Journal
ARTHRITIS RESEARCH & THERAPY
Volume 13, Issue 3, Pages -Publisher
BIOMED CENTRAL LTD
DOI: 10.1186/ar3356
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Categories
Funding
- Health Research Council of New Zealand
- Arthritis New Zealand
- New Zealand National Heart Foundation
- National Heart, Lung and Blood Institute (NHLBI)
- Boston University
- NHLBI [N01-HC-55015, N01 HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021, N01-HC-55022, R01 HL087641, R01 HL59367, R01 HL086694]
- National Human Genome Research Institute [U01HG004402]
- National Institutes of Health (NIH) [HHSN268200625226C, UL1RR025005]
- DIVISION OF EPIDEMIOLOGY AND CLINICAL APPLICATIONS [N01HC055022, N01HC055018, N01HC055015, N01HC055019, N01HC055020, N01HC055016, N01HC055021] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [UL1RR025005] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL086694, R01HL087641, R01HL059367] Funding Source: NIH RePORTER
- NATIONAL HUMAN GENOME RESEARCH INSTITUTE [U01HG004402] Funding Source: NIH RePORTER
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Introduction: The C allele of the nonsynonymous Arg265His (rs3733591) variant of SLC2A9 confers risk for gout in Han Chinese, Solomon Island and Japanese samples, with a stronger role in tophaceous gout. There is no evidence for an association with gout in Caucasian populations. In the present study, we tested rs3733591 for association with gout in New Zealand (NZ) Maori, Pacific Island and Caucasian samples. Methods: Rs3733591 was genotyped across gout patients (n = 229, 232 and 327 NZ Maori, Pacific Island and Caucasian samples, respectively) and non-gout controls (n = 343, 174 and 638 Maori, Pacific Island and Caucasian samples, respectively). Further Caucasian sample sets consisting of 67 cases and 4,712 controls as well as 153 cases and 6,969 controls were obtained from the Framingham Heart Study and the Atherosclerosis Risk in Communities study, respectively. The Polynesian samples were analyzed according to Eastern and Western Polynesian ancestry. Results: No evidence for risk conferred by the C allele of rs3733591 with gout was found in the sample sets of NZ Maori (odd ratio (OR) = 0.98, P = 0.86), Eastern Polynesians (OR = 0.99, P = 0.92), Western Polynesians (OR = 1.16, P = 0.36) or combined Caucasians (OR = 1.15, P = 0.13). The C allele was significantly overrepresented in Maori tophaceous cases compared to cases without tophi (OR = 2.21, P = 0.008), but not in the other ancestral groupings. Conclusions: Noting that our study's power was limited for detecting weak genetic effects, we were unable to replicate associations of rs3733591 with gout in Eastern Polynesian, Western Polynesian and Caucasian samples. However, consistent with a previous study of Han Chinese and Solomon Island populations, our data suggest that rs3733591 could be a marker of severe gout in some populations. Our results also suggest that the effect of this variant is population-specific, further confirming population heterogeneity regarding the association of SLC2A9 with gout.
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