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{{short description|BloodExcess conditionnumber of eosinophil cells in the blood}}
{{Infobox medical condition (new)
| field = [[Infectious disease (medical specialty)|Infectious disease]], [[hematology]]
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== Classification ==
Based on their causes, hypereosinophilias can be sorted into subtypes. However, cases of eosinophilia, which exhibit eosinophil counts between 500 and 1,500/μL, may fit the clinical criteria for, and thus be regarded as falling into, one of these hypereosinophilia categories: the cutoff of 1,500/μL between hypereosinophilia and eosinophilia is somewhat arbitrary. There are at least two different guidelines for classifying hypereosinophilia/eosinophilia into subtypes. The General Haematoloy and Haemato-oncology Task Forces for the British Committee for Standards in Haematology classifies these disorders into '''a)''' Primary, i.e. caused by abnormalities in the eosinophil cell line; '''b)''' Secondary, i.e. caused by non-eosinophil disorders; and '''c)''' Idiopathic, cause unknown.<ref name="pmid28112388"/> The [[World Health Organization]] classifies these disorders into '''a)''' Myeloid and lymphoid neoplasms with eosinophilia and abnormalities of ''PDGFRA, PDGFRB'', or ''FGFR1'' (i.e. high eosinophil blood counts caused by mutations in the eosinophil cell line of one of these three genes), ''''b)''' [[Chronic eosinophilic leukemia]], and '''c)''' the Idiopathic hypereosinophiichypereosinophilic syndrome. In the latter classification, secondary hypereosinophilia/eosinophilia is not viewed as a true disorder of eosinophils.<ref name="pmid29044676"/><ref name="pmid24577808">{{cite journal | vauthors = Gotlib J | title = World Health Organization-defined eosinophilic disorders: 2014 update on diagnosis, risk stratification, and management | journal = American Journal of Hematology | volume = 89 | issue = 3 | pages = 325–337 | year = 2014 | pmid = 24577808 | doi = 10.1002/ajh.23664 | s2cid = 8464735 }}</ref> Here these two classifications are merged and expanded to include the many forms of secondary, i.e. reactive hypereosinophilia/eosinophilia, disorders and also includes another subtype, organ-restricted hypereosinophilias, a disorder in which eosinophil-mediated tissue damage is restricted to one organ and is often but not always associated with increased blood eosinophil counts.{{citation needed|date=July 2020}}
 
=== Primary hypereosinophilia ===
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==== Infections ====
[[Helminths]] are common causes of hypereosinophilia and eosinophilia in areas endemic to these parasites. Helminths infections causing increased blood eosinophil counts include: '''1)''' [[nematodes]], (i.e.g. ''[[Angiostrongylus cantonensis]]'' and [[Hookworm infections]]), [[ascariasis]], [[strongyloidiasis]] [[trichinosis]], [[visceral larva migrans]], [[Gnathostomiasis]], [[cysticercosis]], and [[echinococcosis]]; '''2)''' [[filarioidea]], i.e.g. [[tropical pulmonary eosinophilia]], [[loiasis]], and [[onchocerciasis]]; and '''3)''' [[Fluke (flatworm)|fluke]]s, i.e.g. [[schistosomiasis]], [[fascioliasis]], [[clonorchiasis]], [[paragonimiasis]], and [[fasciolopsiasis]]. Other infections associated with increased eosinophil blood counts include: [[protozoa]]n infections, i.e.g. ''[[Isospora belli]]'' and ''Dientamoeba fragilis'') and [[sarcocystis]]); [[fungus|fungal]] infections (i.e.g. disseminated [[histoplasmosis]], [[cryptococcosis]] [especially in cases with [[central nervous system]] involvement]), and [[coccidioides]]); and viral infections, i.e.g. [[Human T-lymphotropic virus 1]] and [[HIV]].<ref name="pmid27866580"/><ref name="pmid28285268">{{cite journal | vauthors = Nunes MC, Guimarães Júnior MH, Diamantino AC, Gelape CL, Ferrari TC | title = Cardiac manifestations of parasitic diseases | journal = Heart | volume = 103 | issue = 9 | pages = 651–658 | year = 2017 | pmid = 28285268 | doi = 10.1136/heartjnl-2016-309870 | s2cid = 206974794 }}</ref>
 
