Type 1 DM and pulmonary TB

A cross-sectional study was conducted to determine the prevalence of latent tuberculosis (latent TB) among participants with type 1 diabetes mellitus (T1DM). Study participants were recruited from five pediatric and youth diabetes clinics located in Dar es Salaam. A total of 281 participants were included in the study, of whom 144 (51.2%) were females. The mean age of participants was 19 years (±6).[1]

The overall prevalence of latent TB was 14.9%. When stratified by developmental stages, the prevalence was 15% in post-pubertal participants, 19.6% in pubertal participants, and 8.1% in pre-pubertal participants. However, the differences in prevalence across these groups were not statistically significant (p > 0.005). Participants with uncontrolled HbA1c levels had a significantly higher prevalence of latent TB (76.2%) compared to those without latent TB (60.0%; p = 0.046). On the other hand, the duration of diabetes (≥5 years) was similar between participants with and without latent TB. Notably, participants with uncontrolled HbA1c levels were significantly more likely to be diagnosed with latent TB (OR 2.19, 95% CI 1.02–4.71, p = 0.045) compared to those with controlled HbA1c levels.[1]

Observational studies examining the relationship between diabetes and pulmonary tuberculosis (PTB) often face challenges such as reverse causality, confounding factors, and insufficient distinction between diabetes phenotypes, particularly type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). T1DM is notably associated with metabolic disturbances, including impaired glucose and lipid metabolism, obesity, and a heightened susceptibility to PTB infections. Poor glycemic control has been linked to approximately 7.5% of tuberculosis (TB) cases, while PTB patients often exhibit lower levels of HDL-C, LDL-C, and total cholesterol. Furthermore, a log-linear relationship exists between body mass index (BMI) and TB incidence, with a 14% reduction in TB incidence observed for every unit increase in BMI.[2]

Mendelian Randomization (MR), which leverages genetic variants as instrumental variables, provides insights into causal relationships while addressing biases from confounders and reverse causality. MR analyses have identified a positive genetic association between T1DM and PTB, as well as a correlation between genetic predisposition to higher HDL-C levels and increased PTB risk. However, no causal links were found between PTB and other T1DM-related traits such as fasting blood glucose (FBG), HbA1c, fasting insulin (FI), or obesity. Despite these findings, the limitations of MR analyses—such as the lack of stratification by gender and age and the overrepresentation of populations of European ancestry—raise concerns about generalizability. Clinically, these insights emphasize the need for integrated strategies to manage T1DM, control HDL-C levels, and enhance PTB prevention in individuals with T1DM.[2]

References:

1. Majaliwa, E.S., Muze, K., Godfrey, E., Byashalira, K., Mmbaga, B.T., Ramaiya, K. and Mfinanga, S.G., 2023. Latent tuberculosis in children and youth with type 1 diabetes mellitus in Dar es Salaam, Tanzania: a cross section survey. BMC Infectious Diseases, 23(1), p.740.

2. Jiang, Y., Zhang, W., Wei, M., Yin, D., Tang, Y., Jia, W., Wang, C., Guo, J., Li, A. and Gong, Y., 2024. Associations between type 1 diabetes and pulmonary tuberculosis: a bidirectional mendelian randomization study. Diabetology & Metabolic Syndrome, 16(1), pp.1-9.