(A-310) Serum 25-Hydroxyvitamin D Levels and Risk of Diabetes Complications in Sulfonylurea Users: A Linked Database of Kangbuk Samsung Health Study and Nationwide Claims Data

Sunday, August 24, 2025

12:00 PM - 1:30 PM ET

Presenting Author(s)

KJ

Kyungyeon Jung, PharmD

Department of Biohealth Regulatory Science, Sungkyunkwan University, Suwon, South Korea, Republic of Korea

Co-Author(s)

JS

Ju-Young Shin, PharmD, PhD

School of Pharmacy, Sungkyunkwan University, Suwon, South Korea, Republic of Korea
HK

Hwa Yeon Ko, PharmD

School of Pharmacy, Sungkyunkwan University, Suwon, South Korea, Republic of Korea
YC

Yoosoo Chang, MD, PhD

Center for Cohort Studies, Total Healthcare Center, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea, Republic of Korea
SB

Sungho Bea, PharmD, PhD

Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, United States

Background: Sulfonylureas (SUs) stimulate insulin secretion by inhibiting ATP-sensitive K-channels in pancreatic beta cells, potentially regulated by 25-hydroxyvitamin D [25(OH)D]. However, impact of 25(OH)D on cardiovascular risk in SU users remains unexplored.

Objectives: To evaluate whether 25(OH)D levels are associated with the risk of incident cardiovascular outcomes in patients receiving sulfonylurea therapy.

Methods: Using linked data from Kangbuk Samsung Health Study and national claims database (2013–2022), we constructed two distinct cohorts: (1) primary cohort of patients with 25(OH)D measurement during SU treatment, and (2) secondary cohort of SU initiators with prior 25(OH)D measurement. Index date was defined as the date of first 25(OH)D measurement or SU initiation during study period, depending on the cohort. 25(OH)D levels were categorized as deficient ( <20 ng/mL) or normal (≥20 ng/mL). The outcome was a modified composite of major adverse cardiovascular events including myocardial infarction, stroke, and all-cause mortality. Patients were followed up from index date until the earliest of outcome occurrence, SU discontinuation, vitamin D supplementation, death, or study end. Cox proportional hazards models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) in multivariable-adjusted models.

Results: Among 2,739 patients in primary cohort, no association was observed between 25(OH)D levels and MACE. Compared to normal group, deficient group had a higher multivariable-adjusted HR of 1.29 (95% CI, 0.55–3.00). Similarly, in secondary cohort of 1,806 patients, the deficient group showed a multivariable-adjusted HR of 2.50 (0.60–10.50) compared to normal group, though nonsignificant.

Conclusions: While a definitive association was not observed, a modest increase in cardiovascular risk among SU users with lower 25(OH)D levels cannot be ruled out.