ENDO: Cardiovascular Events Occur Less Often With GLP1-RA, SGLT-2i for T2D, Liver Disease

Reduction in cardiovascular events seen with GLP-1 RA, SGLT-2i for type 2 diabetes, metabolic dysfunction-associated steatotic liver disease
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Medically Reviewed By:
Mark Arredondo, M.D.
Published on
Updated on

FRIDAY, June 7, 2024 (HealthDay News) -- For adults with type 2 diabetes (T2D) and metabolic dysfunction-associated steatotic liver disease (MASLD), glucagon-like peptide 1 receptor agonists (GLP-1 RA) and sodium-glucose cotransporter 2 inhibitors (SGLT-2i) are associated with reduced risk of cardiovascular (CV) events compared with dipeptidyl peptidase 4 inhibitors (DPP-4i), according to a study presented at the annual meeting of the Endocrine Society, held from June 1 to 4 in Boston.

Alexander Kutz, M.D., M.P.H., from Brigham and Women's Hospital and Harvard Medical School in Boston, and colleagues used pooled data from Medicare fee-for-service and a large U.S. health insurance database to examine the comparative CV and hepatic effectiveness and safety of GLP-1 RA and SLGT-2i in people with T2D and prevalent MASLD.

The researchers found that the hazard ratio (HR) was 0.67 for the primary CV outcome associated with GLP-1 RA (13,666 initiators) versus DPP-4i (17,084 initiators), corresponding to an incidence rate difference (IRD) of −21.6 per 1,000 person-years. For the primary hepatic outcome, the HR was 0.47 and IRD was −2.1. The CV benefits were similar for SGLT-2i (11,108 initiators) versus DPP-4i (16,979 initiators), with a HR of 0.82 for the primary CV outcome and IRD of −11.0. For the primary hepatic outcome, the HR and IRD were not significant. Compared with DPP-4i, severe adverse events did not occur more often with GLP-1 RA or SGLT-2i.

"Our study shows that GLP-1 receptor agonists and SGLT-2 inhibitors are more beneficial in preventing heart-related events compared to another group of drugs such as dipeptidyl peptidase 4 inhibitors, and GLP-1s also help reduce severe liver events," Kutz said in a statement.

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