SUSPECTED LAMOTRIGINE-INDUCED TOXIC EPIDERMAL NECROLYSIS

OBJECTIVE: To describe a patient who developed toxic epidermal necroly sis (TEN) possibly secondary to lamotrigine use. CASE SUMMARY: A 74-ye ar-old white man with a history of probable complex partial seizures w as admitted to the neurology service for a prolonged postictal state. His antiepileptic regimen was changed while he was in the hospital to include lamotrigine. After 19 days of hospitalization and 14 days of l amotrigine therapy, the patient became febrile. The next day he develo ped a rash which progressed within 4 days to TEN, diagnosed by skin bi opsy. All suspected drugs were discontinued, including lamotrigine. Th e patient was treated with hydrotherapy in the burn unit. His symptoms improved and he was discharged from the hospital 26 days after the ra sh developed. DISCUSSION: During lamotrigine's premarketing clinical t rials, the manufacturer reported several cases of Stevens-Johnson synd rome and TEN. There are several published case reports of lamotrigine- induced severe skin reactions. All of these reports included patients being treated with both valproic acid and lamotrigine. Our patient was exposed to phenytoin, carbamazepine, clindamycin, and lamotrigine, bu t not valproic acid. The patient reported prior use of phenytoin with no skin rash. Carbamazepine was the antiepileptic drug the patient was maintained on prior to his hospital admission, and the symptoms of TE N resolved while he was still receiving carbamazepine. The patient rec eived only two doses of clindamycin, which makes this agent an unlikel y cause of TEN. CONCLUSIONS: Because of the temporal relationship of t he onset of the patient's rash and several drugs that are known to cau se severe rashes, it is not certain which drug was the definite culpri t. However, based on the evidence from the literature, lamotrigine app ears to be the causative agent.