Risk Of Gout Research Articles

Risk of Parkinson\u2019s disease following gout: a population-based retrospective cohort study in Taiwan

BackgroundThe progressive neurodegenerative disorder Parkinson disease (PD) is well-established as the second most common neurodegenerative disease. Associations between the sequential risk of PD and gout have been addressed in other studies, but findings have been inconclusive. Accordingly, we executed the present study with the purpose of assessing PD risk in patients with gout.MethodsFrom Taiwan’s National Health Insurance Research Database, we identified the data of patients newly diagnosed as having gout between January 1, 2000 and December 1, 2000. A cohort of patients without gout, matched for sex and age, was constructed for comparison. Hazard ratios (HRs) and the incidence rate of subsequent PD were calculated for both cohorts and separately for male and female groups. The gout and comparison cohorts consisted of 7900 patients each.ResultsThe HR for PD was not significantly higher in the gout cohort compared with the control cohort (HR 1.01, 95% confidence interval [CI], 0.93–1.31, P = .268), even after adjustment for age, urbanization, monthly income, sex, and comorbidities. We did not observe gender differences in the gout–PD association (male: HR 1.01, 95% CI, 0.88–1.36, P = .400; female: HR 1.11, 95% CI, 0.84–1.46, P = .466).ConclusionsOur study identified that there was no protective effect of gout for the risk of PD in the Taiwanese population.

Effects of Low-Fat, Mediterranean, or Low-Carbohydrate Weight Loss Diets on Serum Urate and Cardiometabolic Risk Factors: A Secondary Analysis of the Dietary Intervention Randomized Controlled Trial (DIRECT).

Weight loss diets may reduce serum urate (SU) by lowering insulin resistance while providing cardiometabolic benefits, something urate-lowering drugs have not shown in trials. We aimed to examine the effects of weight loss diets on SU and cardiometabolic risk factors. This secondary study of the Dietary Intervention Randomized Controlled Trial (DIRECT) used stored samples from 235 participants with moderate obesity randomly assigned to low-fat, restricted-calorie (n = 85); Mediterranean, restricted-calorie (n = 76); or low-carbohydrate, non-restricted-calorie (n = 74) diets. We examined SU changes at 6 and 24 months overall and among those with hyperuricemia (SU ≥416 μmol/L), a relevant subgroup at risk for gout. Among all participants, average SU decreases were 48 μmol/L at 6 months and 18 μmol/L at 24 months, with no differences between diets (P > 0.05). Body weight, HDL cholesterol (HDL-C), total cholesterol:HDL-C ratio, triglycerides, and insulin concentrations also improved in all three groups (P < 0.05 at 6 months). Adjusting for covariates, changes in weight and fasting plasma insulin concentrations remained associated with SU changes (P < 0.05). SU reductions among those with hyperuricemia were 113, 119, and 143 μmol/L at 6 months for low-fat, Mediterranean, and low-carbohydrate diets (all P for within-group comparison < 0.001; P > 0.05 for between-group comparisons) and 65, 77, and 83 μmol/L, respectively, at 24 months (all P for within-group comparison < 0.01; P > 0.05 for between-group comparisons). Nonpurine-focused weight loss diets may simultaneously improve SU and cardiovascular risk factors likely mediated by reducing adiposity and insulin resistance. These dietary options could provide personalized pathways to suit patient comorbidity and preferences for adherence.

Evaluation of the Influence of Genetic Variants of SLC2A9 (GLUT9) and SLC22A12 (URAT1) on the Development of Hyperuricemia and Gout.

Urate transporters, which are located in the kidneys, significantly affect the level of uric acid in the body. We looked at genetic variants of genes encoding the major reabsorption proteins GLUT9 (SLC2A9) and URAT1 (SLC22A12) and their association with hyperuricemia and gout. In a cohort of 250 individuals with primary hyperuricemia and gout, we used direct sequencing to examine the SLC22A12 and SLC2A9 genes. Identified variants were evaluated in relation to clinical data, biochemical parameters, metabolic syndrome criteria, and our previous analysis of the major secretory urate transporter ABCG2. We detected seven nonsynonymous variants of SLC2A9. There were no nonsynonymous variants of SLC22A12. Eleven variants of SLC2A9 and two variants of SLC22A12 were significantly more common in our cohort than in the European population (p = 0), while variants p.V282I and c.1002+78A>G had a low frequency in our cohort (p = 0). Since the association between variants and the level of uric acid was not demonstrated, the influence of variants on the development of hyperuricemia and gout should be evaluated with caution. However, consistent with the findings of other studies, our data suggest that p.V282I and c.1002+78A>G (SLC2A9) reduce the risk of gout, while p.N82N (SLC22A12) increases the risk.

