INTRODUCTIONPTB is associated with weight loss, nutritional deficiency and impaired metabolism [6]. In the prebiotic era, sun exposure, TB sanatorium and cod liver oil were commonly used to treat patients infected with TB. All these incidentally are good sources of Vit D [2,7]. DOTS is the current treatment modality for TB which comprises of administration of anti-tubercular drugs in two phases, intensive phase and continuous phase [8]. With the advent of effective antituberculosis drugs, enthusiasm for treating TB with the earlier Vit D rich modalities subsided [9]. Impaired metabolism in PTB may possibly worsen the effects of VDD [6]. In TB, liver functions may be hampered by diffuse hepatic involvement, granulomatous hepatitis or local abscess formation [10].Previous reports on the interaction between Vit D and anti-tubercular drugs have shown that, rifampicin causes an accelerated loss of Vit D due to increased clearance as it acts as an agonist to pregnane X receptor and inducing the activity of CYP3A4 and limiting the formation of active one alpha 25(OH)2D3 [11]. CYP3A4, a hepatic cytochrome P450 enzyme is involved in drug metabolism, and catabolism of Vit D via a similar pathway as CYP24A1 (an enzyme catalysing the hydroxylation steps of Vit D2 and Vit D3) [12]. Isoniazid causes impairment of 25-hydroxylation leading to impaired Vit D action [13,14], although pyrazinamide, isoniazid and rifampicin have all been associated with hepatotoxicity and the risk is enhanced when these drugs are used in combination. Studies have reported 1-31% of TB patients experience drug related hepatotoxicity following TB treatment [15]. However, isoniazid and ethambutol have been associated with acute kidney injury, rifampin is the most common as reported by most studies [16,17]. Immune responses to TB are influenced by a variety of factors, including younger age [18], diabetes mellitus, tobacco smoking, alcohol, immunosuppressive drugs [19], HIV status, and concurrent infections. Cachexia has been linked to poor prognosis and is a major risk factor for mortality [20]. All these factors are also associated with VDD [21]. The underlying mechanism of how Vit D metabolisms could be linked to the pathophysiology of PTB is complex and not fully understood. This research was carried out to study the changes in Vit D levels in active PTB, the effect of DOTS on Vit D status and alterations in hepatic and renal profiles possibly contributing to the effects.