Hyperuricemia and Its Association with Osteoporosis in a Large Asian Cohort.
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ABSTRACT:
SUBMITTER: Li JY
PROVIDER: S-EPMC9182899 | biostudies-literature | 2022 May
REPOSITORIES: biostudies-literature
Publications
Hyperuricemia and Its Association with Osteoporosis in a Large Asian Cohort.
Li Jhong-You JY Lee Jia-In JI Lu Cheng-Chang CC Su Yu-De YD Chiu Chao-Tse CT Chen Szu-Chia SC Geng Jiun-Hung JH Chen Chung-Hwan CH
Nutrients 20220526 11
In this paper, we aimed to examine the protective role of hyperuricemia in the prevalence of osteoporosis in a large Asian cohort. A total of 119,037 participants from 29 recruitment centers in Taiwan were enrolled onto our study. Participants with serum uric acid greater than 7.0 mg/dL in men and 6.0 mg/dL in women were classified as the hyperuricemia group whereas the others were the control group. The mean age of all participants was 50; there were 23,114 subjects (19%) with hyperuricemia. Os ...[more]
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Project description:Objectives: Genetic variants and obesity are risk factors for hyperuricemia (HUA). Recent genome-wide association studies have identified ABCG2 rs2231142 as one of the most prominent genetic variants for HUA in an East Asian population. Nevertheless, no large-scale studies have demonstrated any interactive effects between this variant and obesity on serum urate level in Asians. This study aimed to determine the interaction of ABCG2 rs2231142 variant and body mass index (BMI) and its effect on risk of HUA in an East Asian population. Methods: The study was conducted using the Taiwan Biobank database, a population-based biomedical research database of patients with Taiwanese Han Chinese ancestry aged 30-70years between September 2014 and May 2017. Detailed physical information on participants were collected by questionnaires and genotyping using Affymetrix TWB 650K SNP chip. The primary outcome was HUA, defined as a serum uric acid level>7.0mg/dl. Odds ratio (OR) of HUA was analyzed using logistic regression models and the effects of interaction between ABCG2 rs2231142 variants and BMI on serum uric acid level were explored. Results: We identified 25,245 subjects, 4,228 (16.75%) of whom had HUA. The prevalence of HUA was 30% in men and 3.8% in women. The risk of HUA was significantly associated with ABCG2 rs2231142 risk T allele, with more HUA in TT genotype (OR: 2.40, 95% CI: 2.11-2.72, p<0.001) and TG genotype (OR: 1.64, 95% CI: 1.51-1.78, p<0.001) in men, and TT genotype (OR: 2.42, 95% CI: 1.83-3.20, p<0.001) and TG genotype (OR: 1.82, 95% CI: 1.46-2.23, p<0.001) in women, compared with their counterparts. Moreover, we found a strong genetic-environmental interaction associated with the risk of HUA. There was increased risk of HUA by the interaction of ABCG2 rs2231142 variant and BMI for TT genotype (OR: 7.42, 95% CI: 2.54-21.7, p<0.001) and TG genotype (OR: 4.25, 95% CI: 2.13-8.47, p<0.001) in men compared with the GG genotype in men, and for TT genotype (OR: 25.43, 95% CI: 3.75-172.41, p<0.001) and TG genotype (OR: 3.05, 95% CI: 0.79-11.71, p=0.011) in women compared with the GG genotype in women. Conclusion: The risk of HUA was markedly increased by the interaction of ABCG2 rs2231142 variant and BMI, both in men and in women. Body weight control and reduction in BMI are recommended in high-risk patients with the ABCG2 rs2231142 risk T allele.
