Abstract

Drug-induced toxic epidermal necrolysis (TEN) is a rare bullous disease characterized by severe epidermal necrosis and sloughing. Soluble TNF-alpha(sTNF-alpha), soluble IL-6 (sIL-6) and their reactive soluble receptors (sTNF-Rp55 or-R1, sTNF-Rp75 or-R2, sIL-6R) were quantified in blister fluid and serum of 6 TEN patients and 13 cases of second-degree burn. The amounts of sTNF-alpha, sTNF-R1 and sTNF-R2 were significantly higher in TEN blisters than in burns reflecting the probable involvement of the TNF-alpha system in the specific pathomechanism of TEN. The ratio sTNF-alpha/sTNF-R2 was significantly lower in TEN blisters than in burns. The concentrations of sTNF-R2 in TEN blisters and serums were significantly greater than those of sTNF-R1. This suggests a potential important role for sTNF-R2 in TEN by enhancing the cytotoxic effect of TNF-alpha. In addition, both sTNF-R1 and sTNF-R2 were significantly more abundant in TEN blisters than in serums, indicating that the TNF-alpha processing was mainly a local event in the TEN skin. No significant difference could be established for sIL-6 and sIL-6R between TEN and burns. Although a role for IL-6 cannot be ruled out, its production has no specific characteristics in TEN compared to burns.

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