Gout develops due to inflammatory arthritis caused by the deposition of monosodium urate in the joints.
Uric acid is the end product of purine metabolism and is excreted primarily by the kidneys as well as cleared by the intestines. When the production of uric acid is greater than the excretion capacity of the kidneys, the blood is oversaturated with urate ions, which in turn causes the deposition of monosodium urate crystals in the joints and tissues.
Monosodium urate crystals can be deposited in small lattice structures on cartilage surfaces and synovial rims. Under the condition that the surrounding environment (uric acid concentration, pH, temperature) does not change drastically, its lattice structure will be more stable. Once the joint environment changes, the lattice structure ruptures causing clinical symptoms.
A typical acute gouty attack is characterized by rapidly progressive redness, swelling, heat, and extreme pain in one or both joints. Acute attacks should be characterized by resting the painful joint and surface icing. The goals of treatment for acute gout are to relieve pain and terminate the attack as soon as possible. Commonly used drugs include non-steroidal anti-inflammatory drugs such as diclofenac sodium, colchicine and glucocorticosteroids such as prednisone acetate.
It is recommended that gout patients go to the rheumatology and immunology department of regular hospitals in a timely manner, and under the guidance of doctors to avoid delays in treatment.