSF).
  • A radiography and a computed tomography scan of the chest revealed a well-limited voluminous and heterogeneous low-density mass of the left lung.
  • The patient died of multiorgan failure related to uncontrolled progressive tumor growth after admission and two cycles of chemotherapy.
  • The G-CSF concentration dramatically increased after the first cycle of chemotherapy and during the subsequent neutropenia, as a result of the tumor lyses as well as of disruption of the physiological negative feedback mechanism.
  • [MeSH-minor] Cell Proliferation. Fatal Outcome. Humans. Leukemia, Neutrophilic, Chronic / etiology. Male. Middle Aged. Multiple Organ Failure

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  • (PMID = 16247754.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
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11. Itzykson R, Ayari S, Vassilief D, Berger E, Slama B, Vey N, Suarez F, Beyne-Rauzy O, Guerci A, Cheze S, Thomas X, Stamatoullas A, Gardembas M, Bauduer F, Kolb A, Chaury MC, Legros L, Damaj G, Chermat F, Dreyfus F, Fenaux P, Ades L, Groupe Francophone des Myelodysplasies (GFM): Is there a role for all-trans retinoic acid in combination with recombinant erythropoetin in myelodysplastic syndromes? A report on 59 cases. Leukemia; 2009 Apr;23(4):673-8
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  • [Title] Is there a role for all-trans retinoic acid in combination with recombinant erythropoetin in myelodysplastic syndromes? A report on 59 cases.
  • Erythropoiesis-stimulating agents (ESAs) remain the first-line treatment of anemia in lower risk myelodysplastic syndromes (MDS) without 5q deletion.
  • A preliminary report suggested that adding all-trans retinoic acid (ATRA) to ESAs may improve their erythroid response, particularly in patients with high endogenous erythropoietin (EPO) level, and may improve other cytopenias.
  • We conducted a prospective multicenter study of EPO-beta and ATRA in anemic MDS patients with marrow blasts <10% and either previous ESA failure or relapse, endogenous EPO >500 U/l or other cytopenia(s) (absolute neutrophilic count <1.0 G/l or platelets <50 G/l).
  • A total of 59 patients were evaluable after 12 weeks of treatment.
  • The erythroid response rates according to IWG 2000 and 2006 criteria, respectively, were as follows: overall: 49 and 36%; patients with previous ESA failure (n=28): 43 and 32%; patients with endogenous EPO >500 U/l (n=18): 11 and 19%; patients transfused >2 red blood cells units/month (n=28) 43 and 39%.
  • Only one neutrophil, but no platelet response, and no major side effect were observed.
  • EPO-beta-ATRA combination appears a possible therapeutic option in anemia of MDS having failed an ESA alone, but not in patients with high endogenous EPO level, and does not improve neutropenia and thrombocytopenia.
  • [MeSH-major] Erythropoietin / therapeutic use. Myelodysplastic Syndromes / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Drug Therapy, Combination. Female. Humans. Leukocyte Count. Male. Middle Aged. Neutropenia / drug therapy. Neutrophils. Platelet Count. Recombinant Proteins. Thrombocytopenia / drug therapy. Treatment Outcome. Young Adult


