Eosinophilia: a pragmatic approach to diagnosis and treatment

Abstract

Eosinophilia is associated with a wide variety of allergic, rheumatologic, infectious, neoplastic, and rare idiopathic disorders. Clinical manifestations range from benign asymptomatic presentations to life-threatening complications, including endomyocardial fibrosis and thromboembolism. The prognosis and choice of treatment depend not only on the degree of eosinophilia and severity of organ involvement, but also on the etiology of the eosinophilia. Unfortunately, despite recent advances in molecular and immunologic techniques, the etiology remains unproven in the overwhelming majority of cases. This review presents a practical approach to the diagnosis and treatment of patients presenting with unexplained marked eosinophilia. A brief overview of the mechanisms of eosinophilia and eosinophil pathogenesis is also provided.

Hypereosinophilic syndrome presenting with multiple organ infiltration and deep venous thrombosis

“…[15] Six clinical variants are designated according to the causes of HES: myeloproliferative HES, lymphocytic variant HES, overlap HES, associated HES, familial HES, and idiopathic HES. [13–14] According to the above criteria of HES, our case can be provisionally diagnosed as idiopathic HES.…”

“…However, the currently accepted definition of HES requires blood EO count greater than 1.5 × 10 9 /L on at least 2 occasions, ideally at minimum 1 month apart, and/or tissue eosinophilia that is considered excessive by the pathologist, and organ damage or dysfunction attributable to tissue EOs. [12–14] However, there are controversies about how to define eosinophilic end organ damage. Evidence of EO-mediated tissue damage using methods other than histology is accepted with highly specific abnormalities that include thrombosis documented by imaging studies.…”

Transcription Factors in Eosinophil Development and As Therapeutic Targets

“…Glucocorticoids are the first-line therapy for eosinophil-associated disorders, such as allergy, asthma, eosinophilic gastrointestinal disorders and hypereosinophilic syndrome (44, 45); yet, there are a subset of individuals with severe asthma with eosinophilia despite high doses of glucocorticoids (46–48) and patients with hypereosinophilic syndrome often become glucocorticoid refractory (49, 50). The TF NFIL3 has recently been shown to be induced by IL-5 stimulation in eosinophils and to protect against glucocorticoid-induced apoptosis (51), suggesting that targeting NFIL3 in patients may restore glucocorticoid sensitivity.…”

65-Year-Old Woman With Chronic Eosinophilia

“…Eosinophils are largely tissue-dwelling cells (>90%), 5 and therefore the amount of eosinophils in the peripheral blood may not reflect their density in organs. 6 In addition, intravascular levels of eosinophils have a diurnal variation that is the reciprocal of the diurnal variation of endogenous steroids, with a trough in the morning hours and a peak value in the late evening.…”