Practical Guidelines for the Prevention and Treatment of Hyperuricemia and Gout: Hazard Identification, Complication Warning, and Low-Purine Dietary Plan

9. What are the dangers of hyperuricemia? Clinically, hyperuricemia is often observed to coexist with impaired glucose tolerance, obesity, type 2 diabetes, dyslipidemia, and hypertension in certain populations.

10. What is Polycystic Ovary Syndrome (PCOS)? Women with PCOS often have insulin resistance and compensatory hyperinsulinemia. Insulin resistance can cause PCOS patients to exhibit certain characteristics of metabolic syndrome, sometimes referred to as the "five highs syndrome": hyperinsulinemia, hyperglycemia-type 2 diabetes, hyperlipidemia with central obesity, hypertension, and hirsutism. The proportion of women with PCOS with impaired glucose tolerance is as high as 20%–40%, significantly higher than the proportion in the general population of women of the same age (5%–10%). Based on the prevalence of impaired glucose tolerance in the general population, the prevalence of impaired glucose tolerance in women with PCOS, and a conservative estimate of the prevalence of PCOS (5%), it can be inferred that approximately 10% of women with impaired glucose tolerance before menopause also have PCOS. The prevalence of type 2 diabetes and cardiovascular disease is also significantly increased in women with PCOS. Women with polycystic ovary syndrome (PCOS) have a 7 times higher risk of heart attack and ischemic heart disease than other women. In addition, PCOS is also a major risk factor for type 2 diabetes in women.

11. What is microvascular angina? Some studies show that patients clinically diagnosed with microvascular angina exhibit more pronounced insulin resistance and higher insulin levels compared to controls; simultaneously, their plasma has higher levels of triglycerides and lower levels of high-density lipoprotein. Since abnormal blood glucose, insulin, and lipid metabolism are actually the main characteristic manifestations of metabolic syndrome, some believe that these two conditions may very well be a syndrome, a metabolic disease associated with ischemic heart disease, affecting both the large and microvascular systems of the heart.

12. What is Hyperuricemia? Hyperuricemia is an elevated level of uric acid in the blood. The normal upper limit of uric acid in men is 417 μmol/L, and in women it is 357 μmol/L. Uric acid levels are also influenced by factors such as race, diet, age, and body type (obesity). Hyperuricemia typically begins in men during puberty and in women after menopause. Hyperuricemia can be caused by excessive uric acid production (75%) or insufficient uric acid excretion (25%). Uric acid is the final metabolic product of purines. Purines are present in nucleic acids and participate in the synthesis of DNA and proteins. Purines originate from: ① increased endogenous purine synthesis, mainly from glutamate synthesized in the liver; ② continuous renewal of endogenous nucleic acid metabolism, eventually breaking down into uric acid; ③ exogenous nucleic acid decomposition, as all proteins are sources of purines. Etiologically, hyperuricemia can be divided into primary and secondary types. Primary hyperuricemia is a congenital hereditary condition, while secondary hyperuricemia is a clinical manifestation that occurs secondary to other diseases or can be caused by certain medications.

13. What factors can cause hyperuricemia? Excessive protein intake in the diet: Hyperuricemia is more common in wealthy individuals. During World War II, gout and hyperuricemia were rare in Western Europe. Their incidence gradually increased after the war. Obese individuals have higher blood uric acid levels than controls of the same age and sex; uric acid levels can be lowered through dietary control. This is because: ① excessive protein intake leads to excessive nucleic acid breakdown; ② abundant carbohydrates, which are substrates for purine synthesis; ③ increased blood fat inhibits uric acid excretion by the kidneys; ④ alcohol can induce hyperuricemia. Hyperuricemia can occur when blood alcohol concentration is close to 0.0022 mmol/L. Increased organic acids in the body: These can competitively inhibit the secretion of uric acid by the renal tubules, causing hyperuricemia. Examples include diabetic ketoacidosis, hyperlactatemia of any cause, and lactic acidosis (infection, shock, etc.). Excessive breakdown of ATP can also be an important cause of excessive uric acid production. For example, acute myocardial infarction, heavy smoking, status epilepticus, and strenuous exercise that is disproportionate to physical strength can all cause a large amount of ATP to be broken down into uric acid.