Diabetes Mellitus Is Associated with a Lower Risk of Gout: A Meta-Analysis of Observational Studies.

Aims Although several epidemiological studies have investigated the relationship between diabetes mellitus (DM) and the risk of gout, the results are inconsistent. Therefore, we systematically retrospected available observational studies to clarify the impact of DM on the risk of gout. Methods Embase, PubMed, Cochrane Library, Scopus, Web of Science, and China National Knowledge Infrastructure were searched for relevant articles from inception to 2 March 2020. The quality of the included studies was assessed using the Newcastle-Ottawa Quality Assessment Scale. The multivariate adjusted relative risks (aRR) and corresponding 95% confidence intervals (CI) were pooled based on a random-effect model. Cochran's Q test and I2 were used to evaluate heterogeneity. Results Five studies involving 863,755 participants were included in our meta-analysis. DM was associated with a lower risk of gout (aRR: 0.66; 95% CI: 0.59 to 0.73) but had a high heterogeneity (I2 = 89.2%). Metaregression analysis revealed that the types of DM were the source of heterogeneity. Subgroup analysis by types of DM showed that the risk of gout was significantly lower in type 1 DM (T1DM) (aRR: 0.42; 95% CI: 0.28 to 0.63) than in type 2 DM (T2DM) (aRR: 0.72; 95% CI: 0.70 to 0.74). Furthermore, when stratified according to gender in DM, sex-specific association was found. The inverse association was observed in males only (aRR: 0.57; 95% CI: 0.43 to 0.77) and not in females (aRR: 0.96; 95% CI: 0.87 to 1.05). Further stratified based on glycated hemoglobin (HbA1c) levels in DM, raised A1C levels were associated with a reduced risk of gout in patients with DM. Conclusions This meta-analysis indicated that DM was related to a lower risk of gout, and the protective effect of DM on the risk of gout was stronger in males, T1DM, or DM with high HbA1c levels. However, more prospective cohort studies are required to confirm these results.

Occupational exposure to inorganic dust and risk of gout: a population-based study

BackgroundRisk factors operating independently of hyperuricemia could be of importance in determining why only a minority of people with hyperuricemia develop gout. Exposure to inorganic dust has been linked to...

Effect modification of hyperlipidemia and hypertension on the association between type 2 diabetes and gout

AimsWe evaluated the association between type 2 diabetes and gout by a retrospective cohort study. MethodsData of 17,259 male and 18,318 female patients with type 2 diabetes were retrieved for the 1998–2010 period. These patients were matched to a comparison group (n=34,518 and n=36,636, respectively) in a 1:2 ratio by age and region. ResultsWe found that patients with type 2 diabetes after adjustment for hyperlipidemia and hypertension had a lower risk of incident gout than the matched population (incidence rate ratio, men: 0.39 [95% CI: 0.36–0.42]; women: 0.78 [0.72–0.84]). Specifically, type 2 diabetes alone without hyperlipidemia and hypertension was associated with a reduced risk of incident gout in men (adjusted relative risk [RR]: 0.29, 95% CI: 0.22–0.39), but not in women (0.86, 95% CI: 0.55–1.36). We found that insulin users with hyperlipidemia and hypertension associated with risk of incident gout and no sex-specific differences were noted (adjusted RR, men: 1.28 [95% CI: 1.11–1.48]; women: 1.32 [95% CI: 1.14–1.53]). Specifically, insulin users alone without hyperlipidemia and hypertension were not statistically significantly associated with gout risk (P≥.0954). ConclusionsThe results of this study indicated that hyperlipidemia and hypertension modified the association between type 2 diabetes and gout.

Global epidemiology of gout: prevalence, incidence, treatment patterns and risk factors.

