Allopurinol was effective in inhibiting uric acid synthesis, and allopurinol allergy was observed in both case 1 and case 2. However, mild allergy with allopurinol is not an absolute contraindication to allopurinol use, and standard desensitization therapy can be used: starting dose of 50 μg/d, increasing to 100 μg, 200 μg, 500 μg, 1 mg, 5 mg, 10 mg, 25 mg every 3 days, and eventually depending on blood uric acid and The dosage will be increased or decreased according to blood uric acid and renal function. In elderly and frail patients with impaired renal function and extensive skin rash, a modified allopurinol desensitization method can be used: start with 10-25 μg/d and increase the dose every 5-10 days. In case of re-sensitization, the drug is stopped immediately and half of the original tolerated dose is given again after it subsides, with longer intervals between dose increases. The usual clinical dose of allopurinol is 300 mg/d, but most studies have shown that long-term low to moderate doses of allopurinol do not reduce the incidence of fatal allergic syndrome and have poor uric acid-lowering efficacy. Recent studies have shown that high doses of allopurinol are effective, with no increase in adverse effects at increasing doses, and that allopurinol above the endogenous creatinine clearance (Ccr)-adjusted dose is safe and effective. The risk of fatal allergic syndrome is reduced by starting allopurinol at a low dose (50-100) mg/d and gradually increasing the dose to a maximum of (800-900) mg/d. Application of new uric acid-lowering drugs Many patients with refractory gout are allergic, ineffective or intolerant to traditional uric acid-lowering drugs and have to seek treatment with other new uric acid-lowering drugs. Febuxostat is a new non-purine, highly effective and selective xanthine oxidase inhibitor, which has a significantly stronger uric acid-lowering effect than allopurinol and rarely causes lethal allergic syndrome, especially for gout patients with renal insufficiency, contraindication to uric acid excretory drugs and allopurinol allergy or intolerance. Case 2 showed a significant decrease in uric acid and rapid dissolution of gout stones with febuxostat. The second-generation uric acid excretory drug (uric acid transporter protein 1 inhibitor RDEA594) is characterized by minimal hepatotoxicity, comparable efficacy to allopurinol, effective in mild to moderate renal insufficiency, minimal risk of kidney stone induction, and no serious adverse events. New drug to promote uric acid decomposition (Precahi) This drug has a rapid rate of uric acid reduction and dissolution of gout stones, and can be used in adult patients with refractory gout who have failed to respond to conventional uric acid-lowering therapy; it is contraindicated in patients with hereditary glucose-6-phosphate dehydrogenase (G6PD) deficiency and used with caution in patients with congestive heart failure. However, the high price, infusion reactions and frequent gout attacks during the initial period of use limit the widespread use of this drug. Combination medication can be used to improve the uric acid-lowering effect in patients for whom single medication is ineffective or not effective. For example, the combination of allopurinol (200-600 mg/d) with benzbromarone (100 mg/d), probenecid (0.5 g/d) or RDEA594 (200-600 mg/d) at stable doses is significantly better than allopurinol alone, and RDEA594 (600 mg/d) is significantly better than allopurinol alone. 600 mg/d) in combination with febuxostat (40-80 mg/d) was also significantly better than febuxostat alone in lowering uric acid. Two drugs that inhibit uric acid synthesis can also be combined, and the combination of allopurinol (100-300 mg/d) with the purine adenosine phosphorylase inhibitor BCX4208 (20-80 mg/d) brought more gout patients to uric acid levels than allopurinol alone, with the rate of attainment increasing with the dose of both drugs. The use of the multiacting uric acid-lowering agents cloxacin and fenofibrate reduced blood uric acid by 15% to 30% while lowering blood pressure and triglycerides, respectively. Atorvastatin lowered blood cholesterol while lowering blood uric acid by 6.4% to 8.2%. Halofenestrol and Arholofenate lowered blood uric acid by 15% to 29% by promoting uric acid excretion while lowering glucose and triglycerides. If the patients of case 1 and case 2 are combined with hypertension, hyperlipidemia and diabetes mellitus, it is recommended to use the above-mentioned drugs with relatively weak uric acid-lowering effect, which are “double (triple) killers”.