Some people still have gout attacks from time to time even after restricting high purine foods, why? First of all, it should be clear that the increase of blood uric acid concentration is not only exogenous, i.e. caused by the breakdown of food metabolism, but also endogenous uric acid production, i.e. the breakdown of amino acids, ribose phosphate and nucleic acid during the normal physiological metabolism in the body also produces blood uric acid. Blood uric acid produced from food sources only accounts for 20% of all blood uric acid, while 80% of blood uric acid is produced from endogenous sources. It has been found that stopping the intake of high purine foods can lead to a significant decrease in blood uric acid levels in the short term, but the decrease can only be about 1 mg per 100 ml. There are three reasons for the increase of uric acid from endogenous blood: 1. The normal physiological process of cell death and nucleic acid decomposition makes uric acid higher; 2. In patients with recurrent gout, the kidney function decreases due to the deposition of uric acid crystals in the kidneys, which makes the kidney excrete uric acid; 3. As gout patients are often combined with obesity, hypertension and atherosclerosis and other disorders, the drugs for treating hypertension, such as diuretics, make When obese people diet to lose weight, the body uses the accumulated fat for energy, and the large amount of ketone bodies produced in fat metabolism can also prevent the excretion of uric acid; 4, certain drugs, such as small doses of aspirin, which can inhibit the excretion of uric acid in the renal tubules, thus increasing the concentration of uric acid in the blood, pyrazinamide and ethambutol in anti-tuberculosis drugs can reduce the renal clearance of uric acid, niacin 5, muscle contraction due to strenuous exercise, as well as surgical treatment and radiotherapy, can cause a sharp increase in adenosine triphosphate (ATP) in energy metabolism, and a significant increase in its metabolites (hypoxanthine and xanthine) leads to conversion imbalance, causing Gout is triggered by an increase in blood uric acid. Therefore, to prevent the onset of gout, drugs that do not affect uric acid excretion should be chosen to treat some coexisting diseases. Angiotensin-converting enzyme inhibitors should be chosen to treat hypertension because they can increase renal blood flow and thus promote uric acid excretion; if calcium antagonists or diuretics are used to treat hypertension, they cause a decrease in renal blood flow, which is not conducive to uric acid excretion. Another example is that lipid-lowering drugs such as lipid-lowering amide, a derivative of phenoxyaromatic acid, have the dual effect of lowering lipids and lowering blood uric acid, so they can be used in gout patients. Diuretics such as dihydrocoumarol and tachyphylaxis can reduce uric acid excretion, while amisulpride, aminoglutethimide and derivatives of diuretic acid, terephalic acid and indolenic acid can both diuretic and uric acid excretion; acetazolamide can both diuretic and alkalinize urine to facilitate uric acid excretion. Insulin for the treatment of diabetes can increase the synthesis of uric acid so that the blood uric acid rises, causing an acute attack of gout, while acetyl benzenesulfonyl hexosemicarbazone has the dual role of lowering blood sugar and lowering blood uric acid can be used.