OVERVIEW

What is gout?

Gout occurs due to a disorder in the body's metabolism of purines or the inability to excrete uric acid normally, leading to the accumulation of urate in the body, particularly in joints and kidneys, which causes inflammatory reactions and tissue damage.

During acute episodes, it manifests as severe pain in one or more joints^[1].

During acute gout attacks, symptoms can be relieved through pain relief and anti-inflammatory treatment.

The most crucial treatment during the remission phase is uric acid-lowering therapy. Adhering to this therapy can prevent recurrent gout attacks, halt joint destruction and deformity, and protect the kidneys from damage caused by hyperuricemia.

Is gout common?

Relatively common. In China, the prevalence of gout ranges from 3 to 28 cases per 1,000 people^[1]. The condition predominantly affects middle-aged and elderly men and postmenopausal women, with men being more affected than women. Among all gout patients, only 5%–20% are female, meaning that out of every 100 gout patients, only 5 to 20 are women^[2].

SYMPTOMS

What are the typical symptoms during an acute gout attack?

Gout initially affects only the joints, commonly occurring at the joint connecting the big toe to the foot (the first metatarsophalangeal joint), though it may also occur in other joints such as the ankle or knee.

Typical attacks often wake the patient at night with joint pain that intensifies rapidly, reaching peak severity within hours. The joint quickly becomes red, hot, and tender. Early episodes usually resolve on their own within 3–10 days, and most patients experience varying intervals between attacks with no lasting effects before the next episode^[2].

Although acute gout attacks may resolve spontaneously, the pain is often severe and unbearable, so seeking medical attention is advisable.

Besides joint pain, does gout cause other complications?

Yes.

• Tophi: Subcutaneous nodules formed by urate crystal deposits, which can occur anywhere in the body. They appear as palpable, tender lumps and, in severe cases, may cause skin redness, swelling, or ulceration.
• Joint dysfunction and deformity: Urate deposits in the toes, ankles, knees, or surrounding tissues can lead to bone erosion and tissue fibrosis, resulting in impaired joint function or deformities.
• Kidney stones: Recurrent gout attacks may cause urate accumulation in the kidneys, leading to kidney stones.
• Increased disease and mortality risks: If blood uric acid levels remain uncontrolled, gout patients face higher risks of cardiovascular disease, metabolic syndrome, type 2 diabetes, hypertension, hyperlipidemia, obesity, chronic kidney disease, and premature death.

Do all gout patients develop tophi?

Not necessarily.

Tophi typically develop 3–40 years after gout onset, averaging around a decade. Not every gout patient will develop tophi. However, their presence indicates progression to chronic gouty arthritis^[3].

Which medical specialties treat gout?

Rheumatology, endocrinology, or nephrology departments are appropriate for gout management. Patients with tophi may require orthopedic consultation, while kidney complications should be addressed by nephrology.

CAUSES

What are the causes of gout?

Gout is associated with hyperuricemia. However, not all patients with hyperuricemia develop gout, as individual differences exist, which may be related to one's genes.
Additionally, certain triggers often lead to gout attacks in hyperuricemia patients.

What is hyperuricemia?

Hyperuricemia is a metabolic disorder primarily caused by purine metabolism dysfunction and/or impaired uric acid excretion.

Purines are naturally occurring substances in biological cells, and many of the foods we consume contain purines. The body metabolizes purines into uric acid. When uric acid production increases or excretion decreases, blood uric acid levels rise.

Under normal dietary conditions, if two separate fasting blood uric acid tests show levels > 420 µmol/L (regardless of gender), hyperuricemia can be diagnosed.

The hyperuricemia we commonly refer to is "primary hyperuricemia."

Some cases of hyperuricemia are caused by other specific diseases (such as kidney disease, blood disorders, etc.), or by certain medications, chemotherapy, or radiation therapy, which are termed "secondary hyperuricemia."

What are the common triggers for gout attacks?

Common triggers for gout attacks include trauma, excessive alcohol consumption, overeating, consuming high-purine foods (such as organ meats, rich meat broths, seafood, etc.), overexertion, cold exposure, and stress. These factors can increase purine levels in the body or specific areas, leading to urate crystal formation and triggering gout^[4].

Is gout hereditary?

It may be hereditary. Gout is a polygenic genetic disorder with a certain hereditary tendency^[1].

Who is more prone to gout?

