Drug Hypersensitivity: Pharmacogenetics and Clinical Syndromes
Identifieur interne : 000A06 ( Ncbi/Curation ); précédent : 000A05; suivant : 000A07Drug Hypersensitivity: Pharmacogenetics and Clinical Syndromes
Auteurs : Elizabeth J. Phillips ; Wen-Hung Chung [Taïwan] ; Maja Mockenhaupt [Allemagne] ; Jean-Claude Roujeau [France] ; Simon A. MallalSource :
- The Journal of allergy and clinical immunology [ 0091-6749 ] ; 2011.
Abstract
Severe cutaneous adverse reactions (SCARs) include syndromes such as drug reaction, eosinophilia and systemic symptoms (DRESS) or drug-induced hypersensitivity syndrome (DIHS) and Stevens-Johnson Syndrome/Toxic epidermal necrolysis (SJS/TEN). An important advance has been the discovery of associations between HLA alleles and many of these syndromes including abacavir hypersensitivity reaction, allopurinol DRESS/DIHS and SJS/TEN and SJS/TEN associated with aromatic amine anticonvulsants. These HLA associations have created the promise for prevention through screening and have additionally shed further light on the immunopathogenesis of SCARs. The roll-out of HLA-B*5701 into routine clinical practice as a genetic screening test to prevent abacavir hypersensitivity provides a translational roadmap for other drugs. Numerous hurdles exist in the widespread translation of several other drugs such as carbamazepine where the positive predictive value of HLA-B*1502 is low and the negative predictive value of HLA-B*1502 for SJS/TEN may not be 100% in all ethnic groups. International collaborative consortia have been formed with the goal of developing phenotype standardization and undertaking HLA and genome-wide analyses in diverse populations with these syndromes.
Url:
DOI: 10.1016/j.jaci.2010.11.046
PubMed: 21354501
PubMed Central: 3061439
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Elizabeth J. Phillips<affiliation><nlm:aff id="A1">Institute for Immunology & Infectious Diseases, Murdoch University</nlm:aff>
<wicri:noCountry code="subfield">Murdoch University</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A2">Department of Clinical Immunology & Immunogenetics, Royal Perth Hospital</nlm:aff>
<wicri:noCountry code="subfield">Royal Perth Hospital</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A3">Department of Clinical Immunology, Infectious Diseases and Clinical Pharmacology/Toxicology, Sir Charles Gairdner Hospital</nlm:aff>
<wicri:noCountry code="subfield">Sir Charles Gairdner Hospital</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A4">School of Pathology & Laboratory Medicine and Biomedical, Biomolecular and Chemical Sciences, University of Western Australia</nlm:aff>
<wicri:noCountry code="subfield">University of Western Australia</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A2">Department of Clinical Immunology & Immunogenetics, Royal Perth Hospital</nlm:aff>
<wicri:noCountry code="subfield">Royal Perth Hospital</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A3">Department of Clinical Immunology, Infectious Diseases and Clinical Pharmacology/Toxicology, Sir Charles Gairdner Hospital</nlm:aff>
<wicri:noCountry code="subfield">Sir Charles Gairdner Hospital</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A4">School of Pathology & Laboratory Medicine and Biomedical, Biomolecular and Chemical Sciences, University of Western Australia</nlm:aff>
<wicri:noCountry code="subfield">University of Western Australia</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A3">Department of Clinical Immunology, Infectious Diseases and Clinical Pharmacology/Toxicology, Sir Charles Gairdner Hospital</nlm:aff>
<wicri:noCountry code="subfield">Sir Charles Gairdner Hospital</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A4">School of Pathology & Laboratory Medicine and Biomedical, Biomolecular and Chemical Sciences, University of Western Australia</nlm:aff>
<wicri:noCountry code="subfield">University of Western Australia</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A4">School of Pathology & Laboratory Medicine and Biomedical, Biomolecular and Chemical Sciences, University of Western Australia</nlm:aff>
<wicri:noCountry code="subfield">University of Western Australia</wicri:noCountry>
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<affiliation><nlm:aff id="A1">Institute for Immunology & Infectious Diseases, Murdoch University</nlm:aff>
<wicri:noCountry code="subfield">Murdoch University</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A2">Department of Clinical Immunology & Immunogenetics, Royal Perth Hospital</nlm:aff>
<wicri:noCountry code="subfield">Royal Perth Hospital</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A2">Department of Clinical Immunology & Immunogenetics, Royal Perth Hospital</nlm:aff>
<wicri:noCountry code="subfield">Royal Perth Hospital</wicri:noCountry>
</affiliation>
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<front><div type="abstract" xml:lang="en"><p id="P1">Severe cutaneous adverse reactions (SCARs) include syndromes such as drug reaction, eosinophilia and systemic symptoms (DRESS) or drug-induced hypersensitivity syndrome (DIHS) and Stevens-Johnson Syndrome/Toxic epidermal necrolysis (SJS/TEN). An important advance has been the discovery of associations between HLA alleles and many of these syndromes including abacavir hypersensitivity reaction, allopurinol DRESS/DIHS and SJS/TEN and SJS/TEN associated with aromatic amine anticonvulsants. These HLA associations have created the promise for prevention through screening and have additionally shed further light on the immunopathogenesis of SCARs. The roll-out of HLA-B*5701 into routine clinical practice as a genetic screening test to prevent abacavir hypersensitivity provides a translational roadmap for other drugs. Numerous hurdles exist in the widespread translation of several other drugs such as carbamazepine where the positive predictive value of HLA-B*1502 is low and the negative predictive value of HLA-B*1502 for SJS/TEN may not be 100% in all ethnic groups. International collaborative consortia have been formed with the goal of developing phenotype standardization and undertaking HLA and genome-wide analyses in diverse populations with these syndromes.</p>
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