在侵袭性CD20(+) B细胞淋巴瘤患者的 RICOVER-60 试验中，NADPH氧化酶多态性与蒽环类药物诱导的心脏毒性的关联
Association of NADPH oxidase polymorphisms with anthracycline-induced cardiotoxicity in the RICOVER-60 trial of patients with aggressive CD20(+) B-cell lymphoma.
作者信息
Reichwagen Annegret, Ziepert Marita, Kreuz Markus, Gödtel-Armbrust Ute, Rixecker Tanja, Poeschel Viola, Reza Toliat Mohammad, Nürnberg Peter, Tzvetkov Mladen, Deng Shiwei, Trümper Lorenz, Hasenfuss Gerd, Pfreundschuh Michael, Wojnowski Leszek
机构信息
Department of Pharmacology, Universitätsmedizin Mainz, Obere Zahlbacher Str. 67, 55101 Mainz, Germany.
出版信息
Pharmacogenomics. 2015;16(4):361-72. doi: 10.2217/pgs.14.179.
AIM
To identify gene variants responsible for anthracycline-induced cardiotoxicity.
PATIENTS & METHODS: Polymorphisms of the NADPH oxidase subunits and of the anthracycline transporters ABCC1, ABCC2 and SLC28A3 were genotyped in elderly patients (61-80 years) treated for aggressive CD20(+) B-cell lymphomas with CHOP-14 with or without rituximab and followed up for 3 years.
RESULTS
The accumulation of RAC2 subunit genotypes TA/AA among cases was statistically significant upon adjustment for gender, age and doxorubicin dose in a multivariate logistic regression analysis (OR: 2.3, p = 0.028; univariate: OR: 1.8, p = 0.077). RAC2 and CYBA genotypes were significantly associated with anthracycline-induced cardiotoxicity in a meta-analysis of this and a similar previous study.
CONCLUSION
Our results support the theory that NADPH oxidase is involved in anthracycline-induced cardiotoxicity. Original submitted 9 July 2014; Revision submitted 19 December 2014.
目的
确定导致蒽环类药物诱导心脏毒性的基因变异。
患者与方法
对接受含或不含利妥昔单抗的CHOP-14方案治疗侵袭性CD20(+)B细胞淋巴瘤的老年患者（61-80岁）进行NADPH氧化酶亚基以及蒽环类药物转运蛋白ABCC1、ABCC2和SLC28A3的基因分型，并随访3年。
结果
在多因素逻辑回归分析中，经性别、年龄和多柔比星剂量校正后，病例组中RAC2亚基基因型TA/AA的累积具有统计学意义（比值比：2.3，p = 0.028；单因素：比值比：1.8，p = 0.077）。在对本研究及之前一项类似研究进行的荟萃分析中，RAC2和CYBA基因型与蒽环类药物诱导的心脏毒性显著相关。
结论
我们的结果支持NADPH氧化酶参与蒽环类药物诱导心脏毒性这一理论。原始稿件于2014年7月9日提交；修订稿于2014年12月19日提交。
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