The goal of gout treatment is to relieve the pain of acute attacks, lower blood uric acid levels, and prevent long-term joint damage and complications. Treatment strategies typically combine medication and non-pharmacological methods, and are personalized based on the patient's age, comorbidities, and severity of the condition. The key during acute attacks is rapid pain relief, while chronic management requires long-term control of uric acid levels to prevent recurrent attacks.
When treating gout, it is important to consider the synergistic effects of medication and lifestyle adjustments, such as dietary control to enhance the efficacy of medications, and regular monitoring of uric acid levels to avoid side effects from excessive medication use. Physicians will develop a phased treatment plan based on the patient's constitution and disease stage, and refer to rheumatology or nephrology specialists for evaluation when necessary.
Treatment during acute attacks focuses on rapidly relieving inflammation and pain. Non-steroidal anti-inflammatory drugs (NSAIDs) are the first-line choice, such as ibuprofen or naproxen, but should be used cautiously in patients with a history of gastric ulcers or renal impairment. Colchicine can inhibit the leukocyte response to uric acid crystals and is usually used in conjunction with NSAIDs to enhance efficacy, but gastrointestinal discomfort and other side effects should be monitored.
For patients who cannot use the aforementioned medications, short-term use of corticosteroids, such as oral prednisone or intra-articular injections, may be considered. While these medications can quickly reduce inflammation, long-term use may lead to 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. Pharmacological treatment is divided into two main categories: uric acid production inhibitors and uric acid excretion promoters. Allopurinol reduces uric acid synthesis by inhibiting xanthine oxidase, while febuxostat is safer for patients with impaired renal function. Probenecid promotes renal excretion of uric acid and should be accompanied by adequate hydration to avoid the risk of kidney stones.
Recently emerging uric acid transporter inhibitors (such as pegloticase) are suitable for refractory cases but require intravenous administration and are more costly. Physicians may choose appropriate medications based on the patient's renal function and comorbidities, and regularly measure blood uric acid levels to adjust dosages.
Non-steroidal anti-inflammatory drugs (NSAIDs) achieve anti-inflammatory and analgesic effects by inhibiting prostaglandin synthesis, and it is recommended to use them within 24 hours of an attack for optimal efficacy. However, patients with heart disease should avoid high doses, as this may induce edema or elevated blood pressure. Colchicine is effective for joint pain at low doses, but overdose may lead to neurotoxicity, so medication instructions must be strictly followed.
Uric acid-lowering medications need to be used continuously for at least 6 months to stabilize uric acid levels. Allopurinol is the first-line choice, but about 5% of patients may develop skin rashes or liver function abnormalities, requiring regular blood monitoring. Febuxostat is safer for patients with renal impairment but may increase the risk of cardiovascular events, requiring physician assessment before use.
Probenecid should be accompanied by a daily intake of at least 2000 c.c. of fluids to reduce the risk of kidney stones. New medications such as uric acid transporter inhibitors (URAT1 inhibitors) increase renal excretion but may induce allergic reactions. All uric acid-lowering medications must be used consistently, as discontinuation may lead to a "rebound effect" causing acute attacks.
Limiting high-purine foods is a fundamental measure, avoiding organ meats (such as liver and roe), alcohol (especially beer), and concentrated meat broths. It is recommended to increase low-fat dairy products, whole grains, and low-fructose diets, as studies suggest that cherry consumption may reduce the risk of attacks. Rapid weight loss should be avoided, as the breakdown of body fat increases endogenous uric acid production.
During an attack, the affected joint should be elevated and cold compresses applied to relieve swelling, while avoiding heat application that may exacerbate pain. Wearing comfortable footwear reduces pressure on the feet, and high-intensity exercise should be paused during the acute phase. Local application of ice packs for 15-20 minutes at a time, 2-3 times a day, can be used in conjunction with medication to enhance effects.
