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.