瑞舒伐他汀
肠道菌群
医学
微生物群
他汀类
内科学
抗生素
胆固醇
相伴的
阿托伐他汀
疾病
冠状动脉疾病
HMG-CoA还原酶
药理学
冠心病
心脏病
内分泌学
免疫学
心脏病学
瑞舒伐他汀钙
作者
Guohui Wang,Yan Luo,Sangcang Song,Xiaodong Li,Yaping Pan,Zhongwen Zhao,Bo Wang,Qiongxiang Yang,Feng Yang,Fuyi Wang
标识
DOI:10.1097/fjc.0000000000001805
摘要
Clinical evidence suggests that the lipid-lowering efficacy of statins may be diminished by concurrent β-lactam administration in patients with coronary heart disease (CHD), yet the mechanisms driving this potential drug-drug interaction, particularly the role of gut microbiota as a mediator, remain undefined. To address this gap, we conducted a retrospective analysis of data from a tertiary hospital spanning 5 years, enrolling 436 CHD patients on statin therapy who had two hospital admissions within a 3-month window. Patients were stratified into β-lactam-treated and antibiotic-free cohorts to assess the correlation between β-lactam exposure and statin efficacy. Additionally, 16S ribosomal RNA gene sequencing was employed to characterize and compare gut microbiota profiles between CHD patients receiving combined rosuvastatin and β-lactam therapy versus those on rosuvastatin monotherapy. Our findings demonstrated that β-lactam exposure was associated with elevated low-density lipoprotein cholesterol and total cholesterol levels. Both rosuvastatin and β-lactams induced significant alterations in gut microbiota composition, with distinct shifts in bacterial taxa abundances: rosuvastatin increased the relative abundance of Faecalibacterium and Dysosmobacter, whereas β-lactams disrupted the abundance of Faecalibacterium, Roseburia, and Dysosmobacter. Collectively, these results indicate that concomitant β-lactam use impairs rosuvastatin efficacy in CHD patients, likely via perturbation of gut microbiota composition. Rosuvastatin may exert a portion of its cardioprotective effects through modulation of gut microbiota, and β-lactams may abrogate this benefit by depleting key bacterial taxa linked to statin-mediated lipid regulation. Notably, Dysosmobacter emerges as a potential mediating species in this interaction, supporting a microbiome-dependent mechanism underlying the reduced lipid-lowering efficacy of rosuvastatin during β-lactam co-administration.
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