==== Autoimmune diseases ====
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==== IgG4-related disease ====
{{main|IgG4-related disease }}
IgG4-related disease or [[Immunoglobulin G4]]-related disease is a condition [[dacryoadenitis]], [[sialadenitis]], lymphadentitis, and [[pancreatitis]] (i.e. inflammation of the [[lacrimal gland]]s, [[salivary gland]]s, [[lymph node]]s, and [[pancreas]], respectively) plus [[retroperitoneal fibrosis]]. Less commonly, almost any other organ or tissue except joints and brain may be beleaguered by the inflammatory disorder. About 1/3 of cases exhibit eosinophilia or, rarely, hypereosinophilia. This increase in blood eosinophil count is often associated with abnormal T-lymphocyte clones (e.g. increased numbers of CD4 negative, CD7 positive T cells, CD3 negative, CD4 positive T cells, or CD3 positive, CD4 negative, CD8 negative T cells) and is thought to be secondary to these immunological disturbances. The disorder often exhibits are recurrent-relapsing course and is highly responsive to [[corticosteroids]] or [[rituximab]] as first-line therapy and [[interferon gamma]] as second-line therapy.<ref name="pmid28005278">{{cite journal | vauthors = Carruthers MN, Park S, Slack GW, Dalal BI, Skinnider BF, Schaeffer DF, Dutz JP, Law JK, Donnellan F, Marquez V, Seidman M, Wong PC, Mattman A, Chen LY | title = IgG4-related disease and lymphocyte-variant hypereosinophilic syndrome: A comparative case series | journal = European Journal of Haematology | volume = 98 | issue = 4 | pages = 378–387 | year = 2017 | pmid = 28005278 | doi = 10.1111/ejh.12842 | doi-access = free }}</ref>
 
==== Angiolymphoid hyperplasia with eosinophilia ====
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** [[Systemic lupus erythematosus]]
** [[Kimura disease]]<ref>{{cite journal|last1=Boyer|first1=DF|title=Blood and Bone Marrow Evaluation for Eosinophilia.|journal=Archives of Pathology & Laboratory Medicine|date=October 2016|volume=140|issue=10|pages=1060–7|doi=10.5858/arpa.2016-0223-RA|pmid=27684977|doi-access=free}}</ref>
** [[Eosinophilic granulomatosis with polyangiitis]]<ref name="White2023">{{cite journal |last1=White |first1=J |last2=Dubey |first2=S |title=Eosinophilic granulomatosis with polyangiitis: A review |journal=Autoimmunity Reviews |date=January 2023 |volume=22 |issue=1 |page=103219 |doi=10.1016/j.autrev.2022.103219 |pmid=36283646 |url=https://www.sciencedirect.com/science/article/pii/S1568997222001896 |access-date=21 September 2024|doi-access=free }}</ref>
** [[Eosinophilic granulomatosis with polyangiitis]]<ref>{{EMedicine|article|333492|Eosinophilic Granulomatosis with Polyangiitis (Churg–Strauss Syndrome)}}</ref>
** [[Eosinophilic fasciitis]]<ref name="pmid22594010">{{cite journal | vauthors = Arlettaz L, Abdou M, Pardon F, Dayer E | title = [Eosinophllic fasciitis (Shulman disease)] | language = fr | journal = Revue Médicale Suisse | volume = 8 | issue = 337 | pages = 854–8 | year = 2012 | doi = 10.53738/REVMED.2012.8.337.0854 | pmid = 22594010 }}</ref>
** Eosinophilic myositis<ref name="pmid27684977">{{cite journal | vauthors = Boyer DF | title = Blood and Bone Marrow Evaluation for Eosinophilia | journal = Archives of Pathology & Laboratory Medicine | volume = 140 | issue = 10 | pages = 1060–7 | year = 2016 | pmid = 27684977 | doi = 10.5858/arpa.2016-0223-RA | doi-access = free }}</ref>
* [[Eosinophilic myocarditis]]<ref name="pmid25858537">{{cite journal | vauthors = Séguéla PE, Iriart X, Acar P, Montaudon M, Roudaut R, Thambo JB | title = Eosinophilic cardiac disease: Molecular, clinical and imaging aspects | journal = Archives of Cardiovascular Diseases | volume = 108 | issue = 4 | pages = 258–68 | year = 2015 | pmid = 25858537 | doi = 10.1016/j.acvd.2015.01.006 | doi-access = free }}</ref>