Calcium and vitamin D play a critical role in maintaining skeletal integrity and regulating immune responses, particularly in tuberculosis (TB). Vitamin D facilitates intestinal calcium absorption by upregulating calcium transport proteins and modulates immunity by regulating Th1 responses and enhancing macrophage-mediated bactericidal activity against Mycobacterium tuberculosis . Despite these protective roles, a paradoxical association of vitamin D deficiency with hypercalcemia is commonly observed in active TB, reported in up to 40% of cases. This hypercalcemia is primarily attributed to extrarenal production of 1,25-dihydroxyvitamin D (calcitriol) by activated macrophages within granulomatous lesions, leading to increased calcium levels independent of circulating 25-hydroxyvitamin D concentrations. This phenomenon is particularly prevalent in TB-endemic regions with extensive granulomatous disease and high mycobacterial burden. Globally, more than half of TB patients exhibit vitamin D deficiency, linked to severe disease manifestations and higher bacillary loads. The interplay between vitamin D metabolism, calcium homeostasis, and immune activation in TB highlights the importance of routine biochemical monitoring. Further studies are needed to elucidate molecular mechanisms and guide individualized therapeutic strategies.
Beniwal et al. (Wed,) studied this question.
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