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Genetic Susceptibility of Delayed Drug Hypersensitivity: Comparison
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Please note this is a comparison between Version 2 by Dean Liu and Version 1 by Shuen-Iu Hung.

The clinical presentations of delayed drug hypersensitivity are various. They range from mild reactions (e.g., maculopapular exanthema (MPE) and fixed drug eruption (FDE)) to drug-induced liver injury (DILI) and severe cutaneous adverse reactions (SCARs) (e.g., Stevens–Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), and drug reaction with eosinophilia and systemic symptoms (DRESS)). The common culprits of delayed drug hypersensitivity include anti-epileptics, antibiotics, anti-gout agents, anti-viral drugs, etc. Delayed drug hypersensitivity is proposed to be initiated by different models of molecular recognition, composed of drug/metabolite antigen and endogenous peptide, HLA presentation, and T cell receptor (TCR) interaction. Increasing genetic variants of HLA loci and drug metabolic enzymes have been identified as responsible for delayed drug hypersensitivity. The genetic susceptibility of delayed drug hypersensitivity showed drug-specific, phenotype-specific, and ethnic variation. 

  • Genetics
  • drug hypersensitivity
  • T lymphocytes
  • HLA
  • Genomics
  • Pharmacogenomics
  • Allergy

1. Genetic Susceptibility of Antiepileptics-Induced Hypersensitivity Reactions

Chung W. H. et al. first reported that HLA-B*15:02 is a genetic marker for carbamazepine (CBZ)-induced SJS/TEN in Han Chinese patient populations in Taiwan in 2004 [36][1] (Table 1). This association has been further validated in other Asian countries, including Hong Kong, Singapore, Vietnam, Thailand, Malaysia, and India [37,38,39,40,41,42,43][2][3][4][5][6][7][8] (Table 1). A prospective study showed that the genetic screening of HLA-B*15:02 before CBZ administration prevented the occurrence of CBZ-induced SJS/TEN [44][9]. None of the 4877 recruited patients who received CBZ treatment with preemptive pharmacogenomic testing developed SJS/TEN [44][9]. Additionally, HLA-B*57:01 was associated with CBZ-induced SJS/TEN in Europeans [45][10] (Table 1). By comparison, HLA-A*31:01 is associated with CBZ-induced MPE and DRESS, which was first reported in Han Chinese in Taiwan in 2006 [46][11]. This genetic susceptibility was then validated in different populations, including Europeans and Japanese [45,46,47,48,49,50,51][10][11][12][13][14][15][16] (Table 1).
Aside from being a risk allele for CBZ-induced SJS/TEN, HLA-B*15:02 has also been associated with SCARs induced by other antiepileptics that have a similar aromatic structure to CBZ, such as oxcarbazepine [52[17][18],53], phenytoin [40[5][18][19][20],53,54,55], and lamotrigine [56][21] (Table 1). In addition, HLA-A*32:01 was reported to be associated with oxcarbazepine-induced MPE in the Eastern Han Chinese population [57][22]. HLA-B*13:01 and B*51:01 are suggested to be related to phenytoin-induced SCARs in different studies in Asians, including Han Chinese, Japanese, and Malaysian patient populations [55,58][20][23] (Table 1). In addition to HLA alleles, the loss of function in the allele of cytochrome P450 2C9 (CYP2C9), CYP2C9*3, affecting drug metabolism, was responsible for phenytoin-induced SCARs in Taiwan [58][23]. The genetic association was validated in the patient populations from Thailand and Japan [58,59,60][23][24][25] (Table 1). For lamotrigine-induced SCARs, HLA-A*31:01 and HLA-B*38:01 were reported to be risk alleles in patients of Asian or European descent [49,61][14][26] (Table 1).
Table 1. Genetic variants associated with antiepileptics-induced hypersensitivity reactions.
Causative Drugs Reactions Genetic Factors Ethnicity OR

(95% CI)		 p-Value Reference
Carbamazepine (CBZ) SJS/TEN HLA-B*15:02 Han Chinese 2504

(126–49,522)		 3.13 × 10−27 ][36][1]
Thai 25.5 (2.68–242.61) 0.0005 [40][
European 80 (34–187) <10−65]
[84][49], and HLA-B*13:01, associated with dapsone-induced DRESS in north-eastern and south-eastern Asians [85,86,87,88,89,90][50][51][52][53][54][55] (Table 3).
Table 3. Genetic variants associated with antibiotics-induced hypersensitivity reactions.
Causative Drugs Reactions Genetic Factors Ethnicity OR

(95% CI)		 p-Value Reference
Amoxicillin MPE HLA-DRB3*02:02 European 8.88 (3.37–23.32) 1 <0.0001 [72][37]
[63][28]
Co-amoxiclav DILI HLA-DRB1*15:01 European 2.59 (1.44–4.68) 0.002 [73 7.27 (2.04–25.97) 4.46 × 10−13 [43][8]
][38] Japanese 62.8 (21.2–185.8) 5.388 × 10−12 [67][32]
Flucloxacillin DILI HLA-B*57:01 European 80.6 (22.8–284.9) 8.97 × 10−19 [74][39] Indian 71.40 (3.0–1698) 0.0014
Sulfamethoxazole (SMX) SJS/TEN HLA-B*38[42][7]
Malaysian
Thai 348.3 (19.2–6336.9) 1.6 × 10−13 [65][30] European 8.6 (3.5–21) <0.003 [63][28] 16.15 (4.57–62.4) 7.87 × 10−6 [41][6]
579.0 (29.5–11,362.7) <0.001 [
Co-trimoxazole (SMX/TMP) SJS/TEN66][31] HLA-B*15:02 Thai 3.91 (1.42–10.92) 0.0037 [75][40] Vietnamese 33.78 (7.55–151.03) <0.0001 [39][4]
DRESS HLA-B*58:01 Han Chinese 47.7 (18.2–125.4) 1.0 × 10−26 [71][36]
HLA-C*06:02 11.84 (1.24–566.04) 0.0131 Singaporean 27.20 (2.67–∞) 0.004 [38][3]
    Thai 430.3 (22.6–8958.9) <0.001 [66][
HLA-C*08:0131] 3.53 (1.21–10.40) 0.0108 HLA-B*57:01 European 9.0 (4.2–19.4) 9.62 × 10−7 [45]
SCARs[10]
SCARs HLA-B*58:01 Korean 97.8 (18.3–521.5) 2.45 × 10−11 [ HLA-A*11:01-B*15:02 haplotype,68 Thai (HIV-infected patients only) 4.36 (1.43–13.34) 0.0108][33] [77][42] DRESS HLA-A*31:01 Han Chinese 23.0 (4.2–125) <0.001
HLA-B*58:01 Han Chinese 44.0 (21.5–90.3) 2.6 × 10
HLA-B*13:01-C*03:04 haplotype 3.77 (1.27–11.19)−41 0.0251[71][
HLA-B*13:01 Han Chinese, Thai, Malaysia 11.7 (5.7–24) 1.3 × 10−13 [76][41]
Vancomycin DRESS HLA-A*32:01 European NA 1 × 10−8 [84][49]
Dapsone SCARs HLA-B*13:01 Thai 39.00 (7.67–198.21) 5.34 × 10−7 [85][50]
54.00 (7.96–366.16) 0.0001 [88][53]
DRESS HLA-B*13:01 Han Chinese 20.53 (11.55–36.48) 6.84 × 10−25 [86][51]
Taiwanese, Malaysian 49.64 (5.89–418.13) 2.92 × 10−4 [87][52]
HLA-B*13:01 Korean 73.67 (2.56–2119.93) 0.012 [89][54]
HLA-B*13:01 Papua 233.46 (1.7–67.7) 7.11 × 10−9 [90][55]
Abbreviations: SJS/TEN, Stevens–Johnson syndrome/toxic epidermal necrolysis; DRESS, drug reaction with eosinophilia and systemic symptoms; SCARs, severe cutaneous adverse reactions; NA, not available; OR, odds ratio. 1 The odds ratio represents the increased risk of delayed type compared to immediate type reaction.