12. Liu KH, Wu CJ, Chou CH, Lee HC, Lee NY, Hung ST, Ko WC: Refractory candidal meningitis in an immunocompromised patient cured by caspofungin. J Clin Microbiol; 2004 Dec;42(12):5950-3
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  • Candidal meningitis is a rare infectious disease that usually leads to substantial morbidity and mortality.
  • We present a case of candidal meningitis refractory to systemic antifungal therapy (amphotericin B and fluconazole).
  • A 63-year-old female with lymphoblastic lymphoma and myelodysplasia with leukemia transformation developed prolonged fever and headache on the seventh day following intrathecal prophylactic chemotherapy.
  • A lumbar puncture showed neutrophilic pleocytosis, and a cerebrospinal fluid culture yielded Candida albicans.
  • Parenteral therapy with amphotericin B alone or amphotericin B in combination with fluconazole or intrathecal administration of amphotericin B failed to eradicate C. albicans in the cerebrospinal fluid.
  • After 7 days of caspofungin therapy, however, the cerebrospinal fluid became sterile and the patient gradually regained consciousness.
  • She was discharged 1 month after completing 4 weeks of caspofungin therapy.
  • There were two critical issues we thought to be relevant to the favorable outcome of this case.
  • First, isolation of C. albicans was achieved by inoculating enriched liquid medium with cerebrospinal fluid.
  • Second, there is a potential therapeutic benefit of caspofungin in treating a fungal infection of the central nervous system.
  • [MeSH-major] Antifungal Agents / therapeutic use. Candida albicans / isolation & purification. Candidiasis / drug therapy. Immunocompromised Host. Meningitis, Fungal / drug therapy. Peptides, Cyclic / therapeutic use
  • [MeSH-minor] Echinocandins. Female. Humans. Middle Aged. Treatment Outcome

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  • (PMID = 15583351.001).
  • [ISSN] 0095-1137
  • [Journal-full-title] Journal of clinical microbiology
  • [ISO-abbreviation] J. Clin. Microbiol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Echinocandins; 0 / Peptides, Cyclic; F0XDI6ZL63 / caspofungin
  • [Other-IDs] NLM/ PMC535248
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13. Yoshida C, Kojima H, Iijima T, Katsura Y, Shimizu S, Suzukawa K, Mukai HY, Hasegawa Y, Abei M, Nagasawa T: Association of non-alcoholic steatohepatitis (NASH) with chronic neutrophilic leukemia. Eur J Haematol; 2004 Mar;72(3):225-8
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  • [Title] Association of non-alcoholic steatohepatitis (NASH) with chronic neutrophilic leukemia.
  • A 54-yr-old female having chronic neutrophilic leukemia (CNL) associated with severe liver injury is presented.
  • Complete blood count showed a hemoglobin level of 9.1 g/dL, platelet count of 25.8 x 10(4)/microL, and white blood cell count of 36.6 x 10(3)/microL with 89.7% neutrophils.
  • Blood chemistry showed hyperbilirubinemia (21.9 mg/dL) with normal transaminase levels.
  • There was no abnormality in serum cholesterol, triglyceride, or glucose levels.
  • Neutrophil alkaline phosphatase activity was significantly elevated.
  • Rearrangement of the bcr/abl was not detected by either polymerase chain reaction or fluorescence in situ hybridization.
  • Human androgen receptor gene assay (HUMARA) of the bone marrow cells showed clonal proliferation of neutrophils.
  • As the patient had no history of alcohol abuse, a diagnosis of non-alcoholic steatohepatitis (NASH) was made.
  • Assuming that the infiltration of abnormal neutrophils into the liver contributed to the development of NASH, she was treated with cytoreductive chemotherapy (cytosine arabinoside: 100 mg/d, 1-3 doses/wk).
  • With decreases in white blood cell counts, serum bilirubin levels decreased gradually to 1.5 mg/mL.
  • To our knowledge, this is the first report describing the development of NASH in a myeloproliferative disorder.
  • [MeSH-major] Fatty Liver / etiology. Leukemia, Neutrophilic, Chronic / complications
  • [MeSH-minor] Antimetabolites, Antineoplastic / therapeutic use. Biopsy. Cytarabine / therapeutic use. Female. Humans. Middle Aged. Treatment Outcome


14. Inuzuka M, Tokura Y: Sterile suppurative folliculitis associated with acute myeloblastic leukaemia. Br J Dermatol; 2002 May;146(5):904-7
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  • [Title] Sterile suppurative folliculitis associated with acute myeloblastic leukaemia.
  • A 20-year-old woman presented with a 4-month history of follicular papules distributed over the trunk and extremities.
  • One month later, routine blood tests were abnormal, showing acute myeloblastic leukaemia (M1 in the French-American-British classification).
  • Skin biopsy demonstrated a dermal infiltrate of a large number of neutrophils with occasional eosinophils and histiocytes in the vicinity of the hair follicle remnants.
  • The follicular eruption improved promptly in response to chemotherapy for the leukaemia.
  • We suggest that this case may represent a rare, follicular variant of neutrophilic dermatosis associated with myelogenous leukaemia.
  • [MeSH-major] Folliculitis / etiology. Leukemia, Myeloid, Acute / complications. Sweet Syndrome / etiology
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Follow-Up Studies. Humans

