{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T17:32:42Z","timestamp":1791567162825,"version":"4.3.4"},"reference-count":42,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2020,5,18]],"date-time":"2020-05-18T00:00:00Z","timestamp":1589760000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["European J of Haematology"],"published-print":{"date-parts":[[2020,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Hypereosinophilia (HE, persistent peripheral blood eosinophilia\u00a0&gt;\u00a01.5\u00a0\u00d7\u00a010\n                      <jats:sup>9<\/jats:sup>\n                      \/L) and hypereosinophilic syndrome (HES, HE with end\u2010organ damage) are classified as primary (due to a myeloid clone), secondary (due to a wide variety of reactive causes), or idiopathic. Diagnostic evaluation of eosinophilia is challenging, in part because secondary causes of HE\/HES such as lymphocyte\u2010variant HES (L\u2010HES) and vasculitis are difficult to diagnose, and emerging causes such as immunoglobulin G4\u2010related disease (IgG4\u2010RD) have rarely been examined.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective and Methods<\/jats:title>\n                    <jats:p>We reviewed 100 consecutive patients with HE\/HES who underwent extensive evaluation for primary and secondary eosinophilia at a single tertiary care center to determine causes of HE\/HES in a modern context.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Six patients had primary HE\/HES, 80 had a discrete secondary cause identified, and 14 had idiopathic HE\/HES. The most common causes of secondary eosinophilia were L\u2010HES\/HES of unknown significance (L\u2010HESus) (20), IgG4\u2010RD (9), and eosinophilic granulomatosis with polyangiitis (EGPA) (8).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>In contrast to other large published series of HE\/HES, most patients in this study were found to have a discrete secondary cause of eosinophilia and only 14 were deemed idiopathic. These findings highlight the importance of extensive evaluation for secondary causes of eosinophilia such as L\u2010HES, IgG4\u2010RD, and EGPA.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/ejh.13437","type":"journal-article","created":{"date-parts":[[2020,5,4]],"date-time":"2020-05-04T11:35:10Z","timestamp":1588592110000},"page":"292-301","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["Causes of hypereosinophilia in 100 consecutive patients"],"prefix":"10.1111","volume":"105","author":[{"given":"Daniel","family":"Moller","sequence":"first","affiliation":[{"name":"Department of Medicine University of British Columbia Vancouver BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia","family":"Tan","sequence":"additional","affiliation":[{"name":"Department of Medicine University of British Columbia Vancouver BC 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