Represents a primary or secondary process.
Defined as an absolute eosinophil count of at least 1500/microL of blood.
Peripheral blood eosinophilia often an incidental finding.
Eosinophilia is never a normal lab finding and efforts should always be made to discover the underlying cause.
The first step and evaluating a patient with eosinophilia is to rule out all secondary non-hematologic causes.
Primary eosinophilia is sub classified into clonal or idiopathic eosinophilia depending upon the presence or absence of cytogenetic abnormalities, acute leukemia or a chronic myeloid disorder.
Primary type may be due to a clonal expansion of eosinophils through acquisition of a somatic mutation such as FIP1L1-PDGFRA, or secondary to exogenous type 2 cytokines such as IL-3, Il-5, and GM-CSF secreted by cells.
Eosinophilic leukemia associated with FIP1L1-PDGFRA fusion gene.
Eosinophilia may be driven by cytokines secreted by aberrant T cells which may be clonal or sometimes related to a lymphoproliferative disorder.
Clonal eosinophilia may accompany AML, ALL, CML, myelodysplastic disorders and myeloproliferative disorders.
Eosinophils may be derived from myeloid stem cells in acute myeloid leukemia, or in association with rearrangement of PDGFRB, chronic myelomonocytic leukemia and systemic mastocytosis.
The myeloproliferative form of hypereosinophilic syndrome is a result of a clonal process involving specific genetic alterations in hematopoiesic stem cell precursor and is similar to classic forms of myeloproliferative neoplasms such as polycythemia vera, myelofibrosis, and essential thrombocythemia.
Eosinophils may be derived from lymphoid-myeloid stem cells such as those associated with the rearrangement of PDGFRA, rearrangement of FGFR1, and BCR-ABL CML.
May be associated with systemic mastocytosis.
Hypereosinophilic syndromes associated with absolute eosinophil counts of greater than 1500/microL for more than 6 months.
Blood and tissue eosinophilia under most circumstances result from production of cytokines IL-5, IL-3 and GM-CSF.
Secondary type may be caused by allergies, adrenal insufficiency, autoimmune disorders, infections-parasitic, fungal, or Michael bacterial. and drug reactions.
Has a major role in allergic and helminth associated eosnophilia.
Secondary type rarely associated with absolute eosinophil count greater than 1500 /microL, except in helminthic infections.
Hypereosinophilia present in less than 1% ofpatients at the time of diagnosis of a malignancy.
Common in cysticercosis, when Taenia solium larvae spread via the blood stream to the brain and other tissues.
Marked eosinophilia rarely seen in malignant disease.
High grade type seen in trichinosis.
Atopy has an inherited predisposition can be associated with mild eosinophilia.
Up to 21% of patients following excretory urography.
Up to 20% of patients have eosinophilia on the second day after administration of various radiographic contrast media.
Occurs in about 15% of patients after administration of oral or rectal iodine contrast media.