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After the exclusion of secondary causes of eosinophilia, diagnostic evaluation of primary eosinophilias relies on a combination of various tests. They include morphologic review of the blood and marrow, standard cytogenetics, fluorescence in situ hybridization, molecular testing and flow immunophenotyping to detect histopathologic or clonal evidence for an acute or chronic hematolymphoid neoplasm.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Risk Stratification<\/jats:title>\n                    <jats:p>Disease prognosis relies on identifying the subtype of eosinophilia. After evaluation of secondary causes of eosinophilia, the 2022 World Health Organization and International Consensus Classification endorse a semi\u2010molecular classification scheme of disease subtypes. This includes the major category \u201cmyeloid\/lymphoid neoplasms with eosinophilia and tyrosine kinase gene fusions\u201d (MLN\u2010eo\u2010TK), and the MPN subtype, \u201cchronic eosinophilic leukemia\u201d (CEL). Lymphocyte\u2010variant HE is an aberrant T\u2010cell clone\u2010driven reactive eosinophila, and idiopathic hypereosinophilic syndrome (HES) is a diagnosis of exclusion.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Risk\u2010Adapted Therapy<\/jats:title>\n                    <jats:p>\n                      The goal of therapy is to mitigate eosinophil\u2010mediated organ damage. For patients with milder forms of eosinophilia (e.g., &lt;1.5\u2009\u00d7\u200910\n                      <jats:sup>9<\/jats:sup>\n                      \/L) without symptoms or signs of organ involvement, a watch and wait approach with close follow\u2010up may be undertaken. Identification of rearranged\n                      <jats:italic>PDGFRA<\/jats:italic>\n                      or\n                      <jats:italic>PDGFRB<\/jats:italic>\n                      is critical because of the exquisite responsiveness of these diseases to imatinib. Pemigatinib was recently approved for patients with relapsed or refractory\n                      <jats:italic>FGFR1<\/jats:italic>\n                      \u2010rearranged neoplasms. Corticosteroids are first\u2010line therapy for patients with lymphocyte\u2010variant HE and HES. Hydroxyurea and interferon\u2010\u03b1 have demonstrated efficacy as initial treatment and in steroid\u2010refractory cases of HES. Mepolizumab, an interleukin\u20105 (IL\u20105) antagonist monoclonal antibody, is approved by the U.S Food and Drug Administration for patients with idiopathic HES. Cytotoxic chemotherapy agents, and hematopoietic stem cell transplantation have been used for aggressive forms of HES and CEL, with outcomes reported for limited numbers of patients. Targeted therapies such as the IL\u20105 receptor antibody benralizumab, IL\u20105 monoclonal antibody depemokimab, and various tyrosine kinase inhibitors for MLN\u2010eo\u2010TK, are under active investigation.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ajh.27287","type":"journal-article","created":{"date-parts":[[2024,3,29]],"date-time":"2024-03-29T09:05:21Z","timestamp":1711703121000},"page":"946-968","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":120,"title":["World Health Organization and International Consensus Classification of eosinophilic disorders: 2024 update on diagnosis, risk stratification, and management"],"prefix":"10.1002","volume":"99","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6500-350X","authenticated-orcid":false,"given":"William","family":"Shomali","sequence":"first","affiliation":[{"name":"Division of Hematology Stanford Cancer Institute\/Stanford University School of Medicine  Stanford California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8253-6156","authenticated-orcid":false,"given":"Jason","family":"Gotlib","sequence":"additional","affiliation":[{"name":"Division of Hematology Stanford Cancer Institute\/Stanford University School of Medicine  Stanford California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2024,3,29]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1002\/ajh.25906"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-97-1-78"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jaci.2009.09.022"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/leu.2008.287"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2006-10-050054"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2004-03-0787"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.leukres.2005.11.011"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1002\/ajh.25945"},{"key":"e_1_2_8_10_1","doi-asserted-by":"publisher","DOI":"10.1002\/ajh.25811"},{"key":"e_1_2_8_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-3476(87)80352-9"},{"key":"e_1_2_8_12_1","doi-asserted-by":"publisher","DOI":"10.1097\/00043426-200301000-00017"},{"key":"e_1_2_8_13_1","doi-asserted-by":"publisher","DOI":"10.1097\/01.mph.0000193467.06938.77"},{"key":"e_1_2_8_14_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa025217"},{"key":"e_1_2_8_15_1","doi-asserted-by":"publisher","DOI":"10.3324\/haematol.11420"},{"key":"e_1_2_8_16_1","first-page":"963","article-title":"Eosinophilia detected by automated blood cell counting in ambulatory north American outpatients. 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