Bisphenol A and its alternatives bisphenol S and F exposure with serum uric acid levels, hyperuricemia, and gout prevalence among US adults: a nationally representative cross-sectional study
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SUBMITTER: Jiang S
PROVIDER: S-EPMC10840165 | biostudies-literature | 2024 Jan
REPOSITORIES: biostudies-literature
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Project description:Urate transporter 1 (URAT1/SLC22A12), a urate transporter gene, is a causative gene for renal hypouricemia type 1. Among several reported nonsynonymous URAT1 variants, R90H (rs121907896) and W258X (rs121907892) are frequent causative mutations for renal hypouricemia. However, no case-control study has evaluated the relationship between gout and these two variants. Additionally, the effect size of these two variants on serum uric acid (SUA) levels remains to be clarified. Here, 1,993 primary gout patients and 4,902 health examination participants (3,305 males and 1,597 females) were genotyped with R90H and W258X. These URAT1 variants were not observed in any gout cases, while 174 subjects had the URAT1 variant in 2,499 health examination participants, respectively (P = 8.3 × 10(-46)). Moreover, in 4,902 health examination participants, the URAT1 nonfunctional variants significantly reduce the risk of hyperuricemia (P = 6.7 × 10(-19); risk ratio = 0.036 in males). Males, having 1 or 2 nonfunctional variants of URAT1, show a marked decrease of 2.19 or 5.42 mg/dl SUA, respectively. Similarly, females, having 1 or 2 nonfunctional variants, also evidence a decrease of 1.08 or 3.89 mg/dl SUA, respectively. We show that URAT1 nonfunctional variants are protective genetic factors for gout/hyperuricemia, and also demonstrated the sex-dependent effect size of these URAT1 variants on SUA (P for interaction = 1.5 × 10(-12)).
| S-EPMC4731750 | biostudies-literature
Project description:ObjectiveTo determine the nationwide prevalence of hyperuricemia in China and evaluate its trends and associated risk factors.MethodsUsing a multi-stage, stratified, cluster-randomized sampling design, two cross-sectional surveys (representative of national and provincial information) were conducted in 31 provinces (autonomous regions and municipalities) in mainland China, with 166, 861 Chinese adults in 2015-16 and 168, 351 in 2018-19. Serum uric acid (SUA) levels of all participants were measured after a >10-hour overnight fast. Hyperuricemia (HUA) was defined when SUA was >420 μmol/L. Prevalence estimates were weighted to represent the total population considering the complex sampling design. Multivariable logistic regression models was used to estimate factors associated with HUA.ResultsThe overall hyperuricemia prevalence in the Chinese adult population was 11.1% (95% confidence interval 10.3% to 11.8%) in 2015-16 and 14.0% (13.1% to 14.8%) in 2018-19; an alarming rise was observed in the three years. Hyperuricemia was more common in men with 19.3% (17.9% to 20.7%) in 2015-16 and 24.4% (23.0% to 25.8%) in 2018-19, although the prevalence also escalated from 2.8% (2.5% to 3.0%) in 2015-16 to 3.6% (3.2% to 4.0%) in 2018-19 in women. The hyperuricemia risk factors include the urban culture, settlement in the East, Zhuang descent, high education, heavy or frequent beer drinking, high red meat intake, physical inactivity, high body mass index, central obesity, hypertension, hyperlipidemia, and low glomerular filtration rate.ConclusionThe estimated hyperuricemia prevalence among Chinese adults was 14.0% in 2018-19; significant escalating trends were observed between 2015-16 and 2018-19.
| S-EPMC8858821 | biostudies-literature
Project description:BackgroundSerum 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.ResultsThree 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.ConclusionsOur findings support the associations of the SLC28A2 gene with the SUA level, the HUA phenotype and gout in Han Chinese.
| S-EPMC6335706 | biostudies-literature
Project description:The effects of serum retinol and α-tocopherol on serum uric acid levels have not been established, especially in Asian people. This study evaluated the independent associations of retinol and α-tocopherol with serum uric acid levels in the Korean population. We included 6023 participants aged ≥ 19 years from the Korean National Health and Nutrition Examination Survey (KNHANES). Serum retinol and α-tocopherol levels were divided into quintiles, and a multivariate linear regression model was used to evaluate the association of serum retinol and α-tocopherol levels with uric acid concentration. Additionally, we used multivariate logistic regression to examine the relationships between the levels of these micronutrients and hyperuricemia. Serum retinol levels were positively associated with uric acid concentrations in a dose-dependent fashion in both sexes (ptrend < 0.001); the difference in serum uric acid levels between the highest and lowest quintiles of retinol levels was 0.57 mg/dL in men and 0.54 mg/dL in women. In the multivariable logistic model, the hyperuricemia risk increased linearly with the increase in serum retinol level, regardless of sex (ptrend < 0.001). Although the serum α-tocopherol level appeared to be significantly associated with increased uric acid levels, this association was nullified after adjusting for serum retinol levels. Serum retinol levels were positively associated with serum uric acid levels and hyperuricemia in a dose-response fashion. Maintaining serum retinol concentrations under sub-toxic levels might be necessary to prevent hyperuricemia-related adverse health outcomes.