4. Genetic Susceptibility of Antiviral Agents-Induced Hypersensiticity

Abacavir is a nucleoside reverse transcriptase inhibitor, usually used in combined therapy for treating patients with HIV infection. Approximately 5–8% of European patients treated with abacavir developed immune-related adverse drug reaction (ADR) during the first six weeks of treatment [91][56]. HLA-B*57:01 was identified as a genetic predisposition for abacavir-related hypersensitivity in Caucasians in 2002 [92,93][57][58] (Table 4). The subsequent randomized clinical trials, recruiting 1956 patients from 19 countries, demonstrated that the carriage of HLA-B*57:01 could be a genetic predictor, in order to prevent abacavir hypersensitivity [94][59].
Nevirapine, a non-nucleoside reverse transcriptase inhibitor to treat HIV infection, has been reported to be associated with a hypersensitivity reaction; it has the clinical presentations of fever, a skin rash, or hepatitis. HLA-B*35:05 and HLA-Cw*04:01 were found to be related to a nevirapine-induced skin rash in Thailand [95,96][60][61] and nevirapine-induced SJS/TEN among Africans, respectively [97][62] (Table 4). Of note, HLA-Cw*04 was also found to be associated with cutaneous adverse reactions in multiple ethnicities [96][61] (Table 4). HLA-DRB1*01:01 was proposed to contribute to nevirapine-induced DRESS in patients in West Australia [98][63] (Table 4). Studies of multiple ethnicities show that the HLA-DRB1*01:01 allele is associated with DILI in white people [96][61] (Table 4). The other studies showed HLA-Cw*08 was associated with Nevirapine-induced hepatitis in Sardinian and Japanese populations [99,100][64][65]. The association between nevirapine-induced hepatotoxicity and HLA-Cw*04 was reported in Han Chinese people; this needs further validation [101][66]. In addition, an SNP (rs3099844) of the HCP gene was proposed to be associated with nevirapine-SJS/TEN in Africans [102][67] (Table 4).
Raltegravir, an HIV integrase inhibitor introduced in 2007, was associated with DRESS in Africans. HLA-B*53:01 was implicated as a risk allele of raltegravir-DRESS in the African population [103][68] (Table 4).
Table 4. Genetic variants associated with antiviral agents-induced hypersensitivity reactions.
Causative Drugs Reactions Genetic Factors Ethnicity OR

(95% CI)		 p-Value Reference
Abacavir DiHS HLA-B*57:01 Caucasians 23.6 (8.0–70.0) <0.0001 [92][57]
117 (29–481) <0.0001 [93][58]
NA NA [94][59]
Nevirapine SJS/TEN rs3099844 (HCP5) Mozambique 2.03 (na) 0.039 [102][67]
HLA-C*04:01 African 4.84 (2.71–8.61) 8.47 × 10−8 [97][62]
DiHS HLA-Cw*04 Thai 2.43(1.22–4.84) 0.17 [96][61]
NA 0.0088 [104][69]
Asians, Blacks, Whites 2.51 (1.73–3.62) 8.7 × 10−6 [96][61]
Han Chinese 3.611 (1.135–11.489) 0.030 [101][66]36][47][12]
HLA-B*35:05 Thai 18.96 (4.87–73.44) 4.6 × 10−6 [95][60]
HLA-B*35 Asians 3.47 (1.58–7.61) 0.053 [96][61]
HLA-DRB1*01 Whites 3.02 (1.66–5.49) 0.0074 [96][61]
4.8 (na) 0.14 [98][63]
HLA-Cw*08 Sardinian NA 0.05 [99][64]
Japanese NA 0.03 [100][65]
Raltegravir DRESS HLA-B*53:01 African NA NA [103][68]
Abbreviations: SJS/TEN, Stevens–Johnson syndrome/toxic epidermal necrolysis; DiHS, drug-induced hypersensitivity syndrome; DRESS, drug reaction with eosinophilia and systemic symptoms; NA, not available; OR, odds ratio.

