Fujisawa S, Togawa J, Tanaka M, Koharazawa H, Aoba M, Fujita H, Murata T, Kanamori H, Matsuzaki M, Mohri H, Ishigatsubo Y
First Department of Internal Medicine, Yokohama City University School of Medicine, Yokohama.
Intern Med. 1999 Jul;38(7):607-11. doi: 10.2169/internalmedicine.38.607.
We describe a rare case of de novo acute myelogenous leukemia with trilineage myelodysplasia (AML/TMDS) associated with t(8;21)(q22;q22). The patient was admitted to our hospital with leukocytopenia. AML/TMDS was diagnosed by excess myeloblasts and morphological findings of bone marrow. The karyotype revealed 45, X, -Y, t(8;21)(q22;q22) in 17 of 20 analyzed mitoses, and also AML1/MTG8 transcripts were detected by the reverse transcription polymerase chain reaction (RT-PCR) method. The patient achieved a complete remission with a combination chemotherapy of daunorubicin, cytarabine, and prednisolone. This case suggests that t(8;21)(q22;q22) may participate in the pathogenesis of AML/TMDS, although this type is usually found as one of the chromosomal abnormalities in de novo acute myelogenous leukemia (AML) with maturation.
我们描述了一例罕见的伴有三系骨髓发育异常的初发急性髓性白血病(AML/TMDS),其与t(8;21)(q22;q22)相关。该患者因白细胞减少症入院。通过骨髓中原始粒细胞增多及形态学表现诊断为AML/TMDS。核型分析显示,在20个分析的有丝分裂中,17个显示为45, X, -Y, t(8;21)(q22;q22),并且通过逆转录聚合酶链反应(RT-PCR)方法检测到AML1/MTG8转录本。该患者通过柔红霉素、阿糖胞苷和泼尼松龙联合化疗实现了完全缓解。该病例提示t(8;21)(q22;q22)可能参与了AML/TMDS的发病机制,尽管这种类型通常是初发急性髓性白血病(AML)伴成熟时发现的染色体异常之一。