TABLE 2.
Variant of HE | Abbreviation | Features |
---|---|---|
Hereditary (familial) HE | HEFA | Familial clustering, often evidence of a hereditary immunodeficiency (inborn errors of immunity with eosinophilia), 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, and no signs or symptoms indicative of HES |
Secondary (reactive) HE | HER | Underlying reactive condition or disease that explains HE, no evidence for a clonal bone marrow disease that explains HE a ; and no signs or symptoms indicative of HES |
Clonal (neoplastic) HE | HEN | Underlying stem cell, myeloid, or eosinophil neoplasm inducing HE a ; no signs/symptoms indicative of HES |
Abbreviations: HE, hypereosinophilia; HES, hypereosinophilic syndrome(s).
In clonal/neoplastic HE (HEN), eosinophils are considered to be clonal cells derived from neoplastic stem cells, whereas in reactive HE (HER), eosinophils are considered to be reactive (non‐clonal) cells triggered by eosinopoietic cytokines such as interleukin‐5.