What is gout? Two reasons need attention

Usually, after people find out that they have gout, they will also understand the cause before treating the disease. So, what is gout?

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.