Yamato H, Yamada K, Koike T, Yoshida M, Tsunogake S, Aoyagi M, Nakamura Y, Watanabe K, Saito K, Enokihara H
Third Department of Internal Medicine Dokkyo University School of Medicine.
Rinsho Ketsueki. 1995 Feb;36(2):128-33.
We report a case of acute myelogenous leukemia (AML), which developed from severe aplastic anemia (SAA) and was successfully treated by low-dose Ara-C and aclarubicin with concomitant use of G-CSF (CAG therapy). A 37-year-old male was admitted for scrutiny of pancytopenia and diagnosed as SAA because of hypocellular bone marrow without abnormal or dysplastic cells. Although hematopoiesis recovered with steroid pulse therapy followed by administration of anabolic steroids, 29 months after initial onset of SAA, he presented as AML (FAB-M6), as his bone marrow Contained 21.6% leukemic myeloblasts and 56% of erythroblasts. Chromosome study revealed 45, XY, -7 in 14 of 20 cells analyzed. Complete remission was achieved by administration of low-dose Ara-C (20 mg/m2 for 7 days) and aclarubicin (14 mg/m2 for 4 days) along with G-CSF (200 micrograms/m2 for 7 days), without any severe complications. In the previous reports in Japan since 1982, 7 out of 8 cases with AML developing from SAA died within a year. Our results indicate that CAG therapy is useful for treatment for this subset of AML with poor prognosis.
我们报告一例急性髓系白血病(AML),其由严重再生障碍性贫血(SAA)发展而来,并通过小剂量阿糖胞苷和阿克拉霉素联合使用粒细胞集落刺激因子(CAG疗法)成功治愈。一名37岁男性因全血细胞减少入院检查,因骨髓细胞减少且无异常或发育异常细胞而被诊断为SAA。尽管在接受类固醇冲击治疗后接着使用同化类固醇,造血功能有所恢复,但在SAA初次发病29个月后,他表现为AML(FAB-M6),因为其骨髓中含有21.6%的白血病原始粒细胞和56%的成红细胞。染色体研究显示,在分析的20个细胞中有14个为45,XY,-7。通过给予小剂量阿糖胞苷(20mg/m²,持续7天)、阿克拉霉素(14mg/m²,持续4天)以及粒细胞集落刺激因子(200μg/m²,持续7天),实现了完全缓解,且无任何严重并发症。在日本自1982年以来的既往报道中,8例由SAA发展而来的AML患者中有7例在一年内死亡。我们的结果表明,CAG疗法对治疗这一预后不良的AML亚组有效。