Background: The risk of incident diabetes following COVID-19 vaccination remains to be elucidated. Also, it is unclear whether the risk of incident diabetes after SARS-CoV-2 infection is modified by vaccination status or differs by SARS-CoV-2 variants.
Objectives: We evaluated the incidence of diabetes following mRNA (BNT162b2), inactivated (CoronaVac) COVID-19 vaccines, and after SARS-CoV-2 infection in Hong Kong.
Methods: In this population-based cohort study, individuals without known diabetes were identified from a population-based electronic health database in Hong Kong. The first cohort included 358,228 people who received ≥1 dose of the COVID-19 vaccine between February and September 2021, and 348,403 people who did not receive any COVID-19 vaccines by September 2021. The second cohort included 145,452 confirmed COVID-19 patients between January 2020 and March 2022, and 653,126 people who were never infected up to March 2022. Both cohorts were followed until August 15, 2022. COVID-19 vaccine recipients and COVID-19 patients were 1:1 matched to their respective controls using propensity score. The propensity score was generated by a logistic regression model conditional on age, sex, prediabetes, Charlson comorbidity index, pre-existing comorbidities and medication use. Since history of SARS-CoV-2 infection and vaccination status may influence incidence of diabetes, we also adjusted for previous SARS-CoV-2 infection when estimating the conditional probability of receiving vaccinations and vaccination status when estimating the conditional probability of contracting SARS-CoV-2 infection. Hazard ratios (HRs) for incident diabetes were estimated using Cox regression models.
Results: In the first cohort, we included 167,337 CoronaVac and 158,378 BNT162b2 recipients with their respective 1:1 matched control. 442 (0.3%) CoronaVac recipients and 693 (0.4%) BNT162b2 recipients were COVID-19 survivors. Upon a median follow-up of one year, CoronaVac or BNT162b2 vaccination was not associated with increased risks of incident diabetes (CoronaVac: HR=0.998 95%CI 0.962–1.035; BNT162b2: HR=0.862 95%CI 0.828–0.897), regardless of type 1 or type 2 diabetes. In the second cohort, we included 145,199 COVID-19 patients and 145,199 matched controls. Among the COVID-19 survivors, 60,348 (41.6%) were fully vaccinated and 25,792 (17.8%) did not receive any COVID-19 vaccines. Upon a median follow-up of 164 days, SARS-CoV-2 infection was associated with significantly higher risk of incident diabetes (1.45% vs 1.22%, HR=1.225 95%CI 1.150–1.305) – mainly type 2 diabetes – regardless of the predominant circulating variants (non-Omicron: HR=1.871 95%CI 1.352–2.589; Omicron: HR=1.209 95%CI 1.134–1.289), albeit lower with Omicron variants (p for interaction=0.009). Subgroup analysis also revealed that fully vaccinated COVID-19 survivors did not have an increased risk of incident diabetes (HR=1.005 95%CI 0.904–1.116).
Conclusions: COVID-19 vaccination was not associated with an increased risk of incident diabetes. The risk of incident diabetes increased following SARS-CoV-2 infection, mainly type 2 diabetes. The excess risk was lower, but still statistically significant, for Omicron variants. Fully vaccinated individuals might be protected from the risk of incident diabetes following SARS-CoV-2 infection.
