**Background:** Tuberculosis (TB) may increase the risk of developing diabetes, but most evidence comes from low-TB prevalence settings. In sub-Saharan Africa, where TB and HIV are common, the relationship is unclear. This study aimed to assess the association between prior treated TB and dysglycemia in a rural South African population with high HIV prevalence.
**Methods:** Data were from the Vukuzazi Study, a cross-sectional population-based cohort in uMkhanyakude District, KwaZulu-Natal, enrolling adults ≥15 years between May 2018 and November 2019. Participants completed questionnaires, had anthropometric measurements, and provided blood for hemoglobin A1c (HbA1c) and HIV testing. Prior TB was defined as self-reported history of TB treatment. Active TB (positive Xpert MTB/RIF, culture, or current TB therapy) was excluded. Dysglycemia was defined as HbA1c ≥6.5% or self-reported diabetes with medication use. Sex-stratified logistic regression models were fitted, adjusted for age, waist circumference, HIV, smoking, alcohol use, and socioeconomic status. Propensity score matching was used to balance age and other confounders between those with and without prior TB. Interactions between prior TB and HIV status were examined.
**Key Results:** The analytic cohort included 17,593 participants (58.7% women; mean age 40.5 years). Prevalence of prior TB was 13.8% in men and 10.7% in women. Dysglycemia was present in 9.1% overall (5.0% men, 11.0% women). HIV prevalence was 34.0%. In propensity score-matched analyses, prior TB was not associated with dysglycemia in men (adjusted OR 0.96, 95% CI 0.59–1.56) or women (adjusted OR 1.05, 95% CI 0.79–1.39). However, a significant qualitative interaction with HIV was found among men: among HIV-negative men, dysglycemia prevalence was higher in those with prior TB (10.1% vs. 4.6%, p=0.0077), while among HIV-positive men, it was lower (3.3% vs. 7.3%, p=0.0073). No such interaction was seen in women. Time since TB diagnosis (mean 11.1 years) and number of TB episodes were not associated with dysglycemia after adjustment.
**Clinical Implications:** This study did not confirm a simple association between prior TB and dysglycemia in a high-burden setting, contrasting with findings from low-TB prevalence regions. The null overall result may be due to the modifying effect of HIV, particularly in men. The interaction suggests distinct pathophysiological mechanisms: in HIV-negative men, prior TB may increase diabetes risk, while in HIV-positive men, competing risks or HbA1c inaccuracies may mask an association. These findings underscore the need for longitudinal studies with careful TB, HIV, and diabetes phenotyping. Clinically, diabetes screening strategies in TB survivors should consider HIV status and sex, and HbA1c may have limitations in HIV-positive individuals.