A whole-genome association study of major determinants for allopurinol-related Stevens–Johnson syndrome and toxic epidermal necrolysis in Japanese patients

Tohkin, Masahiro; Kaniwa, Nahoko; Saito, Yoshiro; Sugiyama, Emiko; Kurose, Kouichi; Nishikawa, Jun; Hasegawa, Ryuichi; Aihara, Michiko; Matsunaga, Kayoko; Abe, Mihoko; Furuya, Hirokazu; Takahashi, Yukitoshi; Ikeda, Hiroko; Muramatsu, Masaaki; Ueta, Mayumi; Sotozono, Chie; Kinoshita, Shigeru; Ikezawa, Zenrō

doi:10.1038/tpj.2011.41

Cited by 164 publications

(120 citation statements)

References 41 publications

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“…Thus, screening for the HLA-B*5801 allele has been proposed to reduce the incidence of these nonimmediate DHRs [33][34][35]. Another promising approach is to genotype the rs9263726 variant in psoriasis susceptibility 1 candidate 1 gene as a surrogate marker [36] that is in absolute linkage disequilibrium with HLA-B*5801 [37].…”

Section: Allopurinolmentioning

confidence: 99%

Update on the Genetic Basis of Drug Hypersensitivity Reactions

Jurado‐Escobar¹,

Perkins²,

García‐Martín³

et al. 2017

J Investig Allergol Clin Immunol

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Drug hypersensitivity reactions (DHRs) are unpredictable, complex responses to medicines in predisposed individuals. They represent a major health problem owing to the number of patients affected and the severity of the clinical conditions they can induce. In addition to environmental factors, the underlying mechanisms of DHRs are also influenced by genetic factors, although considerable gaps remain in our knowledge. Therefore, further study of the genetics of DHRs is necessary to shed light on their underlying mechanisms. In this manuscript, we provide an update on the genetic basis of the most frequent types of DHRs, including those mediated by immunological and nonimmunological mechanisms. For the first group, we will focus on immediate reactions to β-lactam antibiotics, which are associated mainly with the IgE pathway (IL13, IL4R, LGALS3, and NOD2) and antigen presentation (HLA-DRA), and nonimmediate reactions to allopurinol, anticonvulsants, antibiotics, and antiretrovirals, which are often associated with polymorphisms in the HLA system. For the second group, we will focus on nonsteroidal anti-inflammatory drugs, which are mostly associated with genetic variants in enzymes and receptors from the arachidonic acid pathway (eg, ALOX5, ALOX5AP, PTGDR, and CYSLTR1). The information provided here will be of interest for medical practitioners from a range of disciplines who come across these reactions in their clinical practice, as well as for allergologists. Key words: Drug hypersensitivity. Immunologically-mediated reactions. Cross-hypersensitivity. Single-nucleotide polymorphisms. Genomewide association study. ResumenLas reacciones de hipersensibilidad a fármacos (RHFs) son respuestas no predecibles que se producen en algunos sujetos y que representan un serio problema de salud pública debido al número de pacientes implicados y a su potencial gravedad. Además de factores ambientales, en estas reacciones también participan factores genéticos, cuya influencia está, en la mayoría de los casos, aún por dilucidar. En este manuscrito describiremos la información disponible sobre la base genética de los tipos más frecuentes de RHFs, tanto de las mediadas inmunológicamente como de aquellas en las que no se requiere reconocimiento antigénico. En el primer grupo nos ocuparemos de las reacciones inmediatas a antibióticos β-lactámicos, que han sido asociadas con variantes relacionadas con la IgE (IL13, IL4R, LGALS3 y NOD2) y la presentación antigénica (HLA-DRA), y de las reacciones no inmediatas a diferentes grupos de medicamentos (alopurinol, anticonvulsivos, antibióticos y antiretrovirales), relacionadas fundamentalmente con polimorfismos en el sistema HLA. En el segundo grupo nos centraremos en las reacciones inducidas por antiinflamatorios no esteroideos (AINE), que han sido asociadas básicamente con variantes en enzimas y receptores de la vía del ácido araquidónico (ALOX5, ALOX5AP, PTGDR y CYSLTR1, entre otros). Esta revisión puede ser de interés no sólo para alergólogos, sino para los profesionales de otras ...

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Section: Allopurinolmentioning

confidence: 99%

Update on the Genetic Basis of Drug Hypersensitivity Reactions

Jurado‐Escobar¹,

Perkins²,

García‐Martín³

et al. 2017

J Investig Allergol Clin Immunol

View full text Add to dashboard Cite

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“…For example, certain HLA-types such as, HLA-B*1502, HLA-A*3101 and HLA-B*5801 have been to be linked with TEN development when exposed to specific drugs. [17][18][19] As sepsis is the most dreadful complication, drugs that are effective against multi drug resistant bacteria are commonly administered. Currently, no treatment modality has been established as a standard for these patients.…”

Section: Discussionmentioning

confidence: 99%

Amoxicillin induced toxic epidermal necrolysis: a case report

Zachariah

Rao

Noronha

et al. 2016

Int J Basic Clin Pharmacol

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“…Hung et al [8] published the first report of a strong association between allopurinol-induced severe cutaneous adverse reactions [including StevensJohnson syndrome (SJS) and toxic epidermal necrolysis (TEN)] and human leukocyte antigen (HLA)-B*58:01 in Han Chinese patients. A strong association between HLA-B*58:01 and allopurinol-induced SJS and TEN has been reported in Japanese patients [9]. Furthermore, druginduced liver injury (DILI) is the most frequently reported adverse drug event in Japan [10].…”

Section: Discussionmentioning

confidence: 99%

Acute severe liver dysfunction induced by febuxostat in a patient undergoing hemodialysis

Ueda

Miyazawa

et al. 2014

CEN Case Rep

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A 58-year-old man with chronic kidney disease (CKD) was admitted to our hospital for hemodialysis (HD) therapy. He had been administered allopurinol (100 mg/ day) before hospitalization, and we replaced it with febuxostat (10 mg/day), a new xanthine oxidase inhibitor. Levels of aspartate aminotransferase, alanine transaminase (ALT), and lactate dehydrogenase were within the normal ranges in the morning before febuxostat administration, but 6 h after administration, these parameters increased markedly to approximately 10 times the levels before administration. Although we stopped administering febuxostat, his serum potassium levels increased at a rate of 1 mmol/L every 12 h, and he had to undergo HD daily to lower the serum potassium levels. The levels of liver function test parameters peaked on the fourth hospital day (ALT, 1134 IU/L; AST, 1485 IU/L; and LDH, 1869 IU/L) and recovered to normal ranges on the 13th hospital day. In this case, febuxostat appeared to have a relationship with acute liver dysfunction in the clinical course. Therefore, it would be important to check liver function test parameters frequently after febuxostat initiation and also to initiate a lower than usual dose of febuxostat, especially in patients with CKD and those who are undergoing HD.

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A whole-genome association study of major determinants for allopurinol-related Stevens–Johnson syndrome and toxic epidermal necrolysis in Japanese patients

Cited by 164 publications

References 41 publications

Update on the Genetic Basis of Drug Hypersensitivity Reactions

Update on the Genetic Basis of Drug Hypersensitivity Reactions

Amoxicillin induced toxic epidermal necrolysis: a case report

Acute severe liver dysfunction induced by febuxostat in a patient undergoing hemodialysis

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