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


Journal

Arthritis research & therapy
ISSN: 1478-6362
Titre abrégé: Arthritis Res Ther
Pays: England
ID NLM: 101154438

Informations de publication

Date de publication:
03 08 2020
Historique:
received: 21 02 2020
accepted: 20 07 2020
entrez: 5 8 2020
pubmed: 5 8 2020
medline: 22 6 2021
Statut: epublish

Résumé

The aim of this study was to investigate risk factors for cutaneous adverse reactions (CARs) in Kinh Vietnamese. All patients were prospectively recruited in Ho Chi Minh City. Presence of the HLA-B*58:01 allele was determined by real-time PCR-sequence-specific amplification by using the PG5801 Detection Kit (Pharmigene, Taipei). Patients with severe (SCARs) and mild (MCARs) CARs and controls were compared for differences in features prospectively collected, and odds ratios (ORs) with 95% confidence intervals (CIs) were estimated. On comparing 32 patients with SCARs and 395 tolerant controls, we identified eight strong risk factors: increased age (OR 15.1 [95% CI 5.8-40.1], P < 0.0001), female sex (OR 333 [40-43,453], P < 0.0001), allopurinol for asymptomatic hyperuricemia (OR 955 [120-125,847], P < 0.0001), allopurinol starting dose > 150 mg (OR 316 [101-122], P < 0.0001), diuretics intake (OR 304 [35-40,018], P < 0.0001), eGFR < 60 ml/min/1.73 m This study confirmed 8 risk factors, including HLA-B*58:01, for SCARs and identified 3 risk factors for MCARs in Kinh Vietnamese. HLA-B*58:01 genotyping could guide the indication for allopurinol in Kinh Vietnamese patients with gout.

Identifiants

pubmed: 32746911
doi: 10.1186/s13075-020-02273-1
pii: 10.1186/s13075-020-02273-1
pmc: PMC7397637
doi:

Substances chimiques

Gout Suppressants 0
HLA-B Antigens 0
Allopurinol 63CZ7GJN5I

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

182

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Auteurs

Minh Duc Do (MD)

Center for Molecular Biomedicine, University of Medicine and Pharmacy, at Ho Chi Minh City, Vietnam.

Thao Phuong Mai (TP)

Department of Physiology, Pathophysiology and Immunology, Faculty of Medicine, University of Medicine and Pharmacy, Ho Chi Minh City, Vietnam.

Anh Duy Do (AD)

Department of Physiology, Pathophysiology and Immunology, Pham Ngoc Thach University of Medicine, Ho Chi Minh City, Vietnam.

Quang Dinh Nguyen (QD)

French Vietnamese Research Center on Gout and Chronic Diseases, Vien Gut Medical Centre, Ho Chi Minh City, Vietnam.

Nghia Hieu Le (NH)

French Vietnamese Research Center on Gout and Chronic Diseases, Vien Gut Medical Centre, Ho Chi Minh City, Vietnam.

Linh Gia Hoang Le (LGH)

Center for Molecular Biomedicine, University of Medicine and Pharmacy, at Ho Chi Minh City, Vietnam.

Vu Anh Hoang (VA)

Center for Molecular Biomedicine, University of Medicine and Pharmacy, at Ho Chi Minh City, Vietnam.

Anh Ngoc Le (AN)

Department of Scientific Research, Cho Ray Hospital, Ho Chi Minh City, Vietnam.

Hung Quoc Le (HQ)

Department of Tropical Disease, Cho Ray Hospital, Ho Chi Minh City, Vietnam.

Pascal Richette (P)

Université de Paris, U1132, INSERM, 75010, Paris, France.
Department of Rheumatology, AP-HP, Lariboisière hospital, 2 rue A. Paré, 75010, Paris, France.

Matthieu Resche-Rigon (M)

Université de Paris, ECSTRRA Team U1153, INSERM, 75010, Paris, France.
Department of Biostatistics, AP-HP, Saint-Louis hospital, 75010, Paris, France.

Thomas Bardin (T)

French Vietnamese Research Center on Gout and Chronic Diseases, Vien Gut Medical Centre, Ho Chi Minh City, Vietnam. thomas.bardin@aphp.fr.
Université de Paris, U1132, INSERM, 75010, Paris, France. thomas.bardin@aphp.fr.
Department of Rheumatology, AP-HP, Lariboisière hospital, 2 rue A. Paré, 75010, Paris, France. thomas.bardin@aphp.fr.

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