A group of diseases (such as arthritis, gout stone, gouty nephropathy, etc.) caused by genetic and/or acquired causes of purine metabolism disorders, resulting in excessive uric acid production and reduced uric acid excretion. The prerequisite for the development of gout is hyperuricemia.
The principles of gout treatment are.
1, termination of acute arthritis attacks: fast and thorough, the sooner the better, without the use of uric acid-lowering drugs.
2.Control the pain.
3.Prevent recurrence.
Alkalinization of urine: suitable for any period, including asymptomatic hyperuricemia, acute arthritis attacks, intermittent periods of acute attacks. It is necessary to alkalize the urine when using uric acid excreting drugs to prevent urinary stones. Take sodium bicarbonate so that the urine PH is between 6.2 and 6.8, and do not exceed 7.0, otherwise it is easy to cause calcium oxalate or other stone formation.
Asymptomatic hyperuricemia.
1, blood urine elevation is not obvious, no arthritis attack and gout stone, no medication can be used.
2. Find the cause, control diet, lower uric acid and prevent attacks. Actively treat related diseases such as hypertension, hyperlipidemia, coronary heart disease and diabetes, and prevent obesity.
3, to pay attention to long-term uncontrolled can bring harm: women’s blood uric acid greater than 10mg/ml, men greater than 13mg/ml on the kidney function.
Acute arthritis attack period.
1, bed rest, elevate the affected limbs, local cold compresses.
2, timely anti-inflammatory and pain relief: oral 1 non-steroidal anti-inflammatory drugs, the first day the dose doubled, the next day down to the regular amount, the symptoms disappear discontinued, more than less than 2 weeks, and with topical drugs. The following NSAIDs are prohibited: renal insufficiency, recent gastrointestinal ulcer or severe heart failure, selective cyclooxygenase-2 inhibitors are available for patients at risk of gastrointestinal side effects. Reasons for not advocating the first choice of colchicine: high side effects, therapeutic doses similar to toxic doses, easy toxicity. High gastrointestinal reactions, liver and kidney damage, bone marrow suppression. Certain severe allergies.
Intermittent arthritic episodes.
1.If the elevation of blood uric acid is not obvious, there is no gout stone, and arthritis attacks are infrequent, the same asymptomatic hyperuricemia is treated.
2, the use of uric acid-lowering drugs, should be gradually increased from a small dose (1 tablet / day), according to the efficacy and blood uric acid value, gradually increasing, looking for blood uric acid to maintain at 4.0-6.0mg/ml dose, this dose long-term or even lifelong maintenance.
3. Use with caution in the elderly and reduce the dosage by half. There are three major categories: uric acid excretors, propofol, and benzbromarone. Inhibitors of uric acid synthesis, allopurinol. Uric acid dissolving drugs, Lablase. Indications for uric acid synthesis-inhibiting drugs: Uric acid-depleting drugs are ineffective or not tolerated. More than moderate renal impairment. Increased blood uric acid and uric acid > 900 mg/d on a normal diet. presence of gout stones and blood uric acid > 7 mg/d and uric acid > 700 mg/d.
The following conditions should be treated with uric acid-lowering drugs, and the blood uric acid is greater than 9mg/ml even after dietary control, and there are more than 3 acute attacks per year. Have gout stone and kidney function impairment.
The goal of uric acid-lowering control: uric acid-lowering treatment should be lifelong, intermittent treatment or stopping treatment will lead to recurrent gout attacks and increased incidence of related diseases, and blood uric acid should be maintained at the standard stable state.
The new drug for the treatment of gout is febuxostat, which is a new non-purine selective xanthine oxidase inhibitor for the long-term treatment of patients with gout hyperuricemia, but is not recommended for patients with gout without hyperuricemia. It reduces uric acid production by inhibiting the activity of xanthine oxidase, which has a non-purine molecular structure and is more specific in its inhibition of xanthine oxidase, and is therefore more effective than other drugs that inhibit uric acid production. It is indicated for patients who are allergic to drugs that inhibit uric acid production and can reduce uric acid levels in the blood of patients with hyperuricemic gout. The safety and efficacy of febuxostat have been demonstrated in clinical studies and no dose adjustment is required in patients with moderate to severe hepatic or renal insufficiency. The usual starting dose is 4omg once daily. If after 2 weeks the blood uric acid level is still not less than 6mg/dl, the recommended dose is increased to 80mg once daily. The maximum dose used is 120mg/d. This dose is effective for patients with high blood uric acid levels.
Prevention of gout.
1, low purine diet, purine intake less than 150mg/d. can make the blood uric acid drop 1-2mg/ml. reduce the acute attack of gout; shorten the duration of the attack period; reduce uric acid salt deposition to form stones; reduce the application of uric acid-lowering drugs.
2, eat more alkaline food. Normal body fluids are weakly alkaline, alkaline is conducive to the dissolution and discharge of urate crystals, alkaline food is metabolized in the body to generate alkaline substances, mainly vegetables after the fruit, but sugar mung beans, lentils and peanuts to limit. Patients with a family history of gout should change their dietary habits early.