| S-EPMC7353330 | biostudies-literature
Project description:BackgroundEpidemiological evidence of the associations between metal exposure and gout-related outcomes (including serum uric acid [SUA], hyperuricemia and gout) is scarce. The aim of the study is to investigate the associations of metal exposure with SUA, hyperuricemia and gout in general adults.MethodsIn this study, the exposure to five blood metals (mercury, manganese, lead, cadmium and selenium) of general adults was analyzed based on the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2018 (n = 14,871). Linear, logistic and weighted quantile sum (WQS) regression models were applied to examine the associations of blood metals with gout-related outcomes. Possible dose-response relationships were analyzed through restricted cubic spline regression.ResultsCompared with the lowest quartile of blood metals, mercury (quartile 2 and 4), lead (quartile 2, 3, and 4) and selenium (quartile 2 and 4) were found to be positively correlated with SUA and hyperuricemia. Higher levels of mercury and lead were associated with gout, but only those in the fourth quartile had statistical significance (OR [95%CI]: 1.39 [1.10-1.75] and 1.905 [1.41-2.57]) respectively). The WQS index of the blood metals was independently correlated with SUA (β [95%CI]: 0.17 [0.13-0.20]), hyperuricemia (OR [95%CI]: 1.29 [1.16-1.42]) and gout (OR [95%CI]: 1.35 [1.15-1.58]). Among them, lead was the most heavily weighted component (weight = 0.589 for SUA, 0.482 for hyperuricemia, and 0.527 for gout). In addition, restricted cubic spline regression models showed a linear association of lead with the prevalence of hyperuricemia and gout.ConclusionOur results suggested that blood metal mixtures were positively associated with gout-related outcomes, with the greatest effect coming from lead.
| S-EPMC9755211 | biostudies-literature
Project description:BackgroundHyperuricemia has a suspected relationship with hypertension, metabolic syndrome, kidney disease, and cardiovascular disease. Endocrine disruptors may affect uric acid metabolism; however, few epidemiologic studies have been performed in children regarding newly developed bisphenol A (BPA) substitutes. We evaluated the associations between BPA, bisphenol S (BPS), and bisphenol F (BPF) exposure and serum uric acid concentrations in 6-year-old Korean children.MethodsFrom the Environment and Development of Children cohort study, six-year-old children (N = 489; 251 boys) who underwent an examination during 2015-2017 were included. Anthropometry, questionnaires, and biological samples were evaluated. BPA, BPS, and BPF levels were measured from spot urine samples, and log-transformed or categorized into groups for analysis. We constructed linear regression models adjusting for age, sex, urinary creatinine levels, body mass index z-scores, and estimated glomerular filtration rates.ResultsMean serum uric level was 4.2 mg dL-1 (0.8 SD) without sex-differences. Among the three bisphenols, higher BPS exposure was associated with increased serum uric acid concentrations (P-value for trend = 0.002). When BPS levels were categorized into three groups (non-detection < 0.02 μg L-1 vs. medium BPS; 0.02-0.05 μg L-1 vs. high BPS ≥ 0.05 μg L-1), the high BPS group showed higher serum uric acid concentrations (by 0.26 mg dL-1, P = 0.003) than the non-detection group after adjusting for covariates, which was significant in boys but not girls.DiscussionsUrinary BPS levels was positively associated with serum uric acid concentrations in 6-year-old children, and the association was more pronounced in boys. Considering the increasing use of BPS and concerning effect of hyperuricemia on health outcomes, their positive relationship should be investigated further.
| S-EPMC9202957 | biostudies-literature
Project description:ObjectivesTo explore pro-inflammatory cytokines status in the tear fluid of patients with hyperuricemia and gout and its association with uric acid level.MethodsA total of 58 control subjects, 58 hyperuricemia patients including 40 asymptomatic hyperuricemia and 18 gout participants were recruited in this study. For tear analysis, each patient's tears were collected using capillary action microcaps after stimulation. Tear uric acid levels were measured using chemiluminescence. Tear and serum interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) levels were measured using enzyme-linked immunosorbent assay. The correlation of serum and tear uric acid levels with IL-1β and TNF-α were determined.ResultsTear uric acid levels were significantly higher in hyperuricemia group (98.2 ± 51.5 vs. 42.7 ± 24.0 µmol/L, p < .001) than in controls group. IL-1β concentrations were significantly higher in hyperuricemia eyes compared to control eyes (210.2 ± 113.9 vs. 142.6 ± 29.8 pg/mL, p < .001). Multiple linear regression analysis showed that tear uric acid levels were independently positively associated with tear IL-1β concentrations (B = 0.192, p < .001). However, no significant correlations were found between serum or tear uric acid and TNF-α level. Moreover, there were no statistically differences of tear IL-1β and TNF-α levels between the asymptomatic hyperuricemia and gout groups.ConclusionsTear uric acid levels were higher in patients with hyperuricemia and gout than in controls. There was a significant positive correlation between tear uric acid value and tear IL-1β level, implying an interaction between hyperuricemia and ocular inflammation responses.
