Hyperuricemia (HUA) and hypertension? A 2007 study showed that the risk of developing hypertension after 6 years of continuous follow-up in men with normal blood pressure with hyperuricemia was 80% higher in men with HUA compared to men without HUA. Epidemiological studies have all consistently shown that blood uric acid levels are strongly associated with the development of hypertension. Clinical studies have found that 90% of patients with primary hypertension have combined HUA, while only 30% of patients with secondary hypertension have combined HUA, suggesting a causal relationship between HUA and primary hypertension. Hyperuricemia and diabetes Long-term HUA can destroy the function of pancreatic beta cells and induce diabetes. A German analysis of HUA patient data found that the most common comorbidity in patients with gout was diabetes mellitus. Two prospective clinical studies from Korea and Japan enrolled 2951 middle-aged HUA patients with 6-7 years of follow-up and found that those with baseline blood uric acid levels >398umo/l had a 78% increased risk of developing abnormal long-term glucose tolerance and type 2 diabetes compared to those with <280umo/l. It is suggested that there may be some association between glucose metabolism and hyperuricemia. Hyperuricemia and hypertriglyceridemia Epidemiological data, both nationally and internationally, consistently show a correlation between blood uric acid and triglycerides. There is only one prospective cohort study on the relationship between uric acid and triglycerides, which was followed for 8 years and found basal triglycerides to be an independent predictor of future HUA. Animal tests observed that blood triglyceride levels were significantly higher in rats with artificially formed hyperuricemia than in rats with normal blood uric acid, suggesting an effect of uric acid on blood triglyceride metabolism. However, the mechanism of the interaction between uric acid and triglycerides and the causal relationship between uric acid and triglycerides are not well understood. HUA and metabolic syndrome The pathophysiological basis of metabolic syndrome is hyperinsulinemia and insulin resistance. Insulin resistance increases the production of blood uric acid during glycolysis and free fatty acid metabolism, and directly leads to hyperuricemia by increasing the reabsorption of uric acid by the kidneys. Since 70% of patients with metabolic syndrome also have HUA, Professor Reaven, the father of metabolic syndrome, proposed to include HUA in metabolic syndrome. Recent studies have shown that HUA can precede obesity, diabetes and hyperinsulinemia in the metabolic syndrome. A cross-sectional study in Taiwan, which included 28745 adults aged 20-49 years, found a 145% increased risk of developing metabolic syndrome in men and a 447% increased risk in women with HUA. A study of progression to metabolic syndrome in a non-obese population found that the risk of developing metabolic syndrome was 10 times higher in the HUA population than in the normal uric acid population. There is also evidence that lowering blood uric acid levels may reverse the metabolic syndrome state. This further confirms that blood uric acid is an independent risk factor for the metabolic syndrome.