What is gout? What are the causes and types of gout?

Health is something that each of us is concerned about. Many people attach great importance to health, but diseases will always find us. Gout is a common disease, so what is gout? What causes gout?

gout

Gout is a crystal-related arthritis caused by the deposition of monosodium urate (MSU), which is directly related to hyperuricemia caused by purine metabolism disorders and/or decreased uric acid excretion. It specifically refers to acute characteristic arthritis and chronic tophi disease, mainly including acute onset arthritis, tophi formation, tophi-induced chronic arthritis, urate nephropathy and uric acid urinary stones. In severe cases, joint disability and renal insufficiency may occur. Gout is often accompanied by abdominal obesity, hyperlipidemia, hypertension, type 2 diabetes and cardiovascular disease.

Causes

The most important biochemical basis of gout is hyperuricemia. A normal adult produces about 750 mg of uric acid per day, of which 80% is endogenous and 20% is exogenous. This uric acid enters the uric acid metabolic pool (about 1200 mg). About 60% of the uric acid in the metabolic pool is metabolized daily, of which 1/3, about 200 mg, is broken down and metabolized through the intestines, and 2/3, about 400 mg, is excreted through the kidneys, thus maintaining the stability of uric acid levels in the body. Problems in any link can lead to hyperuricemia.

1. Primary gout

It is mostly hereditary, but clinically only 10% to 20% of people have a family history of gout. Excessive uric acid production accounts for 10% of the causes of primary hyperuricemia. The main causes are purine metabolic enzyme defects, hypoxanthine guanine phosphoribosyltransferase (HGPRT) deficiency and hyperactivity of phosphoribosyl pyrophosphate (PRPP) synthetase. Primary renal reduced uric acid excretion accounts for about 90% of primary hyperuricemia. The specific pathogenesis is unclear and may be a multi-gene genetic disease, but organic renal diseases should be ruled out.

2. Secondary gout

Refers to a clinical manifestation secondary to other disease processes and may also be caused by certain drugs. Myeloproliferative diseases such as leukemia, lymphoma, multiple myeloma, polycythemia, hemolytic anemia and cancer can lead to accelerated cell proliferation, increased nucleic acid conversion and increased uric acid production. Malignant tumors cause massive cell destruction after radiotherapy and chemotherapy, and nucleic acid conversion also increases, leading to increased uric acid production. Kidney diseases including chronic glomerulonephritis, pyelonephritis, polycystic kidney disease, lead poisoning and advanced hypertension can cause impaired glomerular filtration function, which can reduce uric acid excretion and lead to increased blood uric acid concentration. Drugs such as thiazide diuretics, furosemide, ethambutol, pyrazinamide, low-dose aspirin and niacin can competitively inhibit the excretion of uric acid by the renal tubules and cause hyperuricemia. In addition, renal transplant patients who take immunosuppressants for a long time may also develop hyperuricemia, which may be related to the fact that immunosuppressants inhibit the excretion of uric acid in the renal tubules.