Vitamin D and calcium levels in Ugandan adults with human immunodeficiency virus and tuberculosis

Human Immunodeficiency Virus (HIV) infected individuals have increased susceptibility to and greater morbidity and mortality due to tuberculosis (TB).1–5 These observations may in part be related to hypovitaminosis D, as low vitamin D levels are associated with decreased macrophage production of the peptide cathelicidin6 that exerts antimicrobial properties. Cathelicidin, part of the innate immune system, plays a critical role in the fight against TB. Mycobacterium tuberculosis binds to toll-like receptors (TLR 2/1) on macrophages, leading to upregulation of 1α-hydroxylase gene expression to promote greater conversion of 25(OH)D to 1,25(OH)2D.6 Intracellular 1,25(OH)2D binds to the vitamin D receptor and induces production of the antimicrobial peptide cathelicidin.6 Cathelicidin localizes to monocytes infected with M. tuberculosis, where it has a direct antimicrobial effect.7 Low vitamin D levels could potentially blunt cathelicidin production, limiting the host's ability to fight TB.2 It was observed that serum containing lower 25(OH)D3 levels demonstrated lower production of c athelicidin mRNA than serum with higher 25(OH)D levels.6 When serum with low 25(OH)D3 was supplemented with 25(OH)D3, cathelicidin mRNA production increased. These findings suggest that vitamin D therapy among individuals with suboptimal levels might induce production of cathelicidin mRNA and improve the immune response to TB infection. Vitamin D could therefore be used as inexpensive adjunctive therapy among HIV patients, especially in settings where TB is highly prevalent, to reduce TB-related morbidity and mortality. In the present study, we describe the serum vitamin D, calcium and albumin levels in HIV-infected Ugandans with and without TB.