Gout is a chronic disease closely related to abnormal uric acid metabolism, characterized mainly by acute arthritis attacks and long-term hyperuricemia. The incidence of this disease is gradually increasing in modern society and is closely associated with dietary habits, lifestyle, and genetic factors. The key to gout lies in excessively high uric acid levels in the body, leading to the deposition of urate crystals in joints or surrounding tissues, triggering inflammatory responses that cause severe pain and swelling.
According to medical research, the pathogenesis of gout involves a metabolic imbalance of uric acid, which may be caused by excessive production or insufficient excretion of uric acid. Common factors in modern individuals include high-purine diets, obesity, and metabolic syndrome, all of which exacerbate the problem. Early diagnosis and treatment not only alleviate acute symptoms but also effectively reduce joint damage and complication risks. Understanding the full picture of gout helps patients and healthcare teams develop long-term management strategies.
The core cause of gout is a disorder in uric acid metabolism, leading to persistently elevated serum uric acid levels (hyperuricemia). Uric acid is the final product of purine metabolism, normally excreted by the kidneys. When uric acid production is excessive or excretion is insufficient, the surplus uric acid forms urate crystals that deposit in joints or soft tissues, triggering inflammatory immune responses.
Genetic factors play a crucial role in the development of gout. About 10-20% of gout patients have a family history, and genetic differences may affect renal uric acid excretion capacity. Additionally, gender and age are important risk factors; men are more commonly affected between the ages of 30-50, while women’s risk increases after menopause. Obesity, excessive alcohol consumption (especially beer), high-purine diets (such as organ meats and seafood), and certain medications (like diuretics) can all trigger gout attacks.
The most typical symptom of gout is an acute onset of arthritis, commonly affecting the base of the big toe (metatarsophalangeal joint), but it can also involve the ankle, knee, or fingers. During an attack, patients experience intense pain in the affected joint, often waking them up at night. The joint becomes red, swollen, hot, and tender; in severe cases, even light pressure (such as contact with bedding) causes significant discomfort.
Acute episodes usually last 3-10 days, but if not properly treated, the frequency and duration of attacks may increase over time. Chronic gout patients may develop visible nodules (tophi) on the earlobes, around joints, or under the skin, which are signs of long-term urate crystal deposition. Some patients may also experience systemic symptoms such as fever, fatigue, or mild leukocytosis.
Diagnosis of gout requires a combination of clinical symptoms, laboratory tests, and imaging results. Physicians typically perform a physical examination to assess inflammation indicators such as redness, swelling, and warmth of the affected joint. Blood tests measure serum uric acid levels, but it is important to note that during acute attacks, uric acid levels may temporarily decrease due to inflammatory responses; thus, measurements should be taken several weeks after an attack for accurate baseline data.
Key diagnostic procedures include joint fluid analysis, observing urate sodium crystals under polarized light microscopy (which exhibit birefringence). Imaging studies such as X-rays can show chronic bone erosions, including "punched-out" lesions or osteopenia. Ultrasound or dual-energy computed tomography (DECT) can detect crystal deposits early, improving diagnostic accuracy.
According to the 2015 American College of Rheumatology diagnostic standards, a diagnosis can be confirmed if any of the following are met:
Gout treatment is divided into two main phases: "acute attack control" and "long-term uric acid management." During an acute attack, the primary goal is pain relief and anti-inflammatory treatment, commonly using non-steroidal anti-inflammatory drugs (NSAIDs), colchicine, or corticosteroids. These medications should be chosen carefully based on the patient’s cardiovascular and renal health, for example, NSAIDs should be used cautiously in patients with renal impairment.
Long-term uric acid management aims to lower serum uric acid levels to target (usually <6 mg/dL), mainly using medications such as:
Lifestyle modifications are fundamental to treatment, including:
Effective prevention of gout attacks involves multiple approaches. Dietary control is key; a low-purine diet with increased intake of low-fat dairy products and vegetables (such as cherries and spinach) is recommended. Studies suggest that vitamin C supplements (500-1500 mg/day) may help reduce attack frequency but should be used under medical supervision.
Regular exercise and weight management significantly lower attack risks. It is recommended to engage in at least 150 minutes of moderate-intensity aerobic activity weekly, avoiding sudden weight loss that can disrupt metabolism. Alcohol intake should be carefully monitored; beer, which contains purine nucleotides and alcohol itself, is considered high risk. Regular monitoring of blood uric acid levels is advised, especially for those with a family history, starting from age 40, with annual checks recommended.
Establishing the following daily habits can reduce attack risk:
If you experience the following, seek medical attention immediately:
Follow-up is needed in the following situations:
If you experience the following symptoms, seek emergency medical care immediately:
Yes, studies show that daily intake of low-fat milk or yogurt can lower serum uric acid levels. The proteins and calcium in dairy products may promote uric acid excretion. It is recommended that gout patients incorporate these into their daily diet, but they should avoid high-fat or sugary 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 prescribed uric acid-lowering medications (such as allopurinol), while also using anti-inflammatory or colchicine medications to relieve symptoms. Abrupt discontinuation can cause fluctuations in uric acid levels and potentially trigger more severe attacks. Always follow your doctor’s instructions for medication adjustments.
Do intermittent gout patients need long-term medication?It depends on the severity of the condition. If serum uric acid remains high over a long period or if kidney stones or joint destruction have occurred, doctors may recommend long-term medication to prevent recurrent attacks. Mild cases may initially be managed with dietary control and regular monitoring, with medication added if necessary.
How should I safely exercise if I experience toe or joint pain?Choose low-impact activities such as swimming or cycling, and avoid prolonged running or intense joint loading exercises. During an acute attack, exercise should be temporarily stopped. Once symptoms subside, gentle water-based rehabilitation can gradually restore activity levels. Wearing comfortable shoes to reduce joint pressure is also advised.
Does recurrent gout attack within a short period indicate treatment failure?It may be related to medication methods or lifestyle factors. During initial uric acid-lowering therapy, attacks can be triggered by crystal movement; in such cases, your doctor may adjust medication doses or add drugs to inhibit crystal movement. Continued high-purine diets, dehydration, or alcohol consumption can also cause recurrent attacks, requiring lifestyle adjustments.
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