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This study aimed to investigate the association of serum uric acid (SUA) levels with dyslipidemia and its components and to further explore the age- and gender-specific association of SUA levels with dyslipidemia in Chinese adults.A cross-sectional study was performed among 8642 adults who underwent health examinations. A meta-analysis covering 17 studies was conducted to confirm the results.The prevalence of hyperuricemia and dyslipidemia was 9.25% and 20.44%, respectively. Participants with hyperuricemia had higher prevalence of dyslipidemia than those without hyperuricemia (34.42% vs 19.01%, P < .005). Compared with participants with SUA in the first quintile, the odds ratio (OR) (95% confidence interval) of dyslipidemia in the second, third, fourth, and fifth quintiles of SUA were 1.095 (0.901-1.332), 1.582 (1.315-1.904), 2.095 (1.752-2.505), and 3.212 (2.702-3.818), respectively. Subgroup analysis showed that SUA quintiles were significantly correlated with the likelihood of dyslipidemia in females aged > 50 years and in males, but not in females aged ≤50 years. The meta-analysis also showed that hyperuricemia increased the likelihood of dyslipidemia and the pooled OR for the highest uric acid level vs the lowest uric acid level was 1.84 (1.49-2.28).SUA levels are significantly associated with dyslipidemia, and this association is impacted by age and gender.

Nonalcoholic fatty liver disease (NAFLD) is a common form of chronic liver disease, and serum uric acid is observed to be significantly elevated in NAFLD patients. However, whether this elevation is causal, a bystander, or a consequence of NAFLD remains unclear. We performed a population-based prospective study among the employees of Zhenhai Refining & Chemical Company Ltd., Ningbo, China to investigate whether the elevation of serum uric acid has a casual role for NAFLD. A total of 6890 initially NAFLD-free subjects were followed up for 3 years. Overall, 11.80% (813/6890) subjects developed NAFLD over 3 years of follow-up. The cumulative incidence of NAFLD increased with progressively higher baseline serum uric acid levels (the cumulative incidence was 7.2%, 9.5%, 11.5%, 13.8%, and 17.2% in quintile 1, quintile 2, 3, 4 and 5, respectively; P value for trend <0.001). Cox proportional hazards regression analyses showed that serum uric acid levels were independently and positively associated with the risk for incident NAFLD; the age-, gender- and metabolic syndrome adjusted hazard ratio (95% CI) for the subjects in quintile 2, 3, 4 and 5 versus quintile 1 was 1.18 (0.91-1.54), 1.32 (1.03-1.70), 1.39 (1.09-1.78) and 1.50 (1.18-1.92), respectively. Taken together, our prospective observational study showed that elevation of serum uric acid levels independently predicts increase risk for incident NAFLD.

Background/aim: Serum uric acid level has been suggested to be associated with factors that contribute to the metabolic syndrome. The aim of this study was to investigate the association of serum uric acid level with non-alcoholic fatty liver disease (NAFLD)., Methods: A cross-sectional study was performed among the employees of Zhenhai Refining & Chemical Company Ltd., Ningbo, China., Results: The study included 8925 subjects (6008 men) with a mean age of 43 years. The prevalence rates of NAFLD and hyperuricemia were 11.78% and 14.71%, respectively. NAFLD patients had significantly higher serum uric acid levels than controls (370.3+/-86.6 vs. 321.1+/-82.6 micromol/L; P<0.001). The prevalence rate of NAFLD was significantly higher in subjects with hyperuricemia than in those without hyperuricemia (24.75% vs. 9.54%; P<0.001), and the prevalence rate increased with progressively higher serum uric acid levels (P value for trend <0.001). Multiple regression analysis showed that hyperuricemia was associated with an increased risk of NAFLD (odds ratio [OR]: 1.291, 95% confidence interval [CI]: 1.067-1.564; P<0.001)., Conclusion: Serum uric acid level is significantly associated with NAFLD, and elevated serum uric acid level is an independent risk factor for NAFLD.