Gout is the most common inflammatory arthritis and occurs when hyperuricaemia, sustained elevation of serum urate levels resulting in supersaturation of body tissues with urate, leads to the formation and deposition of monosodium urate crystals in and around the joints. Recent reports of the prevalence and incidence of gout vary widely according to the population studied and methods employed but range from a prevalence of <1% to 6.8% and an incidence of 0.58-2.89 per 1,000 person-years. Gout is more prevalent in men than in women, with increasing age, and in some ethnic groups. Despite rising prevalence and incidence, suboptimal management of gout continues in many countries. Typically, only a third to half of patients with gout receive urate-loweringtherapy, which is a definitive, curative treatment, and fewer than a half of patients adhere to treatment. Many gout risk factors exist, including obesity, dietary factors and comorbid conditions. As well as a firmly established increased risk of cardiovascular disease and chronic kidney disease in those with gout, novel associations of gout with other comorbidities have been reported, including erectile dysfunction, atrial fibrillation, obstructive sleep apnoea, osteoporosis and venous thromboembolism. Discrete patterns of comorbidity clustering in individuals with gout have been described. Increasing prevalence and incidence of obesity and comorbidities are likely to contribute substantially to the rising burden of gout.

Do Serum Urate-Associated Genetic Variants Differentially Contribute to Gout Risk According to Body Mass Index? Analysis of the UK Biobank.

To examine whether urate-associated genetic variants differ in their influence on gout risk according to body mass index (BMI). This research was conducted using the UK Biobank Resource (n = 358,728). Participants were divided into 3 groups: BMI <25 kg/m2 (low/normal), BMI ≥25 kg/m2 -<30 kg/m2 (overweight), and BMI ≥30 kg/m2 (obese). Gene-BMI interactions for gout association were tested by logistic regression using a urate genetic risk score (GRS). Compared to participants with a GRS less than the mean, the prevalence of gout was higher in those with a GRS greater than or equal to the mean in the low/normal BMI group (0.27% versus 0.77%), in the overweight BMI group (1.02% versus 3.02%), and in the obese BMI group (2.49% versus 6.23%). A GRS greater than or equal to the mean was positively associated with gout compared to a GRS less than the mean in the low/normal BMI group (odds ratio [OR] 2.89 [95% confidence interval (95% CI) 2.42-3.47]), in the overweight BMI group (OR 3.09 [95% CI 2.84-3.36]), and in the obese BMI group (OR 2.65 [95% CI 2.46-2.86]). There was a mildly attenuated effect of the GRS on gout risk in the obese BMI group compared to the overweight BMI group, but no difference in the effect of the GRS between the low/normal BMI and overweight BMI groups, nor between the low/normal BMI and obese BMI groups. The association of a urate GRS with gout is mildly attenuated in obese individuals compared to overweight individuals. However, genetic variants have a strong effect on gout risk in those with overweight and obese BMIs, with an effect similar to that observed in low/normal BMI.

The effects of antihypertensive class on gout in older adults: secondary analysis of the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial.

Gout is a common complication of blood pressure management and a frequently cited cause of medication nonadherence. Little trial evidence exists to inform antihypertensive selection with regard to gout risk. The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) was a randomized clinical trial on the effects of first-step hypertension therapy with amlodipine, chlorthalidone, or lisinopril on fatal coronary heart disease or nonfatal myocardial infarction (1994-2002). Trial participants were linked to CMS and VA gout claims (ICD9 274.XX). We determined the effect of drug assignment on gout with Cox regression models. We also determined the adjusted association of self-reported atenolol use (ascertained at the 1-month visit for indications other than hypertension) with gout. Claims were linked to 23 964 participants (mean age 69.8 ± 6.8 years, 45% women, 31% black). Atenolol use was reported by 928 participants at the 1-month visit. Over a mean follow-up of 4.9 years, we documented 597 gout claims. Amlodipine reduced the risk of gout by 37% (hazard ratio 0.63; 95% CI 0.51--0.78) compared with chlorthalidone and by 26% (hazard ratio 0.74; 95% CI 0.58--0.94) compared with lisinopril. Lisinopril nonsignificantly lowered gout risk compared with chlorthalidone (hazard ratio 0.85; 95% CI 0.70--1.03). Atenolol use was not associated with gout risk (adjusted hazard ratio 1.18; 95% CI 0.78--1.80). Gout risk reduction was primarily observed after 1 year of follow-up. Amlodipine lowered long-term gout risk compared with lisinopril or chlorthalidone. This finding may be useful in cases where gout risk is a principal concern among patients being treated for hypertension.This trial is registered at clinicaltrials.gov, number: NCT00000542.

