Cephazolin-Induced Toxic Epidermal Necrolysis Treated with Intravenous Immunoglobulin and N-Acetylcysteine

Toxic epidermal necrolysis is the most severe form of drug-induced skin reaction and includes denudation of >30% of total body surface area. The mechanism of disease is not completely understood, but immunologic mechanisms, cytotoxic reactions, and delayed hypersensitivity seem to be involved. We report a case of cephazolin-induced toxic epidermal necrolysis treated with intravenous immunoglobulin and N-acetylcysteine with excellent response. 1. Introduction Drug-induced toxic epidermal necrolysis (TEN), also known as Lyell’s syndrome, remains one of the most dramatic dermatological emergencies characterized by extensive destruction of the epidermis and mucosal epithelia that often can be caused by drugs [1]. TEN affects between 0.4 and 1.5 cases per million people every year [1, 2] with a mortality rate from 15% to 40%, with a large portion of patients dying from infections or multiorgan failure [3, 4]. The pathogenesis of drug-induced TEN is unknown, although several theories have been developed. Recent discoveries have shown that keratinocytes in TEN undergo apoptosis, not simply necrosis [5, 6]. Further research has elucidated that this apoptosis can be induced by interactions between cell surface death receptor Fas and its ligand, FasL or CD95L. The management of these patients is primarily supportive, although use of corticosteroids and intravenous immunoglobulin (IVIG) therapy has been widely used with controversy. We report a case of Cephazolin-induced toxic epidermal necrolysis with excellent response to N-acetylcysteine. Immunopathogenesis and current imputability of antibiotics in TEN will be discussed together with a review of the literature. 2. Case Report A 38-year-old woman with a long history of type I diabetes was hospitalized in our institution for an acute episode of complicated urinary tract infection. She reported no history of allergy to antibiotics. Upon admission, physical examination revealed a temperature of 38°C, a pulse of 120 beats/min, and a blood pressure of 85/50. The patient developed septic and hypovolemic shock requiring aggressive fluid resuscitation and dopamine. Laboratory findings were white blood cells, 24？900/mm3 (85.8% segmented, 7.6% lymphocyte, 5.7% monocyte, 0.4% eosinophil, and 0.5% basophil); red blood cells, 435 × 104/mm3; hemoglobin, 14.0？g/dL; platelets, 23.2 × 104/mm3. Blood chemistry documented: glucose level, 305？mg/dL; blood urea nitrogen (BUN), 27？mg/dL; creatinine, 1.6？mg/dL; C-reactive protein, 70？mg/dL; IgG, 1050？mg/dL; IgA, 290？mg/dL; IgM, 132？mg/dL. She was first administered cephazolin