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  • (PMID = 12000394.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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15. Chevalier N, Solari ML, Becker H, Pantic M, Gärtner F, Maul-Pavicic A, Hübner J, Wäsch R, Schmitt-Gräff A, Lübbert M: Robust in vivo differentiation of t(8;21)-positive acute myeloid leukemia blasts to neutrophilic granulocytes induced by treatment with dasatinib. Leukemia; 2010 Oct;24(10):1779-81
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  • [Title] Robust in vivo differentiation of t(8;21)-positive acute myeloid leukemia blasts to neutrophilic granulocytes induced by treatment with dasatinib.
  • [MeSH-major] Cell Differentiation / drug effects. Granulocytes / cytology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / pathology. Neutrophils / cytology. Pyrimidines / therapeutic use. Thiazoles / therapeutic use. Translocation, Genetic
  • [MeSH-minor] Blast Crisis / drug therapy. Blast Crisis / genetics. Blast Crisis / pathology. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Dasatinib. Flow Cytometry. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Survival Rate. Treatment Outcome

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  • (PMID = 20811401.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.10.1 / Protein-Tyrosine Kinases; RBZ1571X5H / Dasatinib
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16. Gómez Vázquez M, Peteiro C, Toribio J: Neutrophilic eccrine hidradenitis heralding the onset of chronic myelogenous leukaemia. J Eur Acad Dermatol Venereol; 2003 May;17(3):328-30
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  • [Title] Neutrophilic eccrine hidradenitis heralding the onset of chronic myelogenous leukaemia.
  • Neutrophilic eccrine hidradenitis was initially described in acute myelogenous leukaemic patients undergoing chemotherapy, suggesting a drug-induced mechanism.
  • However, most the reported cases have been described in acute myelogenous leukaemic cases receiving chemotherapy.
  • We describe a neutrophilic eccrine hidradenitis case unassociated with chemotherapy in a woman with chronic myelogenous leukaemia.
  • [MeSH-major] Hidradenitis / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis
  • [MeSH-minor] Aged. Aged, 80 and over. Axilla. Diagnosis, Differential. Female. Humans

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  • (PMID = 12702078.001).
  • [ISSN] 0926-9959
  • [Journal-full-title] Journal of the European Academy of Dermatology and Venereology : JEADV
  • [ISO-abbreviation] J Eur Acad Dermatol Venereol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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17. Cohen PR: Sweet's syndrome--a comprehensive review of an acute febrile neutrophilic dermatosis. Orphanet J Rare Dis; 2007;2:34
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  • [Title] Sweet's syndrome--a comprehensive review of an acute febrile neutrophilic dermatosis.
  • Sweet's syndrome (the eponym for acute febrile neutrophilic dermatosis) is characterized by a constellation of clinical symptoms, physical features, and pathologic findings which include fever, neutrophilia, tender erythematous skin lesions (papules, nodules, and plaques), and a diffuse infiltrate consisting predominantly of mature neutrophils that are typically located in the upper dermis.
  • Sweet's syndrome presents in three clinical settings: classical (or idiopathic), malignancy-associated, and drug-induced.
  • Classical Sweet's syndrome (CSS) usually presents in women between the age of 30 to 50 years, it is often preceded by an upper respiratory tract infection and may be associated with inflammatory bowel disease and pregnancy.
  • Approximately one-third of patients with CSS experience recurrence of the dermatosis.
  • The malignancy-associated Sweet's syndrome (MASS) can occur as a paraneoplastic syndrome in patients with an established cancer or individuals whose Sweet's syndrome-related hematologic dyscrasia or solid tumor was previously undiscovered; MASS is most commonly related to acute myelogenous leukemia.
  • The dermatosis can precede, follow, or appear concurrent with the diagnosis of the patient's cancer.
  • Hence, MASS can be the cutaneous harbinger of either an undiagnosed visceral malignancy in a previously cancer-free individual or an unsuspected cancer recurrence in an oncology patient.
  • Drug-induced Sweet's syndrome (DISS) most commonly occurs in patients who have been treated with granulocyte-colony stimulating factor, however, other medications may also be associated with DISS.
  • Systemic corticosteroids are the therapeutic gold standard for Sweet's syndrome.
  • After initiation of treatment with systemic corticosteroids, there is a prompt response consisting of dramatic improvement of both the dermatosis-related symptoms and skin lesions.
  • Topical application of high potency corticosteroids or intralesional corticosteroids may be efficacious for treating localized lesions.
  • The symptoms and lesions of Sweet's syndrome may resolved spontaneously, without any therapeutic intervention; however, recurrence may follow either spontaneous remission or therapy-induced clinical resolution.
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged

