The goals of gout treatment are to relieve acute pain, lower blood uric acid levels, and prevent long-term joint damage and complications. Treatment strategies typically combine medication and non-pharmacological approaches, tailored to the patient's age, comorbidities, and severity of the condition. The key during the acute phase is rapid pain relief, while in the chronic phase, long-term control of uric acid levels is essential to prevent recurrent attacks.
Managing gout requires attention to the synergistic effects of medication and lifestyle adjustments. For example, dietary control can enhance medication efficacy, and regular monitoring of uric acid levels can prevent side effects caused by overuse of drugs. Physicians will develop phased treatment plans based on the patient's constitution and disease stage, and refer to rheumatology or nephrology specialists for further evaluation when necessary.
During an acute attack, treatment focuses on quickly alleviating inflammation and pain. Non-steroidal anti-inflammatory drugs (NSAIDs) are first-line options, such as ibuprofen or naproxen, but should be used cautiously in patients with gastric ulcers or renal impairment. Colchicine can inhibit leukocyte response to urate crystals, often used with NSAIDs to enhance efficacy, but watch for gastrointestinal side effects.
For patients unable to use the above medications, short-term corticosteroids, such as oral prednisone or intra-articular injections, may be considered. While these drugs can rapidly reduce inflammation, long-term use may cause blood sugar fluctuations or immune suppression, requiring strict monitoring by a physician.
Long-term management of uric acid is key to preventing recurrent gout attacks. Medications are divided into two main categories: uric acid synthesis inhibitors and uric acid excretion enhancers. Allopurinol reduces uric acid production by inhibiting xanthine oxidase, with febuxostat being safer for patients with renal impairment. Probenecid promotes renal uric acid excretion and should be taken with sufficient water intake to prevent kidney stones.
Emerging drugs like uric acid transporter inhibitors (e.g., Pegloticase) are used for refractory cases, administered via intravenous infusion and are more costly. Physicians may choose appropriate medications based on renal function and comorbidities, with regular blood uric acid level monitoring to adjust doses.
NSAIDs achieve anti-inflammatory and analgesic effects by inhibiting prostaglandin synthesis. They are recommended within 24 hours of attack onset for optimal results. Patients with heart disease should avoid high doses due to potential for edema or increased blood pressure. Colchicine is effective at low doses for joint pain but can cause neurotoxicity if overdosed, so strict adherence to dosing instructions is essential.
Uric acid-lowering medications should be used continuously for at least 6 months to stabilize levels. Allopurinol is the first choice, but about 5% of patients may develop skin rashes or liver function abnormalities, requiring regular blood tests. Febuxostat is safer for patients with renal impairment but may increase cardiovascular risk, so use should be evaluated by a doctor.
Probenecid must be taken with at least 2000 ml of water daily to reduce kidney stone risk. Newer drugs like URAT1 inhibitors increase renal uric acid excretion but may cause allergic reactions. All uric acid-lowering drugs require persistent use; discontinuation may lead to rebound effects and acute attacks.
Limiting high-purine foods is fundamental, avoiding organ meats (like liver, fish roe), alcohol (especially beer), and concentrated meat broths. Increasing intake of low-fat dairy products, whole grains, and low-fructose foods is recommended. Studies suggest cherry consumption may reduce attack risk. Rapid weight loss should be avoided, as fat breakdown increases endogenous uric acid production.
During an attack, elevate the affected joint and apply cold compresses to reduce swelling, avoiding hot packs which may worsen pain. Wear comfortable shoes to reduce foot pressure, and temporarily stop high-impact activities. Use ice packs for 15-20 minutes per session, 2-3 times daily, possibly combined with medication to enhance relief.
Adopt the DASH diet principles, emphasizing vegetables, whole grains, and low-fat dairy. Prioritize high-quality protein sources like eggs and low-fat dairy, and limit red meat and seafood such as sardines and squid. Research indicates that daily intake of 1.6-2.5 grams of low-fat dairy may reduce attack risk by 35%.
Regular aerobic exercise improves insulin sensitivity and promotes uric acid metabolism. Aim for at least 150 minutes of moderate-intensity exercise per week, such as brisk walking or swimming. Reducing BMI by 1 unit can lower blood uric acid by 0.12 mmol/L. Avoid intense joint-loading exercises to prevent triggering acute attacks.
Research focuses on new uric acid metabolism regulators, including selective URAT1 inhibitors and CRTH2 antagonists. Advances in genetic screening enable personalized treatment, such as adjusting allopurinol doses for HLA-B*5801 positive individuals to prevent severe skin reactions. Biologics like IL-1β antibodies are in clinical trials, offering potential non-steroidal anti-inflammatory options.
Minimally invasive techniques like uricase implantation are under investigation, and AI-based predictive models can forecast drug responses and side effects based on genetic and biochemical data. Future developments may include oral uricase enzymes to reduce renal burden.
Seek immediate medical attention if: (1) joint swelling with fever persists for over 48 hours, (2) kidney stones or renal dysfunction are present, or (3) pain persists despite self-medication. Patients with long-term uric acid levels over 480 μmol/L and tophi should have their uric acid management goals set by a rheumatologist.
Patients with hypertension or diabetes should be cautious of drug interactions, such as diuretics raising uric acid levels. Symptoms like skin rash or difficulty breathing require prompt discontinuation of medication and medical consultation. Regular monitoring of renal function and blood counts every 3-6 months is recommended for long-term uric acid-lowering therapy.
Applying cold packs (15-20 minutes per session) to the affected area can reduce redness and swelling. Elevating the limb above the heart helps decrease renal load. Avoid hot packs or massage, which may worsen inflammation. If pain is severe, a doctor may recommend short-term NSAIDs or colchicine, following proper dosing instructions.
Does consuming low-fat dairy products help reduce the risk of gout attacks?Studies show that daily intake of 1-2 servings of low-fat dairy (such as skim milk or yogurt) can enhance uric acid excretion and lower blood uric acid levels. Choosing low-fat options is advised to prevent high-fat-induced insulin resistance, which can indirectly affect uric acid metabolism. This approach can be combined with dietary control and medication but should not be relied upon solely.
Why can diuretics used for hypertension trigger gout attacks?Some diuretics (like hydrochlorothiazide) decrease renal uric acid excretion, leading to increased blood uric acid levels. For patients with both hypertension and gout, physicians may switch to selective ADH2 antagonists or calcium channel blockers, with monitoring of uric acid levels. Caution is advised when using diuretics in patients on uric acid-lowering therapy.
Is it necessary to continue uric acid-lowering medication if blood levels are normal?Even if blood uric acid levels are within target (<6 mg/dL), patients with recurrent attacks or tophi may be advised to continue medication for 3-5 years to prevent urate crystal deposition. Discontinuation should be evaluated by a doctor, with regular follow-up of uric acid levels and joint imaging. Stopping medication independently may cause uric acid rebound and trigger relapse.
Do gout and chronic kidney disease influence each other?Long-term hyperuricemia can damage renal tubules, increasing the risk of chronic kidney disease, while impaired renal function can hinder uric acid excretion, worsening gout. Treatment should involve low-nephrotoxicity drugs (like febuxostat), blood pressure control, adequate hydration, and avoidance of high-purine foods to improve both conditions.
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