Vitamin D Status in HIV-Infected Patients With and Without Tuberculosis

Abstract

Tuberculosis (TB) is a leading cause of death in human immunodeficiency virus (HIV)-infected individuals. Efforts to reduce the burden of TB include isoniazid prophylactic therapy (IPT) for latent TB infection (LTBI).1 However, IPT confers a risk of hepatotoxicity and requires at least six months of therapy.2 Therefore, additional strategies to reduce the burden of active TB are needed. Vitamin D supplementation may decrease the progression of LTBI to active TB. Primarily, in vitro studies demonstrate that 1,25-dihydroxyvitamin D (1,25[OH]2D) enhances macrophage function, thereby augmenting immunologic control of mycobacteria.3 The benefit of vitamin D supplementation is suggested by the observation of increased rates of clearance of TB from sputum in HIV-uninfected individuals.4 Vitamin D, however, may have detrimental effects in HIV-infected patients. In vitro, vitamin D depresses cell mediated immune function, 5 which could hasten progression of LTBI to active disease. This may limit vitamin D supplementation as an adjunct for TB control. Given vitamin D’s conflicting mechanisms of action on the immune system, we conducted a study in Botswana, an area of high TB and HIV prevalence,6 to determine if there was evidence for differences in 25-hydroxyvitamin D (25-OHD) levels in HIV-infected individuals with and without active TB. We hypothesized that 25-OHD levels would be significantly lower in HIV-infected individuals with active TB as compared to those without active TB.