| S-EPMC8438144 | biostudies-literature
Project description:Hyperuricemia (HUA) is a metabolic abnormality syndrome caused by disorders of purine metabolism. This study aimed to investigate the predictive value of the low-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio (LHR) for the risk of developing HUA. We extracted data from the China Health and Retirement Longitudinal Study (CHARLS) database from 2011 to 2016. Multivariable logistic regression, restricted cubic splines (RCSs) analysis, and linear correlation analysis were conducted to evaluate the association between LHR and risk of developing HUA. Subgroup analyses and interaction tests were also performed. A higher LHR was associated with an increased incidence of HUA (7.8% vs. 9.9% vs. 13.9, p < 0.001). The LHR was also higher in the HUA group compared to the non-HUA group (2.64 ± 1.07 vs. 2.40 ± 0.91, p < 0.001). When assessed as a continuous variable, LHR was independently associated with the risk of HUA (OR = 1.27, 95% CI = 1.16-1.39, p < 0.001). The risk of developing HUA was significantly higher among individuals with the highest LHR subgroup than those with the lowest LHR subgroup (OR = 1.81, 95% CI = 1.47-2.23, p < 0.001). RCS analysis revealed a significant nonlinear association between an increased LHR and a higher risk of developing HUA. The predictive abilities of LHR for HUA were 0.577. The composite variable comprising LHR and other traditional risk factors could significantly enhance the ability to predict HUA (C statistic = 0.677). In conclusion, a higher LHR was associated with an increased risk of developing HUA. Further studies on LHR could be beneficial for preventing and treating HUA.
| S-EPMC11711105 | biostudies-literature
Project description:ContextMutations in the low-density lipoprotein receptor-related protein 5 (LRP5) gene cause rare syndromes characterized by altered bone mineral density (BMD). More common LRP5 variants may affect osteoporosis risk in the general population.ObjectiveTo generate large-scale evidence on whether 2 common variants of LRP5 (Val667Met, Ala1330Val) and 1 variant of LRP6 (Ile1062Val) are associated with BMD and fracture risk.Design and settingProspective, multicenter, collaborative study of individual-level data on 37,534 individuals from 18 participating teams in Europe and North America. Data were collected between September 2004 and January 2007; analysis of the collected data was performed between February and May 2007. Bone mineral density was assessed by dual-energy x-ray absorptiometry. Fractures were identified via questionnaire, medical records, or radiographic documentation; incident fracture data were available for some cohorts, ascertained via routine surveillance methods, including radiographic examination for vertebral fractures.Main outcome measuresBone mineral density of the lumbar spine and femoral neck; prevalence of all fractures and vertebral fractures.ResultsThe Met667 allele of LRP5 was associated with reduced lumbar spine BMD (n = 25,052 [number of participants with available data]; 20-mg/cm2 lower BMD per Met667 allele copy; P = 3.3 x 10(-8)), as was the Val1330 allele (n = 24,812; 14-mg/cm2 lower BMD per Val1330 copy; P = 2.6 x 10(-9)). Similar effects were observed for femoral neck BMD, with a decrease of 11 mg/cm2 (P = 3.8 x 10(-5)) and 8 mg/cm2 (P = 5.0 x 10(-6)) for the Met667 and Val1330 alleles, respectively (n = 25 193). Findings were consistent across studies for both LRP5 alleles. Both alleles were associated with vertebral fractures (odds ratio [OR], 1.26; 95% confidence interval [CI], 1.08-1.47 for Met667 [2001 fractures among 20 488 individuals] and OR, 1.12; 95% CI, 1.01-1.24 for Val1330 [1988 fractures among 20,096 individuals]). Risk of all fractures was also increased with Met667 (OR, 1.14; 95% CI, 1.05-1.24 per allele [7876 fractures among 31,435 individuals)]) and Val1330 (OR, 1.06; 95% CI, 1.01-1.12 per allele [7802 fractures among 31 199 individuals]). Effects were similar when adjustments were made for age, weight, height, menopausal status, and use of hormone therapy. Fracture risks were partly attenuated by adjustment for BMD. Haplotype analysis indicated that Met667 and Val1330 variants both independently affected BMD. The LRP6 Ile1062Val polymorphism was not associated with any osteoporosis phenotype. All aforementioned associations except that between Val1330 and all fractures and vertebral fractures remained significant after multiple-comparison adjustments.ConclusionsCommon LRP5 variants are consistently associated with BMD and fracture risk across different white populations. The magnitude of the effect is modest. LRP5 may be the first gene to reach a genome-wide significance level (a conservative level of significance [herein, unadjusted P < 10(-7)] that accounts for the many possible comparisons in the human genome) for a phenotype related to osteoporosis.