5. Genetic Susceptibility of Hypersensitivity Reactions to Anti-Thyroid Drugs and Methazolamide

Anti-thyroid drugs (ATD), including carbimazole and methimazole, have been reported to induce agranulocytosis, and their association with HLA genotypes has been found in different ethnicities. Table 5 lists the genetic variants associated with drug-induced agranulocytosis (DIA). Methimazole-induced agranulocytosis was associated with HLA-DRB1*08:03:02 in Japanese people [105][70] (Table 5). HLA-B*27:05, HLA-B*38:02, and HLA-DRB1*08:03 alleles were found to be related to ATD-induced agranulocytosis in Taiwan [106][71] (Table 5). HLA-B*38:02 and HLA-DRB1*08:03 alleles were reported to be associated with ATD-induced agranulocytosis in Han Chinese people [107,108][72][73] (Table 5). HLA-B*27:05 was reported in a European population [109][74], as well as in Han Chinese people from northern China [110][75] (Table 5).
Methazolamide, an intraocular pressure-lowering drug, may cause SJS/TEN in Asians. HLA-B*59:01 has been proposed to be associated with methazolamide-induced SJS/TEN in Korean, Japanese, and Han Chinese patients [111,112,113,114][76][77][78][79] (Table 5).
Table 5. Genetic variants associated with hypersensitivity reactions to anti-thyroid drugs and methazolamide.
Causative Drugs Reactions Genetic Factors Ethnicity OR//break//(95% CI) p-Value Reference
Methimazole DIA HLA-DRB1*08:03:02 Japanese 5.42 (na) 0.002 [105][70]
HLA-B*38:02, DRB1*08:03 haplotype Han Chinese 48.41 (21.66–108.22) 3.32 × 10−21 [107][72]
HLA-B*38:02 21.48 (11.13–41.48) 6.75 × 10−32
HLA-DRB1*08:03 6.13 (3.28–11.46) 1.83 × 10−9
Carbimazole/Methimazole DIA HLA-B*38:02:01 Han Chinese 265.5 (27.87–2528.0) 2.5 × 10−14 [108][73]
Carbimazole, Methimazole, Propylthiouracil DIA HLA-B*27:05 Caucasian 7.30 (3.81–13.96) 1.91 × 10−9 [109][74]
Methimazole, Propylthiouracil DIA HLA-B*27:05 Han Chinese 60.11 (3.27–1104.4) 1.1 × 10−4 [110][75]
HLA-B*38:02 6.55 (2.11–20.36) 2.41 × 10−4
HLA-DRB1*08:03 3.95 (1.60–9.79) 6.86 (2.4–19.9) 2.7 × 10−3 [50][15
1.57 × 10−3 European]
39.11 (4.49–340.51) 5.9 × 10−4 [64][29]
Methazolamide SJS/TEN HLA-B*59:01 Han Chinese 305.0 (11.3–8259.9) 6.3 × 10−7 [111][76] European 49.9 (12.9–193.6) 4.0 × 10
Korean−8 249.8 (13.4–4813.5)[45][10]
<0.001 [112][77] 13.2 (8.4–20.8) <0.001 [47][12]
Japanese NA NA [114][79] 12.41 (1.27–121.03) 3.5 × 10
HLA-B*59:01−8 Han Chinese[48][13]
146.00 (16.12–1321.98) 6.19 × 10−10 [113][78] 22.00 (1.03–1190.36) 0.047 [49][14]
Japanese 10.8 (5.9–19.6) 3.64 × 10−15
20.86 (9.03–48.20)
1.22 × 10
−13
DILI HLA-B*58:01, HLA-B*53:01 cluster African-American, Caucasian, Hispanic NA 0.0007 [69][34]
MPE HLA-B*58:01 Thai 144.0 (13.9–1497.0) <0.001 [66][31] [
Han Chinese 8.5 (4.2–17.5) 2.3 × 10−9 [51][16]
HLA-B*55:02 MPE/DRESS HLA-A*31:01 Han Chinese 17.5 (4.6–66.5) 0.0022 [46][11]
[ MPE HLA-B*15:02 Thai 7.27 (2.04–25.97) 0.0022 [43][8]
71][ Oxcarbazepine (OXC) SJS/TEN HLA-B*15:02 Han Chinese 27.90 (7.84–99.23) 1.12 × 10−9 [52][17]
71.00 (7.84–643.10)  1.43 × 10−4 80.7 (3.8–1714.4) 8.4 × 10−4 [53][18]
MPE HLA-A*32:01 Han Chinese 15.877 (1.817–138.720) 0.004 [57][22]
Phenytoin (PHT) SCARs CYP2C9*3 Taiwanese 14.00 (6.75–29.02) 0.00001 [58][23]
Japanese 8.88 (2.20–35.83)
Malaysian 5.60 (0.56–56.20)
  Thai 4.30 (1.41–13.09) <0.05 [59][24]
 60][25]
36] Taiwanese, Japanese, Thai HLA-B*15:02 Asian (Han Chinese, Japanese, Malaysian) 5.0 (2.0–13) 0.025 [58][23]
SJS/TEN HLA-B*15:02 Han Chinese 5.1 (1.8–15.1) 0.0041 [53][18]
3.50 (1.10–11.18) 0.045 [55][20]
Thai 18.5 (1.82–188.40) 0.005 [40][5]
Malaysian 5.71 (1.41–23.10) 0.016 [54][19]
Lamotrigine (LTG) SCARs HLA-A*31:01 Korean 11.43 (1.95–59.77) 0.0037 [61][26]
HLA-B*38:01 European 147.00 (1.88–483) 0.001 [49][14]
SJS/TEN HLA-B*15:02 Han Chinese 4.98 (1.43–17.28) 0.01 [56][21]
AEDs (CBZ, LTG, PHT, etc.) SCARs HLA-B*15:02 Han Chinese 17.6 (2.9–105.2) 0.001 [37][2]
Abbreviations: SJS/TEN, Stevens–Johnson syndrome/toxic epidermal necrolysis; DRESS, drug reaction with eosinophilia and systemic symptoms; MPE, maculopapular exanthema; OR, odds ratio; SCARs, severe cutaneous adverse reactions.

2. Genetic Susceptibility of Allopurinol Hypersensitivity

Allopurinol, a xanthine oxidase inhibitor, is the first-line drug to treat hyperuricemia and gout. Allopurinol is also one of the common culprit drugs to induce drug hypersensitivity. Hung S.I. et al. first found HLA-B*58:01 to be associated with allopurinol-induced SCARs in Han Chinese people in Taiwan in 2005 [62][27] (Table 2). This association was further replicated and validated among various ethnicities, including European [63[28][29],64], Thai [65,66][30][31], Japanese [67][32], Korean [68][33], and African American [69][34] (Table 2). HLA-B*58:01 genetic screening has been shown to be a promising strategy for preventing allopurinol SCARs [70][35]. The renal dysfunction and increased plasma levels of the metabolite of allopurinol, i.e., oxypurinol, deteriorate the severity of allopurinol hypersensitivity [71][36]. This might explain the higher mortality rate of allopurinol-induced SCARs in patients with chronic kidney disease, because of the delayed clearance of oxypurinol. Furthermore, allopurinol-induced liver injury (DILI) was found to be associated with HLA-A*34:02, HLA-B*53:01, and HLA-B*58:01 [66,69][31][34] (Table 2). Some genomics studies validated the attribution of HLA-B*58:01 and proposed that other genetic variants, out of the HLA region, might also contribute to the development of allopurinol hypersensitivity [67][32] (Table 2).
Table 2. Genetic variants associated with allopurinol-induced hypersensitivity reactions.
Reactions Genetic Factors Ethnicity OR

(95% CI)		 p-Value Reference
SJS/TEN HLA-B*58:01 Han Chinese 580.3 (34.4–9780.9) 4.7 × 10−24 [62][27
Abbreviations: SJS/TEN, Stevens–Johnson syndrome/toxic epidermal necrolysis; DRESS, drug reaction with eosinophilia and systemic symptoms; DILI, drug-induced liver injury; SCARs, severe cutaneous adverse reactions; MPE, maculopapular exanthema; NA, not available; OR, odds ratio.

