Gout is a crystal-associated arthropathy caused by urate deposition, the onset of which is directly related to hyperuricemia due to disturbances in purine metabolism and/or reduced uric acid excretion. Since hyperuricemia is the basis for the pathogenesis of gout, any medication that causes elevated uric acid or interferes with uric acid metabolism is something that should be avoided by gout patients whenever possible. Purines are one of the constituent substances of the human body and exist mainly in the form of purine nucleotides. Purines are metabolized in the body and eventually converted into uric acid, which is the final metabolite of purines. Uric acid is excreted from the body through the intestine and urine. However, many drugs can cause uric acid to rise or interfere with uric acid metabolism, such as pyrazinamide, ethambutol, isoniazid and other anti-tuberculosis drugs, whose metabolites can compete with uric acid for organic acid excretion channels and reduce uric acid excretion, thus causing uric acid to rise. Further, tab diuretics and thiazide diuretics and antihypertensive drugs containing diuretic components, such as compound reserpine, can increase glomerular uptake of urate and decrease secretion of uric acid salts. It has also been suggested that aspirin also has an interfering effect on the metabolism of blood uric acid in humans. Therefore, for gout patients, the usual medication must be rigorous and standardized, avoiding as much as possible drugs that can cause uric acid to rise or interfere with uric acid metabolism. If you have to take it because of a certain disease, then you must adjust it under the guidance of your physician and use it in a reasonable and standardized manner.