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. 2019 Jan 16:156:4.
doi: 10.1186/s41065-018-0078-0. eCollection 2019.

Common variants in the SLC28A2 gene are associated with serum uric acid level and hyperuricemia and gout in Han Chinese

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Common variants in the SLC28A2 gene are associated with serum uric acid level and hyperuricemia and gout in Han Chinese

Zhaowei Zhou et al. Hereditas. .

Abstract

Background: Serum uric acid (SUA), hyperuricemia (HUA) and gout are complex traits with relatively high heritability. This study aims to identify whether a candidate gene, SLC28A2, exerts susceptibility for SUA fluctuation and incidence of HUA and gout in the Han Chinese population.

Results: Three sample sets of 1376 gout patients, 1290 long-term HUA subjects (no gout attack) and 1349 normouricemic controls were recruited for this study. Eight polymorphisms in the SLC28A2 gene were genotyped using the ligase detection reaction-polymerase chain reaction (LDR-PCR) technology. Rs16941238 showed the most significant associations with SUA level (minor allele "A", BETA = - 13.84 μmol/L, P = 0.0041, Pperm = 0.0042) and HUA (OR = 0.7734, P = 0.0033, Pperm = 0.0020), but not with gout (OR = 0.8801, P = 0.1315, Pperm = 0.1491). Rs2271437 was significantly associated with gout (minor allele "G", OR = 1.387, P = 0.0277, Pperm = 0.0288), and was further confirmed in the meta-analysis with the previously published gout GWAS dataset (OR = 1.3221, P = 0.0089). Each variant basically conferred consistent OR direction on gout and HUA, compared with the normouricemic control.

Conclusions: Our findings support the associations of the SLC28A2 gene with the SUA level, the HUA phenotype and gout in Han Chinese.

Keywords: Gout; Hyperuricemia (HUA); Polymorphisms; SLC28A2; Serum uric acid (SUA).

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Conflict of interest statement

The study was approved by the Ethics Committee of Shanghai Jiao Tong University and the Affiliated Hospital of Qingdao University, and in accordance with the principles of the Declaration of Helsinki. All participants gave their written informed consent to take part in the present study.Not applicable.The authors declare no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

Fig. 1
Fig. 1
Forest plot of the association between the seven SNPs and gout
Fig. 2
Fig. 2
Linkage disequilibrium plot of the eight SNPs in the samples of gout patients (a), HUA cohort (b), normouricemic controls (c) and the overall (d)

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