Gout in immigration physical examination

At present, the incidence of gout and hyperuricemia is still high. I feel that more and more friends pay attention to gout and hyperuricemia in the process of popular science writing. So what is gout? Today I will explain its definition and harm.

What is gout?

Gout is a kind of metabolic rheumatism, which is a crystal-related joint disease caused by the deposition of monosodium urate. Its pathogenesis is closely related to hyperuricemia caused by purine metabolism disorder and/or decreased uric acid excretion. Uric acid deposits in joints to form tophi, which is common in spiral, metatarsophalangeal, interphalangeal and metacarpophalangeal joints. Involve multiple joints, showing swelling, stiffness and deformity of joints, fibrosis and degeneration of surrounding tissues. In severe cases, the affected skin is shiny and thin, and white bean dregs-like substances can be discharged when it is broken.

Harm of gout

Gout is very harmful, and joints bear the brunt. Once tophi is formed, it is not easy to eliminate, and it is easy to have repeated acute attacks, which are characterized by redness, swelling, heat, pain and dysfunction of the affected joint. There are not a few patients who are disabled due to joint injury and deformation caused by gout for many years. Followed by renal function damage, renal function damage caused by gout is mainly gouty nephropathy and uric acid kidney calculi. Gouty nephropathy can appear intermittent proteinuria in the early stage and renal insufficiency in the late stage, which is characterized by edema, hypertension, elevated blood urea nitrogen and creatinine. However, about 10% ~ 25% of gout patients have uric acid stones in their kidneys, which are sediment-like. Larger stones may cause renal colic and hematuria, and may also cause hydronephrosis and pyelonephritis. Furthermore, gout is often accompanied by hyperlipidemia, hypertension, diabetes, arteriosclerosis and coronary heart disease.

Drug treatment of gout

1. Treatment of acute attack

The main therapeutic drugs for acute gout attack are non-steroidal anti-inflammatory drugs, colchicine and glucocorticoid. The guidelines suggest that NSAIDs are the first choice to relieve symptoms during acute attacks. For patients with contraindications to NSAIDs, it is recommended to use small doses of colchicine alone. Because colchicine tablets has many adverse reactions, it is recommended to take it under the guidance of a doctor or pharmacist. If NSAIDs and colchicine are intolerant, short-term glucocorticoid alone (equivalent to prednisone 30mg/ day for 3 days) can achieve the same analgesic effect as NSAIDs.

2. Hypouricemic therapy

Gout is caused by hyperuricemia, so the treatment of reducing uric acid is also very important. The goal of uric acid reduction therapy is to prevent the acute recurrence of gouty arthritis and the formation of tophus, and to help tophus dissolve. Keeping the patient's blood uric acid level below 360μmol/L is helpful to relieve symptoms and control the disease. Commonly used drugs for reducing uric acid include allopurinol and febuxostat which inhibit uric acid production, and benbromarone and probenecid which promote uric acid excretion. It should be specially reminded that during the acute attack of gout, it is strictly forbidden to carry out uric acid reduction treatment, because it will promote the dissolution of tophus and aggravate the symptoms of acute attack. The uric acid reduction treatment should start 2 weeks after the acute attack is relieved.

How to prevent it in life?

Adjusting lifestyle is helpful to the prevention and treatment of gout. Gout patients should follow the following principles: (1) alcohol restriction; (2) reduce the intake of high purine food; (3) prevent strenuous exercise or sudden cold; (4) reduce the intake of fructose-rich beverages; (5) Drink plenty of water (more than 2000ml per day); (6) control weight; (7) Increase the intake of fresh vegetables; (8) Diet and routine; (9) Regular exercise; No smoking.

In short, gout can be severely disabling, so if hyperuricemia is found in physical examination, it should be intervened in time, and uric acid should be controlled at 360μmol/L through diet adjustment and drugs to avoid the formation of gout stones and gout attacks.