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  • (PMID = 17655751.001).
  • [ISSN] 1750-1172
  • [Journal-full-title] Orphanet journal of rare diseases
  • [ISO-abbreviation] Orphanet J Rare Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 435
  • [Other-IDs] NLM/ PMC1963326
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18. Uhara H, Saida T, Nakazawa H, Ito T: Neutrophilic dermatoses with acute myeloid leukemia associated with an increase of serum colony-stimulating factor. J Am Acad Dermatol; 2008 Aug;59(2 Suppl 1):S10-2
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  • [Title] Neutrophilic dermatoses with acute myeloid leukemia associated with an increase of serum colony-stimulating factor.
  • We report a case of acute myeloid leukemia with folliculitis, Sweet's syndrome, and neutrophilic panniculitis after remission induction chemotherapy for acute myeloid leukemia.
  • The level of endogenous granulocyte colony-stimulating factor was closely associated with disease activity.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / blood. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / metabolism. Sweet Syndrome / complications. Sweet Syndrome / metabolism
  • [MeSH-minor] Antibiotics, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / administration & dosage. Cytarabine / administration & dosage. Folliculitis / complications. Folliculitis / metabolism. Humans. Idarubicin / administration & dosage. Male. Middle Aged. Remission Induction

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  • (PMID = 18625369.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; ZRP63D75JW / Idarubicin
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19. Kim MJ, Choe YH: EPONYM. Sweet syndrome. Eur J Pediatr; 2010 Dec;169(12):1439-44
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  • Sweet syndrome, also referred to as acute febrile neutrophilic dermatosis, is characterized by tender, red inflammatory nodules or papules that occur in association with infection, malignancy, connective tissue disease, or following exposure to certain drugs.
  • Although drug-induced Sweet syndrome is rare, granulocyte colony-stimulating factor, all-trans-retinoic acid, and miscellaneous drugs have been implicated in causing this disorder in adults.
  • In pediatric patients, granulocyte colony-stimulating factor, all-trans-retinoic acid, trimethoprim-sulfamethoxazole, and azathioprine have been implicated as potential causes of drug-induced Sweet syndrome.
  • [MeSH-major] Azathioprine / adverse effects. Granulocyte Colony-Stimulating Factor / adverse effects. Sweet Syndrome / chemically induced. Tretinoin / adverse effects. Trimethoprim, Sulfamethoxazole Drug Combination / adverse effects
  • [MeSH-minor] Adult. Child. Connective Tissue Diseases / complications. Connective Tissue Diseases / drug therapy. Erythema / chemically induced. Erythema / physiopathology. Fever / physiopathology. Humans. Infection / complications. Infection / drug therapy

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  • (PMID = 20445990.001).
  • [ISSN] 1432-1076
  • [Journal-full-title] European journal of pediatrics
  • [ISO-abbreviation] Eur. J. Pediatr.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor; 5688UTC01R / Tretinoin; 8064-90-2 / Trimethoprim, Sulfamethoxazole Drug Combination; MRK240IY2L / Azathioprine
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