Vitamin D receptor BsmI haplotype BB linked to lower 25(OH)D levels in tuberculosis patients

Adequate micronutrient status is crucial for effective immune responses, particularly in the context of tuberculosis (TB), a global health challenge. Vitamin D plays a key immunomodulatory role, primarily through the vitamin D receptor (VDR), influencing the production of antimicrobial peptides like cathelicidin (LL-37). While vitamin D deficiency is common in TB patients, the impact of genetic variations in the VDR on vitamin D levels and disease susceptibility remains underexplored. Understanding these genetic links could inform more personalized adjunctive therapies for TB.

This pilot cross-sectional study evaluated vitamin D receptor polymorphisms and their relationship with vitamin D and cathelicidin levels in pulmonary tuberculosis (PTB) patients (n=80) and healthy controls (HC) (n=50) from Colon, Panama. Researchers measured total 25-hydroxyvitamin D (25(OH)D) and cathelicidin (LL-37) levels using enzyme-linked immunosorbent assays (ELISA). Vitamin D receptor (VDR) polymorphisms (FokI, TaqI, and BsmI) were analyzed via PCR-RFLP. Comparisons were made across demographic groups and associations with VDR polymorphisms were explored.

Overall, no significant difference in 25(OH)D levels was observed between PTB and HC groups (median 36.6 ng/mL vs. 32.5 ng/mL, p=0.067). However, 25(OH)D levels in women with PTB were significantly higher than in HC women (median 33.9 ng/mL vs. 19.5 ng/mL, p=0.002). Regarding LL-37, unemployed PTB participants showed higher levels compared to HC (median 59.4 ng/mL vs. 28.2 ng/mL, p=0.048), as did Hispanic PTB patients (median 59.6 ng/mL vs. 38.9 ng/mL, p=0.014). PTB patients within 1 month of treatment had higher 25(OH)D levels than HC, particularly in women (median 41.4 ng/mL vs. 19.5 ng/mL, p=0.01).

A statistically significant association was observed between the BsmI VDR polymorphism and serum 25(OH)D levels, with a significant difference between PTB and HC (p=0.004). This indicates that specific VDR genetic variants may influence vitamin D status in the context of tuberculosis.