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Hypereosinophilic syndrome

The hypereosinophilic syndrome is a disease process characterized by a persistently elevated eosinophil count (≥ 1500 eosinophils/mm3) in the blood for at least six months without any recognizable cause after a careful workup, with evidence of involvement of either the heart, nervous system, or bone marrow. more...

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There are two forms of the hypereosinophilic syndrome: Endomyocardial fibrosis and Loeffler's endocarditis. Endomyocardial fibrosis (also known as Davies disease) is seen in Africa and South America, while Loeffler's endocarditis does not have any geographic predisposition.

In both forms of the hypereosinophilic syndrome, the eosinophilia causes infiltration of the myocardium of the heart, which leads to fibrotic thickening of portions of the heart. The portions of the heart most effected by this disease are the apex of the left and right ventricles, fibrotic infiltrations may involve the mitral or tricuspid valves. Because of the infiltrative nature of the disease process, the cavity of the ventricles of the heart diminish in size, causing an obliterative cardiomyopathy and restriction to the inflow of blood in to the chambers of the heart. Ventricular mural thromb may develop.

Chronic eosinophilic leukemia (CEL) is a myeloproliferative disease which shares many common characteristics with hypereosinophilic syndrome. Many cases of CEL have a characteristic gene rearrangement , FIP1L1/PDGFRA, caused by a sub-micoscopic deletion of ~800 thousand base pairs of DNA on chromosome 4. The FIP1L1/PDGFRA fusion gene causes consitutive activation of the platelet derived growth factor receptor - alpha (PDGFRA). FIP1L1/PDGFRA-positive patients respond well to treatment with the tyrosine kinase inhibitor drug, imatinib mesylate (Gleevec® or Glivec®).

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Intravenous mepolizumab in subjects with hypereosinophilic syndromes
From Journal of Drugs in Dermatology, 1/1/05

This study is currently recruiting patients.

Sponsored by GlaxoSmithKline.

Hypereosinophilic syndrome (HES) is a rare disease with broad clinical signs and symptoms which is diagnosed based on a persistent blood eosinophil count of greater than 1500 cells, various end-organ damages (including skin, heart, lung, nervous system and digestive system etc.), and with exclusion of known secondary causes of hypereosinophilia. HES has a high morbidity/mortality rate. The major treatment of HES has been systemic corticosteroid and other chemotherapeutic drugs (for example, hydroxyurea and interferon) with the intention to lower eosinophil counts and therefore to slow down the progression of disease. Even though corticosteroid and other therapies can effectively reduce eosinophilia in some patients, some may eventually become nonresponsive and intolerable to the amount of side effects of the long-term therapy with these medications. Mepolizumab is a humanized monoclonal antibody that binds specifically to human interleukin 5 (hIL-5) and inhibits its activity. Previous human experience has shown it has been effective in reducing blood eosinophilia in atopic and HES patients and has alleviated some HES clinical signs and symptoms. This study intends to further evaluate the corticosteroid-sparing and clinical benefit of mepolizumab in HES.

Study ID Numbers: 100185

ClinicalTrials.gov Identifier: NCT00086658

COPYRIGHT 2005 Journal of Drugs in Dermatology
COPYRIGHT 2005 Gale Group

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