Uric acid is the end product of purine metabolism and is mainly produced by the enzymatic breakdown of nucleic acids and other purine-like compounds from cellular metabolism and purines from food. The saturation and concentration of uric acid in the body at 37°C is about 420μmol/L (7mg/dl) for men and 357μmol/L for women, and exceeding this concentration is considered hyperuricemia. Uric acid in the body is produced 80% by endogenous purine metabolism and 20% from external purine dietary intake. The body has a self-regulatory function for uric acid, which can maintain it at a certain stable level. If the endogenous purine production is excessive or the excretion of uric acid is reduced, the blood uric acid level will rise, resulting in hyperuricemia. When uric acid exceeds the saturation concentration, urate crystals are precipitated and can be deposited directly in the joints and surrounding soft tissues, renal tubules and blood vessels. Most patients with primary hyperuricemia have no clinical symptoms, but some patients have manifestations of metabolic syndrome. Chronic hyperuricemia may lead to gout and therefore manifest the symptoms of gout. Gout may manifest as follows: 1. Asymptomatic phase: only fluctuating or persistent hyperuricemia. 2, gouty arthritis: often first in the first metatarsophalangeal joint, or ankle, knee joints, the onset of the disease is rapid, repeated attacks. 3, gout stone: the first symptoms appear in untreated patients, after many years about 70% can appear gout stone. 4, renal lesions: mainly manifested as both gouty nephropathy and uric acid kidney stones. 5. Eye lesions: gout stones, recurrent conjunctivitis, keratitis and sclerositis may occur. So, hyperuricemia is when the metabolite of purines, uric acid, exceeds its saturation concentration, which is the upper limit of blood uric acid level that we mentioned is different for men and women, and exceeds this concentration, it is hyperuricemia.