3. Genetic Susceptibility of Antibiotics-Induced Hypersensitivity Reactions

Antibiotics can cause either immediate-type or delayed-type drug hypersensitivity. Antibiotic hypersensitivity has shown an immune-related genetic predisposition. The HLA-DRB3*02:02 allele, absent in Europeans, accounts for 83% of amoxicillin-induced MPE cases in Italy [72][37] (Table 3). A high level of HLA-DRB1*15:01 was observed in Europeans with amoxicillin-clavulanate-induced liver injury [73][38], and a high level of HLA-B*57:01 was observed in flucloxacillin-induced liver injury [74][39].
Co-trimoxazole, a combination of sulfamethoxazole (SMX) and trimethoprim (TMP), is associated with delayed drug hypersensitivity. HLA-B*38 was reported to be related to sulfamethoxazole-induced SJS/TEN in Europeans [63][28]. Kongpan T. et al. reported that carriers with HLA-B*15:02, HLA-C*06:02, or HLA-C*08:01 had an increased risk of co-trimoxazole-induced SJS/TEN (odds ratio: 11) [75][40]. By whole genome sequencing (WGS), the recent multi-country case-control study showed that HLA-B*13:01 was strongly associated with co-trimoxazole-induced SCARs in patients from Taiwan, Thailand, and Malaysia [76][41]. Notably, HLA-B*13:01 contributed to 85.4% of patients with co-trimoxazole-induced DRESS [76][41]. A multicentric study of the Thai population showed that HLA-B*15:02 and HLA-C*08:01 are associated with cotrimoxazole-SJS/TEN and HLA-B*13:01 in DRESS. Additionally, the haplotypes of HLA-A*11:01-B*15:02 and HLA-B*13:01-C*03:04 are associated with co-trimoxazole-induced SJS/TEN and DRESS, respectively [77][42]. Earlier studies indicate that gene variants involved in drug metabolisms, such as NAT2 [78,79,80,81,82][43][44][45][46][47] and GSTM1 [83][48] null genotypes, were associated with sulfonamide-induced hypersensitivity reactions. However, the associations were weak and lacked validation.
Other significant discoveries, regarding pharmacogenomic associations with antibiotics-induced SCARs, include HLA-A*32:01, is associated with vancomycin-induced DRESS in Caucasians
Abbreviations: DIA, drug-induced agranulocytosis; SJS/TEN, Stevens–Johnson syndrome/toxic epidermal necrolysis; NA, not available; OR, odds ratio.

