Sulfonamides causing Stevens-Johnson syndrome/TEN corresponds to which type of hypersensitivity ADR?

Sulfonamides causing Stevens-Johnson syndrome/TEN corresponds to which type of hypersensitivity ADR?

• A. Type IV
• B. Type III
• C. Type II
• D. Type I

Answer: (A)

Type IV hypersensitivity is a delayed, cell-mediated immune response driven by T cells rather than antibodies. Stevens-Johnson syndrome and toxic epidermal necrolysis are severe, life-threatening mucocutaneous reactions in which drug-specific T cells recognize the drug or drug-modified peptides in the skin and mucosa. These T cells release cytokines and cytotoxic mediators (including perforin/granzyme pathways and Fas-FasL interactions) that induce apoptosis of keratinocytes, leading to widespread epidermal necrosis. This process typically appears days to weeks after exposure, which is characteristic of a delayed-type reaction. Other hypersensitivity types involve antibodies or immune complexes (Type I is IgE-mediated immediate reactions, Type II is antibody-dependent cytotoxicity, and Type III involves immune complex–mediated damage). Those mechanisms don’t explain SJS/TEN, which is driven by T-cell–mediated cytotoxicity, hence it aligns with Type IV.

Type IV hypersensitivity is a delayed, cell-mediated immune response driven by T cells rather than antibodies. Stevens-Johnson syndrome and toxic epidermal necrolysis are severe, life-threatening mucocutaneous reactions in which drug-specific T cells recognize the drug or drug-modified peptides in the skin and mucosa. These T cells release cytokines and cytotoxic mediators (including perforin/granzyme pathways and Fas-FasL interactions) that induce apoptosis of keratinocytes, leading to widespread epidermal necrosis. This process typically appears days to weeks after exposure, which is characteristic of a delayed-type reaction.

Other hypersensitivity types involve antibodies or immune complexes (Type I is IgE-mediated immediate reactions, Type II is antibody-dependent cytotoxicity, and Type III involves immune complex–mediated damage). Those mechanisms don’t explain SJS/TEN, which is driven by T-cell–mediated cytotoxicity, hence it aligns with Type IV.