A 28-year-old woman presents with fever, painful oral ulcers, and a widespread blistering rash involving <10% of body surface area. She had started trimethoprim-sulfamethoxazole for a urinary tract infection 2 weeks ago. What is the most common causative drug class implicated in Stevens-Johnson Syndrome?

Explanation

## Most Common Drug Causes of SJS/TEN **High-Yield:** Sulfonamides (including trimethoprim-sulfamethoxazole) are the most frequently implicated drug class in Stevens-Johnson Syndrome globally, accounting for 20–30% of drug-induced cases. ### Top Offenders by Class | Drug Class | Relative Frequency | Examples | |---|---|---| | **Sulfonamides** | Highest | TMP-SMX, sulfasalazine | | **NSAIDs** | High | Ibuprofen, naproxen, oxicams | | **Anticonvulsants** | High | Phenytoin, carbamazepine, lamotrigine | | **Antibiotics (other)** | Moderate | Fluoroquinolones, macrolides | | **Penicillins/Cephalosporins** | Lower | β-lactams are less common triggers | | **Antiretrovirals** | Moderate | Nevirapine, abacavir | **Key Point:** In India, TMP-SMX remains the single most common drug trigger for SJS/TEN, particularly in patients with HIV/AIDS and UTIs. ### Clinical Pearl **Warning:** The latency period between drug exposure and SJS onset is typically **1–8 weeks** (average 2–3 weeks), making a careful drug history essential. The patient in this case fits the classic timeline with TMP-SMX exposure 2 weeks prior. **Mnemonic — "SCAN":** **S**ulfonamides, **C**arbamazepine, **A**llopurinol, **N**SAIDs — the four most common drug triggers in SJS/TEN. ### Pathophysiology Sulfonamides undergo hepatic acetylation and conjugation. Slow acetylators and patients with genetic polymorphisms in drug-metabolizing enzymes (CYP2C9, NAT2) have increased risk of accumulating toxic metabolites that trigger CD8+ T-cell-mediated keratinocyte apoptosis.