• Middle-aged and elderly men: This group often includes individuals with affluent lifestyles, obesity, frequent social engagements, high alcohol and meat consumption, and comorbidities such as hypertension, diabetes, or hyperlipidemia, which disrupt uric acid metabolism.
• Postmenopausal women: Due to declining estrogen levels, uric acid excretion is affected, increasing the risk of gout.
• Coastal populations: Their dietary habits (high seafood intake) lead to greater purine consumption, raising the likelihood of gout.
• Obese individuals: Obesity disrupts metabolic processes, increasing susceptibility to gout.
• People with metabolic disorders: Conditions like diabetes and hyperlipidemia can impair uric acid metabolism, predisposing them to gout.

DIAGNOSIS

What tests are needed for suspected gout?

• Blood test: When gout is suspected, the most direct method is a blood test to measure uric acid levels. If two separate blood tests on different days show uric acid levels exceeding 420 μmol/L, hyperuricemia can be diagnosed^[5].
• Ultrasound: Doctors can assess the severity of the condition by performing an ultrasound on the affected joint. Ultrasound imaging may reveal a "double contour sign," urate crystal deposits, tophi, or bone erosion^[6].
• Joint fluid analysis: If acute gout is suspected, joint fluid can be extracted and examined for crystals. The presence of monosodium urate crystals strongly suggests a gout flare. This test can also check for bacterial infection to rule out infectious arthritis^[5].
• Colchicine diagnostic trial: Colchicine is the first-line treatment for acute gout. Doctors may use it diagnostically—if pain improves after administration, gout is likely. However, this method is not 100% accurate and misdiagnosis is possible^[1].

Does hyperuricemia always lead to gout?

Not necessarily.

Elevated uric acid is the foundation and most direct risk factor for gout. Higher uric acid levels increase the likelihood of gout.

Studies show that in mainland China, the prevalence of hyperuricemia is 13.3%, while gout occurs in 1.1% of cases—meaning roughly 11 out of 133 hyperuricemia patients develop gout^[7].

Is joint swelling with high uric acid always gout?

Not always.

Joint swelling can result from osteoarthritis, rheumatoid arthritis, infections, etc. Even with elevated uric acid, it may not indicate gout. Gout is considered only when characteristic arthritis (sudden nighttime pain peaking within hours, rapid swelling) coincides with hyperuricemia.

Is uric acid always high during a gout attack?

No.

Some gout patients have normal serum uric acid levels during flares^[8]. Ruling out gout solely based on normal uric acid may lead to misdiagnosis.

Does higher uric acid mean worse gout?

Not necessarily.

Theoretically, higher uric acid increases the risk and severity of gout attacks. However:

• Some patients have severe arthritis but near-normal uric acid levels.
• Others show markedly high uric acid without gout flares.
• Uric acid may rise during remission but not during attacks.

Thus, uric acid levels alone don’t determine gout severity.

TREATMENT

How to Reduce Pain During an Acute Gout Attack?

During an acute gout attack, pain-relieving and anti-inflammatory medications should be used as early as possible to alleviate discomfort. Commonly used drugs include colchicine, ibuprofen, etoricoxib, prednisone, and dexamethasone.

General treatments can also be applied, such as elevating the affected area, immobilizing the involved joint (reducing joint movement), or bed rest.

Is Medication Still Needed After a Gout Attack Subsides? How to Treat It?

It depends on the specific situation.

After using nonsteroidal anti-inflammatory drugs (NSAIDs) or colchicine during an acute gout attack, the pain usually subsides. If lifestyle changes alone can maintain normal uric acid levels and prevent further gout attacks, medication may not be necessary.

However, for patients with recurrent gout attacks, uric acid-lowering drugs should be used under the guidance of a specialist to maintain normal uric acid levels and reduce flare-ups.

What Is the Ideal Uric Acid Level for Gout Patients?

For gout patients, uric acid levels should be kept below 360 µmol/L. If gout attacks occur more than twice, or if tophi or kidney uric acid stones are present, levels should be reduced to below 300 µmol/L^[5].

Is Lower Uric Acid Always Better for Gout Patients?

No.

Uric acid is the end product of purine metabolism in the body, and at normal levels, it has antioxidant effects. Both excessively high and low uric acid levels may increase the risk of cardiovascular disease. Therefore, uric acid should not be too low but maintained within an appropriate range, not below 180 µmol/L^[5].

Are Antibiotics Like Cephalosporins Needed During a Gout Attack?

Usually not.

During an acute gout attack, the affected joint often shows significant redness, swelling, heat, pain, and limited mobility. Severe cases may even present with fever and elevated white blood cell counts, leading to the mistaken belief that an infection is present and antibiotics are needed.

