Strong association between HLA-B*5801 and allopurinol-induced Stevens–Johnson syndrome and toxic epidermal necrolysis in a Thai population

Tassaneeyakul, Wichittra; Jantararoungtong, Thawinee; Chen, Pei‐Jer; Lin, Pao-Yu; Tiamkao, Somsak; Khunarkornsiri, Usanee; Chucherd, Pachadaporn; Konyoung, Parinya; Vannaprasaht, Suda; Choonhakarn, Charoen; Pisuttimarn, Pornrith; Sangviroon, Alisara; Tassaneeyakul, Wongwiwat

doi:10.1097/fpc.0b013e328330a3b8

Cited by 347 publications

(267 citation statements)

References 19 publications

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“…In line with these results, other studies linked variants in HLA genes on chromosome 6 with autoimmune diseases [62,63]. Additionally, several HLA-B alleles were associated with small molecule drug allergy and adverse reactions [64][65][66][67][68][69]. Specifically, HLA-DRB1*07 : 01 allele was associated with elevated levels of serum alanine transferase during ximelagatrn and lapatinib treatment through a drug-induced adaptative immune response [70,71].…”

Section: Pharmacogeneticssupporting

confidence: 73%

Review of pharmacogenetics studies of L-asparaginase hypersensitivity in acute lymphoblastic leukemia points to variants in the GRIA1 gene

Lopez-Santillan

Iparraguirre

Martín-Guerrero

et al. 2017

Drug Metabolism and Personalized Therapy

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Acute lymphoblastic leukemia (ALL) is a major pediatric cancer in developed countries. Although treatment outcome has improved owing to advances in chemotherapy, there is still a group of patients who experience severe adverse events. L-Asparaginase is an effective antineoplastic agent used in chemotherapy of ALL. Despite its indisputable indication, hypersensitivity reactions are common. In those cases, discontinuation of treatment is usually needed and anti-asparaginase antibody production may also attenuate asparaginase activity, compromising its antileukemic effect. Till now, six pharmacogenetic studies have been performed in order to elucidate possible genetic predisposition for inter-individual differences in asparaginase hypersensitivity. In this review we have summarized the results of those studies which describe the involvement of four different genes, being polymorphisms in the glutamate receptor, ionotropic, AMPA 1 (GRIA1) the most frequently associated with asparaginase hypersensitivity. We also point to new approaches focusing on epigenetics that could be interesting for consideration in the near future.

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Section: Pharmacogeneticssupporting

confidence: 73%

Review of pharmacogenetics studies of L-asparaginase hypersensitivity in acute lymphoblastic leukemia points to variants in the GRIA1 gene

Lopez-Santillan

Iparraguirre

Martín-Guerrero

et al. 2017

Drug Metabolism and Personalized Therapy

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“…Regarding the association in other southeast Asian populations, a similar strong association between HLA-B*5801 and allopurinol-induced SJS ⁄ TEN was shown in a case-control study in a Thai population. 32 The association of HLA-B*5801 with allopurinolinduced SJS ⁄ TEN was observed in a European study as well (P < 10…”

Section: Association Between Hla-b*5801 and Allopurinol-induced Cutanmentioning

confidence: 92%

Pharmacogenetics of cutaneous adverse drug reactions

Aihara

2011

The Journal of Dermatology

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Drug-induced hypersensitivity reactions are of major medical concern because they are associated with high morbidity and high mortality. In addition, individual patients' reactions are impossible to predict in each patient. In the field of severe cutaneous adverse drug reactions (cutaneous ADR) such as Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), and drug-induced hypersensitivity syndrome (DHIS) or drug rash with eosinophilia and systemic symptoms (DRESS), major advances have recently been gained through studies of an association between HLA alleles and drug hypersensitivity induced by specific drugs. The results of these pharmacogenomic studies allow prediction of the risk of adverse reactions in patients treated with certain drugs, including carbamazepine and other aromatic antiepileptic drugs, allopurinol and abacavir. However, different ethnic populations show variations in the genetic associations. A strong association between carbamazepine-induced SJS ⁄ TEN and HLA-B*1502 has been found in Southeast Asian patients but not in Caucasian and Japanese patients. Moderate associations between aromatic amine anticonvulsants and other HLA alleles have been proposed in Japanese patients. In contrast, HLA-B*5801 was found to be associated with allopurinol-induced cutaneous ADR, including SJS ⁄ TEN and DIHS ⁄ DRESS, in Caucasian and Asian patients, including the Japanese. These differences may, at least in part, be due to the differences in allele frequency in different ethnic populations. This article reviews the progress in pharmacogenomics, associated mainly with carbamazepine and allopurinol in different ethnic populations. Pharmacogenetic screening based on associations between adverse reactions and specific HLA alleles helps to avoid serious conditions associated with drug hypersensitivity.

