A group of diseases (e.g., arthritis, gout stones, gouty nephropathy, etc.) caused by genetic and/or acquired causes of disorders of purine metabolism, resulting in excessive uric acid production and decreased uric acid excretion. The prerequisite for the development of gout is hyperuricemia.
Gout treatment principles
1. termination of acute arthritic attacks: rapid and complete, the sooner the better, without the use of uric acid-lowering drugs.
2. control of pain.
3. Prevention of recurrence.
Alkalinization of urine: suitable for any period, including asymptomatic hyperuricemia, acute arthritis attacks, and intermittent periods of acute attacks. It is necessary to alkalize the urine when using uric acid detoxification 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 will easily cause calcium oxalate or other stone formation.
Asymptomatic hyperuricemia.
1, blood urine elevation is not obvious, no arthritis attack and gout stone, no medication may 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, elevation of 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 elevated blood uric acid is not obvious, no gout stones, and arthritis attacks are infrequent, treated with asymptomatic hyperuricemia.
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 dose by half. Divided into three major categories: uric acid excretory drugs, propofol, 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 usual starting dose is 40 mg once daily. If the blood uric acid level is not less than 6 mg/dl after 2 weeks, the recommended dose is increased to 80 mg 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 human 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.