However, gout is a non-infectious inflammatory condition—antibiotics like cephalosporins have no therapeutic effect on gout itself. Antibiotics should only be considered if tophi rupture and become infected, and renal toxicity should be minimized when selecting them.

Can Uric Acid-Lowering Drugs Be Used During a Gout Attack?

It depends.

• Using uric acid-lowering drugs during an attack may cause a rapid drop in blood uric acid levels, leading to a disparity between joint and systemic uric acid levels, which can worsen inflammation and prolong the attack. Therefore, the decision should be based on individual circumstances:
• For patients who have never used uric acid-lowering drugs: Acute symptoms should be managed with anti-inflammatory and pain-relieving medications like colchicine or corticosteroids. Uric acid-lowering drugs can be started two weeks after pain control.
• For patients already on long-term uric acid-lowering therapy: The medication should not be stopped during an acute attack.

Does a Gout Attack During Uric Acid-Lowering Treatment Mean the Treatment Is Ineffective?

No.

Gout attacks are more frequent in the early stages of uric acid-lowering therapy because the decrease in blood uric acid levels causes urate crystals in tissues to redistribute and deposit in joints, rather than indicating worsening symptoms.

To prevent attacks during this phase, NSAIDs (e.g., ibuprofen) or colchicine can be used alongside uric acid-lowering drugs without discontinuing them. Symptoms will improve once uric acid levels stabilize over time.

Should Medication Continue After Uric Acid Levels Are Lowered in Gout Patients?

Yes.

Gout primarily results from abnormal purine metabolism, making it a chronic condition like diabetes or hypertension that requires long-term medication to maintain target uric acid levels. Stopping medication may lead to rising uric acid levels and disease recurrence.

Under a specialist's guidance, the minimal effective dose can be used to control uric acid levels, reducing potential side effects and treatment costs. Generally, the longer the disease duration and the more tophi present, the longer uric acid-lowering therapy may be needed^[5].

How Are Tophi Treated?

• Medication: Uric acid-lowering drugs can prevent tophi from growing if blood uric acid is maintained below 300 µmol/L.
• Minimally invasive surgery: Recurrent or stubbornly painful tophi can be treated with minimally invasive surgery to remove urate crystals from joints and surrounding tissues, reducing future attacks.
• Pain and anti-inflammatory treatment: Acute tophi flare-ups can be managed with colchicine or ibuprofen.
• Surgical removal: Tophi may erode bones, cartilage, synovium, tendons, or ligaments, causing deformities or joint dysfunction, necessitating surgical excision.

Can Gout Be Cured?

Currently, gout cannot be cured^[1].

Gout is a lifelong metabolic disorder with no definitive cure. However, lifestyle changes and medication to control uric acid levels can significantly reduce attack frequency and prevent further organ damage.

Do Western Medications for Gout Have Side Effects?

Yes. Potential side effects include exfoliative dermatitis and kidney stones. Doctors should evaluate and adjust treatment plans accordingly.

Does Long-Term Use of Uric Acid-Lowering Drugs Cause Dependence?

First, uric acid-lowering drugs are not addictive, so there is no risk of dependence or withdrawal symptoms upon discontinuation.

Second, the misconception of dependence arises when uric acid levels rise after stopping medication. This occurs because gout patients inherently have abnormal uric acid metabolism, requiring long-term drug control.

DIET & LIFESTYLE

Can patients with gout and hyperuricemia drink alcohol?

It is recommended to abstain from alcohol completely.

Whether it's white wine, red wine, yellow wine, or beer, the main component is ethanol (alcohol), which slows down the excretion of uric acid, leading to its accumulation and triggering gout. Beer also contains large amounts of substances that can be converted into uric acid.

Simply put, drinking alcohol increases uric acid intake and reduces its excretion, which can induce or worsen gout attacks.

Therefore, gout patients should abstain from alcohol.

How should gout patients drink water?

Daily water intake should be maintained at 2 to 3 liters (4–6 standard 500ml bottles of mineral water), with a daily urine output of at least 1.5 liters to facilitate uric acid excretion.

Drink water regularly and proactively, avoiding excessive intake only when thirsty. It is also not advisable to drink large amounts of water shortly before or immediately after meals.

The best times to drink water are between meals, in the evening (from 45 minutes after dinner until bedtime), and in the morning (from waking up until half an hour before breakfast).

What dietary restrictions and precautions should gout patients follow?

