NOT JUST A RASH. B. Kinder 1 , P. Basaviah 1 ; 1 University of California at San Francisco, San Francisco, CA LEARNING OBJECTIVES: 1) Recognize the clinical features of Anticonvulsant Hypersensitivity Syndrome (AHS). 2) Manage a potentially fatal adverse drug reaction. CASE INFORMATION: A 36 year old Caucasion female reported a four day history of a progressive maculopapular rash associated with a mouth ulcer. On day 2 of the rash, she developed mucosal sloughing and presented to an emergency room (ER). At that time she denied drug allergies or use of new detergents or skin products. Of note, three weeks prior to this presentation, the patient had been prescribed phenytoin by her psychiatrist for treatment of refractory bipolar affective disorder. In the ER she was treated with hydroxizine, prednisone, and analgesics and told to discontinue the phenytoin. Progression of her skin lesions to blisters over the next two days prompted a medical admission. Exam revealed a temperature of 38.2, pulse of 100, injected, desquamating conjunctivae, oral and vaginal erosions, a confluent maculopapular rash involving her face and trunk, and no hepatosplenomegaly or lymphadenopathy. Data were remarkable for a WBC of 2.4, AST of 70, and ALT of 81. Intravenous hydration, methylprednisolone, morphine, diphenhydramine, and local wound care were initiated. The rash progressed to bullae affecting her face and upper body,were limited to 10 ± 15 % of body surface area, and gradually improved over several days. Her elevated transaminases normalized within twenty-four hours of steroid initiation. Steroids were tapered. The patient was discharged with outpatient follow-up. DISCUSSION: AHS is a potentially fatal drug reaction induced by arene oxide-producing anticonvulsants, including phenytoin, carbamazepine, and phenobarbital. It occurs in 0.01%-0.1% of the population and is fatal in 5 ± 50% of cases if toxic epidermonecrolysis (TEN) or hepatitis develop. The mechanism apparently involves an inability to detoxify arene oxide metabolites which then bind to proteins and elicit an immune response. AHS may be genetically determined, conferring increased risk to siblings. The hallmark clinical features include fever, rash, and lymphadenopathy which can be associated with hepatitis, hematologic abnormalities, and interstitial nephritis. The skin eruption typically begins as a morbilliform rash involving the upper trunk, face and upper extremities. The cutaneous manifestations can be variable, including target lesions, bullae, and skin sloughing and mucosal involvement resembling Stevens-Johnson Syndrome and TEN. AHS usually occurs 2 ± 6 weeks after initial drug exposure, later than most other skin reactions. Steroid therapy is controversial and has not demonstrated benefit in randomized control trials. However, some experts recommend steroid use if there is evidence of hepatic or renal involvement and if skin desquamation is limited. Essentials of management include prompt discontinuation of the offending drug, supportive management, avoidance of cross-reactive drugs in the future, and counselling regarding potential genetic implications to family members. LEARNING OBJECTIVE: To recognize that in the face of renal dysfunction, azotemia may reflect non-renal causes. CASE INFORMATION: A 76 year-old white male presented with shortness of breath and hypoglycemia. He had vomited that morning and had nothing further to eat or drink. His history was significant for diabetes mellitus (27 years), COPD, CHF, and stable chronic renal insufficiency (BUN 54, creatinine 1.6). The patient' home medications included aspirin qd, acetominophen #3 prn pain, potassium 20 mg qd, glyburide 2.5 mg qd, furosemide 20 mg bid, prednisone 10 mg qd, and lisinopril/HCTZ 20/25 mg qd (started three weeks previously). Physical exam revealed bilateral wheezing. Lab studies showed BUN 93, creatinine 3.2, Hgb 9.4, U/A showed 2+ protein and no casts. On ultrasound, the kidneys were normal size with no hydronephrosis. The patient had good urine output. The patient was admitted with an exacerbation of COPD, hypoglycemia and renal failure. Hypoglycemia was considered to be secondary to inadequate clearance of glyburide and poor oral intake. Glyburide, furosemide, and lisinopril were held. The patient was treated with albuterol, ipratropium, fluticasone, salmeterol inhalers and IV solumedrol for the COPD exacerbation. Over several days the BUN increased to 115 while the creatinine declined to 1.9 . Because of persistent azotemia, other non-renal causes were considered. Colonoscopy revealed several large, hyperemic polyps which were removed. Eventually the BUN declined to 46 and the creatinine returned to baseline. DISCUSSION: This case illustrates the multifactorial nature of illnesses in the elderly and emphasizes the importance of considering alternate or confounding hypotheses when making a diagnosis. Although this patient had underlying renal failure, focusing on this alone would have missed such potentially life-threatening problems as dehydration, steroid-induced azotemia, and GI bleeding from colonic polyps, all of which could have contributed to this patient' condition.