| S-EPMC3282142 | biostudies-literature
Project description:BackgroundHypertension and high triglyceride are two of the most important risk factors for hyperuricemia. Epidemiological records show that hypertension and dyslipidemia often coexist and may significantly increase the risk of target organ damage. However, their combined effect on incident hyperuricemia is poorly understood. Thus, we aimed to investigate the separate and combined effect of hypertension and hypertriglyceridemia on the incidence of hyperuricemia.MethodsA prospective cohort study of 6424 hyperuricemia-free participants aged 20 to 94 years between August 2009 and October 2017 was performed at Tianjin General Hospital of China. Participants were categorized into four groups by combining hypertension and hypertriglyceridemia status at baseline. The restricted cubic spline fitting Cox regression model was used to evaluate the relationship between blood pressure and triglyceride and hyperuricemia. Cox regression models were performed to calculate hazard ratios (HRs) and 95% confident intervals (CIs) to estimate baseline factors and their association with the incidence of hyperuricemia. A Kaplan-Meier survival analysis was performed to compare the incidence of hyperuricemia among subjects in each separate and combined hypertension and hypertriglyceridemia group.ResultsDuring the 8-year follow-up period, 1259 subjects developed hyperuricemia (20.6%). There existed positive relationships between blood pressure and triglyceride levels and hyperuricemia. This risk factor arising from a combination of the two (HR, 3.02; 95% CI 2.60-3.50) is greater than that from hypertension (HR, 1.48; 95% CI 1.28-1.71) or hypertriglyceridemia (HR, 1.84; 95% CI 1.55-2.18) separately. The Kaplan-Meier survival analysis indicated that combined effect of hypertension and hypertriglyceridemia may predict higher onset of hyperuricemia.ConclusionThe combined effect of hypertension and hypertriglyceridemia on the risk of hyperuricemia is much stronger than that by hypertension or hypertriglyceridemia separately. Hypertension combined with hypertriglyceridemia may be an independent and powerful predictor for hyperuricemia.
| S-EPMC7603698 | biostudies-literature
Project description:BackgroundMore than 11 million people were estimated to be infected by Schistosoma japonicum in China before the 1950s. However, seldom studies have been conducted to evaluate the longitudinal effects of previous schistosome infection (PSI). We aimed to investigate the association between PSI and hyperuricemia in China.MethodsFrom February 2013 to October 2013, 3,517 Chinese subjects (908 persons with PSI and 2,609 persons without PSI) were recruited from a prospective cohort study of "135". After two years, 113 and 462 participants had developed hyperuricemia in the persons with and without PSI, respectively. Multivariable logistic models were used to estimate Relative Ratios (RR) and 95% confidence intervals (CIs) for hyperuricemia.ResultsThe PSI participants had a decreased risk of hyperuricemia compared with those without PSI [adjusted RR (95%CI): 0.73 (0.55, 0.97)]. Within the PSI group, higher level of fasting plasma glucose was significantly associated with the reduced incidence of hyperuricemia in PSI population (RR: 0.40, 95% CI: 0.26-0.63). For females, hypertension, increased levels of serum creatinine and triglycerides were the risk factors for incident hyperuricemia in the PSI group.ConclusionsOur results suggest that PSI is significantly associated with the lower incidence of hyperuricemia. Moreover, elevated fasting plasma glucose might prevent the onset of hyperuricemia in PSI population.
