To the best of our knowledge, there is no systematic VE-822 1232416-25-9 prospective observational study that compared and contrasted the incidence, severity, predictors and clinical pattern of HAART and/or antiTB DILI using the same case definition and study population thereby controlling the GANT61 effect of genetic variation. In the present study we performed a prospective observational study to evaluate the incidence, severity, pattern and predictors of HAART and/or anti-TB DILI in a large well defined cohort, four arm parallel treatment groups using the DILI case definition set by international DILI expert working group. Effect of disease type, type of treatment received, baseline and follow up biochemical parameters on DILI were investigated in HIV patients receiving efavirenz based HAART alone, HIV negative TB patients receiving anti-TB drugs alone, HIV-TB coinfected patients receiving anti-TB drugs alone, and HIV-TB coinfected patients receiving both anti-TB drugs and HAART. The result indicates Antiretroviral and anti-TB drugs are more associated with cholestatic and hepatocellular liver toxicity, respectively and TB-HIV patients receiving concomitant antiTB-HIV therapy have the highest risk of developing severe DILI. We performed a prospective parallel assignment observational study to evaluate the incidence, type, severity and predisposing risk factors of DILI as well as effect of DILI on HAART efficacy outcome in a large well defined TB and/or HIV patient cohort receiving either anti-TB therapy alone, HAART alone or concomitant anti-TB and antiretroviral therapy. Our major finding includes i) ARV induced liver injury is associated mainly with cholestatic and mild injury. In contrast hepatocellular or mixed type of liver injury pattern with severity grade $ 2 is more common among TB patients receiving anti-TB drugs with or without HAART ii) TB-HIV co-infection and disease severity exacerbates the risk of DILI. iii) although lower BMI, higher HIV viral load, and abnormal liver enzymes level at baseline were implicated as independent risk factors in the univariate model, a multivariate analysis indicated disease status and type of treatment received, low hemoglobin, CD4 cell count, high AST and direct bilirubin at baseline as predictors of DILI. To the best of our knowledge this is the first systematic study to investigate the incidence, type, severity and predictors of DILI stratified by disease status and type of treatment received in the same population there by controlling for effect of genetic predisposition to DILI from Africa. Evaluations of the incidence, type of injury, severity grade and identification of prognostic markers for DILI requires parallel and equivalent assessment of the aminotransferases and use of the same DILI phenotype classification. Inconsistent definitions and terminology related to the clinical phenotypes of DILI, lack of a reference upper limit of normal for serum aminotransferase levels and inter-laboratory variability in the expression ULN and use of ethnically diverse study population is a challenge for crossstudy comparisons of DILI association studies. The use of same DILI case definition across the different parallel treatment groups in ethnically the same study population makes our study ideal to compare the incidence, pattern, severity grade and risk factors of ARV and/or anti-TB DILI between HIV, TB and TBHIV infected patients.