Murata T, Motomura S, Harano H, Kanamori H, Miyasita H, Ogawa K, Ookubo T
First Department of Internal Medicine, Yokohama City University School of Medicine.
Rinsho Ketsueki. 1990 Feb;31(2):177-82.
We describe a patient with CML who developed hypercalcemia in his course of blast crisis. A 25-years-old man was diagnosed as CML with priapism in April 1985, and controlled with BHAC-DVP, VMP, busulfan therapy. In December 1987, he readmitted to our hospital with abdominal pain. Investigations at that time showed: white blood cell count 11600/microliters (blast cells 9%); hemoglobin 8.4 g/microliters; platelets 19.0 X 10(4)/microliters; serum calcium 13.2 mg/dl; BUN 44 mg/dl; creatinine 2.7 mg/dl. Treatment with predonine, 6-MP and vincristine was begun. But serum calcium level rose gradually up to 16.5 mg/dl. So we tried middle dose Ara-c therapy, serum calcium decreased to 6.8 mg/dl. At once he was in a chronic phase, but he relapsed and died of heart failure. Necropsy showed extensive leukemic blast-cell infiltration of the bone marrow, liver, spleen, lung, and kidney. The cause of hypercalcemia in our case was suspected of local osteolytic hypercalcemia, because multiple bone destruction was found.
我们描述了一名慢性粒细胞白血病（CML）患者，其在急变期出现了高钙血症。一名25岁男性于1985年4月被诊断为CML并伴有阴茎异常勃起，先后接受了BHAC - DVP、VMP及白消安治疗。1987年12月，他因腹痛再次入院。当时的检查结果显示：白细胞计数11600/微升（原始细胞9%）；血红蛋白8.4克/微升；血小板19.0×10⁴/微升；血清钙13.2毫克/分升；血尿素氮44毫克/分升；肌酐2.7毫克/分升。开始使用泼尼松、6 - 巯基嘌呤及长春新碱进行治疗。但血清钙水平逐渐升至16.5毫克/分升。于是我们尝试中剂量阿糖胞苷治疗，血清钙降至6.8毫克/分升。患者随即进入慢性期，但之后复发并死于心力衰竭。尸检显示骨髓、肝脏、脾脏、肺和肾脏有广泛的白血病原始细胞浸润。我们病例中高钙血症的原因怀疑是局部溶骨性高钙血症，因为发现了多处骨质破坏。
