The word gout is of Latin origin (gutta) meaning “a drop” of malignant body fluid that attacks weakened joints. Gout is a clinical syndrome of one or more lesions caused by the deposition of sodium urate or uric acid crystals in tissues from supersaturated extracellular fluid due to disorders of purine metabolism and or reduced uric acid excretion due to genetic or acquired causes. To put it bluntly, either too much uric acid is produced or too little uric acid is excreted, resulting in hyperuricemia, the main cause of gout. What is meant by hyperuricemia? It is defined as blood uric acid >420umol/L for men and >360umol/L for women, when the blood is saturated with uric acid, beyond which urate crystals are precipitated from the blood and deposited in the connective tissue, which can cause gout attacks when stimulated by certain factors. But asymptomatic hyperuricemia is not a disease state, do not be afraid of hyperuricemia, the relationship between uric acid concentration and gout incidence: uric acid 540umol/L, gout incidence rate of 8%, it can be seen that simple hyperuricemia is not equal to gout, most do not need to eat uric acid drugs, mainly to control risk factors, such as dietary control, drinking more water, exercise, weight loss, control blood pressure, blood lipids, blood sugar, etc., uric acid will naturally come down. The conditions that require uric acid-lowering treatment are: gout patients with dietary control of blood uric acid >420μmol/L, patients with simple hyperuricemia with dietary control of blood uric acid >780μmol/L, and those with gout stones, uric acid kidney stones or kidney damage, and other studies have shown that the benefits obtained from uric acid-lowering drugs used in patients with more than 2 gout attacks per year outweigh the the risk of inducing gout attacks and drug side effects.