Why do some patients get toxic epidermal necrolysis? The etiology is not completely understood, but recent evidence has found a genetic predisposition in at least some classes of drugs (e.g., association of aromatic antiepileptic drugs and HLA-B*1502 in the Han Chinese). It is likely that continued research will uncover more ties to a genetic predisposition. The molecular and immunologic events are still not fully elucidated; however, the recent demonstration of very high levels of soluble FasL interacting with Fas, which is expressed on the keratinocytes in toxic epidermal necrolysis, may provide insight into the pathophysiology of this life-threatening disorder. In one series, 77% of cases were clearly established as druginduced. Since the average patient with TEN is on 4.4 drugs, identifying the offending drug can be problematic. Frequent offenders include allopurinol, ampicillin, amoxicillin, carbamazepine, NSAIDs, phenobarbital, phenytoin, sulfonamides, and carbamazepine. Abe R: Toxic epidermal necrolysis and Stevens-Johnson syndrome: soluble Fas ligand involvement in the pathomechanisms of these diseases, J Dermatol Sci 52:151–159, 2008. Chung WH, Hung SI, Chen YT: Genetic predisposition of life-threatening antiepileptic-induced skin reactions, Expert Opin Drug Saf 9:15–21, 2010. |
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