A Systematic Review on Anti-tubercular Therapy Induced Hepatotoxicity

Tuberculosis is the leading cause of major morbidities and mortalities around the globe. One in every three persons suffers fromtubercular infection in their lifetime. Antitubercular therapy-induced hepatitis occurs due to toxicity from the primary compound,metabolite, or an immunologically mediated response. Risk factors associated with hepatotoxicity are age, sex, low BMI,hypoalbuminemia, alcohol consumption, HIV, hepatitis B, and C. There are 6 major pathways by which anti-TB drugs are involved inhepatotoxicity including hampering of intracellular calcium homeostasis, derangement of actin fibril assembly that occurs next to thecanaliculus, the drug binds to the heme-containing cytochrome p-450 and forms enzyme-drug adduct and produces an immuneresponse, The enzyme- drug addict when gets incorporated to vesicle acts as antigen for the production antibodies, some drugs alsoinhibit the ? oxidation and respiration and hence reduction in ATP production hence damaging cell and mitochondrial DNA, and somedirectly leads to apoptosis. Isoniazid is being metabolized to acetyl-isoniazid followed by hydrolysis to acetyl hydrazine via cytochromeP450 enzyme which produces toxic metabolites responsible for hepatotoxicity. Rifampicin activates the cytochrome enzyme andhence stimulates the production of harmful toxic materials leading to ATT-induced hepatotoxicity. It is the duty of the he pharmacist/ medical staff has to provide the patient with adequate education about diseases and to inform them about their therapy regardingpossible side effects and side effects. Pharmacists / medical staff must also train patients to comply with medication.