Association Between Gout and Injury Risk: A National Retrospective Cohort Study.

The association between gout and injury remains unclear. This study aimed to investigate the injury risk in patients with gout. Using the Longitudinal Health Insurance Database (LHID) from 2000 to 2010 in Taiwan, patients with gout (group CFG) and those without gout (group C) were enrolled for further analysis. The CFG group was separated into two subgroups (with and without medication) to determine whether the risk of injury was reduced with drug intervention. The follow-up period was defined as the time from the initial diagnosis of gout to the date of injury. A total of 257,442 individuals were enrolled in this study, with 85,814 people in group CFG and 171,628 people in group C. Using Cox regression analysis, group CFG showed a significant increase in the risk of injury. Traffic injuries, poisoning, falls, crushing/cutting/piercing injury, and suicides were prominent among these injuries. Furthermore, when urate-lowing drugs were used to treat the CFG group, there were no significant differences in the occurrence of injury. Patients with gout had an increased risk of injury overall, and drug intervention did not lower the risk of injury in these patients.

Obstructive sleep apnea and the risk of gout: a population-based case-control study

BackgroundPatients with obstructive sleep apnea (OSA) might be at risk of gout because of pathophysiological mechanisms that can lead to hyperuricemia and eventually gout or because of shared risk factors between both diseases. The objective of the present study was to investigate the risk of gout in patients with OSA.MethodsA population-based case-control study using the UK Clinical Practice Research Datalink GOLD including all patients aged 40 years and older with a first diagnosis of gout between 1987 and 2014. Gout cases were matched by year of birth, sex, and practice to non-gout controls. Conditional logistic regression estimated the risk of gout with an earlier diagnosis of OSA. Analyses were adjusted for lifestyle factors, comorbidities, and recent drug use.ResultsOne hundred eleven thousand five hundred nine cases were matched with 210,241 controls. Patients with OSA were at increased risk of gout (OR 1.86; 95%CI (1.71–2.02). However, this association disappeared (OR 1.05; 95% CI 0.96–1.16) after adjustment for smoking status, body mass index (BMI), alcohol use, a history of heart failure, diabetes mellitus, renal function, and recent use of diuretics and other medications. Among females with OSA and patients with OSA associated with heart failure, renal impairment, or higher BMI, the risk of gout was however still increased when compared to the total control population.ConclusionThis study showed that the observed association between OSA and gout disappeared after adjustment.

Lowering the risk of gout: Another benefits from the use of sodium-glucose cotransporter2 inhibitors.

Lowering the risk of gout: Another benefits from the use of sodium-glucose cotransporter2 inhibitors.

Socioeconomic differences in hyperuricemia and gout: a systematic review and meta-analysis.

There are multiple risk factors have different influence on the disorder. However, the risk of hyperuricemia and gout in different socioeconomic status (SES) remains unclear. Recent studies provided results that contradicted to former studies. We aimed to perform a systematic review and meta-analysis of evidence to date and to assess the associations between SES and hyperuricemia or gout worldwide. We searched MEDLINE, EMBASE, and Web of Science databases to identify studies that investigated the association between SES and hyperuricemia or gout. Studies that presented risk estimates were included. We conducted meta-analyses using random effects to combine unadjusted and adjusted effect estimates. Data from 14 studies were included, 9 provided data about hyperuricemia and 5 provided gout. Overall, there was an association between higher educational level and a higher risk of hyperuricemia (POR = 1.38, 95% CI 1.04-1.73) but lower risk of gout (POR = 0.59, 95% CI 0.47-0.71). Subgroup meta-analysis showed no association between all SES measures and hyperuricemia or gout in males or females. Our study suggested that the associations between SES and hyperuricemia gout are different. Higher educational level was related to a higher risk of hyperuricemia but lower risk of gout. Given the limitations of our study, future studies are needed to investigate specific mechanisms underlying the relationship among SES differences in hyperuricemia and gout. Strategies to prevent and control SES inequalities in hyperuricemia and gout should be explored and adopted.

