Another study, which was hospital-based, enrolled 54 325 Taiwanese subjects who underwent a health-screening program, and these individuals were classified into eight groups according to their UA level and gout status (≤ 4.9, 5.0–6.9, 7.0–8.9, and ≥ 9.0 mg/dL, with and without gout) to examine the association between gout and NAFLD.[19] The prevalence of NAFLD was significantly higher in subjects with gout (23.1%, n = 445) than in those without gout (10.9%, n = 5724, P < 0.001).

Gout remained associated with an increased risk for NAFLD (OR 1.42; 95% CI 1.25–1.60; P < 0.001) after adjusting for age, gender, presence of metabolic syndrome, and low eGFR. The results showed an independent association between gout and the risk of NAFLD and a dose–response relationship between UA levels and the presence of NAFLD in subjects with and without gout, with UA ≤ 4.9 mg/dL Regorafenib in the absence of gout as a reference: OR (95% CI) 2.16 (1.94–2.41)–5.99 (5.19–6.90) without gout and 2.61 (1.39–4.91)–6.31 (5.12–7.77) with gout (Table 1). An investigation was conducted to examine whether elevated levels of serum UA play a causal role in NAFLD. This investigation was a population-based

prospective study among the employees of a Chinese company.[26] The study investigators followed a total of selleck screening library 6890 initially NAFLD-free subjects for 3 years and showed that UA levels were independently and positively associated with a risk for the onset of NAFLD through the use of Cox proportional hazards regression analyses; the age-, gender-, and metabolic selleck syndrome-adjusted HR

(95% CI) for the subjects in quintiles 2, 3, 4, and 5 versus quintile 1 were 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 (Table 2). Another study examined the incidence of NAFLD in 4954 apparently healthy subjects who participated in a health-screening program. The incidence of NAFLD over a 5-year period was assessed according to the individuals’ baseline UA levels, categorized into quartiles.[27] Multiple logistic regression analysis showed that hyperuricemia was associated with the development of NAFLD. When compared with subjects in quartile 1, the ORs for the incidence of NAFLD in subjects in quartiles 2, 3, and 4 were 1.53 (95% CI 1.09–2.16; P = 0.014), 1.69 (95% CI 1.17–2.44; P = 0.005), and 1.84 (95% CI 1.25–2.71; P = 0.002), respectively (Table 2). On the basis of the findings from many of these large studies, more attention should be paid to UA levels than was previously appreciated. Further studies examining the mechanism of this association are desired. Subjects with metabolic syndrome often develop NAFLD, and this has led to an examination into the influence of metabolic syndrome on the onset of NAFLD.