Abstract
Article history: Severe or pertinent hepatic toxicity interferes with antituberculotic chemotherapy resulting in dose reductions, treatment delays or cessation of therapy. Hepatic toxicity by antituberculotic agents is due to anaphylactic reactions (acetylaor phenotype polymorphism) and is relative to the cumulative dose intensity. Risk of hepatic toxicity is higher in the elderly and alcoholic patients. Patients with previous hepatic diseases such as hepatitis and comorbidities i.e. HIV infections, malnutrition and renal damages are prone to an added risk of hepatic toxicity. This review consolidates the pattern of hepatic adverse effects associated with each component of the antimyobacterial regimen e.g. isoniazid, rifampicin and pyrazinamaide. Higher propensities of hepatic adverse effects are associated with the first line agents, intensified by the incorporation of second line antibiotics, primarily metabolized in the liver. In conclusion the hepatic biomarkers should be monitored in the patient under a tuberculosis treatment plan as well as purposefully assessed during follow-up visits of the patients.
Highlights
Tuberculosis (TB) is a global health problem and considered as a second leading cause of death
Severe or pertinent hepatic toxicity interferes with antituberculotic chemotherapy resulting in dose reductions, treatment delays or cessation of therapy
This review consolidates the pattern of hepatic adverse effects associated with each component of the antimyobacterial regimen e.g. isoniazid, rifampicin and pyrazinamaide
Summary
Tuberculosis (TB) is a global health problem and considered as a second leading cause of death. The structure comprises of hydrazine group and a pyridine ring (Jindani et al, 2004, Kass and shandera, 2010) It is a pro-drug, activated by tuberculosis catalase-peroxidase enzyme (Kat G) and results in production of per oxy nitrate and hydrogen peroxide (both are oxygen free radical). These radicals inhibit the mycolic acid, responsible for DNA damage and the death of the bacillus (Kass and Shandera, 2010, Flynn et al, 1993). Isoniazid INH causes severe hepatic toxicity as it is metabolized in the liver by N-acetyl transfers by acetylation, produces isonicotinic acid and acetyl INH It is mainly (70-90%) excreted by kidney mostly in feces (Singh et al, 2012). It is recommended that antacids containing ranitidine and aluminum hydroxide should be taken after one hour of INH administration
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