药物诱导的高乳酸血症和乳酸性酸中毒:文献系统综述

Zachary R. Smith, Michelle Horng, M. Rech
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引用次数: 23

摘要

高乳酸血症和乳酸酸中毒是两种与发病率和死亡率相关的综合征。药物诱导的高乳酸血症和乳酸性酸中毒是排除性诊断,有可能被忽视。本系统综述的目的是识别已发表的药物诱导乳酸水平升高的报告,以帮助临床医生诊断和理解这种罕见药物不良反应的潜在机制,并提供管理策略。PubMed数据库检索了1950年1月至2017年6月间发表的病例报告、病例系列、回顾性研究和前瞻性研究,这些研究描述了药物诱导的乳酸水平升高的病例,包括乳酸酸中毒和高乳酸血症。采用标准化的检索策略,确定的文章由两名审稿人进行两轮独立评估,以评估是否纳入。如果文章描述了至少一名12岁以上的患者由美国食品和药物管理局(FDA)批准的药物引起的高乳酸血症或乳酸性酸中毒,并且排除了其他病因导致的乳酸水平升高,则文章被纳入。二甲双胍和核苷/核苷酸逆转录酶抑制剂被排除在外,因为这些药物的病理生理和乳酸酸中毒的发生率已经得到了很好的证实。总共鉴定了1918篇文章,其中101篇符合纳入标准。共有286名患者经历了药物诱导的乳酸水平升高,从中确定了59种独特的药物。最常见的药物是肾上腺素和沙丁胺醇。药物诱导的乳酸水平升高分为乳酸性酸中毒(64.0%)、高乳酸血症(31.1%)或未明确的(4.9%)。摄入的剂量包括FDA标签剂量(86%)、故意过量剂量(10.8%)或处方剂量超过FDA标签剂量(3.1%)。无变化继续用药(40.8%),永久停药(34.4%),减少剂量继续用药(11.6%),或最初停药,乳酸水平正常化后恢复用药(2.9%);其余10.0%患者的用药管理未见报道。46例患者死亡(16%)。治疗临床医生将6例死亡归因于药物诱导的乳酸酸中毒。管理策略是不同的,治疗包括支持性护理、外源性碳酸氢盐治疗、药物特异性解毒剂和净化策略。原因不明的乳酸水平升高应促使临床医生评估药物诱导的乳酸水平升高。药剂师是医疗保健团队的成员,在药物诱导的乳酸水平升高的诊断和管理方面具有良好的定位。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Medication‐Induced Hyperlactatemia and Lactic Acidosis: A Systematic Review of the Literature
Hyperlactatemia and lactic acidosis are two syndromes that are associated with morbidity and mortality. Medication‐induced hyperlactatemia and lactic acidosis are diagnoses of exclusion and have the potential to be overlooked. The purposes of this systematic review are to identify published reports of medication‐induced lactate level elevations to aid clinicians in diagnosing and comprehending the underlying mechanism of this rare adverse drug effect and to provide management strategies. The PubMed database was searched for case reports, case series, retrospective studies, and prospective studies describing cases of medication‐induced lactate level elevation, including lactic acidosis and hyperlactatemia, published between January 1950 and June 2017. A standardized search strategy was used, and the articles identified underwent two rounds of independent evaluation by two reviewers to assess for inclusion. Articles were included if they described at least one patient older than 12 years with hyperlactatemia or lactic acidosis caused by a medication with United States Food and Drug Administration (FDA) approval and if alternative etiologies for an elevated lactate level were ruled out. Metformin and nucleoside/nucleotide reverse transcriptase inhibitors were excluded since the pathophysiology and incidence of lactic acidosis have been well established for these agents. Overall, 1918 articles were identified, and 101 met inclusion criteria. A total of 286 patients experienced medication‐induced lactate level elevations, from which 59 unique medications were identified. The most commonly identified agents were epinephrine and albuterol. Medication‐induced lactate level elevation was classified as lactic acidosis (64.0%), hyperlactatemia (31.1%), or not specified (4.9%). The doses ingested included FDA‐labeled doses (86%), intentional overdoses (10.8%), or prescribed doses exceeding the FDA‐labeled dose (3.1%). Medications were continued without a change (40.8%), were permanently discontinued (34.4%), were continued with a dosage reduction (11.6%), or were initially withheld then resumed after lactate level normalized (2.9%); medication management for the remaining 10.0% was not reported. Forty‐six patients died (16%). Six deaths were attributed by treating clinicians to be secondary to medication‐induced lactic acidosis. Management strategies were heterogeneous, and treatment included supportive care, exogenous bicarbonate therapy, medication specific antidotes, and decontamination strategies. Unexplained lactate level elevations should prompt clinicians to assess for medication‐induced lactate level elevations. Pharmacists are members of the health care team that are well positioned to serve as experts in the diagnosis and management of medication‐induced lactate level elevations.
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