• Avoid high-purine foods: During acute gout attacks, opt for low-purine foods such as dairy products, eggs, vegetables, fruits, and refined grains. During remission, avoid high-purine foods like organ meats, seafood, and rich meat broths.
• Pay attention to cooking methods: Proper cooking can reduce purine content, such as boiling meat first and discarding the broth before further cooking.
• Limit sweets: Avoid consuming desserts, fruit juices, carbonated drinks, etc.

Food-induced gout triggers vary individually, so it's important to identify personal dietary patterns. If a certain food consistently triggers gout attacks, avoid it.

Additionally, limiting high-purine intake does not mean completely avoiding moderate or high-purine foods. Instead, focus on keeping daily purine intake below 200 mg, maintaining nutritional balance, and avoiding a monotonous diet.

Can gout patients eat whole grains?

No, this is a misconception.

No studies have proven that whole grains increase gout risk. Some whole grains have low purine content. For example, corn and millet contain less than 10 mg/100 g of purines, while refined rice contains 20 mg—more than double.

Moreover, gout patients need sufficient B vitamins and potassium, which are much lower in refined white rice due to processing. Corn and millet contain several times more potassium and B vitamins than refined rice.

Therefore, it is recommended to diversify staple foods, moderately replacing refined grains with whole grains and tubers, which aids weight management, improves metabolic function, and helps control uric acid levels to prevent gout attacks.

Can gout patients eat soy products?

Neither excessive consumption nor strict avoidance is recommended^[5].

By weight, dried beans have purine levels similar to lean meat, but wet beans (e.g., tofu) contain less purine. Additionally, during processing, cooking, and preparation, a significant portion of purines dissolve into water and are removed.

Thus, consuming the same weight of soy products results in much lower purine intake compared to eating whole soybeans.

Furthermore, the types of purines in soy products differ from those in meat, leading to relatively less uric acid production even when consumed in equal amounts.

Therefore, there is no need to fear soy products. Moderate intake does not raise blood uric acid levels or trigger gout attacks. Soaking and rinsing solid soy products in hot water before consumption can further reduce purine intake.

What lifestyle precautions should gout patients take?

Obese individuals should aim for weight loss to achieve a normal BMI, adopt a healthy diet, and engage in moderate exercise.

Avoid the aforementioned factors that trigger gout attacks.

Actively manage conditions like hypertension, diabetes, and hyperlipidemia to prevent mutual exacerbation of these "four highs."

PREVENTION

Can Gout and Hyperuricemia Be Prevented?

Before gout develops, hyperuricemia often has no noticeable symptoms, making it difficult to detect and easy to overlook. Most cases are only discovered after an acute gout attack occurs. To prevent gout, it is necessary to stop hyperuricemia from progressing and causing further harm, such as recurrent gout attacks, joint dysfunction, joint deformities, kidney damage, or kidney stones. Specific measures include:

• Losing weight and maintaining a healthy body shape.
• Quitting alcohol and reducing sugary drinks.
• Avoiding excessive consumption of meat and seafood.
• Avoiding prolonged sitting and engaging in moderate exercise.

Can Frequent Gout Attacks Be Prevented?

Frequent gout attacks not only cause more suffering for patients but also accelerate disease progression. Therefore, those who have experienced gout can try the following methods to reduce or prevent future attacks.

• Weight loss: Maintain a healthy weight within the normal range. You can calculate your Body Mass Index (BMI): weight (kg) ÷ height (m) ÷ height (m). A result between 18.5 and 24 is considered normal. Values below or above this range indicate an unhealthy state. For example, a person weighing 64 kg and standing 1.7 m tall has a BMI of 22.1, which falls within the healthy range.
• Quitting alcohol: Alcohol slows down the body's ability to metabolize uric acid, leading to its accumulation and increasing the risk of gout. Therefore, it is crucial to avoid alcohol.
• Healthy diet: Maintain a balanced and varied diet. Avoid excessive intake of high-purine foods like meat or seafood while neglecting fresh fruits and vegetables. Focus on low-purine foods such as vegetables, dairy products, and fruits, and limit high-purine foods like meat and seafood. Drinking plenty of water helps dilute uric acid levels and promotes its excretion.
• Moderate exercise: Exercise aids in weight control and overall health. Suitable activities include brisk walking, jogging, and swimming. However, avoid excessive intensity to prevent injuries, which can trigger gout attacks.
• Managing other conditions: Diseases like diabetes, hyperlipidemia, and hypertension increase the risk of hyperuricemia. Actively treating these conditions helps prevent their mutual influence.
• Uric acid-lowering treatment: For those already diagnosed with hyperuricemia or gout, long-term, proper uric acid-lowering therapy is essential to prevent recurrent attacks.