A 36-year-old man was transfered to Kinki University Hospital with complaints of splenomegaly, motor and sensory dysfunction of lower extremities.
The leukocytosis of this patient was pointed out five years previously in another hospital when he was treated with duodenal ulcer. The diagnosis of CML with Ph
1 positive chromosome was made and he was treated with Busulfan intermittently. Two years before admission a gastrojejunostomy was performed because of the perforation of duodenal ulcer. Five months before entry motor and sensory disturbance of lower extremities and incontinence developed abruptly and he was readmitted to the Kansai Denryoku Hospital. Partial obstruction of the Th
6 myeloid cavity on myelography and marked splenomegaly were observed. He was treated with VEMP to the blast crisis of CML. Thereafter neurologic findings disappered gradually and he was transfered to our hospital on March 25, 1977. Patient was chronically ill and splenomegaly was presented. Hematological findings were as follows; Hb 5.1g/d
l, WBC 19,500 with 37% myeloblast, and 1.5% eosinophils, erythroblast 31/200, platelet 4.0×10
4, NAP score 206. Bone marrow; cc 22.1×10
4, myeloblast 14%, erythroblast 63.4% with 37.6% immature erythroblast in Wright-Giemsa staining, Peroxidase (-), PAS (+). The patient was treated with MTX and blood transfusions, subsequently immature erythroblast in bone marrow decreased to 6%, but rose to 42.5% thereafter. Patient died on 33th hospital day inspite of intensive chemotherapy and supportive therapy.
At autopsy, bone marrow and lymph nodes were extremely infiltrated with blast cells and eosinophils. Spleen was markedly enlarged (1,500g) due to moderate cell infiltration. Spinal cord showed no infiltration of blast cells.
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