Polymorphism in folate cycle genes in patients with gout in the Russian population of Trans-Baikal Territory

Objective. To study the frequency distribution of genotypes and alleles of polymorphic loci of folate cycle genes ( MTHFR C677T, MTHFR A1298G, MTR A2756G, MTRR A66G) in patients with gout and to evaluate their association with the risk of the disease. Material and Methods. 80 patients (69 men and 11 women) with gout were examined. The diagnosis of gout was made according to the classification criteria ACR/EULAR, 2015. DNA isolated from white blood cells of whole peripheral blood was the material used in the genetic analyses. All patients were genotyped to detect polymorphisms of the MTHFR C677T, MTHFR A1298G, MTR A2756G, MTRR A66G gene loci. Statistical data processing was performed using the software package Statistiсa 10.0. Results. Genetic polymorphisms of the MTHFR C677T and MTR A2756G genes are involved in the development of gout in individuals of Russian ethnicity in the population of the Trans-Baikal Territory. Minor T allele (χ 2 = 4.65, p = 0.03, OR = 1.83, CI95% = 1.05–3.17) and the T/T genotype (χ 2 = 6.5, p = 0.01, OR = 5.94, CI95% = 1.3–27.00) of the C677T locus of the MTHFR gene, minor G allele (χ 2 = 6.46, p = 0.01, OR = 2.38, CI95% = 1.2–4.69) and the A/G genotype of the MTR A2756G gene (χ 2 = 5.78, p = 0.01, OR = 2.66, CI95% = 1.18–5.98 ) were identified as alleles and genotypes having increased risk for developing gout. While the C allele (χ 2 = 4.65, p = 0.03, OR = 0.55, CI95% = 0.31–0.94) of the MTHFR C677T gene, and allele A (χ 2 = 6.46, p = 0.01, OR = 0.42, CI95% = 0.21–0.83) and genotype A/A (χ 2 = 7.58, p = 0.006, OR = 0.33, CI95% = 0.15–0.74) of the A2756G locus of the MTR gene were determined as genotypes and alleles having a protective effect. Conclusion. Significant differences were found in the frequency distribution of genotypes and alleles of the MTHFR C677T and MTR A2756G genes in gout patients compared with the control group. The presence of minor T allele and the T/T genotype of MTHFR C677T gene, the minor G allele and the A/G genotype of MTR A2756G gene was associated with an increased risk of gout. In contrast, the carriage of the C allele of MTHFR C677T gene, allele A and the genotype A/A of MTR A2756G gene had a potentially protective effect.

Dapansutrile: a new hope?

The beginning of the 21st century was a time of mini-Renaissance in the science and care of gout. A PubMed Search of the term “gout” retrieves 159 papers in 1999, but 1005 papers by 2019. Key discoveries have driven, and in turn been driven by, increasing interest in gout. Epidemiological studies showed that gout prevalence has increased substantially since the 1970s, and gout is now the most common inflammatory arthritis.1 Genetic studies uncovered a series of renal transporters that are largely determinant of serum urate levels and subsequently the risk of gout.

Differential DNA Methylation of Networked Signaling, Transcriptional, Innate and Adaptive Immunity, and Osteoclastogenesis Genes and Pathways in Gout.

In gout, autoinflammatory responses to urate crystals promote acute arthritis flares, but the pathogeneses of tophi, chronic synovitis, and erosion are less well understood. Defining the pathways of epigenomic immunity training can reveal novel pathogenetic factors and biomarkers. The present study was undertaken to seminally probe differential DNA methylation patterns utilizing epigenome-wide analyses in patients with gout. Peripheral blood mononuclear cells (PBMCs) were obtained from a San Diego cohort of patients with gout (n = 16) and individually matched healthy controls (n = 14). PBMC methylome data were processed with ChAMP package in R. ENCODE data and Taiji data analysis software were used to analyze transcription factor (TF)-gene networks. As an independent validation cohort, whole blood DNA samples from New Zealand Māori subjects (n = 13 patients with gout, n = 16 control subjects without gout) were analyzed. Differentially methylated loci clearly separated gout patients from controls, as determined by hierarchical clustering and principal components analyses. IL23R, which mediates granuloma formation and cell invasion, was identified as one of the multiple differentially methylated gout risk genes. Epigenome-wide analyses revealed differential methylome pathway enrichment for B and T cell receptor signaling, Th17 cell differentiation and interleukin-17 signaling, convergent longevity regulation, circadian entrainment, and AMP-activated protein kinase signaling, which are pathways that impact inflammation via insulin-like growth factor 1 receptor, phosphatidylinositol 3-kinase/Akt, NF-κB, mechanistic target of rapamycin signaling, and autophagy. The gout cohorts overlapped for 37 (52.9%) of the 70 TFs with hypomethylated sequence enrichment and for 30 (78.9%) of the 38 enriched KEGG pathways identified via TFs. Evidence of shared differentially methylated gout TF-gene networks, including the NF-κB activation-limiting TFs MEF2C and NFATC2, pointed to osteoclast differentiation as the most strongly weighted differentially methylated pathway that overlapped in both gout cohorts. These findings of differential DNA methylation of networked signaling, transcriptional, innate and adaptive immunity, and osteoclastogenesis genes and pathways suggest that they could serve as novel therapeutic targets in the management of flares, tophi, chronic synovitis, and bone erosion in patients with gout.

