4. CONCLUSION
The hepatotoxicity of dapsone appears to occur by several mechanisms including injury to hepatocytes, induction of oxidative stress by DDS-NOH metabolite via N- hydroxylation pathway, induction of cholestasis via bile duct and bile flow obstruction, cholangitis due to focal bile ducts destruction, aggravation of hepatitis and hepatic fibrogenesis by iron overload due to the hemolysis. Clinically, early recognition of DIH is important based on mucocutaneous findings to minimize injury. Laboratory monitoring should be frequently performed during treatment, including complete blood counts and liver function tests. Early detection, prompt withdrawal of dapsone, and minimal use of other sulfa drugs need to be emphasized for the management of DHS. Patient should be on regular follow up and slow, gradual introduction of antileprotics may improve clinical outcome and patient compliance.