他汀类药物与糖尿病高风险:发病率、拟议机制和临床意义。

PubMed ID
发表日期 年月

原始出处 回顾心脏病学
Cardiology in review
作者 Guber  Kenneth  Pemmasani  Gayatri  Malik  Aaqib  Aronow  Wilbert S  Yandrapalli  Srikanth  Frishman  William H 

文献标题 他汀类药物与糖尿病高风险:发病率、拟议机制和临床意义。
Statins and Higher Diabetes Mellitus Risk: Incidence, Proposed Mechanisms, and Clinical Implications.

文献摘要

3-羟基-3-甲基戊二酰辅酶A还原酶抑制剂广泛用于心血管疾病(CVD)的预防和治疗。然而,他汀类药物的使用与新发糖尿病(NODM)的发生有关,这可能会增加未来CVD的风险。这种现象需要明确讨论这种关系的可能病因及其更广泛的临床后果。我们通过对随机对照试验荟萃分析数据的严格审查,讨论了他汀类药物使用者中NODM的报告发病率。我们还强调了他汀类药物诱发糖尿病的各种可能机制。最后,我们研究了这种影响对未来CVD风险的临床意义,并确定了可用于风险分层策略的特定患者因素。14项随机对照试验的数据荟萃分析表明,使用他汀类药物的NODM风险高9-33%。一些细胞、分子和遗传机制以及生活习惯已被确定为导致这种高风险的潜在潜在因素。他汀类药物致糖尿病作用的主要模式尚不清楚,尽管这可能是胰腺和胰腺外效应复杂相互作用的结果。据了解,糖尿病易感性较高的患者群体和心外膜脂肪较厚的患者更容易发生他汀类药物诱导的NODM。尽管有这些观察结果,但来自各种研究的可靠数据表明,他汀类药物治疗的心血管疾病预防益处明显大于与NODM发展相关的风险。然而,进一步的研究必须更好地确定这一过程中涉及的致病机制、其自然史和独特的因素,以帮助临床医生对服用他汀类药物的患者进行风险分层和适当监测。


3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors are ubiquitously prescribed for cardiovascular disease (CVD) prevention and treatment. However, the use of statins has been linked to the development of new-onset diabetes mellitus (NODM), which could possibly increase future CVD risk. This phenomenon necessitates a clear discussion of the possible etiologies of this relationship and its broader clinical consequences. We discuss the reported incidence of NODM in statin users through a rigorous review of data from metaanalyses of randomized control trials examining this association. We also highlight the various possible mechanisms responsible for the development of statin-induced diabetes mellitus. Finally, we examine the clinical implications of this effect on future CVD risk and identify specific patient factors that can be used for risk-stratification strategies. Data from 14 randomized control trials metaanalyses suggest a 9-33% higher risk of NODM with statin use. Several cellular, molecular, and genetic mechanisms, as well as lifestyle habits, have been identified as potential underlying factors responsible for this elevated risk. The principle mode of the diabetogenic action of statins is still unclear, though it is likely the result of a complex interplay of pancreatic and extrapancreatic effects. It is understood that patient populations with a greater predisposition to diabetes mellitus, and those with thicker epicardial adiposity are more at risk for the development of statin-induced NODM. Despite these observations, robust data from a variety of investigations suggest that the CVD preventative benefits of statin treatment significantly outweigh the risks associated with the development of NODM. Nevertheless, further study must better identify the causative mechanisms involved in this process, its natural history, and the unique factors that will help clinicians risk stratify and appropriately monitor patients on statin therapy.


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