Table 5.

Classification of hypereosinophilia (HE)

Variant of HE	Abbreviation	Features
Hereditary (familial) HE	HEFA	Familial clustering, no evidence of a hereditary immunodeficiency, no evidence of a reactive or neoplastic underlying disease, and no signs or symptoms indicative of HES
HE of unknown significance	HEUS	No known underlying etiology of HE, no positive family history, no evidence of a reactive or neoplastic condition or disorder underlying HE
Secondary (reactive) HE	HER	Underlying reactive condition or disease that explains HE, no evidence for a clonal bone marrow disease that explains HE*
Primary (clonal/neoplastic) HE	HEN	Underlying stem cell, myeloid, or eosinophil neoplasm inducing HE*

^*In primary, neoplastic HE (HE_N), eosinophils are considered to be clonal cells derived from neoplastic stem cells, whereas in reactive HE (HE_R), eosinophils are considered to be reactive (non-clonal) cells triggered by eosinophiliopoietic cytokines such as interleukin-5

HE hypereosinophilia, HES hypereosinophilic syndrome