HLA-B*5801 allele as a genetic marker for severe cutaneous adverse reactions caused by allopurinol.

By S. Hung, W. Chung, L. Liou, C. Chu, Marie Lin, H. Huang, Yen-Ling Lin, J. Lan, Li-cheng Yang, H. Hong and 9 more. Proceedings of the National Academy of Sciences of the United States of America, 2005

1,123 citations recorded by the source corpus.

Subfields: Pharmacology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/bb7966a93075869516458afeebf1bebd97ebb1a3

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Pharmacology

1. M. Eichelbaum
2. Magnus Ingelman-Sundberg
3. William E. Evans
4. Shufeng Zhou

Citations in the corpus

• Toxic epidermal necrolysis and Stevens-Johnson syndrome (2010, background): “Indeed, 100% of Han Chinese patients with a severe adverse drug reaction to allopurinol were HLA-B*5801 positive [37].”
• Granulysin is a key mediator for disseminated keratinocyte death in Stevens-Johnson syndrome and toxic epidermal necrolysis (2008, background): “The major histocompatibility complex–restricted presentation of a drug or its metabolite for T cell activation is now supported by our recent findings of strong genetic association between human leukocyte antigen-B alleles and reactions to specific drug”
• HIBAG – HLA Genotype Imputation with Attribute Bagging (2013, neutral): “29 Our results show that the predictions of B*57:01 and B*58:01 have 100% sensitivities and specificities with call rates 4 95% for Europeans.”
• Pharmacogenomics and individualized drug therapy. (2006, background): “Indeed, genetic susceptibility is implicated in various idiosyncratic ADRs, including hypersensitivity to abacavir (9), Stevens-Johnson syndrome induced by carbamazepine (10), and severe cutaneous ADRs caused by allopurinol (11).”