BackgroundSerum uric acid (SUA) interferes with lipid metabolism and is considered an independent risk factor for atherosclerosis, a major complication in patients with hyperlipidemia. However, the effects of uric acid levels on mortality in hyperlipidemic patients has yet to be sufficiently determined. In this study, we aimed to assess the association between all-cause mortality and SUA in a hyperlipidemic population.MethodsTo determine mortality rates, we obtained data for 20,038 hyperlipidemia patients from the U.S. National Health and Nutrition Examination Surveys (NHANES) 2001–2018 and National Death Index. To examine the all-cause mortality effect of SUA, multivariable Cox regression models, restricted cubic spline models, and two pairwise Cox regression models were used.ResultsOver a median follow-up of 9.4 years, a total of 2079 deaths occurred. Mortality was examined according to SUA level quintiles: <4.2, 4.3–4.9, 5.0–5.7, 5.8–6.5, and >6.6 mg/dl. In multivariable analysis using 5.8–6.5 mg/dl SUA as a reference, the hazard ratios (95% confidence interval) of all-cause mortality across the five groups were 1.24 (1.06–1.45), 1.19 (1.03–1.38), 1.07 (0.94–1.23), 1.00 (reference), and 1.29 (1.13–1.48), respectively. According to a restricted cubic spline, we noted a U-shaped relationship between SUA and all-cause mortality. The inflection point was approximately 6.30 mg/dl, with hazard ratios of 0.91 (0.85–0.97) and 1.22 (1.10–1.35) to the left and right of the inflection point, respectively. In both sexes, SUA was characterized by a U-shaped association, with inflection points at 6.5 and 6.0 mg/dl for males and females, respectively.ConclusionUsing nationally representative NHANES data, we identified a U-shaped association between SUA and all-cause mortality in participants with hyperlipidemia.

Purpose In the anaerobic metabolic pathway, lactate dehydrogenase (LDH) plays an important role in hypoxia, inflammation, and cell damage, making it a potential biomarker for the progression of chronic obstructive pulmonary disease (COPD). We aimed to examine the relationship between LDH levels and all-cause mortality in participants with COPD. Patients and Methods Data of participants in the US National Health and Nutrition Examination Surveys (NHANES) 2007–2012 aged ≥20 years who underwent spirometry tests were examined, and follow-up mortality data were obtained. According to serum LDH levels, participants with COPD were divided into five groups (59–111, 112–123, 124–135, 136–150, and 151–344 U/L). To evaluate whether LDH levels were independently associated with COPD mortality, we used multivariate Cox regression analysis and smooth curve fitting. Results We included 1320 subjects, 64 with stage III or IV COPD and 541 with stage II COPD. Over a median follow-up of 9.7 years (IQR: 7.8, 11.2), 252 of the 1320 subjects died. The mean LDH level was 132.5 U/L (standard deviation [SD], 27.0). A U-shaped relationship was observed between LDH levels and all-cause mortality. Below and above the inflection point, which was approximately 110 U/L, we found different slopes for the correlation between LDH and all-cause mortality of patients with COPD. Below the threshold, per 1-standard deviation (1SD) increase in LDH resulted in a 68% reduced risk of all-cause mortality (hazard ratio [HR] 0.32, 95% confidence interval [CI] 0.13–0.81, P=0.016); conversely, above the threshold, per 1SD increase in LDH accelerated the risk of all-cause mortality (HR 1.23, 95% CI: 1.08–1.41, P= 0.002). Conclusion Using the nationally representative NHANES data, we found a U-shaped association between LDH level and all-cause mortality in participants with COPD. An optimal LDH level of approximately 110 U/L was associated with the lowest risk of all-cause mortality.