14. What are the complications of hyperuricemia? (1) Obesity. Common weight is 10% to 30% above the standard weight. (2) Diabetes. 2% to 50% of hyperuricemia patients have diabetes. Among gout patients, 7% to 74% have impaired glucose tolerance. Those with clinical diabetes manifestations are generally type 2 diabetes. (3) Hyperlipidemia. 75% to 84% of gout patients have high triglycerides. Among patients with high triglycerides, 82% have high uric acid. (4) Hypertension. 22% to 38% of untreated hypertensive patients have hyperuricemia, which is significantly higher than the incidence of hyperuricemia in the general population. The incidence of gout in hypertensive patients is 2% to 12%. Blood urate concentration is inversely proportional to renal blood flow and urate clearance. Therefore, hypertension with hyperuricemia may be related to the reduced renal blood flow in hypertensive patients. (5) Arteriosclerosis. The incidence of hyperuricemia is significantly increased in patients with arteriosclerosis, and hyperuricemia is considered a risk factor for coronary heart disease. Based on the above, hyperuricemia is associated with obesity, diabetes, hyperlipidemia, hypertension, and arteriosclerosis. In patients with hyperuricemia, the combined effects of hypertension, diabetes, hyperlipidemia, and obesity lead to both hyperuricemia and arteriosclerosis.

15. How to prevent hyperuricemia (1) Examine suspected patients with metabolic syndrome symptoms, such as those who are obese, have primary hypertension, hyperlipidemia, type 2 diabetes, hypercoagulability, hyperinsulinemia, and middle-aged and elderly people, to detect hyperuricemia early. (2) Reduce exogenous purine sources, i.e., dietary control. (3) Adjust diet to prevent obesity. (4) Increase uric acid excretion: drink more water, more than 2000 ml per day. (5) Avoid factors that promote the formation of urate crystals: catching a cold, overwork, stress, and drinking alcohol.

16. What are the dietary treatment principles for hyperuricemia? (1) Weight loss. Reduce total calories and maintain or reach ideal weight, preferably 10% to 15% below ideal weight, and give 6440 to 8280 kJ/day depending on the situation. Weight loss measures for obese patients should be gradual and take several months. Avoid losing weight too quickly, as a sudden reduction in calorie intake can lead to ketosis. Ketones compete with uric acid for excretion, reducing uric acid excretion and promoting acute gout attacks. (2) Protein. Protein intake should be moderate. Give 0.8 to 1.0 grams of protein per kilogram of body weight, or 50 to 70 grams of protein per day. Choose milk, cheese, eggs, grains and vegetables as the main sources of protein. (3) Fat. Reduce fat intake. Because fat can reduce the normal excretion of uric acid, it is recommended to use a moderate or low amount of fat, generally controlled at about 50 grams per day. (4) Sugar. It accounts for a large proportion of food. Since sugar can prevent tissue breakdown and the production of ketone bodies, and also tends to increase uric acid excretion, it should be the main source of calories. Fructose can increase the production and excretion of uric acid, so the proportion of fructose in carbohydrates should not be too large. (5) Alcohol. Do not drink alcohol. Although it was previously thought that small or moderate drinking of alcohol by patients with hyperuricemia would not necessarily cause harm, alcohol can cause lactic acid to accumulate in the body, and lactic acid has a competitive inhibitory effect on uric acid excretion, so it is best not to drink alcohol. (6) Water. Drink plenty of water, fruit juice and mineral water, etc., at least 2000 ml per day, to keep urine diluted. (7) Vitamins. Vitamins should be sufficient, especially vitamin B and vitamin C. Uric acid is easily dissolved in an alkaline environment. Vegetables and fruits are both alkaline-forming foods and can provide rich vitamins and inorganic salts. (8) Purines. In the past, it was advocated to use purine-free or strictly purine-restricted foods, but this also restricted the intake of protein, and long-term consumption had an adverse effect on nutritional intake. Currently, the recommendation is to only avoid foods high in purines, and to determine the purine content in the diet based on different medical conditions.

17. What are the dietary requirements for hyperuricemia? The dietary requirements for hyperuricemia are a normal, balanced diet to maintain an ideal weight. Since high protein intake can accelerate the biosynthesis of uric acid in patients with hyperuricemia, daily protein intake should not exceed 80 grams. Foods are divided into three categories based on their purine content (see Table 3) to help patients with hyperuricemia manage their diet. Table 3

Patients with hyperuricemia should avoid Group 1 foods, which are high in purines. They can choose Group 2 foods, which contain moderate amounts of purines, in limited quantities. The intake of meat, fish, and poultry in Group 2 should be 60-90 grams per day (or 5 times per week, depending on the condition). Cooked meat that has been boiled in broth can be used instead of raw meat. Vegetables should be limited to a small portion. They can freely choose Group 3 foods, which are low in purines. Group 3 foods can be consumed daily.