Michael Fralick1, Sarah K Chen2, Elisabetta Patorno2, Seoyoung C Kim2. 1. Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, and Sinai Health System and the University of Toronto, Toronto, Ontario, Canada (M.F.). 2. Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts (S.K.C., E.P., S.C.K.).
Abstract
Background: Hyperuricemia is common in patients with type 2 diabetes mellitus and is known to cause gout. Sodium-glucose cotransporter-2 (SGLT2) inhibitors prevent glucose reabsorption and lower serum uric acid levels. Objective: To compare the rate of gout between adults prescribed an SGLT2 inhibitor and those prescribed a glucagon-like peptide-1 (GLP1) receptor agonist. Design: Population-based new-user cohort study. Setting: A U.S. nationwide commercial insurance database from March 2013 to December 2017. Patients: Persons with type 2 diabetes newly prescribed an SGLT2 inhibitor were 1:1 propensity score matched to patients newly prescribed a GLP1 agonist. Persons were excluded if they had a history of gout or had received gout-specific treatment previously. Measurements: The primary outcome was a new diagnosis of gout. Cox proportional hazards regression was used to estimate hazard ratios (HRs) of the primary outcome and 95% CIs. Results: The study identified 295 907 adults with type 2 diabetes mellitus who were newly prescribed an SGLT2 inhibitor or a GLP1 agonist. The gout incidence rate was lower among patients prescribed an SGLT2 inhibitor (4.9 events per 1000 person-years) than those prescribed a GLP1 agonist (7.8 events per 1000 person-years), with an HR of 0.64 (95% CI, 0.57 to 0.72) and a rate difference of -2.9 (CI, -3.6 to -2.1) per 1000 person-years. Limitation: Unmeasured confounding, missing data (namely incomplete laboratory data), and low baseline risk for gout. Conclusion: Adults with type 2 diabetes prescribed an SGLT2 inhibitor had a lower rate of gout than those prescribed a GLP1 agonist. Sodium-glucose cotransporter-2 inhibitors may reduce the risk for gout among adults with type 2 diabetes mellitus, although future studies are necessary to confirm this observation. Primary Funding Source: Brigham and Women's Hospital.
Background: Hyperuricemia is common in patients with type 2 diabetes mellitus and is known to cause gout. Sodium-glucose cotransporter-2 (SGLT2) inhibitors prevent glucose reabsorption and lower serum uric acid levels. Objective: To compare the rate of gout between adults prescribed an SGLT2 inhibitor and those prescribed a glucagon-like peptide-1 (GLP1) receptor agonist. Design: Population-based new-user cohort study. Setting: A U.S. nationwide commercial insurance database from March 2013 to December 2017. Patients: Persons with type 2 diabetes newly prescribed an SGLT2 inhibitor were 1:1 propensity score matched to patients newly prescribed a GLP1 agonist. Persons were excluded if they had a history of gout or had received gout-specific treatment previously. Measurements: The primary outcome was a new diagnosis of gout. Cox proportional hazards regression was used to estimate hazard ratios (HRs) of the primary outcome and 95% CIs. Results: The study identified 295 907 adults with type 2 diabetes mellitus who were newly prescribed an SGLT2 inhibitor or a GLP1 agonist. The gout incidence rate was lower among patients prescribed an SGLT2 inhibitor (4.9 events per 1000 person-years) than those prescribed a GLP1 agonist (7.8 events per 1000 person-years), with an HR of 0.64 (95% CI, 0.57 to 0.72) and a rate difference of -2.9 (CI, -3.6 to -2.1) per 1000 person-years. Limitation: Unmeasured confounding, missing data (namely incomplete laboratory data), and low baseline risk for gout. Conclusion: Adults with type 2 diabetes prescribed an SGLT2 inhibitor had a lower rate of gout than those prescribed a GLP1 agonist. Sodium-glucose cotransporter-2 inhibitors may reduce the risk for gout among adults with type 2 diabetes mellitus, although future studies are necessary to confirm this observation. Primary Funding Source: Brigham and Women's Hospital.
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