The Hypereosinophilic Syndrome

Chusid, Michael J.; Dale, David C.; West, Burton C.; Wolff, Sheldon M.

doi:10.1097/00005792-197501000-00001

Cited by 1,056 publications

(105 citation statements)

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“…Chusid et al (15) defined the syndrome more precisely restricting the diagnosis to patients with 1) persistent eosinophilia (>1.5xlO9/l), 2) a lack of evidence for any known cause, and 3) evidence for multi-organ disease. The present patient with eosinophilia and periodic angioedema showed no evidence of parasitic, allergic or other disease which could cause eosinophilia.…”

Section: Discussionmentioning

confidence: 99%

Periodic Angioedema with Eosinophilia: Increased Serum Level of Interleukin 5.

et al. 1995

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A 48-year-old man developed episodic non pitting edema and eosinophilia. Symptoms were alleviated promptly when treated with prednisolone. However, major basic protein (MBP), eosinophil cationic protein (ECP), and eosinophil-derived neurotoxin (EDN)levels in the serum as well as the total numberof eosinophils remained high. During periods of attack serum levels of interleukin-5 (IL-5) were elevated, but the levels were lowered following treatment, suggesting that IL-5 is involved in periodic angioedema with eosinophilia. (Internal Medicine 34: 108-111, 1995)

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Section: Discussionmentioning

confidence: 99%

Periodic Angioedema with Eosinophilia: Increased Serum Level of Interleukin 5.

et al. 1995

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“…Eosinophils were obtained from four patients with hypereosinophilia of unknown etiology (11) and differing degrees (30-85%) and one patient with hypereosinophilia secondary to Strongyloides stercoralis infestation. Heparinized blood from these patients was diluted 1:4 in phosphate-buffered saline (PBS).…”

Section: Methodsmentioning

confidence: 99%

The selective eosinophil chemotactic activity of histamine.

Clark¹,

Gallin²,

Kaplan³

1975

The Journal of Experimental Medicine

244

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Histamine diphosphate was shown to selectively attract human eosinophils from mixed granulocyte populations when over 20% eosinophils were used in a modified Boyden chamber chemotactic assay system. This effect of histamine is abolished by incubation with diamine oxidase (histaminase) and was generated by decarboxylation of L-histidine. A linear dose dependent increase in eosinophil migration was observed between 3 X 10(-7) M and 1.25 X 10(-6) M, while higher concentrations of histamine inhibited the migration of eosinophils. The attractant activity of histamine was not inhibited by H-1 or H-2 receptor antagonists, however, the inhibition of migration observed at higher histamine concentrations was reversed by metiamine, an H-2 receptor antagonist. The effects of histamine upon eosinophil migration were demonstrable using three different assays: (a) counting cells that had traversed 5-mum pore, 12-mum thick polycarbonate filters, (b) counting cells that had migrated various distances into a 3-mum pore, 145-mum cellulose nitrate filters, or (c) measuring the number of cells that had traversed an upper polycarbonate filter and migrated into a lower cellulose nitrate filter using 15Cr-labeled cells. The ability of histamine to enhance eosinophil migration was shown to be dependent upon the presence of a concentration gradient; histamine did not cause a dose-dependent increase in random motility. Furthermore, preincubation of the eosinophils with histamine deactivate the cells to further stimulation by histamine or by C5a. It is concluded that in low doses histamine is a chemoattractant for human eosinophils, while in higher doses histamine inhibits eosinophil migration. These observations may relate to the influx and localization of eosinophils in immediate hypersensitivity reactions.

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“…The hypereosinophilic syndromes, first described by Chusid et al in 1970s, [1] comprise a heterogeneous group of nonhematologic (secondary or reactive) and hematologic (primary or clonal) diseases. The diagnosis is united by a persistently elevated eosinophil count of greater than 1,500/mm 3 , and resultant end-organ damage from eosinophilic tissue infiltration.…”

Section: Introductionmentioning

confidence: 99%

“…hydroxyurea, with profoundly disappointing high mortality and morbidity rates. [1] The discovery of the fusion protein FIP1L1-PDGFRA revolutionized treatment and outcome for patients, as the presence of the FIP1L1-PDGFRA fusion correlates to an exquisite sensitivity to the tyrosine kinase inhibitor (TKI) Imatinib. [3] Whilst well described in adults, pediatric hypereosinophilia is rare, with only four cases of FIP1L1-PDGFRA fusion in children reported.…”

Section: Introductionmentioning

confidence: 99%

Pediatric hypereosinophilia: FIP1L1-PDGFRA myeloproliferative disease in a 14-year-old male

Wang

Conyers

2016

CRIM

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Hypereosinophilic myeloproliferative disease is a rare entity in the pediatric population. We report the fifth known pediatric case of FIP1L1-PDFGRA hypereosinophilia. This fusion drives hypereosinophilia, and often neutrophilia, with the propensity for T-cell or myeloid transformation. The exquisite sensitivity of the FIP1L1-PDGFRA fusion to the tyrosine kinase inhibitor Imatinib, abrogates the short-term life threatening complications of hyper-eosinophilia. The issues arising from long-term treatment with Imatinib, including optimal dosing, length of treatment, and bone marrow transplantation, are explored in the accompanying discussion. These issues are particularly relevant in pediatric patients facing life-long therapy.

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The Hypereosinophilic Syndrome

Cited by 1,056 publications

References 0 publications

Periodic Angioedema with Eosinophilia: Increased Serum Level of Interleukin 5.

Periodic Angioedema with Eosinophilia: Increased Serum Level of Interleukin 5.

The selective eosinophil chemotactic activity of histamine.

Pediatric hypereosinophilia: FIP1L1-PDGFRA myeloproliferative disease in a 14-year-old male

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