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Chokri Ben Lamine: High-Yield Differentiation of Eosinophilic Disorders

AI Generated

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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