Background/Aims: To examine the cross-sectional and longitudinal associations of serum ferritin levels with hyperuricemia. Methods: A cross-sectional and subsequently prospective study was performed among the employees of Zhenhai Refining and Chemical Company, Ningbo, China. In a cross-sectional study, the association between serum ferritin levels and the prevalence of hyperuricemia was analyzed. Subjects who were free of hyperuricemia at baseline were followed up annually to explore the prospective association between serum ferritin levels and hyperuricemia incidence. Results: Of the 10,074 subjects enrolled at baseline, 1,731 (17.18%) fulfilled the diagnostic criteria of hyperuricemia. Subjects with hyperuricemia presented significantly higher serum ferritin levels, and the levels were positively correlated with the prevalence of hyperuricemia. During a total of 22,367 person-years of follow-up, 502 subjects developed hyperuricemia. The overall incidence of hyperuricemia for 1,000 person-years of follow-up was 22.4, ranging from 17.6 in subjects with baseline serum ferritin levels in the first quintile to 19.2, 21.7, 23.9, and 30.7 in subjects in quintiles 2, 3, 4, and 5, respectively (p for trend < 0.001). Cox regression analyses showed that serum ferritin levels were positively associated with the risk of incident hyperuricemia. Conclusions: Our cross-sectional and longitudinal results indicate that high serum ferritin levels increase the risk of hyperuricemia. © 2014 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

OBJECTIVES:The precise prevalence and risk factors for the development of nonalcoholic fatty liver disease (NAFLD) in nonobese adults remains unclear. The objective of this study was to investigate the prevalence of NAFLD and risk factors for its development in a nonobese Chinese population.METHODS:We firstly investigated the prevalence and factors associated with the presence of NAFLD in nonobese (body mass index (BMI) <25 kg/m2) Chinese subjects via a cross-sectional study, and then analyzed the risk factors for the development of NAFLD via a subsequent prospective 5-year follow-up of the same population.RESULTS:A total of 6,905 nonobese subjects were enrolled in the cross-sectional study. Baseline evaluation revealed that the prevalence of NAFLD was 7.27%. A total of 5,562 subjects who were free of NAFLD at baseline completed the follow-up study, and 494 (8.88%) had developed NAFLD during the 5-year follow-up. Further analyses revealed that age, gender, BMI, waist circumference, triglyceride, high-density lipoprotein (HDL) cholesterol, serum uric acid, hemoglobin, and platelet count were independently associated with the presence and development of NAFLD.CONCLUSIONS:NAFLD is prevalent in the nonobese Chinese population, and a substantial proportion of subjects developed NAFLD over the 5-year follow-up period. Special attention should be paid to the factors associated with the presence and development of NAFLD in nonobese subjects, to improve prevention and management of NAFLD. [ABSTRACT FROM AUTHOR]

Background & Aims Hyperuricemia is a common feature of patients with non-alcoholic fatty liver disease (NAFLD). This study aimed to explore the causal relationship and underlying mechanisms between NAFLD and hyperuricemia. Methods We evaluated the impact of NAFLD on the development of hyperuricemia in a cohort of 5541 baseline hyperuricemia-free individuals. We further analyzed xanthine oxidase (XO), a rate-limiting enzyme that catalyzes uric acid production, as a candidate to link NAFLD and hyperuricemia. Results In the first study, a 7-year prospective analysis found that NAFLD was strongly associated with subsequent development of hyperuricemia. Cox proportional hazards regression analyses showed that age, gender, and body mass index adjusted hazard ratio (95% confidence interval) for incident hyperuricemia was 1.609 (1.129–2.294) in individuals with NAFLD, as compared with those without NAFLD at baseline. In the second study, we observed that expression and activity of XO were significantly increased in cellular and mouse models of NAFLD. Knocking down XO expression or inhibiting XO activity significantly decreases uric acid production and attenuates free fatty acids-induced fat accumulation in HepG2 cells. Inhibiting XO activity also significantly prevents the development of and ameliorates established hepatic steatosis induced by a high-fat diet in mice. Further experiments indicated that XO regulates activation of the NLRP3 inflammasome, which may be essential for the regulatory effect of XO on NAFLD. Conclusions NAFLD significantly increases the risk of incident hyperuricemia. XO is a mediator of the relationship between NAFLD and hyperuricemia, and may serve as a novel therapeutic target for the two linked diseases. [ABSTRACT FROM AUTHOR]