# Severe Cutaneous Adverse Reaction to Lamotrigine: A Case of Stevens-Johnson Syndrome in a Psychiatric Patient

## TL;DR

A psychiatric patient developed Stevens-Johnson syndrome after increasing lamotrigine dosage, highlighting the drug's risk of severe skin reactions.

## Contribution

This case report highlights lamotrigine's potential to cause SJS and emphasizes the importance of early detection and management.

## Key findings

- Lamotrigine was identified as the probable cause of SJS using the WHO-UMC causality assessment scale.
- The patient's condition improved with drug discontinuation and supportive care, though hyperpigmentation remained.
- The case underscores the need for vigilance during lamotrigine dose escalation and improved pharmacovigilance.

## Abstract

Stevens-Johnson syndrome (SJS) is a severe and potentially life-threatening mucocutaneous reaction often triggered by medications. Antiepileptic drugs, particularly lamotrigine, are recognized as significant causative agents. Early identification and management are crucial to improve patient outcomes.

We report the case of a 26-year-old male diagnosed with schizoaffective bipolar disorder who developed SJS following the dose escalation of lamotrigine. He presented with multiple well-defined erythematous lesions, targetoid macular lesions, oral erosions, and fever. Based on clinical findings and a detailed medication history, lamotrigine was identified as the probable causative agent using the World Health Organization (WHO)-Uppsala Monitoring Centre (UMC) causality assessment scale. Laboratory investigations revealed elevated inflammatory markers and Severity-of-Illness Score for Toxic Epidermal Necrolysis (SCORTEN) assessment predicted a significant mortality risk. Management included immediate discontinuation of lamotrigine, systemic corticosteroids, antihistamines, antibiotics, and topical agents for symptomatic relief. Supportive care led to gradual re-epithelialization, resolution of mucosal lesions, and eventual discharge with residual post-inflammatory hyperpigmentation.

This case emphasizes the risk of severe cutaneous adverse reactions with lamotrigine, particularly within the initial weeks of treatment. The pathophysiology of SJS involves immune-mediated keratinocyte apoptosis, with granulysin playing a key role. Current treatment strategies remain debated, with corticosteroids, cyclosporine, and tumor necrosis factor α (TNF-α) inhibitors showing potential benefits. Early drug discontinuation, vigilant monitoring, and multidisciplinary management are crucial in reducing morbidity and mortality.

This report underscores the need for heightened vigilance when prescribing lamotrigine, particularly during dose escalation. Strengthening pharmacovigilance, patient education, and screening for genetic predispositions may help mitigate the risk of drug-induced SJS. Further research into optimal therapeutic strategies is warranted to improve clinical outcomes in affected patients.