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“…HLA-B*1502 were reported to be associated with carbamazepine-induced Stevens-Johnson syndrome in Asian populations (33)(34)(35) and HLA-A*3101 in European, North American, and Mexican mestizo populations (36)(37)(38). HLA-B*5801 were reported to be associated with allopurinol-induced Stevens-Johnson syndrome or drug-induced hypersensitivity syndrome (39,40), and HLA-B*5701 were reported to be associated with abacavir-induced hypersensitivity reaction (41,42). There were also a few studies showing an association between HLA II alleles and drug allergy; for instance, HLA-DRB1*0701 was related to asparaginase allergy in people of European descent (43), and HLA-DRB9 was related to penicillin-induced immediate hypersensitive reaction in Chinese Han populations (44).…”

Section: Discussionmentioning

confidence: 99%

HLA-DQA1, -DQB1, and -DRB1 Alleles Associated with Acute Tubulointerstitial Nephritis in a Chinese Population: A Single-Center Cohort Study

Jia

et al. 2018

The Journal of Immunology

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Acute tubulointerstitial nephritis (ATIN) is a common cause of acute kidney injury with various origins. HLA-DQA1, -DQB1, and -DRB1 have been associated with development of tubulointerstitial nephritis and uveitis (TINU) syndrome in case reports and small case series, but information about HLA genetic susceptibility to drug hypersensitivity–related ATIN (D-ATIN) or other types of ATIN is limited. In this article, we genotyped 154 patients with ATIN of different causes and 200 healthy controls at HLA-DQA1, -DQB1, and -DRB1 loci. We found that there was no difference between patients with D-ATIN and TINU in the carrier’s frequency of HLA-DQA1, -DQB1, or -DRB1. Patients with Sjogren’s syndrome–ATIN and IgG4-related ATIN presented a different pattern of tested HLA alleles. HLA-DQA1*0104 (p value corrected by false discovery rate method [Pc] = 4.72 × 10−22, odds ratio [OR] = 13.81), -DQB1*0503 (Pc = 1.95 × 10−14, OR = 9.51), and -DRB1*1405 (Pc = 8.06 × 10−19, OR = 12.80) were significant risk alleles for the occurrence of D-ATIN and TINU. There were no significant associations between tested HLA alleles and ATIN induced by other causes. Patients with D-ATIN/TINU carrying HLA-DQA1*0104/DQB1*0503/DRB1*1405 had higher peak serum creatinine and more severe renal tubulointerstitial inflammatory impairment. They also had significantly higher levels of tubular HLA-DR and HLA-DQ expression, which were correlated with the numbers of interstitial CD4+ T lymphocytes (r = 0.975, p < 0.001 and r = 0.832, p = 0.005, respectively) and monocytes/macrophages (r = 0.721, p = 0.004 and r = 0.615, p = 0.02, respectively). In conclusion, patients with D-ATIN or TINU have genetic susceptibility in HLA-DQA1, -DQB1, and -DRB1 alleles. HLA-DQA1*0104/DQB1*0503/DRB1*1405 serves as a significant risk haplotype for development of D-ATIN and TINU, which might facilitate renal tubulointerstitial inflammation by enhancing Ag-presenting capacity of renal tubular cells.

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Strong association between HLA-B*5801 and allopurinol-induced Stevens–Johnson syndrome and toxic epidermal necrolysis in a Thai population

Abstract: A strong association of allopurinol-induced SJS/TEN with the HLA-B5801 allele was observed in a Thai population. The results suggest that HLA-B5801 is a valid genetic marker for screening Thai individuals who may be at risk for allopurinol-induced life-threatening SJS and TEN.

Cited by 347 publications

References 19 publications

Review of pharmacogenetics studies of L-asparaginase hypersensitivity in acute lymphoblastic leukemia points to variants in the GRIA1 gene

Review of pharmacogenetics studies of L-asparaginase hypersensitivity in acute lymphoblastic leukemia points to variants in the GRIA1 gene

Pharmacogenetics of cutaneous adverse drug reactions

HLA-DQA1, -DQB1, and -DRB1 Alleles Associated with Acute Tubulointerstitial Nephritis in a Chinese Population: A Single-Center Cohort Study

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Strong association between HLA-B*5801 and allopurinol-induced Stevens–Johnson syndrome and toxic epidermal necrolysis in a Thai population

Abstract: A strong association of allopurinol-induced SJS/TEN with the HLA-B*5801 allele was observed in a Thai population. The results suggest that HLA-B*5801 is a valid genetic marker for screening Thai individuals who may be at risk for allopurinol-induced life-threatening SJS and TEN.

Cited by 347 publications

References 19 publications

Review of pharmacogenetics studies of L-asparaginase hypersensitivity in acute lymphoblastic leukemia points to variants in the GRIA1 gene

Review of pharmacogenetics studies of L-asparaginase hypersensitivity in acute lymphoblastic leukemia points to variants in the GRIA1 gene

Pharmacogenetics of cutaneous adverse drug reactions

HLA-DQA1, -DQB1, and -DRB1 Alleles Associated with Acute Tubulointerstitial Nephritis in a Chinese Population: A Single-Center Cohort Study

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Abstract: A strong association of allopurinol-induced SJS/TEN with the HLA-B5801 allele was observed in a Thai population. The results suggest that HLA-B5801 is a valid genetic marker for screening Thai individuals who may be at risk for allopurinol-induced life-threatening SJS and TEN.