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Dexrazoxane Significantly Reduces Anthracycline-Induced Cardiotoxicity in Pediatric Solid Tumor Patients - A Systematic Review

机译:右雷佐生显着降低小儿实体瘤患者蒽环类药物引起的心脏毒性-系统评价

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摘要

Cardiotoxicity is a dose-limiting and potentially lethal complication of anthracycline administration. Previous studies failed to determine definitive toxic doses or cardioprotective factors. Current dosing strategies may utilize unnecessarily high anthracycline doses, such that survival benefit may not outweigh increased toxicity rates. A systematic review of randomized controlled trials and prospective/retrospective studies investigating anthracycline treatment in pediatric solid tumors was performed from PubMed/MEDLINE and Cochrane databases. Generalized linear models mapping survival, cardiotoxicity and cardiotoxicity-free survival adjusted for male-to-female ratio, follow-up time, and concomitant chemotherapeutic drugs or cardioprotective agents (dexrazoxane) were generated using R. Survival rose linearly with increasing cumulative anthracycline dose while cardiotoxicity demonstrated exponential increases both without (dose >200mg/m2) and with (dose >400mg/m2) dexrazoxane. Maximum cardiotoxicity-free survival was 268.2 mg/m2 without and 431.8 mg/m2 with dexrazoxane. Despite increasing cardiotoxicity-free dose by >150mg/m2, dexrazoxane minimally improved projected survival (71.9% vs. 75.4%). Cardiotoxicity increased linearly as a function of follow-up time with rates doubling from 5 to 20 years, without evidence of plateau. Based on our model, current dosing regimens — doxorubicin doses >375 mg/m2 without dexrazoxane — overvalue increased anthracycline administration and may contribute to devastating cardiotoxicity. The linear increase of cardiotoxicity without evidence of plateau confirms the necessity for lifelong cardiac monitoring.
机译:心脏毒性是蒽环类药物给药的剂量限制和可能致命的并发症。先前的研究未能确定确定的毒性剂量或心脏保护因子。当前的给药策略可能会使用不必要的高蒽环类药物剂量,以使生存获益可能不超过增加的毒性率。从PubMed / MEDLINE和Cochrane数据库中进行了对蒽环类药物治疗小儿实体瘤的随机对照试验和前瞻性/回顾性研究的系统评价。使用R生成了针对生存率,心脏毒性和无心脏毒性生存率(按男女比例,随访时间以及伴随的化疗药物或心脏保护剂(右雷佐生)进行调整)的通用线性模型。生存率随着蒽环类药物累积累积剂量的增加而线性上升在未使用(剂量> 200mg / m 2 )和使用(剂量> 400mg / m 2 )右雷佐生时,心脏毒性均呈指数增加。无心脏毒性时的最大无生存期为268.2 mg / m 2 ,与右雷佐生相比为431.8 mg / m 2 。尽管无心毒性剂量增加了> 150mg / m 2 ,但右雷佐生的预期生存率仍微不足道(71.9%对75.4%)。心脏毒性随随访时间呈线性增加,从5年到20年增加一倍,无明显的平稳期。根据我们的模型,当前的给药方案(阿霉素剂量> 375 mg / m 2 而不使用右雷佐生)高估了蒽环类药物的使用,可能会导致破坏性的心脏毒性。心脏毒性呈线性增加而无平台期的迹象,证实了终生心脏监测的必要性。

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