Eosinophilia

Question 1

Myeloid/lymphoid neoplasm with Eosinophilia (Primary Hypereosinophilia) [3] [4 new]

Answer 1

I. M/L with PDGFRA
* Respond to TKI
* Increase B12, Neutros and Eos
* Basos and Monos Normal
* ↑BM Mast cells and ↑Serum tryptase

**II. M/L with PDGFRB **
* Eosinophilia t(5;12)(q32;p13.2)
* Respond to TKI
* Mimics Overlaps Clinically and BM
* Monocytosis mimicking CMML and ↑Basos
* AbN Megs and MF
* Spindle shaped Mast cells

III. M/L with FGFR1
* Poor prognosis. Do not respond to TKI
* Often presents as CML-BP, ALL or AML

IV. M/L with JAK2
* ?MPN, CEL, PMF, Overlap
* HSM
* May respond to JAK2 inhibitors

V. M/L wih FLT3

VI. M/L with ETV6::ABL1 t(9;12)

VII. M/L with other TK fusions

Question 2

Definitions of Eosinophilia, HE and HES

Answer 2

I. Eosinophilia
* Mild >0.5 - 1
* Mod >1 - 1.5
* Severe >1.5 (HE)

II. HE
* Eos >1.5 x 2mo
* ± Tissue HE (>20% Eos in BM, Extensive tissue infiltration, Deposition of eosinophil granules in Tissue

III. HES
* >1.5
* With Eosinophilic organ damage (oher cause of damage excluded)

Question 3

Differential diagnosis of Eosinophilia (9)

Answer 3

1. Reactive (Drugs, Allergy/Infection, Solid tumour/LPD)
2. M/L with TK mutation
3. CML
4. AML inv16
5. Mastocytosis
6. MPN/Overlap
7. B-ALL t(5;14)
8. L-HES / M-HES
9. CEL

Question 4

Causes for secondary HE

Answer 4

I. M-HES
* Cardiac involvement

II. L-HES
* T-cells CD3-, CD4+ or CD3+, DN
* Produce IL5
* Could evolve to LPD

III. Familial
* AD and from birth

IV. Idiopathic

V. HE with US
* No Tissue damage

VI. Organ restricted
* Single organ (Cradiac, Derma, Pulmo, GI and Neuro)

VII. S/D associated with HES
* Gleich s/d - Episodic angiooedema and Eos
* Eosinophilic granulomatosis with polyangitis