Gout is a chronic disease closely related to abnormal uric acid metabolism, characterized primarily by acute arthritis attacks and long-term hyperuricemia. The incidence of this disease is gradually rising in modern society, closely associated with dietary habits, lifestyle, and genetic factors. The key to gout lies in the excessively high concentration of uric acid in the body, leading to the deposition of urate crystals in the joints or surrounding tissues, triggering inflammatory responses, resulting in severe pain and swelling.
According to medical research, the pathogenesis of gout involves an imbalance in uric acid metabolism, which may be caused by excessive uric acid production or insufficient excretion. Common factors in modern individuals, such as a high-purine diet, obesity, and metabolic syndrome, can exacerbate this issue. Early diagnosis and treatment can not only relieve acute symptoms but also effectively reduce the risk of joint damage and complications. Understanding the full picture of gout helps patients and healthcare teams collaboratively develop long-term management strategies.
The core cause of gout is the disorder of uric acid metabolism in the body, leading to prolonged high levels of uric acid in the blood (hyperuricemia). Uric acid is the final product of purine metabolism and is normally excreted through the kidneys. When uric acid is produced excessively or not excreted adequately, the excess uric acid forms urate crystals, which deposit in the joints or soft tissues, triggering inflammatory responses from the immune system.
Genetic factors play a key role in the development of gout. About 10-20% of gout patients have a family history, and genetic differences may affect the kidneys' ability to excrete uric acid. Additionally, gender and age are also important risk factors, with men having a higher incidence between the ages of 30 and 50, while women's risk gradually increases after menopause. Obesity, excessive alcohol consumption (especially beer), high-purine diets (such as organ meats and seafood), and certain medications (such as diuretics) may all trigger gout attacks.
The most typical symptom of gout is the sudden onset of acute arthritis, commonly occurring at the base of the big toe (metatarsophalangeal joint), but it can also affect the ankle, knee, or fingers. During an attack, patients experience severe pain in the affected joint, often waking up at night due to the pain. The joint may exhibit redness, swelling, heat, and tenderness, and in severe cases, even slight pressure (such as contact with bed sheets) can cause intense discomfort.
The acute attack phase usually lasts 3-10 days, but if not properly treated, the frequency and duration of attacks may gradually increase. Chronic gout patients may develop white nodules (tophi) in the earlobes, around joints, or under the skin, which are clear signs of long-term deposition of urate crystals. Some patients may also experience systemic symptoms such as fever, fatigue, or a slight increase in white blood cell count.
The diagnosis of gout requires a combination of clinical symptoms, laboratory tests, and imaging results. Physicians typically begin with a physical examination to assess inflammatory indicators such as redness, swelling, and heat in the affected joint. Blood tests measure serum uric acid levels, but it is important to note that during an acute attack, inflammatory responses may temporarily lower uric acid levels, necessitating retesting several weeks after the attack for accurate baseline values.
Key diagnostic procedures include joint fluid analysis, where sodium urate crystals are observed under polarized light microscopy (which have birefringent properties). Imaging tests such as X-rays can reveal destructive changes in the bones during chronic stages, including bone calcification or osteoporosis. Ultrasound or dual-energy computed tomography (DECT) can detect crystal deposits early, improving diagnostic accuracy.
According to the 2015 American College of Rheumatology diagnostic criteria, a diagnosis can be confirmed if any of the following conditions are met:
Gout treatment is divided into two main directions: "acute phase control" and "long-term uric acid management." During an acute attack, the primary goal is to relieve pain and inflammation, with commonly used medications including non-steroidal anti-inflammatory drugs (NSAIDs), colchicine, or corticosteroids. These medications should be chosen based on the patient's heart and kidney health; for example, NSAIDs should be used with caution in patients with renal insufficiency.
Long-term uric acid management focuses on lowering serum uric acid levels to target values (usually <6mg/dL), with main medications including:
Lifestyle adjustments are fundamental to treatment, including:
Effective prevention of gout attacks requires a multi-faceted approach. Dietary control is a key strategy, recommending a low-purine diet and increasing the intake of low-fat dairy products and vegetables (such as cherries and spinach). Studies have shown that vitamin C supplements (500-1500mg/day) may help reduce the frequency of attacks, but should be used under medical supervision.
Regular exercise and weight management can significantly lower the risk of attacks. It is recommended to engage in at least 150 minutes of moderate-intensity aerobic exercise weekly, avoiding sudden weight loss that could cause metabolic disturbances. Alcohol consumption should be particularly monitored, as beer is considered a high-risk beverage due to its purine nucleotide content and the alcohol itself inhibiting uric acid excretion. Regular monitoring of serum uric acid levels is essential, especially for those with a family history, who should start annual checks from age 40.
Establishing the following daily habits can reduce the risk of attacks:
If any of the following conditions occur, immediate medical attention is required:
The following conditions require regular follow-up:
If any of the following symptoms occur, immediate medical attention is required:
Yes, studies have shown that daily intake of low-fat milk or yogurt can lower blood uric acid levels. The proteins and calcium in dairy products may help promote uric acid excretion, and gout patients are advised to include them in their daily diet, but should avoid high-fat or added sugar products.
Should all uric acid-lowering medications be stopped immediately during an acute attack?No, during an acute attack, it is important to continue taking uric acid-lowering medications prescribed by the doctor (such as allopurinol), but they should be combined with anti-inflammatory pain relief medications or colchicine to alleviate symptoms. Sudden discontinuation of medication may lead to fluctuations in blood uric acid levels, potentially triggering more severe attacks, so it is essential to follow the doctor's instructions for medication adjustments.
Do patients with intermittent gout need to take medication long-term?It depends on the severity of the condition. If blood uric acid levels remain high for an extended period or if kidney stones or joint damage have occurred, the doctor may recommend long-term medication to prevent recurrent attacks. Mild cases may initially focus on dietary control, with regular monitoring of indicators to decide whether medication intervention is necessary.
What safe physical activities can be done if experiencing toe or joint pain during exercise?It is recommended to choose low-impact exercises such as swimming or cycling, avoiding prolonged running or intense weight-bearing exercises. During the acute phase of an attack, exercise should be paused, and once symptoms improve, activities can be gradually resumed through water rehabilitation, ensuring comfortable footwear to reduce joint pressure.
Does experiencing recurrent gout attacks in a short period indicate treatment failure?This may be related to medication methods or lifestyle factors. If uric acid-lowering treatment has begun, initial attacks may be triggered by the movement of uric acid crystals, and the doctor may adjust medication dosages or add medications to inhibit crystal movement. Continued high-purine diets, dehydration, or alcohol abuse may also lead to recurrent attacks, necessitating lifestyle adjustments.
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