References

  1. Chung, W.H.; Hung, S.I.; Hong, H.S.; Hsih, M.S.; Yang, L.C.; Ho, H.C.; Wu, J.Y.; Chen, Y.T. Medical genetics: A marker for Stevens-Johnson syndrome. Nature 2004, 428, 486.
  2. Man, C.B.; Kwan, P.; Baum, L.; Yu, E.; Lau, K.M.; Cheng, A.S.; Ng, M.H. Association between HLA-B*1502 allele and antiepileptic drug-induced cutaneous reactions in Han Chinese. Epilepsia 2007, 48, 1015–1018.
  3. Chong, K.W.; Chan, D.W.; Cheung, Y.B.; Ching, L.K.; Hie, S.L.; Thomas, T.; Ling, S.; Tan, E.C. Association of carbamazepine-induced severe cutaneous drug reactions and HLA-B*1502 allele status, and dose and treatment duration in paediatric neurology patients in Singapore. Arch. Dis. Child. 2014, 99, 581–584.
  4. Nguyen, D.V.; Chu, H.C.; Nguyen, D.V.; Phan, M.H.; Craig, T.; Baumgart, K.; van Nunen, S. HLA-B*1502 and carbamazepine-induced severe cutaneous adverse drug reactions in Vietnamese. Asia Pac. Allergy 2015, 5, 68–77.
  5. Locharernkul, C.; Loplumlert, J.; Limotai, C.; Korkij, W.; Desudchit, T.; Tongkobpetch, S.; Kangwanshiratada, O.; Hirankarn, N.; Suphapeetiporn, K.; Shotelersuk, V. Carbamazepine and phenytoin induced Stevens-Johnson syndrome is associated with HLA-B*1502 allele in Thai population. Epilepsia 2008, 49, 2087–2091.
  6. Chang, C.C.; Too, C.L.; Murad, S.; Hussein, S.H. Association of HLA-B*1502 allele with carbamazepine-induced toxic epidermal necrolysis and Stevens-Johnson syndrome in the multi-ethnic Malaysian population. Int. J. Dermatol. 2011, 50, 221–224.
  7. Mehta, T.Y.; Prajapati, L.M.; Mittal, B.; Joshi, C.G.; Sheth, J.J.; Patel, D.B.; Dave, D.M.; Goyal, R.K. Association of HLA-B*1502 allele and carbamazepine-induced Stevens-Johnson syndrome among Indians. Indian J. Dermatol. Venereol. Leprol. 2009, 75, 579–582.
  8. Sukasem, C.; Chaichan, C.; Nakkrut, T.; Satapornpong, P.; Jaruthamsophon, K.; Jantararoungtong, T.; Koomdee, N.; Sririttha, S.; Medhasi, S.; Oo-Puthinan, S.; et al. Association between HLA-B Alleles and Carbamazepine-Induced Maculopapular Exanthema and Severe Cutaneous Reactions in Thai Patients. J. Immunol. Res. 2018, 2018, 2780272.
  9. Chen, P.; Lin, J.J.; Lu, C.S.; Ong, C.T.; Hsieh, P.F.; Yang, C.C.; Tai, C.T.; Wu, S.L.; Lu, C.H.; Hsu, Y.C.; et al. Carbamazepine-induced toxic effects and HLA-B*1502 screening in Taiwan. N. Engl. J. Med. 2011, 364, 1126–1133.
  10. Mockenhaupt, M.; Wang, C.W.; Hung, S.I.; Sekula, P.; Schmidt, A.H.; Pan, R.Y.; Chen, C.B.; Dunant, A.; Gouvello, S.L.; Schumacher, M.; et al. HLA-B*57:01 confers genetic susceptibility to carbamazepine-induced SJS/TEN in Europeans. Allergy 2019, 74, 2227–2230.
  11. Hung, S.I.; Chung, W.H.; Jee, S.H.; Chen, W.C.; Chang, Y.T.; Lee, W.R.; Hu, S.L.; Wu, M.T.; Chen, G.S.; Wong, T.W.; et al. Genetic susceptibility to carbamazepine-induced cutaneous adverse drug reactions. Pharm. Genom. 2006, 16, 297–306.
  12. Genin, E.; Chen, D.P.; Hung, S.I.; Sekula, P.; Schumacher, M.; Chang, P.Y.; Tsai, S.H.; Wu, T.L.; Bellón, T.; Tamouza, R.; et al. HLA-A*31:01 and different types of carbamazepine-induced severe cutaneous adverse reactions: An international study and meta-analysis. Pharmacogenom. J. 2014, 14, 281–288.
  13. McCormack, M.; Alfirevic, A.; Bourgeois, S.; Farrell, J.J.; Kasperavičiūtė, D.; Carrington, M.; Sills, G.J.; Marson, T.; Jia, X.; De Bakker, P.I.; et al. HLA-A*3101 and carbamazepine-induced hypersensitivity reactions in Europeans. N. Engl. J. Med. 2011, 364, 1134–1143.
  14. Ramírez, E.; Bellón, T.; Tong, H.Y.; Borobia, A.M.; De Abajo, F.J.; Lerma, V.; Moreno Hidalgo, M.A.; Castañer, J.L.; Cabañas, R.; Fiandor, A.; et al. Significant HLA class I type associations with aromatic antiepileptic drug (AED)-induced SJS/TEN are different from those found for the same AED-induced DRESS in the Spanish population. Pharmacol. Res. 2017, 115, 168–178.
  15. Hsiao, Y.H.; Hui, R.C.; Wu, T.; Chang, W.C.; Hsih, M.S.; Yang, C.H.; Ho, H.C.; Chang, Y.G.; Chen, M.J.; Lin, J.Y.; et al. Genotype-phenotype association between HLA and carbamazepine-induced hypersensitivity reactions: Strength and clinical correlations. J. Dermatol. Sci. 2014, 73, 101–109.
  16. Ozeki, T.; Mushiroda, T.; Yowang, A.; Takahashi, A.; Kubo, M.; Shirakata, Y.; Ikezawa, Z.; Iijima, M.; Shiohara, T.; Hashimoto, K.; et al. Genome-wide association study identifies HLA-A*3101 allele as a genetic risk factor for carbamazepine-induced cutaneous adverse drug reactions in Japanese population. Hum. Mol. Genet. 2011, 20, 1034–1041.
  17. Chen, C.B.; Hsiao, Y.H.; Wu, T.; Hsih, M.S.; Tassaneeyakul, W.; Jorns, T.P.; Sukasem, C.; Hsu, C.N.; Su, S.C.; Chang, W.C.; et al. Risk and association of HLA with oxcarbazepine-induced cutaneous adverse reactions in Asians. Neurology 2017, 88, 78–86.
  18. Hung, S.I.; Chung, W.H.; Liu, Z.S.; Chen, C.H.; Hsih, M.S.; Hui, R.C.; Chu, C.Y.; Chen, Y.T. Common risk allele in aromatic antiepileptic-drug induced Stevens-Johnson syndrome and toxic epidermal necrolysis in Han Chinese. Pharmacogenomics 2010, 11, 349–356.
  19. Chang, C.C.; Ng, C.C.; Too, C.L.; Choon, S.E.; Lee, C.K.; Chung, W.H.; Hussein, S.H.; Lim, K.S.; Murad, S. Association of HLA-B*15:13 and HLA-B*15:02 with phenytoin-induced severe cutaneous adverse reactions in a Malay population. Pharmacogenom. J. 2017, 17, 170–173.
  20. Cheung, Y.K.; Cheng, S.H.; Chan, E.J.; Lo, S.V.; Ng, M.H.; Kwan, P. HLA-B alleles associated with severe cutaneous reactions to antiepileptic drugs in Han Chinese. Epilepsia 2013, 54, 1307–1314.
