Volumen: 19 # Number : 2
Publication Date : Mayo - Agosto Year: 2015
Hypereosinophilia:clonal or not? A vital question
Authors: Agamennoni L, Almada D, Colombi Martínez F, Reynoso J.
Abstract: We present a clinical case of a 46 year old male patient
with eosinophilia and thrombocytopenia, who
also presented signs of an underlying myeloproliferative
syndrome. We built a diagnostic analysis
using eosinophilia as a trigger, always keeping in
mind that reactive causes are still the most prevalent
worldwide and therefore should be the first to rule
out. On the other hand, diagnostic studies seeking
for organ damage by eosinophils should always be
undertaken as part of the first round of studies. In
this case, our primary diagnostic approach was of
a clonal eosinophilia, as the patient also presented
leukocytosis with a left shift, splenomegaly and a
bone marrow with myeloid hyperplasia. The 2008
WHO classification system for hematologic malignancies
recognizes two distinct subcategories of
clonal eosinophilia: chronic eosinophilic leukemia,
not otherwise specified and mutations involving
platelet-derived growth factor receptor α o β (PDGFRA/
PDGRFB) or fibroblastgrowth factor receptor
1 (FGF). A series of specific complementary studies,
including a bone marrow biopsy, cytogenetic
analysis, FISH and molecular studies for FIP1L1/
PDGFRA were performed in order to rule out these
diseases. After analyzing all the available data we
reached the conclusion that this particular case was
indeed a clonal eosinophilia, without molecular evidence,
at least with the available technology. The
clinical condition of the patient deteriorated during
the first few days since his admission and there was
no improvement with glucocorticoid therapy. At
this point we decided to practice a therapeutic test
with TKI. Imatinib at 400 mg per day was started,
achieving clinical improvement within days and accomplishing
a sustained hematologic remission, until
present day. This favorable outcome has been observed
in other case reports which describe similar
positive results with Imatinib in patients who were
also negative for the mutation FIP1L1/PDGFRA.
Key words: Eosinophilia,
Hypereosinophilic syndrome,
FIP1L1/PDGFRA,
Imatinib.
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