| S-EPMC10022423 | biostudies-literature
Project description:IntroductionSmoking status based solely on self-reporting is unreliable and might be inaccurate, particularly among women. This study investigated the association between urinary cotinine-verified smoking status and hyperuricemia in a nationwide Korean population.MethodsThis study included 5329 participants aged ≥19 years with information on smoking status, urine cotinine levels and serum uric acid. We determined smoking status according to self-reports and urinary cotinine levels. Multivariate linear regression analysis was used to measure the association between smoking exposure and serum uric acid levels. The effects of smoking on hyperuricemia were evaluated by multivariate logistic regression analysis.ResultsBiochemically verified active and passive smokers comprised 22% (38.7% of men and 8.8% of women) and 12.3% (11.9% of men and 12.6% of women) of the study population, respectively. While reclassification rate of active smokers was 1.4% in men, 31.8% of cotinine-verified female active smokers were self-reported never smokers. Higher uric acid levels were observed with increased tobacco exposure among women (p-trend=0.007) but not among men. After adjusting for confounders, the risk of hyperuricemia increased with tobacco exposure only in women (p-trend=0.016).ConclusionsCotinine-verified smoking status was associated with increased serum uric acid and hyperuricemia in a dose-response manner only in women. This study might provide evidence to support the importance of smoking cessation in women with gout and further studies are necessary to elucidate the underlying mechanism of the observed association.
| S-EPMC7557215 | biostudies-literature
Project description:ObjectivesThe present study evaluated the association of electronic cigarette (EC) exposure with serum uric acid (UA) level and hyperuricemia (HUA) using a nationally representative sample of South Korea.MethodsThis study included 10,692 participants (9,905, 609, and 178, never, ever, and current EC users, respectively). Urinary cotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) levels were used to determine conventional smoking exposure among EC users. The association between EC use and UA level was evaluated by linear regression analysis. Multivariable logistic regression analysis was used to assess the association between EC and HUA. Subgroup analysis confined to cotinine-verified active smokers was performed to address the association between the dual use of EC and combustible cigarettes and serum UA levels.ResultsThe serum UA level was highest among current EC users, followed by ever and never EC users. The prevalence of HUA was 26.2%, 19.3%, and 10.8% in current, ever, and never EC users, respectively. Although EC exposure was positively associated with HUA in a dose-dependent manner only in men (Ptrend = 0.04), a similar tendency was also observed in women with marginal significance (Ptrend = 0.102). The positive association of HUA with EC exposure was more apparent among dual users (odds ratio [OR] = 1.96, 95% confidence interval [CI]: 1.29-2.99) than among those who only smoked combustible cigarettes.ConclusionsEC exposure was associated with higher serum UA level and higher OR of HUA. The positive association between EC exposure and HUA was more prominent in dual users who concurrently consumed EC and combustible cigarettes.
| S-EPMC7920355 | biostudies-literature
Project description:BackgroundThe ABCG2 Q141K (rs2231142) and rs10011796 variants associate with hyperuricaemia (HU). The effect size of ABCG2 rs2231142 on urate is ~ 60% that of SLC2A9, yet the effect size on gout is greater. We tested the hypothesis that ABCG2 plays a role in the progression from HU to gout by testing for association of ABCG2 rs2231142 and rs10011796 with gout using HU controls.MethodsWe analysed 1699 European gout cases and 14,350 normouricemic (NU) and HU controls, and 912 New Zealand (NZ) Polynesian (divided into Eastern and Western Polynesian) gout cases and 696 controls. Association testing was performed using logistic and linear regression with multivariate adjusting for confounding variables.ResultsIn Europeans and Polynesians, the ABCG2 141K (T) allele was associated with gout using HU controls (OR = 1.85, P = 3.8E- 21 and ORmeta = 1.85, P = 1.3E- 03, respectively). There was evidence for an effect of 141K in determining HU in European (OR = 1.56, P = 1.7E- 18) but not in Polynesian (ORmeta = 1.49, P = 0.057). For SLC2A9 rs11942223, the T allele associated with gout in the presence of HU in European (OR = 1.37, P = 4.7E- 06), however significantly weaker than ABCG2 rs2231142 141K (PHet = 0.0023). In Western Polynesian and European, there was epistatic interaction between ABCG2 rs2231142 and rs10011796. Combining the presence of the 141K allele with the rs10011796 CC-genotype increased gout risk, in the presence of HU, 21.5-fold in Western Polynesian (P = 0.009) and 2.6-fold in European (P = 9.9E- 06). The 141K allele of ABCG2 associated with increased gout flare frequency in Polynesian (Pmeta = 2.5E- 03).ConclusionThese data are consistent with a role for ABCG2 141K in gout in the presence of established HU.
| S-EPMC7069001 | biostudies-literature