For a study, it was determined that Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) were serious adverse medication responses that can be fatal. Despite the fact that such reactions were once assumed to be idiosyncratic and unpredictable, great progress had been made in understanding the pathomechanism and pharmacogenetics of such reactions. Researchers wanted to go over these developments as well as their clinical implications.
The human leukocyte antigen (HLA) association in SJS/TEN was recognized to play a functional role in addition to being a genetic marker. In an HLA-restricted manner, cytotoxic T lymphocytes (CTLs) mediated this response. Due to drug-modified HLA-peptide repertoire, certain medicines bonded directly to the HLA complex as well as encouraging the formation of self-reactivity. The function of drug-specific T cells and T-cell receptors had also been determined in the study. Granulysin, which is a cytotoxic protein generated by CTLs or natural killer cells and thought to be the primary mediator in the response, had been used to decipher downstream cytotoxic signals.
Pre-drug pharmacogenetic screening of the HLA alleles had previously been demonstrated to be effective in preventing various adverse responses. Other advancements in the disease process served as the foundation for a more effective prevention and treatment measure.