It is recommended to adopt the DASH dietary principles, emphasizing the intake of vegetables, whole grains, and low-fat dairy products. Quality protein sources should prioritize eggs and low-fat dairy products, while avoiding excessive red meat and seafood such as sardines and squid. Studies show that daily intake of 1.6-2.5 grams of low-fat dairy products may reduce the risk of attacks by 35%.
Regular aerobic exercise can improve insulin sensitivity and promote uric acid metabolism, with a recommendation of 150 minutes of moderate-intensity exercise such as brisk walking or swimming each week. A decrease of 1 unit in body mass index (BMI) can lower blood uric acid levels by 0.12 mmol/L. Vigorous weight-bearing exercises should be avoided to prevent triggering acute attacks.
Drug development is focusing on new regulators of uric acid metabolism pathways, including selective URAT1 receptor inhibitors and CRTH2 antagonists. Advances in genetic screening technology have made personalized treatment possible, such as adjusting the dosage of allopurinol for those with the HLA-B*5801 gene to avoid severe skin reactions. Biologics such as IL-1β antibodies are in clinical trials and may provide new non-steroidal anti-inflammatory options.
Minimally invasive treatment techniques such as uricase implantation therapy are still under research, while AI-assisted treatment prediction models can predict drug responses and side effect risks based on the patient's genotype and biochemical indicators. Future developments may include oral uricase enzymes to avoid the renal burden of existing medications.
Immediate medical attention should be sought in the following situations: (1) joint swelling accompanied by fever lasting more than 48 hours, (2) history of kidney stones or renal dysfunction, (3) pain not relieved by self-medication. Patients with long-term blood uric acid levels exceeding 480 μmol/L and with gouty tophi formation should have their uric acid treatment goals set by a rheumatology specialist.
Patients with concurrent hypertension or diabetes should pay special attention to drug interactions, as diuretics may elevate blood uric acid levels. If symptoms of drug allergies such as skin rashes or difficulty breathing occur, medication should be stopped immediately and medical attention sought. Long-term users of uric acid-lowering medications should have their renal function and blood counts monitored every 3-6 months.
Applying ice to the affected area (for 15-20 minutes each time) can reduce redness and swelling, while elevating the affected limb above the heart to reduce renal burden. Avoid heat application or massage, as they may exacerbate inflammation. If the pain is severe, the physician may recommend short-term use of NSAIDs or colchicine, but medication instructions must be followed.
Does consuming low-fat dairy products help reduce the risk of gout attacks?Studies show that consuming 1-2 servings of low-fat dairy products (such as low-fat milk or yogurt) daily can enhance uric acid excretion and help lower blood uric acid levels. It is recommended to choose low-fat products to avoid high-fat-induced insulin resistance, which indirectly affects uric acid metabolism. This approach can be combined with dietary control and pharmacological treatment but should not be relied upon solely.
Why might using diuretics for hypertension trigger gout attacks in patients with gout?Certain diuretics (such as hydrochlorothiazide) reduce renal uric acid excretion, leading to elevated blood uric acid levels. If a patient has both hypertension and gout, the physician may switch to selective ADH2 antagonists or calcium channel blockers and monitor uric acid levels. For those receiving uric acid-lowering treatment, careful dosage adjustments of diuretics are necessary.
If blood uric acid levels are normal, do I still need to continue taking uric acid-lowering medications?Even if blood uric acid levels are within the target range (usually <6mg/dL), if the patient has a history of recurrent attacks or gouty tophi, the physician may recommend continuing medication for at least 3-5 years to avoid urate deposition. Discontinuation of medication should be evaluated by a physician, with regular follow-up on uric acid levels and joint imaging. Stopping medication on one's own may lead to a rebound in uric acid levels and trigger a relapse.
Is there a relationship between gout and chronic kidney disease?Long-term hyperuricemia can damage renal tubular function, increasing the risk of chronic kidney disease; conversely, renal impairment can hinder uric acid excretion, potentially exacerbating gout. When treating, it is necessary to choose medications with low nephrotoxicity (such as febuxostat) and manage blood pressure, fluid intake, and avoid high-purine diets to improve the course of both conditions.
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