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Chokri Ben Lamine: High-Yield Differentiation of Eosinophilic Disorders
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Apr 21, 2026, 15:51

Chokri Ben Lamine: High-Yield Differentiation of Eosinophilic Disorders

Chokri Ben Lamine, Adult Hematology and SCT Assistant Consultant at Oncology Center of Excellence at King Faisal Specialist Hospital and Research Center, shared a post on X:

“Hes vs other eosinophilic disorders –  high – yield differentiation

Hypereosinophilic Syndrome (HES)

  • AEC greater than or equal to 1.5 multiplied by ten to the power of nine per liter persistently
    Organ damage heart skin lungs central nervous system
  • No secondary cause and no defined clonal malignancy
  • Subtypes myeloid for example PDGFRA lymphocytic idiopathic
  • Treatment steroids then imatinib if PDGFRA positive then anti interleukin five such as mepolizumab or benralizumab off label

Reactive (Secondary) Eosinophilia

  • Cause identified
  • Parasites (helminths)
  • Drugs (DRESS)
  • Allergic diseases (asthma, eczema)
  • No primary clonal disorder
  • Rx: treat underlying cause

Clonal Eosinophilia Myeloid Neoplasm

  • Genetic driver present
  • PDGFRA, PDGFRB, FGFR1, PCM1, JAK2
  • Often splenomegaly and dysplasia
  • Can evolve to acute myeloid leukemia
  • Treatment targeted tyrosine kinase inhibitors for example imatinib shows a dramatic response in PDGFRA

EGPA (Churg – Strauss)

  • Asthma and sinusitis plus eosinophilia
  • Vasculitis features including neuropathy and purpura
  • ANCA positive or negative
  • Treatment steroids and biologics such as benralizumab or mepolizumab (Food and Drug Administration approved)

Lymphocytic Variant HES (L-HES)

  • Aberrant T cells leading to interleukin five overproduction
  • Skin predominant disease and high immunoglobulin E
  • Risk of T cell lymphoma
  • Treatment steroids with or without immunosuppression

Eosinophilic Leukemia (CEL)

  • Blasts increased or clonal markers present
  • Aggressive clinical course
  • Severe organ infiltration
  • Treatment leukemia type therapy with or without tyrosine kinase inhibitor

Key Clinical Differentiation Pearls

  • Organ damage means consider hypereosinophilic syndrome or eosinophilic leukemia
  • Identifiable trigger suggests reactive eosinophilia
  • Mutation indicates clonal disease (test all patients)
  • Asthma and vasculitis suggests EGPA
  • Skin involvement and increased immunoglobulin E suggests lymphocytic variant HES

Workup Snapshot

  • Complete blood count and peripheral blood smear
  • Fluorescence in situ hybridization and polymerase chain reaction testing for PDGFRA, PDGFRB, FGFR1 and JAK2
  • Bone marrow examination
  • Parasite screening
  • T cell clonality assessment using flow cytometry or T cell receptor studies

MCQ

  • Patient with absolute eosinophil count 3.0, asthma, sinusitis, neuropathy leads to best diagnosis
  • Answer EGPA (vasculitis plus asthma plus eosinophilia)

OSCE

  • Patient with persistent eosinophilia plus cardiac involvement and no secondary cause
  • Next step molecular testing for PDGFRA before labeling idiopathic hypereosinophilic syndrome.”

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