| S-EPMC6384030 | biostudies-literature
Project description:BackgroundDespite several muscle mass measures being used in the current definitions of sarcopenia, their usefulness is uncertain because of limited data on their association with health outcomes. The aim of the study was to compare the performance of different muscle mass measures for predicting incident osteoporosis in postmenopausal women.MethodsThis study included data from 149 166 participants (aged 60.3 ± 5.5 years) as part of the UK Biobank cohort. Body composition was assessed using bioelectrical impedance. The muscle mass measures included were total body skeletal muscle mass (SMM) and appendicular SMM (aSMM) divided by height squared (ht2 ), derived residuals, SMM, SMM adjusted for body mass (SMM/bm × 100), and aSMM normalized for body mass index (aSMM/BMI). Diagnoses of the events were confirmed by primary care physicians and coded according to the World Health Organization's International Classification of Diseases 10th Revision (ICD-10: M80-M82).ResultsOver a median follow-up of 6.75 (5th to 95th percentile interval, 1.53 to 8.37) years, 394 newly diagnosed cases of osteoporosis occurred, with 40 (10.2%) cases being associated with a pathological fracture. SMM/ht2 , aSMM/ht2 residual, and SMM were lower in postmenopausal women with osteoporosis compared with women without (all P < 0.0001), while SMM/bm × 100 (P = 0.003), but not aSMM/BMI (P = 0.59), was higher in the osteoporosis group. The unadjusted rates of osteoporosis increased with decreasing quintiles for SMM/ht2 , aSMM/ht2 , residuals, and SMM (all P trend <0.0001), while the incidence of osteoporosis increased with increasing SMM/bm × 100 (P trend =0.001), but not for aSMM/BMI (P = 0.45). After minimally adjusting for age and after full adjustment, SMM/ht2 , aSMM/ht2 , and SMM were the only measure that consistently predicted osteoporosis in the total group of postmenopausal women [hazard ratio (HR) 0.65-0.67, all P ≤ 0.0001], in lean women (HR 0.62-0.68; all P ≤ 0.001), and women with increased adiposity (HR 0.64-0.68; all P ≤ 0.01). In fully adjusted models, the changes in the R2 statistic were 13.4%, 11.6%, and 15.3% for the SMM/ht2 (aSMM/ht2 ), residual, and SMM, but only 4.9% and 1.3% for SMM/bm × 100 and aSMM/BMI.ConclusionsMuscle mass measures adjusted for height only (SMM/ht2 , aSMM/ht2 ) appear to be better muscle-relevant risk factors for incident osteoporosis in postmenopausal women, including when stratified into lean participants and participants with increased adiposity.
| S-EPMC6438341 | biostudies-literature
Project description:Dendritic cell immunoreceptor (DCIR) has been implicated in development of autoimmune disorders in rodent and DCIR polymorphisms were associated with anti-citrullinated proteins antibodies (ACPA)-negative rheumatoid arthritis (RA) in Swedish Caucasians. This study was undertaken to further investigate whether DCIR polymorphisms are also risk factors for the development of RA in four Asian populations originated from China and Malaysia.We genotyped two DCIR SNPs rs2377422 and rs10840759 in Han Chinese population (1,193 cases, 1,278 controls), to assess their association with RA. Subsequently, rs2377422 was further genotyped in three independent cohorts of Malaysian-Chinese subjects (MY_Chinese, 254 cases, 206 controls), Malay subjects (MY_ Malay, 515 cases, 986 controls), and Malaysian-Indian subjects (MY_Indian, 378 cases, 285 controls), to seek confirmation of association in various ethnic groups. Meta-analysis was preformed to evaluate the contribution of rs2377422 polymorphisms to the development of ACPA-negative RA in distinct ethnic groups. Finally, we carried out association analysis of rs2377422 polymorphisms with DCIR mRNA expression levels.DCIR rs2377422 was found to be significantly associated with ACPA -negative RA in Han Chinese (OR 1.92, 95% CI 1.27-2.90, P=0.0020). Meta-analysis confirms DCIR rs2377422 as a risk factor for ACPA-negative RA across distinct ethnic groups (OR(overall)?=1.17, 95% CI 1.06-1.30, P=0.003). The SNP rs2377422 polymorphism showed significant association with DCIR mRNA expression level, i.e. RA-risk CC genotype exhibit a significant increase in the expression of DCIR (P=0.0023, Kruskal-Wallis).Our data provide evidence for association between DCIR rs2377422 and RA in non-Caucasian populations and confirm the influence of DCIR polymorphisms on RA susceptibility, especially on ACPA-negative RA.
