Literature DB >> 29653927

Racial/ethnic variation and risk factors for allopurinol-associated severe cutaneous adverse reactions: a cohort study.

Sarah F Keller1, Na Lu1, Kimberly G Blumenthal1, Sharan K Rai1, Chio Yokose1, Jee Woong J Choi1, Seoyoung C Kim2,3, Yuqing Zhang1, Hyon K Choi1.   

Abstract

OBJECTIVES: To examine associations of race/ethnicity and purported risk factors with hospitalised allopurinol-associated severe cutaneous adverse reactions (AASCARs).
METHODS: We used US Medicaid data to identify incident allopurinol users between 1999 and 2012. We examined the risk of hospitalised AASCARs according to race/ethnicity and purported key risk factors and calculated relative risks (RR).
RESULTS: Among 400 401 allopurinol initiators, we documented 203 hospitalised AASCAR cases (1 in 1972 initiators). The average AASCAR hospitalisation was 9.6 days and 43 individuals (21%) died. The multivariable-adjusted RRs for AASCARs among blacks, Asians and Native Hawaiians/Pacific Islanders compared with whites or Hispanics were 3.00 (95% CI 2.18 to 4.14), 3.03 (95% CI 1.72 to 5.34) and 6.68 (95% CI 4.37 to 10.22), respectively. Female sex, older age (≥60 years), chronic kidney disease and initial allopurinol dose (>100 mg/day) were independently associated with a 2.5-fold, 1.7-fold, 2.3-fold and 1.9-fold higher risk of AASCAR, respectively. In our combined demographic analysis, older women (≥60 years) of a high-risk race/ethnicity (blacks, Asians or Native Hawaiians/Pacific Islanders) had over a 12-fold higher risk of hospitalised AASCARs than younger men of a low-risk race/ethnicity (whites or Hispanics) (multivariable-adjusted RR, 12.25; 95% CI 6.46 to 23.25).
CONCLUSIONS: This racially diverse (yet mostly white) cohort study indicates that the risk of hospitalised AASCAR is rare overall, although blacks, Asians and Native Hawaiians/Pacific-Islanders have a substantially higher risk of hospitalised AASCARs, particularly among older women. These data also support the practice of initiating allopurinol at a low dose (eg, ≤100 mg/day). © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

Entities:  

Keywords:  epidemiology; gout; health services research

Mesh:

Substances:

Year:  2018        PMID: 29653927      PMCID: PMC6045437          DOI: 10.1136/annrheumdis-2017-212905

Source DB:  PubMed          Journal:  Ann Rheum Dis        ISSN: 0003-4967            Impact factor:   19.103


  25 in total

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4.  Allopurinol pharmacogenetics: assessment of potential clinical usefulness.

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5.  Insights into the poor prognosis of allopurinol-induced severe cutaneous adverse reactions: the impact of renal insufficiency, high plasma levels of oxypurinol and granulysin.

Authors:  Wen-Hung Chung; Wan-Chun Chang; Sophie L Stocker; Chiun-Gung Juo; Garry G Graham; Ming-Han H Lee; Kenneth M Williams; Ya-Chung Tian; Kuo-Chang Juan; Yeong-Jian Jan Wu; Chih-Hsun Yang; Chee-Jen Chang; Yu-Jr Lin; Richard O Day; Shuen-Iu Hung
Journal:  Ann Rheum Dis       Date:  2014-08-12       Impact factor: 19.103

6.  Severe cutaneous reactions requiring hospitalization in allopurinol initiators: a population-based cohort study.

Authors:  Seoyoung C Kim; Craig Newcomb; David Margolis; Jason Roy; Sean Hennessy
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7.  Positive and negative associations of HLA class I alleles with allopurinol-induced SCARs in Koreans.

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9.  Allopurinol is the most common cause of Stevens-Johnson syndrome and toxic epidermal necrolysis in Europe and Israel.

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Review 10.  Association of HLA-B*5801 allele and allopurinol-induced Stevens Johnson syndrome and toxic epidermal necrolysis: a systematic review and meta-analysis.

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6.  Risk of Acute Myocardial Infarction Among New Users of Allopurinol According to Serum Urate Level: A Nested Case-Control Study.

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9.  Risk factors for cutaneous reactions to allopurinol in Kinh Vietnamese: results from a case-control study.

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