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Non-selective nonsteroidal anti-inflammatory drugs and cardiovascular events: is aldosterone the silent partner in crime?

机译:非选择性非甾体抗炎药和心血管事件:醛固酮是犯罪的沉默伴侣吗?

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Non-selective nonsteroidal anti-inflammatory drugs (NSAIDs) have long been known to cause gastrointestinal and renal toxicity. More recently, adverse cardiovascular effects have been associated with the selective COX-2 inhibitors. However, current studies that show an increased cardiovascular risk with non-selective NSAIDs raise the question of the exclusive contribution of COX-2 to this type of toxicity. Aldosterone, a key cardiovascular hormone, can induce deleterious effects, such as myocardial fibrosis and vascular stiffening. Non-selective NSAIDs inhibit the metabolism of aldosterone in vitro by human renal tissue, predicating an increased plasma aldosterone concentration in vivo. The question remains whether inhibition of aldosterone metabolism by non-selective NSAIDs is a casual or causal factor in NSAID-induced cardiovascular toxicity.
机译:长期以来,非选择性非甾体抗炎药(NSAIDs)会引起胃肠道和肾脏毒性。最近,心血管不良反应与选择性COX-2抑制剂有关。但是,目前的研究表明,非选择性NSAIDs会增加心血管疾病的风险,提出了COX-2对这种毒性的独家贡献的问题。醛固酮是一种重要的心血管激素,可引起有害作用,例如心肌纤维化和血管僵硬。非选择性NSAIDs可在体外通过人肾组织抑制醛固酮的代谢,提示体内血浆醛固酮浓度升高。问题仍然在于,非选择性NSAID抑制醛固酮代谢是NSAID诱导的心血管毒性的偶然因素还是因果因素。

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