Pleiotropic effect of the ABCG2 gene in gout: involvement in serum urate levels and progression from hyperuricemia to gout

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.

Effect of tart cherry juice on risk of gout attacks: protocol for a randomised controlled trial

IntroductionGout is a painful form of inflammatory arthritis associated with several comorbidities, particularly cardiovascular disease. Cherries, which are rich in anti-inflammatory and antioxidative bioactive compounds, are proposed to be efficacious...

Effect of mixing lard with soybean oil in cooking on hepatic antioxidative ability and renal metabolic activity

A simulate daily oriental dietary pattern (a blend of lard and soybean oil) was performed in this research to investigate influence on liver and kidney function. Sixty mice were randomly divided into 6 groups with diets of different fat added oils respectively for 12 weeks. Malondialdehyde and uric acid contents in mice fed with blended oil were significantly lower than in those fed only with soybean oil and lard due to the improved activities of antioxidant enzymes. Daily use of a blend of lard with soybean oil significantly increased antioxidant capacity, reduced lipid peroxidation of liver and serum uric acid production, thus protected liver and renal function. It also suggests that the oriental dietary pattern might reduce the risk of gout.

The prevalence of the gout-associated polymorphism rs2231142 G>T in ABCG2 in a pregnant female Filipino cohort.

Gout is a metabolic disorder and one of the most common arthritic conditions. Hyperuricemia is the hallmark of developing gout and mostly caused by uric acid underexcretion. Gout disproportionately affects people of specific races and ethnicities. Filipinos are the second-largest Asian population in the USA and reported to have a higher prevalence of gout and hyperuricemia than non-Filipino counterparts and Filipinos residing in the Philippines. The genetic polymorphism rs2231142 G>T in the ABCG2 has been strongly associated with hyperuricemia and gout across multiple populations. However, the prevalence of this variant in Filipinos is unknown. Therefore, assessing the prevalence of this variant may provide insights on the high prevalence of hyperuricemia and gout in Filipinos. A total of 190 DNA samples from pregnant females who self-identified as a Filipino from the Hawaii Biorepository Bank were genotyped for rs2231142 G>T in the ABCG2. The prevalence of the gout risk allele (T) (46%) was significantly higher in Filipinos than in samples of Caucasians (12%, p < 0.001), Han Chinese (29%, p = 0.014), and African Americans (3%, p < 0.001). Similarly, the prevalence of the gout-risk genotype (TT) (21%) was significantly higher in Filipinos than in samples of Caucasians (1%, p < 0.001), Han Chinese (9%, p = 0.002), and African Americans (0.1%, p < 0.001). Though there were no gout cases in this cohort, these findings are suggestive of a genetic basis to the high prevalence of hyperuricemia and gout in Filipinos. This might also explain the reported reduced urinary uric acid excretion in Filipinos compared with Caucasians. Key Points • The Filipinos have the highest prevalence of the gout-associated risk allele (T) of the rs2231142 G>T in ABCG2. • The high prevalence of the risk allele (T) of the rs2231142 G>T in ABCG2 may partly explain the reduced urinary urate excretion and early-onset gout in Filipinos. • The high prevalence of the risk allele (T) of the rs2231142 G > T in ABCG2 may predispose Filipinos to hyperuricemia and gout when acculturated to high-purine diet.