  21. Zeng, T.; Long, Y.S.; Min, F.L.; Liao, W.P.; Shi, Y.W. Association of HLA-B*1502 allele with lamotrigine-induced Stevens-Johnson syndrome and toxic epidermal necrolysis in Han Chinese subjects: A meta-analysis. Int. J. Dermatol. 2015, 54, 488–493.
  22. Xu, J.; Shi, X.; Qiu, Y.; Zhang, Y.; Chen, S.; Shi, Y.; Deng, Y. Association between HLA-A*3201 allele and oxcarbazepine-induced cutaneous adverse reactions in Eastern Han Chinese population. Seizure 2019, 65, 25–30.
  23. Chung, W.H.; Chang, W.C.; Lee, Y.S.; Wu, Y.Y.; Yang, C.H.; Ho, H.C.; Chen, M.J.; Lin, J.Y.; Hui, R.C.; Ho, J.C. Genetic variants associated with phenytoin-related severe cutaneous adverse reactions. JAMA 2014, 312, 525–534.
  24. Tassaneeyakul, W.; Prabmeechai, N.; Sukasem, C.; Kongpan, T.; Konyoung, P.; Chumworathayi, P.; Tiamkao, S.; Khunarkornsiri, U.; Kulkantrakorn, K.; Saksit, N.; et al. Associations between HLA class I and cytochrome P450 2C9 genetic polymorphisms and phenytoin-related severe cutaneous adverse reactions in a Thai population. Pharm. Genom. 2016, 26, 225–234.
  25. Su, S.C.; Chen, C.B.; Chang, W.C.; Wang, C.W.; Fan, W.L.; Lu, L.Y.; Nakamura, R.; Saito, Y.; Ueta, M.; Kinoshita, S.; et al. HLA Alleles and CYP2C9*3 as Predictors of Phenytoin Hypersensitivity in East Asians. Clin. Pharmacol. Ther. 2019, 105, 476–485.
  26. Kim, B.K.; Jung, J.W.; Kim, T.B.; Chang, Y.S.; Park, H.S.; Moon, J.; Lee, S.T.; Jung, K.H.; Jung, K.Y.; Chu, K.; et al. HLA-A*31:01 and lamotrigine-induced severe cutaneous adverse drug reactions in a Korean population. Ann. Allergy Asthma Immunol. 2017, 118, 629–630.
  27. Hung, S.I.; Chung, W.H.; Liou, L.B.; Chu, C.C.; Lin, M.; Huang, H.P.; Lin, Y.L.; Lan, J.L.; Yang, L.C.; Hong, H.S.; et al. HLA-B*5801 allele as a genetic marker for severe cutaneous adverse reactions caused by allopurinol. Proc. Natl. Acad. Sci. USA 2005, 102, 4134–4139.
  28. Lonjou, C.; Borot, N.; Sekula, P.; Ledger, N.; Thomas, L.; Halevy, S.; Naldi, L.; Bouwes-Bavinck, J.N.; Sidoroff, A.; de Toma, C.; et al. A European study of HLA-B in Stevens-Johnson syndrome and toxic epidermal necrolysis related to five high-risk drugs. Pharm. Genom. 2008, 18, 99–107.
  29. Goncalo, M.; Coutinho, I.; Teixeira, V.; Gameiro, A.R.; Brites, M.M.; Nunes, R.; Martinho, A. HLA-B*58:01 is a risk factor for allopurinol-induced DRESS and Stevens-Johnson syndrome/toxic epidermal necrolysis in a Portuguese population. Br. J. Dermatol. 2013, 169, 660–665.
  30. Tassaneeyakul, W.; Jantararoungtong, T.; Chen, P.; Lin, P.Y.; Tiamkao, S.; Khunarkornsiri, U.; Chucherd, P.; Konyoung, P.; Vannaprasaht, S.; Choonhakarn, C.; et al. Strong association between HLA-B*5801 and allopurinol-induced Stevens-Johnson syndrome and toxic epidermal necrolysis in a Thai population. Pharm. Genom. 2009, 19, 704–709.
  31. Sukasem, C.; Jantararoungtong, T.; Kuntawong, P.; Puangpetch, A.; Koomdee, N.; Satapornpong, P.; Supapsophon, P.; Klaewsongkram, J.; Rerkpattanapipat, T. HLA-B (*) 58:01 for Allopurinol-Induced Cutaneous Adverse Drug Reactions: Implication for Clinical Interpretation in Thailand. Front. Pharmacol. 2016, 7, 186.
  32. Tohkin, M.; Kaniwa, N.; Saito, Y.; Sugiyama, E.; Kurose, K.; Nishikawa, J.; Hasegawa, R.; Aihara, M.; Matsunaga, K.; Abe, M.; et al. A whole-genome association study of major determinants for allopurinol-related Stevens-Johnson syndrome and toxic epidermal necrolysis in Japanese patients. Pharmacogenom. J. 2013, 13, 60–69.
  33. Kang, H.R.; Jee, Y.K.; Kim, Y.S.; Lee, C.H.; Jung, J.W.; Kim, S.H.; Park, H.W.; Chang, Y.S.; Jang, I.J.; Cho, S.H.; et al. Positive and negative associations of HLA class I alleles with allopurinol-induced SCARs in Koreans. Pharm. Genom. 2011, 21, 303–307.
  34. Fontana, R.J.; Li, Y.J.; Phillips, E.; Saeed, N.; Barnhart, H.; Kleiner, D. Allopurinol hepatotoxicity is associated with human leukocyte antigen Class I alleles. Liver Int. 2021, 41, 1884–1893.
  35. Ko, T.M.; Tsai, C.Y.; Chen, S.Y.; Chen, K.S.; Yu, K.H.; Chu, C.S.; Huang, C.M.; Wang, C.R.; Weng, C.T.; Yu, C.L.; et al. Use of HLA-B*58:01 genotyping to prevent allopurinol induced severe cutaneous adverse reactions in Taiwan: National prospective cohort study. BMJ 2015, 351, h4848.
  36. Ng, C.Y.; Yeh, Y.T.; Wang, C.W.; Hung, S.I.; Yang, C.H.; Chang, Y.C.; Chang, W.C.; Lin, Y.J.; Chang, C.J.; Su, S.C.; et al. Impact of the HLA-B(*)58:01 Allele and Renal Impairment on Allopurinol-Induced Cutaneous Adverse Reactions. J. Investig. Dermatol. 2016, 136, 1373–1381.
  37. Romano, A.; Oussalah, A.; Chery, C.; Gueant-Rodriguez, R.M.; Gaeta, F.; Cornejo-Garcia, J.A.; Rouyer, P.; Josse, T.; Mayorga, C.; Torres, M.J.; et al. Next-generation sequencing and genotype association studies reveal the association of HLA-DRB3*02:02 with delayed hypersensitivity to penicillins. Allergy 2021, 77, 1827–1834.
  38. Donaldson, P.T.; Daly, A.K.; Henderson, J.; Graham, J.; Pirmohamed, M.; Bernal, W.; Day, C.P.; Aithal, G.P. Human leucocyte antigen class II genotype in susceptibility and resistance to co-amoxiclav-induced liver injury. J. Hepatol. 2010, 53, 1049–1053.
  39. Daly, A.K.; Donaldson, P.T.; Bhatnagar, P.; Shen, Y.; Pe’er, I.; Floratos, A.; Daly, M.J.; Goldstein, D.B.; John, S.; Nelson, M.R.; et al. HLA-B*5701 genotype is a major determinant of drug-induced liver injury due to flucloxacillin. Nat. Genet. 2009, 41, 816–819.