| S-EPMC3400585 | biostudies-literature
Project description:BackgroundStatins are one of the most widely prescribed medicines in clinical practice. Their benefits have extended beyond cardiovascular applications to reduce serum uric acid levels. This study aims to investigate the relationship of hyperuricemia with the risk of all-cause mortality among individuals taking statins.MethodA retrospective cohort study was performed using data from the National Health and Nutrition Examination Survey (NHANES) database between 2005 and 2018. The weighted Cox proportional hazards models were used to investigate the relationship between hyperuricemia and all cause-mortality.ResultsA total of 1,958 participants were enrolled for analysis. Of them 1,429 participants were with normal uric acid levels and 529 people were with hyperuricemia. After 12 years of follow-up, there were 267 participants who died from all-cause mortality in the non-hyperuricemia group and 136 died in the hyperuricemia group. Additionally, 32.49% of participants took more than five kinds of medicines in the non-hyperuricemia group compared to 42.05% participants in the hyperuricemia group. Even after adjusting for confounding factors, we found that the serum uric acid (SUA) level was significantly correlated with all-cause mortality among statin users (HR = 1.13, 95% CI:1.02-1.24, p = 0.0161). Additionally, hyperuricemia resulted in significant increases in all-cause mortality relative to non-hyperuricemia participants in three models (HR = 1.51, 95% CI:1.16-1.96, P = 0.0023).ConclusionAlthough statins have been shown to reduce uric acid levels, hyperuricemia is still significantly associated with the all-cause mortality in people taking statins. Those taking statins and having hyperuricemia should pay special attention to their SUA level.
| S-EPMC11883159 | biostudies-literature
Project description:[This corrects the article DOI: 10.1371/journal.pone.0041228.].
| S-EPMC5699237 | biostudies-literature
Project description:Previous studies do not widely support hyperuricemia as a risk factor for stroke and other cardiovascular diseases. We assessed the relationship between hyperuricemia and ischemic stroke (≈900 cases) using a large data set from the REGARDS study (Reasons for Geographic and Racial Differences in Stroke). We employed a case-cohort design (incident stroke cases and randomly selected cohort participants) and weighted Cox-proportional hazard models to estimate the association of serum urate level ≥6.8 mg/dL (ie, hyperuricemia) and 6.0 to <6.8 mg/dL versus <6.0 mg/dL (reference) with incident stroke. Analyses were stratified by race, gender, and age. Mediation of cardiovascular disease comorbidities on the serum urate-stroke association was tested. Hyperuricemia was associated with stroke (hazard ratio, 1.40 [95% CI, 1.10-1.78]) after adjustment for demographic variables and systolic and diastolic blood pressure. This association was substantially attenuated (hazard ratio, 1.17 [95% CI, 0.90-1.51]) by additional covariate adjustment. In particular, apparent treatment-resistant hypertension (systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg on 3 antihypertensive medications or use of ≥4 antihypertensive medications) and the count of antihypertensive medication classes significantly reduced the effect of hyperuricemia on ischemic stroke. Specifically, apparent treatment-resistant hypertension and number of antihypertensive, respectively, mediate 45% and 43% of the association. There was no effect modification in the association between hyperuricemia and stroke by age, race, or gender. We conclude that hyperuricemia may be a risk factor for stroke. The substantial attenuation of this association by apparent treatment-resistant hypertension and number of antihypertensive suggests that severe hypertension may be a mediator.
| S-EPMC7122733 | biostudies-literature