ABSTRACT
I. INTRODUCTION Tuberculosis is a major public health problem in the developing countries and there is ample evidence for its resurgence in the developed countries during the last few years (1). However, effective treatment is available to treat most of the cases with tuberculosis. The currently recommended treatment regimen for tuberculosis includes four first-line drugs-isoniazid, rifampicin, ethambutol or streptomycin, and pyrazinamide-for a period of 3 months followed by continuation of a “core” of isoniazid and rifampicin for the next 6 months (2). The response to the treatment is generally very good and gratifying but at times it may be poor and frustrating, e.g., in patients with coexistent HIV infection, infection with resistant strains of Mycobacterium tuberculosis, poor drug compliance, and
506 Garg and Tandon
development of serious toxicity necessitating stoppage of drugs. The antituberculous treatment (ATT)-associated side effects may involve almost all systems in the body such as the gastrointestinal tract, liver, skin, nervous system, otovestibular apparatus, eyes, etc. Of these, drug-induced hepatotoxicity is the most important and common adverse effect observed (3,4). The underlying mechanisms of ATT-induced hepatotoxicity are not clearly understood (3,4). Development of hepatotoxicity usually has a benign course, but may result in serious morbidity and even mortality (2-5). In addition, it has important implications with regard to the treatment of the underlying tuberculosis, i.e., how to use these effective antituberculous drugs with potential hepatotoxicity in patients who have developed ATT-induced hepatotoxicity. In this review we shall discuss the incidence, course, and pathophysiology of hepatotoxicity associated with different antituberculous drugs, predisposing factors for the development of antituberculous drugs-induced hepatotoxicity, and the management of such hepatotoxicity as well as of underlying tuberculosis.
