Pages Menu
TwitterRssFacebook
Categories Menu

Posted by on Jun 14, 2013 in Medical Journals |

Pathogenesis, classification, and therapy of eosinophilia and eosinophil disorders.

Head for The Masto Townhall forum to debate this paper.
This article may be copyrighted. Notice to copyright holders.
You can view the full article at the publisher here
There is a fee associated with downloading this article.
Blood Rev. 2009 Jul;23(4):157-65. doi: 10.1016/j.blre.2009.01.001. Epub 2009 Feb 25.

Pathogenesis, classification, and therapy of eosinophilia and eosinophil disorders.

Valent P.

Abstract

Eosinophilia is a recurrent feature and diagnostic clue in several hematologic malignancies. In stem cell- and myelopoietic neoplasms, eosinophils are derived from the malignant clone, whereas in lymphoid neoplasms and reactive states, eosinophilia is usually triggered by eosinopoietic cytokines. Myeloid neoplasms typically presenting with eosinophilia include chronic myeloid leukemia, chronic eosinophilic leukemia (CEL), other myeloproliferative neoplasms, some acute leukemias, advanced mast cell disorders, and rare forms of myelodysplastic syndromes. Diagnostic evaluations in unexplained eosinophilia have to take these diagnoses into account. In such patients, a thorough hematologic work-up including bone marrow histology and immunohistochemistry, cytogenetics, molecular markers, and a complete staging of potentially affected organ systems has to be initiated. Endomyocardial fibrosis, the most dangerous cardiovascular complication of the hypereosinophilic state, is frequently detected in PDGFR-mutated neoplasms, specifically in FIP1L1/PDGFRA+ CEL, but is usually not seen in other myeloid neoplasms or reactive eosinophilia, even if eosinophilia is recorded for many years. Treatment of hypereosinophilic patients depends on the variant of disease, presence of end organ damage, molecular targets, and the overall situation in each case. In a group of patients, oncogenic tyrosine kinases (TK) such as FIP1L1/PDGFRA, can be employed as therapeutic targets by using imatinib or other TK-blocking agents.

PMID: 19246139 [PubMed – indexed for MEDLINE]