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Chromosomes and causation of human cancer and leukemia. XXXIV. A case of “hypereosinophilic syndrome” with unusual cytogenetic findings in a chloroma, terminating in blastic transformation and CNS leukemia
Author(s) -
Huang Chao Shuo,
Gomez German A.,
Kohno SeiIchi,
Sokal Joseph E.,
Sandberg Avery A.
Publication year - 1979
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(197910)44:4<1284::aid-cncr2820440418>3.0.co;2-n
Subject(s) - medicine , hypereosinophilia , leukemia , pathology , eosinophilia , bone marrow , hypereosinophilic syndrome , biopsy , hepatosplenomegaly , immunology , disease
A 47‐year‐old white male developed massive hepatosplenomegaly, a pleural effusion, leucocytosis, and a left parasternal mass following a relatively symptomfree persistent hypereosinophilia for about 5 years. Bone marrow aspiration and biopsy and peripheral blood differential showed eosinophilia and a shift to the left with immature cells. A high serum B 12 vitamin level and low LAP activity were found. Biopsy of the soft tissue mass revealed a granulocytic sarcoma (chloroma) with a hyperdiploid karyotype (49,XY,+10,+15,+19,3q‐), whereas the bone marrow cells had a normal male karyotype. The patient responded temporarily to chemotherapy but eventually developed CNS leukemia and went on to terminate in a frank blastic phase. This case illustrates hypereosinophilia and a myeloproliferative syndrome characterized by a somewhat indolent chronic course evolving into “eosinophilic leukemia” and granulocytic sarcoma, CNS involvement by leukemic cells and, finally, blastic transformation. It is possible that this case represents a variant of Ph 1 ‐negative CML to which the term “chronic eosinophilic leukemia” could be justifiably applied.