A patient develops blistering and full-thickness epidermal necrosis affecting 45% body surface area 21 days after starting phenytoin. This clinical picture (TEN - toxic epidermal necrolysis) is primarily mediated by:
- A IgE-mediated mast cell degranulation
- B Cytotoxic CD8+ T-cells and NK cells releasing granulysin causing keratinocyte apoptosis ✓
- C Immune complex deposition in dermal blood vessels
- D Direct toxic effect of drug metabolites on keratinocytes
Correct answer: B. Cytotoxic CD8+ T-cells and NK cells releasing granulysin causing keratinocyte apoptosis
Explanation
TEN/SJS is mediated by CD8+ cytotoxic T lymphocytes and NK cells that secrete granulysin — a cytotoxic protein that induces widespread keratinocyte apoptosis. FasL, perforin/granzyme, and TNF-alpha also contribute. Granulysin is considered the most important mediator (found in high concentrations in blister fluid). Genetic predisposition: HLA-B*1502 (phenytoin/carbamazepine TEN risk in Southeast Asians, including Indians), HLA-B*5701 (abacavir hypersensitivity). IgE-mediated reactions cause urticaria/anaphylaxis, not TEN.
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.