Fixed drug eruption (FDE) characteristically recurs at the same site with re-exposure to the offending drug. The immunological mechanism responsible for site-specific recurrence is:

• A Tissue-resident memory CD8+ T cells (TRM) at the site retaining drug-specific cytotoxic capacity ✓
• B IgE sensitization in mast cells localised to the skin at the site of prior reaction
• C Persistent drug-protein depot at previous reaction sites triggering local immune complex formation
• D Upregulated COX-2 expression in keratinocytes at the site mediating prostaglandin-driven inflammation

Explanation

Fixed drug eruption is mediated by tissue-resident memory CD8+ T lymphocytes (TRM, CD103+/CD69+ phenotype) that persist at the reaction site after resolution. Upon drug re-exposure, these TRM cells are rapidly reactivated in a non-MHC-restricted manner, releasing perforin, granzyme B, and TNF-α, causing keratinocyte apoptosis and the characteristic dusky hyperpigmented oval lesion with central blister. The commonest causative drugs include NSAIDs (particularly naproxen), trimethoprim-sulfamethoxazole, tetracyclines, and metronidazole.

Reference: Neena Khanna Illustrated Synopsis of Dermatology & STD, 6th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.