Abstract Background Serum uric acid (SUA) levels have been reported to be associated with various diseases, with both high and low levels potentially influencing inflammatory processes. However, epidemiological studies investigating the relationship between SUA levels, and the risk of ulcerative colitis (UC) and Crohn’s disease (CD) are still limited. Methods This cohort study recruited 438155 participants from the UK Biobank, with follow-up 2006 to 2010. During a mean follow-up of 12.6 years, we diagnosed 1904 cases of UC and 913 cases of CD. To assess the relationship between SUA levels and the incidence of UC and CD we categorized SUA levels (mg/dL) into six gender-specific quartiles (Q1–Q6) and performed Cox regression analysis with restricted cubic splines. Subsequently, we used Cox proportional hazards regression to analyze the effects of SUA levels on the risk of UC and CD. Results In the analysis of UC, low SUA level-Q1 (SUA < 4.0 mg/dL) was consistently linked to an elevated risk across both statistical models (Model 1: HR = 1.27, 95% CI 1.03–1.56, P = 0.025; Model 2: HR = 1.30, 95% CI 1.04–1.62, P = 0.020). For CD, high SUA level-Q6 (SUA ≥ 8.0 mg/dL) was significantly associated with an increased risk (HR = 1.50, 95% CI 1.11–2.03, P = 0.008). In subgroup analyses, low SUA levels were significantly associated with an increased risk of UC, particularly among males. Conversely, high SUA levels were significantly linked to an elevated risk of CD, especially in females. These associations were also observed in several specific subgroups, including participants aged 60 years or older, individuals with a body mass index (BMI) ≥ 25 kg/m 2 , alcohol drinkers, and never-smokers. Conclusion This study is the first to propose that SUA levels may serve as differential risk factors for UC and CD. Specifically, low SUA levels were associated with an increased risk of UC, whereas high levels were linked to a higher risk of CD. Subgroup analyses further identified additional risk factors. These findings provide novel insights into the distinct roles of SUA in the pathogenesis of UC and CD.
Tie et al. (Thu,) studied this question.