目的 增加对治疗相关性继发白血病的认识。 方法 报道非霍奇金淋巴瘤治疗后2年继发急性髓细胞白血病M6型1例，结合文献讨论治疗相关性白血病的发病机制、治疗、预后。 结果 1例73岁非霍奇金淋巴瘤患者接受R（Rituxmab，利妥昔单抗）－CHOP环磷酰胺+多柔比星+长春新碱+泼尼松方案规律化学治疗。治疗结束24+个月后，经骨髓涂片及细胞免疫分型诊断为急性髓细胞白血病M6型，染色体检查为：44～48，XY，del（5）（q12q33），-8，-10，der（12）t（4；12）（q11-q12；p13），其一般情况急剧恶化并死亡。 结论 治疗相关性白血病的发生可能与烷化剂等化疗药物使用和免疫受损等有关，利妥昔单抗导致第二肿瘤的发生暂时不能除外。治疗相关性白血病常伴有复杂染色体核型，其病情发展迅速，治疗效果差，生存期明显缩短。Objective To improve the understanding of secondary therapy-related leukemia. Methods The clinical data of one patient with non-Hodgkin lymphoma which transformed into acute myeloid leukemia M6 2 years after chemotherapy were studied. We discussed the pathogenesis, treatment and prognosis of therapy-related leukemia with literature review. Results A 73-year-old patient diagnosed to have non-Hodgkin’s lymphoma accepted R-CHOP chemotherapy.Two years after the treatment, the disease finally developed into acute myeloid leukemia M6 confirmed by cytogenetics, bone marrow morphology and flowcytometry analysis. The chromosome analysis demonstrated complex karyotypes as 44-48, XY, del (5) (q12q33), -8, -10, der (12) t (4; 12) (q11-q12; p13). His general status deteriorated rapidly and soon after the patient died. Conclusions Occurrence of therapy-related leukemia may be due to the administration of alkylating agents, topoisomerase inhibitors and damage of immune function. Therapy-related leukemia often occurs with complex karyotypes and progresses rapidly with poor treatment response.
ObjectiveTo analyze the clinical efficacy of decitabine contained chemotherapy regimens in the treatment of relapsed or refractory acute myeloid leukemia (AML) patients.MethodsA total of 101 patients with relapsed or refractory AML from May 2014 to December 2017 were collected retrospectively. Three schemes with a relatively larger number of users were included: 15 cases were treated with decitabine monotherapy (DAC regime); 37 cases were treated with decitabine, anthracycline antibiotic, and cytarabine (D-DA regime); and 49 cases were treated with decitabine, cytarabine, aclarubicin, and granulocyte colony-stimulatingfactor (G-CSF) (D-CAG regimen). The remission rate, blood products support strength, degree and duration of bone marrow suppression, adverse reaction, and survival time were compared.ResultsThe complete remission (CR) rates of DAC, D-DA and D-CAG regimen group were 40.0%, 48.6%, and 71.4%, respectively; the overall respond rates (ORR) were 46.7%, 54.1%, and 79.6%, respectively. The ORR in D-CAG regimen group was higher than those in the other two groups (P<0.017). The dosage of G-CSF in D-CAG regimen group were lower than those in DAC regimen group [ (1 363.0±1 037.9) vs. (2 517.0±1 163.4) μg, P<0.05]; the mean number of erythrocyte transfusion and the dosage of G-CSF were lower than those in D-DA regimen group [(6.7±4.0) vs. (14.8±10.1) U, P<0.05; (1 363.0±1 037.9) vs. (2 786.0±1474.0) μg, P<0.05]; the time to the suppression of hemoglobin and platelet in D-CAG regimen group were later than those in D-DA regimen group [(11.5±2.6) vs. (8.8±2.5) days, P=0.007; (10.9±2.6) vs. (7.6±2.5) days, P=0.002]; the time to the suppression of platelet was later than that in DAC regimen group [(10.9±2.6) vs. (7.6±1.6) days, P=0.003]. There was no statistically significant difference in the incidence of adverse reations among the three group (P>0.05). The median overall survival of D-CAG regimen group was longer than that in DAC regimen group (11.6 vs. 8.8 months, P=0.013).ConclusionAmong the three chemotherapy regimens containing decitabine, the CR and ORR of D-CAG regimen are higher, the tolerance is better, and further promotion can be attempted in qualified medical institutions.