Gout has many dangers, statistics say that gout patients “gouty nephropathy – clinical 20% – 40%, autopsy 100%” fear.
40%, autopsy 100%” fear. Gout to be visible to the naked eye gout stone, chronic gouty nephropathy or X-ray visible joint destruction before starting uric acid treatment has been late, in order to avoid kidney function, joints and other serious damage, regular treatment and diet is still needed. Hyperuricemia is increasing in adults, with a proportion of about 10% in people over 30 years of age, and some may be higher. Acute attacks of gout Control acute inflammation (treat the symptoms first) NSAIDs: generally very effective (aspirin is prohibited) Colchicine: 0.5mg/tablet, 1/h until relief or GI symptoms (nausea vomiting diarrhea), max <12 tablets/d. Maintain 1 tablet, tid. Can also be applied intravenously
(Special effects, but part of the literature considers that the side effects and efficacy are limited, so NSAIDs should be chosen in sufficient quantity first, and then colchicine should be chosen if they are not effective) Glucocorticoids: the above are not effective! Not tolerated! Symptoms are more severe! The rapid fluctuation of uric acid (increase or decrease) can lead to aggravation of arthritis, sudden decrease can lead to dissolution of gout stone surface, release of crystals, release of chemokines after being engulfed by leukocytes, and attract more leukocytes, release of lysosomal enzymes, and destruction of joints.
It is recommended to use it after the acute attack is completely controlled (mostly 3-6 weeks after the termination of the attack). The more effective the initial uric acid lowering therapy is, the more frequent the gout attacks may be. To prevent acute attacks, the use of NSAIDs or colchicine is also considered: at least 4-6 weeks or even more than half a year (see above). Promote uric acid excretion drugs Domestic currently mainly uric acid excretion drugs and inhibit inhibit uric acid synthesis drugs, the former propofol ward seems to have no drugs, and instead of safer benzbromarone. The former seems to have been replaced by the safer benzbromarone. It seems that allopurinol is the only drug that inhibits uric acid. The incidence of allopurinol allergic reaction syndrome is about 10%, manifested by fever, rash, eosinophilia, hepatic necrosis and renal abnormalities, and the death rate is as high as 20-25%, so its use has some restrictions and concerns. Benzbromarone 25mg/tablet, 1-2 tablets/d ,1-3w,no decrease,increase 1-2 tablets/d available 2-4 tablets/d Sodium bicarbonate tablets 1.0 TID Drink plenty of water. Indications: normal or mildly impaired renal function (Ccr>20 ml/min), no kidney stones, uric acid < 600 mg/d (3571 μmol/d) Cautions: drink plenty of water/alkaline drugs (100-fold increase in solubility at urine pH 8), thiazide diuretics/aspirin prohibited / alcohol The third class of drugs for gout; drugs that promote uric acid catabolism including rasburicase and pegloticase, are also being studied and progressed. Clinically, the selection of "double whammy" drugs should be advocated according to the co-morbidities of the gout patient. Gout patients with hypertension can choose coxsartan or amlodipine, which has been confirmed by domestic and international studies to have both uric acid-lowering and antihypertensive effects. Gout patients with hyperlipidemia can choose fenofibrate or atorvastatin. The former is suitable for those with mainly increased triglycerides, while the latter is suitable for those with mainly increased cholesterol. Fenofibrate 200
mg/d for 3 weeks or 160 mg/d for 2 months can reduce blood uric acid by 19% and 23% respectively [P2-23]. Fenofibrate also has some anti-inflammatory properties and is less likely to induce acute attacks of gout when lowering uric acid.