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1.山东大学齐鲁医院临床药学部,济南 250012
2.山东大学齐鲁医院德州医院临床药学科,山东 德州 253000
3.山东大学齐鲁医院肿瘤内科,济南 250012
主管药师,硕士。研究方向:临床药学。E-mail:xln0788@163.com
副主任药师。研究方向:抗肿瘤药物、临床药学。E-mail:fyl1599@126.com
收稿日期:2025-01-14,
修回日期:2025-02-15,
录用日期:2025-04-17,
纸质出版日期:2025-05-30
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徐丽娜,方英立,王向玲,等.1例奥沙利铂联合卡培他滨致严重心脏毒性病例报道及文献复习[J].中国药房,2025,36(10):1248-1253.
XU Lina,FANG Yingli,WANG Xiangling,et al.One case report and literature review of severe cardiotoxicity by oxaliplatin combined with capecitabine[J].ZHONGGUO YAOFANG,2025,36(10):1248-1253.
徐丽娜,方英立,王向玲,等.1例奥沙利铂联合卡培他滨致严重心脏毒性病例报道及文献复习[J].中国药房,2025,36(10):1248-1253. DOI: 10.6039/j.issn.1001-0408.2025.10.17.
XU Lina,FANG Yingli,WANG Xiangling,et al.One case report and literature review of severe cardiotoxicity by oxaliplatin combined with capecitabine[J].ZHONGGUO YAOFANG,2025,36(10):1248-1253. DOI: 10.6039/j.issn.1001-0408.2025.10.17.
目的
2
探讨奥沙利铂联合卡培他滨导致严重心脏毒性与基因多态性的关系,为临床安全用药提供参考。
方法
2
临床药师对山东大学齐鲁医院1例首次应用标准剂量奥沙利铂联合卡培他滨治疗的直肠癌患者出现严重心脏毒性进行相关性鉴别分析。检索中国知网、PubMed等中英文数据库中关于奥沙利铂、卡培他滨导致心脏毒性的个案报道,提取所有病例的基本资料、药物治疗方案和心脏毒性特征等进行汇总分析。结合本例患者铂类、氟尿嘧啶类药物代谢、排泄相关基因多态性检测结果,讨论奥沙利铂、卡培他滨导致心脏毒性的可能机制及防治策略。
结果
2
本例患者存在三磷酸腺苷结合盒转运体B亚家族成员1
C3435T和G2677T/A纯合突变、亚甲基四氢叶酸还原酶 A1298C杂合突变、谷胱甘肽硫转移酶P1 A105G杂合突变,存在奥沙利铂、卡培他滨代谢、排泄障碍。药师建议:患者再次治疗停用奥沙利铂,给予原剂量50%卡培他滨治疗。医师采纳药师建议;患者后续治疗未再出现严重不良反应,且病情稳定。
结论
2
奥沙利铂、卡培他滨可致严重心脏毒性。建议有条件的医疗机构对应用奥沙利铂、卡培他滨的患者进行代谢、排泄相关基因多态性检测;对存在多基因突变的患者给予密切监护,并适当降低药物剂量,以保障患者用药安全、有效。
OBJECTIVE
2
To explore the relationship between severe cardiotoxicity caused by oxaliplatin combined with capecitabine and genetic polymorphism, thereby providing references for safe clinical medication use.
METHODS
2
Clinical pharmacists conducted a correlation analysis on a case of severe cardiotoxicity in a rectal cancer patient at Qilu Hospital of Shandong University following first-time treatment with standard doses of oxaliplatin combined with capecitabine. Case reports of cardiotoxicity caused by oxaliplatin and capecitabine were retrieved from the Chinese and English databases such as CNKI and PubMed.Basic patient information, drug treatment plan, and cardiotoxic manifestations were extracted and summarized. Combined with the patient’s genetic polymorphism test results related to the metabolism and excretion of platinum-based and fluorouracil drugs, potential mechanisms and prevention strategies for cardiotoxicity induced by oxaliplatin and capecitabine were discussed.
RESULTS
2
The patient exhibited homozygous mutations in
ABCB1
C3435T and G2677T/A, a heterozygous mutation in
MTHFR
A1298C, and a heterozygous mutation in
GSTP1
A105G, indicating impaired metabolism and excretion of oxaliplatin and capecitabine. The pharmacists recommended discontinuing oxaliplatin and reducing capecitabine to 50% of the original dose for subsequent treatment. The physicians adopted this advice, and the patient experienced no further severe adverse reactions with stable disease progression.
CONCLUSIONS
2
Oxaliplatin and capecitabine may cause severe cardiotoxicity. Medical institutions with adequate resources should perform genetic polymorphism test related to drug metabolism and excretion in patients prescribed these agents. For patients with multiple gene mutations, close monitoring and appropriate dose reductions are recommended to ensure medication safety and efficacy.
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