In multibacillary leprosy, clofazimine contributes to the MDT regimen. Its anti-mycobacterial mechanism and a significant adverse effect are:

• A Inhibits RNA polymerase like rifampicin; causes optic neuritis
• B Inhibits dihydrofolate reductase like dapsone; causes hemolytic anemia
• C Binds mycobacterial DNA and generates reactive oxygen species via redox cycling; causes hyperpigmentation and ichthyosis ✓
• D Disrupts mycobacterial cell membrane; causes peripheral neuropathy

Explanation

Clofazimine is a phenazine dye that binds preferentially to mycobacterial DNA. Its main bactericidal action involves redox cycling: clofazimine is reduced by bacterial NADH oxidoreductase, and the reduced form is then re-oxidized by molecular oxygen, generating reactive oxygen species (superoxide, hydrogen peroxide) that damage bacterial DNA and membranes. Due to its dye nature, it accumulates in skin, fat, and reticuloendothelial system, causing a characteristic reddish-brown to slate-grey hyperpigmentation of skin (especially in sun-exposed areas) and ichthyosis. The discoloration may take months to years to resolve after stopping the drug and is cosmetically distressing, contributing to poor compliance.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.