The liver is responsible for concentrating and metabolizing the majority of drugs and toxins introduced into the body, thus it is subject to a wide range of toxic drug effects. Liver metabolism of drugs is mediated through phase I and phase II reactions. Phase I reactions involve addition of polar groups to the lipophilic parent compounds by oxidation, reduction, or hydrolysis to facilitate water-solubility. These reactions are catalyzed by the cytochrome P450 superfamily (CYP). In phase II reactions, readily excretable, nontoxic substances are formed through conjugation of the drug to a large water-soluble polar group. (Ishak, 1998). A variety of clinical presentations may be seen in patients who develop drug hepatotoxicity, which can be classified as:1- Acute hepatic injury: e.g., acetaminophen, amiodarone, captopril(Chitturi and Farrell, 2000).2- Chronic hepatic injury: e.g., diclofenac, phenytoin, sulfonamides, methotrexate, glucocorticoids. (Somani, et al., 1990) 3- Vascular disease: e.g., vitamin A, azathioprine, oral contraceptives. (Ishak, 1993)4- Granulomatous disease: e.g., diazepam, diltiazem, allopurinol. (Zimmerman and Maddrey, 1993)5- Neoplasia: e.g., oral contraceptives and alcohol. (Zimmerman andLewis, 1995)6- Extrahepatic manifestations: e.g., penicillin, phenytoin, erythromycin. (Batt and Ferrari, 1995)Diagnosis of drug induced liver injury requires clinical suspicion, a careful drug history, consideration of temporal relationships between drug ingestion and liver disease, and exclusion of other disorders. Sources of potential hepatotoxins include complementary and alternative medicines, drug abuse and substances taken for self-poisoning. (Maria and Victorino, 1997)With the exception of acetaminophen hepatotoxicity, there is little specific treatment for drug-induced liver disease. Active management includes discontinuation of the offending agent and administration of anti-inflammatory agents. In cases of acute liver failure, hepatic transplantation should be considered. (Schiodt, et al., 1999)Special emphasis should be placed on prevention and early detection of liver injury. This could be achieved through clear and open communication between physicians and their patients and appropriate recommendations about dose limitations. Patients should be warned to report any untoward symptoms, particularly unexplained nausea, malaise, right upper quadrant abdominal pain, lethargy or fever. Routine follow up of liver function tests is sometimes recommended. (Kaplowitz, 1999)