Premium
Bone marrow hypoplasia and aplasia complicating interferon therapy for chronic myelogenous leukemia
Author(s) -
Talpaz Moshe,
Kantarjian Hagop,
Kurzrock Razelle,
Gutterman Jordan U.
Publication year - 1992
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19920115)69:2<410::aid-cncr2820690222>3.0.co;2-v
Subject(s) - pancytopenia , medicine , bone marrow aplasia , chronic myelogenous leukemia , bone marrow , aplasia , hypoplasia , complication , philadelphia chromosome , leukemia , pathology , immunology , surgery , biology , chromosomal translocation , biochemistry , gene
In four patients with Philadelphia chromosome‐positive (Ph 1 ) chronic myelogenous leukemia (CML), bone marrow hypoplasia (three patients) and aplasia (one patient) developed during or after therapy with either al‐pha‐interferon (IFN) or gamma‐IFN. The predominant clinical characteristic of this complication was protracted pancytopenia, which required 2 to 5 months recovery time after treatment and did not resolve in one patient. Bone marrow cytogenetic analysis in two of the patients demonstrated 100% Ph 1 metaphases despite the profound bone marrow suppression. Overall, this complication was uncommon, occurring in less than 2% of the patients with CML treated with various IFN. The possible underlying causes include previous therapy with alkylating agents, lack of “reservoir” or normal stem cells, or pronounced sensitivity of the malignant cell clone to the suppressive effect of IFN.