  40. Kongpan, T.; Mahasirimongkol, S.; Konyoung, P.; Kanjanawart, S.; Chumworathayi, P.; Wichukchinda, N.; Kidkeukarun, R.; Preechakul, S.; Khunarkornsiri, U.; Bamrungram, W.; et al. Candidate HLA genes for prediction of co-trimoxazole-induced severe cutaneous reactions. Pharm. Genom. 2015, 25, 402–411.
  41. Wang, C.W.; Tassaneeyakul, W.; Chen, C.B.; Chen, W.T.; Teng, Y.C.; Huang, C.Y.; Sukasem, C.; Lu, C.W.; Lee, Y.S.; Choon, S.E.; et al. Whole genome sequencing identifies genetic variants associated with co-trimoxazole hypersensitivity in Asians. J. Allergy Clin. Immunol. 2021, 147, 1402–1412.
  42. Sukasem, C.; Pratoomwun, J.; Satapornpong, P.; Klaewsongkram, J.; Rerkpattanapipat, T.; Rerknimitr, P.; Lertpichitkul, P.; Puangpetch, A.; Nakkam, N.; Konyoung, P.; et al. Genetic Association of Co-Trimoxazole-Induced Severe Cutaneous Adverse Reactions Is Phenotype-Specific: HLA Class I Genotypes and Haplotypes. Clin. Pharmacol. Ther. 2020, 108, 1078–1089.
  43. Wolkenstein, P.; Carriere, V.; Charue, D.; Bastuji-Garin, S.; Revuz, J.; Roujeau, J.C.; Beaune, P.; Bagot, M. A slow acetylator genotype is a risk factor for sulphonamide-induced toxic epidermal necrolysis and Stevens-Johnson syndrome. Pharmacogenetics 1995, 5, 255–258.
  44. Pirmohamed, M.; Alfirevic, A.; Vilar, J.; Stalford, A.; Wilkins, E.G.; Sim, E.; Park, B.K. Association analysis of drug metabolizing enzyme gene polymorphisms in HIV-positive patients with co-trimoxazole hypersensitivity. Pharmacogenetics 2000, 10, 705–713.
  45. Zielinska, E.; Niewiarowski, W.; Bodalski, J.; Rebowski, G.; Skretkowicz, J.; Mianowska, K.; Sekulska, M. Genotyping of the arylamine N-acetyltransferase polymorphism in the prediction of idiosyncratic reactions to trimethoprim-sulfamethoxazole in infants. Pharm. World Sci. 1998, 20, 123–130.
  46. O’Neil, W.M.; MacArthur, R.D.; Farrough, M.J.; Doll, M.A.; Fretland, A.J.; Hein, D.W.; Crane, L.R.; Svensson, C.K. Acetylator phenotype and genotype in HIV-infected patients with and without sulfonamide hypersensitivity. J. Clin. Pharmacol. 2002, 42, 613–619.
  47. Alfirevic, A.; Stalford, A.C.; Vilar, F.J.; Wilkins, E.G.; Park, B.K.; Pirmohamed, M. Slow acetylator phenotype and genotype in HIV-positive patients with sulphamethoxazole hypersensitivity. Br. J. Clin. Pharmacol. 2003, 55, 158–165.
  48. Delomenie, C.; Mathelier-Fusade, P.; Longuemaux, S.; Rozenbaum, W.; Leynadier, F.; Krishnamoorthy, R.; Dupret, J.M. Glutathione S-transferase (GSTM1) null genotype and sulphonamide intolerance in acquired immunodeficiency syndrome. Pharmacogenetics 1997, 7, 519–520.
  49. Konvinse, K.C.; Trubiano, J.A.; Pavlos, R.; James, I.; Shaffer, C.M.; Bejan, C.A.; Schutte, R.J.; Ostrov, D.A.; Pilkinton, M.A.; Rosenbach, M.; et al. HLA-A*32:01 is strongly associated with vancomycin-induced drug reaction with eosinophilia and systemic symptoms. J. Allergy Clin. Immunol. 2019, 144, 183–192.
  50. Satapornpong, P.; Pratoomwun, J.; Rerknimitr, P.; Klaewsongkram, J.; Nakkam, N.; Rungrotmongkol, T.; Konyoung, P.; Saksit, N.; Mahakkanukrauh, A.; Amornpinyo, W.; et al. HLA-B*13:01 Is a Predictive Marker of Dapsone-Induced Severe Cutaneous Adverse Reactions in Thai Patients. Front. Immunol. 2021, 12, 661135.
  51. Zhang, F.R.; Liu, H.; Irwanto, A.; Fu, X.A.; Li, Y.; Yu, G.Q.; Yu, Y.X.; Chen, M.F.; Low, H.Q.; Li, J.H.; et al. HLA-B*13:01 and the dapsone hypersensitivity syndrome. N. Engl. J. Med. 2013, 369, 1620–1628.
  52. Chen, W.T.; Wang, C.W.; Lu, C.W.; Chen, C.B.; Lee, H.E.; Hung, S.I.; Choon, S.E.; Yang, C.H.; Liu, M.T.; Chen, T.J.; et al. The Function of HLA-B*13:01 Involved in the Pathomechanism of Dapsone-Induced Severe Cutaneous Adverse Reactions. J. Investig. Dermatol. 2018, 138, 1546–1554.
  53. Tempark, T.; Satapornpong, P.; Rerknimitr, P.; Nakkam, N.; Saksit, N.; Wattanakrai, P.; Jantararoungtong, T.; Koomdee, N.; Mahakkanukrauh, A.; Tassaneeyakul, W.; et al. Dapsone-induced severe cutaneous adverse drug reactions are strongly linked with HLA-B*13: 01 allele in the Thai population. Pharm. Genom. 2017, 27, 429–437.
  54. Park, H.J.; Park, J.W. The HLA-B*13:01 and the dapsone hypersensitivity syndrome in Korean and Asian populations: Genotype- and meta-analyses. Expert Opin. Drug Saf. 2020, 19, 1349–1356.
  55. Krismawati, H.; Irwanto, A.; Pongtiku, A.; Irwan, I.D. Validation study of HLA-B*13:01 as a biomarker of dapsone hypersensitivity syndrome in leprosy patients in Indonesia. PLoS Negl. Trop. Dis. 2020, 14, e0008746.
  56. Hetherington, S.; McGuirk, S.; Powell, G.; Cutrell, A.; Naderer, O.; Spreen, B.; Lafon, S.; Pearce, G.; Steel, H. Hypersensitivity reactions during therapy with the nucleoside reverse transcriptase inhibitor abacavir. Clin. Ther. 2001, 23, 1603–1614.
  57. Hetherington, S.; Hughes, A.R.; Mosteller, M.; Shortino, D.; Baker, K.L.; Spreen, W.; Lai, E.; Davies, K.; Handley, A.; Dow, D.J.; et al. Genetic variations in HLA-B region and hypersensitivity reactions to abacavir. Lancet 2002, 359, 1121–1122.
  58. Mallal, S.; Nolan, D.; Witt, C.; Masel, G.; Martin, A.M.; Moore, C.; Sayer, D.; Castley, A.; Mamotte, C.; Maxwell, D.; et al. Association between presence of HLA-B*5701, HLA-DR7, and HLA-DQ3 and hypersensitivity to HIV-1 reverse-transcriptase inhibitor abacavir. Lancet 2002, 359, 727–732.
  59. Mallal, S.; Phillips, E.; Carosi, G.; Molina, J.M.; Workman, C.; Tomazic, J.; Jägel-Guedes, E.; Rugina, S.; Kozyrev, O.; Cid, J.F.; et al. HLA-B*5701 screening for hypersensitivity to abacavir. N. Engl. J. Med. 2008, 358, 568–579.
