ANTICONVULSANT HYPERSENSITIVITY SYNDROME: A CALL FOR INCREASING AWARENESS. N. Khan 1 , B. Cheong 1 , A. Jaffer 1 ; 1 Cleveland Clinic Foundation, Cleveland, OH LEARNING OBJECTIVES: 1. Diagnose the distinct entity of hypersensitivity reaction to anticonvulsants. 2. Recognize the prevelance of cross-reactivity between different anticonvulsant medications. CASE INFORMATION: A 27 year-old lady with a history of multiple sclerosis was initiated on oral phenytoin for tonic spasms of extremities. Two weeks later she noted a mild maculopapular erythematous rash on her extremities. Concerns for drug induced rash and minimal response to treatment, led to a change in regimen from phenytoin to carbamazepine. One week later the patient was hospitalized with worsening pruritic maculopapular rash, more prominent on the trunk and extremities, and recurrent fevers. Except for a temperature of 101.5 Å F, her vital signs were within normal limits. Notable changes on physical exam included mild facial edema, with 1.5 to 2cm bilateral, tender, mobile jugulodigastric and submandibular lympadenopathy (LAD). Laboratory abnormalities on admission included peripheral eosinophilia and elevated hepatic enzymes: AST=271 (7 ± 40 U/L), ALT=324 (5 ± 45 U/L). Other hepatic enzymes were normal. A CBC with differential revealed WBC=15.63 (4 ± 11.0 K/uL) with neutrophils 59% (40 ± 70%), lymphocytes 27% (22 ± 44%), eosinophils 11% (0 ± 4%), monocytes 2% (0 ± 7%), and atypical lymphocytes 1%. Carbamezepine level= 9.0 (8 ± 12 ug/mL) Blood and urine cultures were normal. Titers for Epstein-Barr virus and cytomegalovirus were normal. Given the rash, pyrexia, eosinophilia, lymphadenopathy and recent treatment with anticonvulsants the patient was diagnosed with anticonvulsant hypersensitivity syndrome (AHS). Progressive resolution of the dermatological changes and hepatitis was noted with discontinuation of anticonvulsants and treatment with corticosteroids for 1week. DISCUSSION: AHS is an adverse drug reaction associated with medications such as phenytoin, carbamezepine and phenobarbital. Originally cited prevelance of 15% is increasing with broader spectrum of use of anticonvulsants, such as for treatment of neuropathic pain. This patient exhibited a typical presentation including hepatitis and eosinophilia. The pathogenesis of AHS involves inadequate function of epoxide hydroxylase enzyme, leading to decreased inactivation of toxic metabolites of anticonvulsant drugs. Current data indicates allergic cross-reactivity between these medications to be as high as 80%. Treatment involves discontinuing the medication and initiating steroid therapy. With a mortality rate suggested at 40% (mostly due to hepatic necrosis), it is important for general practitioners to recognize AHS; its presentation, cross-reactivity of medications, and treatment options. A high index of suspicion based on the patient's history and exam will enable an astute primary care provider to make the diagnosis early.