Lymphocytic Variant Hypereosinophilic Syndrome: Case Series From a Tertiary Referral Center in Canada

ABSTRACT Background Lymphocytic variant hypereosinophilic syndrome (L‐HES) is a rare disorder characterized by persistent eosinophilia driven by aberrant T‐cell populations. Diagnosis remains challenging due to the lack of standardized diagnostic criteria. Methods We retrospectively analyzed 18 pati...

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Main Authors: Xiu Qing Wang, Kevin Shopsowitz, Jack Lofroth, Xuehai Wang, Erica Peterson, Andrew P. Weng, Luke Y. C. Chen
Format: Article
Language:English
Published: Wiley 2025-04-01
Series:eJHaem
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Online Access:https://doi.org/10.1002/jha2.1109
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author Xiu Qing Wang
Kevin Shopsowitz
Jack Lofroth
Xuehai Wang
Erica Peterson
Andrew P. Weng
Luke Y. C. Chen
author_facet Xiu Qing Wang
Kevin Shopsowitz
Jack Lofroth
Xuehai Wang
Erica Peterson
Andrew P. Weng
Luke Y. C. Chen
author_sort Xiu Qing Wang
collection DOAJ
description ABSTRACT Background Lymphocytic variant hypereosinophilic syndrome (L‐HES) is a rare disorder characterized by persistent eosinophilia driven by aberrant T‐cell populations. Diagnosis remains challenging due to the lack of standardized diagnostic criteria. Methods We retrospectively analyzed 18 patients diagnosed with L‐HES between 2016 and 2023. Comprehensive flow cytometry was performed on peripheral blood samples. Results Nine patients demonstrated the classic sCD3−CD4+CD5+CD2+CD45RO+CD45RA− immunophenotype, ranging from 0.6% to 70% of total lymphocytes. Two patients showed variant sCD3−CD4+ phenotypes, five had expanded (> 10%) sCD3+CD4+CD7− T‐cells, and two displayed aberrant CD8+ T‐LGL populations. Clonality was established in all patients with nonclassic phenotypes by molecular TCR testing or based on uniform TRBC1. We assessed a serial gating strategy to quantify the classic L‐HES phenotype and found this to be highly sensitive and specific with an estimated limit of detection of 0.06% of lymphocytes. Using this strategy, we identified decreased but detectable abnormal T‐cells in all classic phenotype patients reassessed posttreatment, down to as low as 0.3% of lymphocytes. The identification of T‐LGL phenotypes with eosinophilia is a novel finding. Conclusion Our study highlights the diverse immunophenotypic spectrum of L‐HES, emphasizing the importance of comprehensive flow cytometry analysis for accurate diagnosis.
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spelling doaj-art-6aea239d12da4dfd90cb627b21e4d35e2025-08-20T02:18:28ZengWileyeJHaem2688-61462025-04-0162n/an/a10.1002/jha2.1109Lymphocytic Variant Hypereosinophilic Syndrome: Case Series From a Tertiary Referral Center in CanadaXiu Qing Wang0Kevin Shopsowitz1Jack Lofroth2Xuehai Wang3Erica Peterson4Andrew P. Weng5Luke Y. C. Chen6Department of Pathology and Laboratory Medicine University of British Columbia Vancouver British Columbia CanadaDepartment of Pathology and Laboratory Medicine University of British Columbia Vancouver British Columbia CanadaFaculty of Medicine University of British Columbia Vancouver British Columbia CanadaDepartment of Pathology and Laboratory Medicine University of British Columbia Vancouver British Columbia CanadaDivision of Hematology Dalhousie University Halifax Nova Scotia CanadaDepartment of Pathology and Laboratory Medicine University of British Columbia Vancouver British Columbia CanadaDivision of Hematology Dalhousie University Halifax Nova Scotia CanadaABSTRACT Background Lymphocytic variant hypereosinophilic syndrome (L‐HES) is a rare disorder characterized by persistent eosinophilia driven by aberrant T‐cell populations. Diagnosis remains challenging due to the lack of standardized diagnostic criteria. Methods We retrospectively analyzed 18 patients diagnosed with L‐HES between 2016 and 2023. Comprehensive flow cytometry was performed on peripheral blood samples. Results Nine patients demonstrated the classic sCD3−CD4+CD5+CD2+CD45RO+CD45RA− immunophenotype, ranging from 0.6% to 70% of total lymphocytes. Two patients showed variant sCD3−CD4+ phenotypes, five had expanded (> 10%) sCD3+CD4+CD7− T‐cells, and two displayed aberrant CD8+ T‐LGL populations. Clonality was established in all patients with nonclassic phenotypes by molecular TCR testing or based on uniform TRBC1. We assessed a serial gating strategy to quantify the classic L‐HES phenotype and found this to be highly sensitive and specific with an estimated limit of detection of 0.06% of lymphocytes. Using this strategy, we identified decreased but detectable abnormal T‐cells in all classic phenotype patients reassessed posttreatment, down to as low as 0.3% of lymphocytes. The identification of T‐LGL phenotypes with eosinophilia is a novel finding. Conclusion Our study highlights the diverse immunophenotypic spectrum of L‐HES, emphasizing the importance of comprehensive flow cytometry analysis for accurate diagnosis.https://doi.org/10.1002/jha2.1109eosinophiliahypereosinophilic syndromelymphocyte immunophenotypinglymphocytic hypereosinophilic syndromeT‐cell receptor gene rearrangement
spellingShingle Xiu Qing Wang
Kevin Shopsowitz
Jack Lofroth
Xuehai Wang
Erica Peterson
Andrew P. Weng
Luke Y. C. Chen
Lymphocytic Variant Hypereosinophilic Syndrome: Case Series From a Tertiary Referral Center in Canada
eJHaem
eosinophilia
hypereosinophilic syndrome
lymphocyte immunophenotyping
lymphocytic hypereosinophilic syndrome
T‐cell receptor gene rearrangement
title Lymphocytic Variant Hypereosinophilic Syndrome: Case Series From a Tertiary Referral Center in Canada
title_full Lymphocytic Variant Hypereosinophilic Syndrome: Case Series From a Tertiary Referral Center in Canada
title_fullStr Lymphocytic Variant Hypereosinophilic Syndrome: Case Series From a Tertiary Referral Center in Canada
title_full_unstemmed Lymphocytic Variant Hypereosinophilic Syndrome: Case Series From a Tertiary Referral Center in Canada
title_short Lymphocytic Variant Hypereosinophilic Syndrome: Case Series From a Tertiary Referral Center in Canada
title_sort lymphocytic variant hypereosinophilic syndrome case series from a tertiary referral center in canada
topic eosinophilia
hypereosinophilic syndrome
lymphocyte immunophenotyping
lymphocytic hypereosinophilic syndrome
T‐cell receptor gene rearrangement
url https://doi.org/10.1002/jha2.1109
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