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1.
Pharmacogenomics ; 22(1): 1-12, 2021 01.
Article in English | MEDLINE | ID: mdl-33356553

ABSTRACT

Aims: To determine genetic susceptibility markers for carbamazepine (CBZ) and allopurinol-induced severe cutaneous adverse reactions (SCARs) in Vietnamese. Methods: A case-control study was performed involving 122 patients with CBZ or allopurinol-induced SCARs and 120 drug tolerant controls. Results:HLA-B*58:01 was strongly associated with allopurinol-induced SCARs and strongly correlated with SNP rs9263726. HLA-B*15:02 was associated with CBZ-induced Stevens-Johnson syndrome/toxic epidermal necrolysis but not with drug-induced hypersensitivity syndrome/drug rash with eosinophilia and systemic symptoms. No association was found between HLA-A*31:01 and CBZ-induced SCARs. HLA-B*58:01 and rs3909184 allele A with renal insufficiency were shown to increase the risk of allopurinol-induced SCARs. Conclusion:HLA-B*58:01 and HLA-B*15:02 confer susceptibility to allopurinol-induced SCARs and CBZ-induced SJS/TEN in Vietnamese. SNP rs9263726 can be used as a surrogate marker in identifying HLA-B*58:01.


Subject(s)
Allopurinol/adverse effects , Asian People/genetics , Carbamazepine/adverse effects , Genetic Predisposition to Disease/genetics , HLA-B Antigens/genetics , Stevens-Johnson Syndrome/genetics , Adolescent , Adult , Aged , Aged, 80 and over , Anticonvulsants/adverse effects , Case-Control Studies , Female , Forecasting , Genetic Predisposition to Disease/epidemiology , Gout Suppressants/adverse effects , Humans , Male , Middle Aged , Severity of Illness Index , Stevens-Johnson Syndrome/diagnosis , Stevens-Johnson Syndrome/epidemiology , Vietnam/epidemiology , Young Adult
2.
Pharmacogenomics ; 21(14): 985-994, 2020 09.
Article in English | MEDLINE | ID: mdl-32896208

ABSTRACT

Aim: To examine gene expression in different clinical phenotypes of allopurinol-induced severe cutaneous adverse reactions (SCARs). Materials & methods: Gene expression profiling was performed using microarray on 11 RNA samples (four controls, three hypersensitivity syndrome/drug rash with eosinophilia and systemic symptoms, four Stevens-Johnson syndrome/toxic epidermal necrolysis) followed by quantitative real-time PCR in a total of 11 SCARs patients and 11 controls. Results: The biological pathways which were significantly enriched in differentially expressed genes in Stevens-Johnson syndrome/toxic epidermal necrolysis compared with hypersensitivity syndrome/drug rash with eosinophilia and systemic symptoms patients included; cell surface interactions at the vascular wall, immunoregulatory interactions at the immunological synapse and MyD88 signaling pathways. Overexpression of miR146a occurred in allopurinol-tolerant HLA-B*58:01 carriers. Conclusion: Biological pathways are identified which appear to be implicated in determining clinical phenotypes in allopurinol-induced SCARs. Overexpression of miR146a is potentially important for allopurinol tolerance in HLA-B*58:01 carriers.


Subject(s)
Allopurinol/adverse effects , Asian People/genetics , Drug Eruptions/genetics , Gene Expression/genetics , Skin/drug effects , Adolescent , Adult , Aged , Aged, 80 and over , Anticonvulsants/adverse effects , Exanthema/chemically induced , Exanthema/genetics , Female , Gene Expression Profiling/methods , Gout Suppressants/adverse effects , HLA-B Antigens/genetics , Humans , Male , Middle Aged , Signal Transduction/genetics , Stevens-Johnson Syndrome/genetics
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