  60. Chantarangsu, S.; Mushiroda, T.; Mahasirimongkol, S.; Kiertiburanakul, S.; Sungkanuparph, S.; Manosuthi, W.; Tantisiriwat, W.; Charoenyingwattana, A.; Sura, T.; Chantratita, W.; et al. HLA-B*3505 allele is a strong predictor for nevirapine-induced skin adverse drug reactions in HIV-infected Thai patients. Pharm. Genom. 2009, 19, 139–146.
  61. Yuan, J.; Guo, S.; Hall, D.; Cammett, A.M.; Jayadev, S.; Distel, M.; Storfer, S.; Huang, Z.; Mootsikapun, P.; Ruxrungtham, K.; et al. Toxicogenomics of nevirapine-associated cutaneous and hepatic adverse events among populations of African, Asian, and European descent. AIDS 2011, 25, 1271–1280.
  62. Carr, D.F.; Bourgeois, S.; Chaponda, M.; Takeshita, L.Y.; Morris, A.P.; Castro, E.M.; Alfirevic, A.; Jones, A.R.; Rigden, D.J.; Haldenby, S.; et al. Genome-wide association study of nevirapine hypersensitivity in a sub-Saharan African HIV-infected population. J. Antimicrob. Chemother. 2017, 72, 1152–1162.
  63. Martin, A.M.; Nolan, D.; James, I.; Cameron, P.; Keller, J.; Moore, C.; Phillips, E.; Christiansen, F.T.; Mallal, S. Predisposition to nevirapine hypersensitivity associated with HLA-DRB1*0101 and abrogated by low CD4 T-cell counts. AIDS 2005, 19, 97–99.
  64. Littera, R.; Carcassi, C.; Masala, A.; Piano, P.; Serra, P.; Ortu, F.; Corso, N.; Casula, B.; La Nasa, G.; Contu, L.; et al. HLA-dependent hypersensitivity to nevirapine in Sardinian HIV patients. AIDS 2006, 20, 1621–1626.
  65. Gatanaga, H.; Yazaki, H.; Tanuma, J.; Honda, M.; Genka, I.; Teruya, K.; Tachikawa, N.; Kikuchi, Y.; Oka, S. HLA-Cw8 primarily associated with hypersensitivity to nevirapine. AIDS 2007, 21, 264–265.
  66. Gao, S.; Gui, X.E.; Liang, K.; Liu, Z.; Hu, J.; Dong, B. HLA-dependent hypersensitivity reaction to nevirapine in Chinese Han HIV-infected patients. AIDS Res. Hum. Retroviruses 2012, 28, 540–543.
  67. Borgiani, P.; Di Fusco, D.; Erba, F.; Marazzi, M.C.; Mancinelli, S.; Novelli, G.; Palombi, L.; Ciccacci, C. HCP5 genetic variant (RS3099844) contributes to Nevirapine-induced Stevens Johnsons Syndrome/Toxic Epidermal Necrolysis susceptibility in a population from Mozambique. Eur. J. Clin. Pharmacol. 2014, 70, 275–278.
  68. Thomas, M.; Hopkins, C.; Duffy, E.; Lee, D.; Loulergue, P.; Ripamonti, D.; Ostrov, D.A.; Phillips, E. Association of the HLA-B*53:01 Allele With Drug Reaction With Eosinophilia and Systemic Symptoms (DRESS) Syndrome During Treatment of HIV Infection With Raltegravir. Clin. Infect. Dis. 2017, 64, 1198–1203.
  69. Likanonsakul, S.; Rattanatham, T.; Feangvad, S.; Uttayamakul, S.; Prasithsirikul, W.; Tunthanathip, P.; Nakayama, E.E.; Shioda, T. HLA-Cw*04 allele associated with nevirapine-induced rash in HIV-infected Thai patients. AIDS Res. Ther. 2009, 6, 22.
  70. Tamai, H.; Sudo, T.; Kimura, A.; Mukuta, T.; Matsubayashi, S.; Kuma, K.; Nagataki, S.; Sasazuki, T. Association between the DRB1*08032 histocompatibility antigen and methimazole-induced agranulocytosis in Japanese patients with Graves disease. Ann. Intern. Med. 1996, 124, 490–494.
  71. Chen, W.T.; Chi, C.C. Associations of HLA genotypes with antithyroid drug-induced agranulocytosis: A systematic review and meta-analysis of pharmacogenomics studies. Br. J. Clin. Pharmacol. 2019, 85, 1878–1887.
  72. Chen, P.L.; Shih, S.R.; Wang, P.W.; Lin, Y.C.; Chu, C.C.; Lin, J.H.; Chen, S.C.; Chang, C.C.; Huang, T.S.; Tsai, K.S.; et al. Genetic determinants of antithyroid drug-induced agranulocytosis by human leukocyte antigen genotyping and genome-wide association study. Nat. Commun. 2015, 6, 7633.
  73. Cheung, C.L.; Sing, C.W.; Tang, C.S.; Cheng, V.K.; Pirmohamed, M.; Choi, C.H.; Hung, C.S.; Lau, E.Y.; Lee, K.F.; Mak, M.W.; et al. HLA-B*38:02:01 predicts carbimazole/methimazole-induced agranulocytosis. Clin. Pharmacol. Ther. 2016, 99, 555–561.
  74. Hallberg, P.; Eriksson, N.; Ibanez, L.; Bondon-Guitton, E.; Kreutz, R.; Carvajal, A.; Lucena, M.I.; Ponce, E.S.; Molokhia, M.; Martin, J.; et al. Genetic variants associated with antithyroid drug-induced agranulocytosis: A genome-wide association study in a European population. Lancet Diabetes Endocrinol. 2016, 4, 507–516.
  75. He, Y.; Zheng, J.; Zhang, Q.; Hou, P.; Zhu, F.; Yang, J.; Li, W.; Chen, P.; Liu, S.; Zhang, B.; et al. Association of HLA-B and HLA-DRB1 polymorphisms with antithyroid drug-induced agranulocytosis in a Han population from northern China. Sci. Rep. 2017, 7, 11950.
  76. Yang, F.; Xuan, J.; Chen, J.; Zhong, H.; Luo, H.; Zhou, P.; Sun, X.; He, L.; Chen, S.; Cao, Z.; et al. HLA-B*59:01: A marker for Stevens-Johnson syndrome/toxic epidermal necrolysis caused by methazolamide in Han Chinese. Pharm. J. 2016, 16, 83–87.
  77. Kim, S.H.; Kim, M.; Lee, K.W.; Kim, S.H.; Kang, H.R.; Park, H.W.; Jee, Y.K. HLA-B*5901 is strongly associated with methazolamide-induced Stevens-Johnson syndrome/toxic epidermal necrolysis. Pharmacogenomics 2010, 11, 879–884.
  78. Jiang, M.; Yang, F.; Zhang, L.; Xu, D.; Jia, Y.; Cheng, Y.; Han, S.; Wang, T.; Chen, Z.; Su, Y.; et al. Unique motif shared by HLA-B*59:01 and HLA-B*55:02 is associated with methazolamide-induced Stevens-Johnson syndrome and toxic epidermal necrolysis in Han Chinese. J. Eur. Acad. Dermatol. Venereol. 2022, 36, 873–880.
  79. Shirato, S.; Kagaya, F.; Suzuki, Y.; Joukou, S. Stevens-Johnson syndrome induced by methazolamide treatment. Arch. Ophthalmol. 1997, 115, 550–553.
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