Pathogenesis

There are many reported causes of SJS, but drugs represent the most common association. Among the most frequent offenders are nonsteroidal anti-inflammatory drugs (NSAIDs), sulfonamides, anticonvulsants, penicillins, doxycycline, and tetracyclines. In contrast to EM, infectious causes are not as frequently implicated (12). Other reported causative factors include fungal and viral infections, X-irradiation, and inflammatory bowel disease.

The mechanism through which NSAIDs, sulfonamides, and anticonvulsants may lead to SJS involves accumulation of arene oxides due to a deficiency in epoxide hydrolase in susceptible individuals (13). Genetic differences in the detoxification of drugs may be responsible and several enzymes have been implicated, including those responsible for acetylation and arene hydroxylation. Mucosal lesions follow ingestion of the drug by 14 to 56 days in drug-associated SJS, and drugs administered a few days prior to the onset of SJS are usually not implicated.

The pathogenesis of SJS in infectious-related disease remains unknown. Auto-antibodies to desmoplakin I and II, causing cell separation through disruption in the keratin cytoskeleton, have been detected in patients with SJS, but it is not known if these autoantibodies are primarily involved in the pathogenesis of SJS or merely play a role in the evolution of the disease.

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