Active TB needs to be excluded before considering treatment of latent infection, which is usually with isoniazid monotherapy for 6 months or isoniazid/rifampicin ABT-263 concentration for 3 months. Starting HAART reduces the risk of reactivation of latent TB infection and is effective at reducing the incidence of new TB. We recommend that all HIV-positive patients should be offered HAART in line with the British HIV Association (BHIVA) treatment guidelines [2]. We recommend daily TB treatment whenever possible. Treatment

may be given 5 days per week, but should be intensively supervised. This option may be useful in hospital or other highly supervised settings. Three-times-per-week directly observed therapy (DOT) should only be given to patients who are stable and clinically well and where local logistics

enable this to be undertaken successfully. We do not recommend twice-weekly Selleckchem Autophagy inhibitor DOT for treatment of HIV/TB coinfected patients, especially in those with CD4 counts <100 cells/μL, as it has been associated with unacceptably high rates of rifamycin resistance. In cases where multiple drug resistance is not suspected, treatment should be started with four drugs (typically rifampicin, isoniazid, pyrazinamide and ethambutol) until sensitivities are known. We recommend a 6-month treatment regimen for drug-sensitive TB outside of the central nervous system (CNS). This is usually four drugs for 2 months, followed by isoniazid and rifampicin for a further 4 months (at least 182 doses of isoniazid and rifampicin and 56 doses of pyrazinamide and ethambutol in total). In drug-sensitive TB affecting Celastrol the CNS we recommend 9 months of treatment. This usually consists of four drugs for 2 months, followed by 7 months of isoniazid and rifampicin [3]. Drug-resistant disease should be treated only by specialists with experience in such cases, in line with NICE guidelines [1]. Careful attention should be paid to drug interactions between TB drugs, HAART and other therapy. Rifampicin is a powerful inducer of cytochrome 450 (CYP450)

and has effects on several metabolic pathways and P-glycoprotein (PgP). Rifampicin interacts with protease inhibitors (PIs), NNRTIs, chemokine (C-C motif) receptor 5 (CCR5) antagonists, and antimicrobials such as fluconazole. Rifabutin is a less potent inducer of CYP450 and may be used as an alternative to overcome some of these difficulties (for up-to-date drug interaction data go to http://www.hiv-druginteractions.org). Toxicity profiles of antiretrovirals and anti-tuberculosis drugs overlap and make it difficult to determine the causative drug. For example, rashes occur with NNRTIs, rifampicin and isoniazid. Isoniazid and stavudine both cause peripheral neuropathy. All patients on isoniazid should take pyridoxine to try and prevent this complication.