SGLT-2 Inhibitor use and liver-related and mortality outcomes in patients with type 2 diabetes and compensated cirrhosis

SGLT-2抑制剂的使用与2型糖尿病合并代偿性肝硬化患者的肝脏相关结局和死亡率之间的关系

阅读:1

Abstract

BACKGROUND: Sodium-glucose cotransporter-2 (SGLT-2) inhibitors with pleiotropic effects beyond glycemic control potentially improve clinical outcomes in cirrhosis; however, large-scale human evidence remains limited. We aimed to compare liver outcomes and mortality risk in adults with type 2 diabetes and compensated cirrhosis, who initiated either SGLT-2 inhibitors or dipeptidyl peptidase-4 (DPP-4) inhibitors. METHODS: Using the TriNetX Global Collaborative Network and a target trial emulation framework, we identified adults with compensated cirrhosis and type 2 diabetes initiating an SGLT-2- or DPP-4 inhibitor between 2016 and 2024. Baseline demographics, laboratory information, comorbidities and concomitant medications were matched by propensity scores. The primary outcome was a composite of incident hepatic decompensation, hepatocellular carcinoma and all-cause mortality. We used Cox proportional hazards models to estimate the hazard ratios (HR) with 95% confidence intervals (CI). RESULTS: We included 5,398 patients (mean [SD] age: 63.9 [10.3] years), receiving SGLT-2 inhibitors, matched to 5,398 DPP-4 inhibitor users, with an overall mean follow-up of 49.8 months. Compared to DPP-4 inhibitors, SGLT-2 inhibitors were associated with a lower risk of the primary composite outcome (HR: 0.85, 95% CI: 0.79-0.91), with similar results for all-cause mortality (HR: 0.77, 95% CI: 0.69-0.85) and incident hepatic decompensation (HR: 0.89, 95% CI: 0.82-0.96), but not for hepatocellular carcinoma (HR: 0.96, 95% CI: 0.82-1.14). CONCLUSIONS: Among adults with compensated cirrhosis and type 2 diabetes, SGLT-2 inhibitors were associated with lower risk of all-cause mortality and incident hepatic decompensation, compared to DPP-4 inhibitors. Future clinical trials are warranted to confirm this observation.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。