The diagnosis of gout is a complex process that requires the integration of various assessment methods. Physicians typically begin by confirming whether the patient exhibits typical symptoms such as acute arthritis attacks, joint redness, swelling, heat, and pain through detailed medical history inquiries and clinical observations. Further combination of blood tests, joint fluid analysis, and imaging studies is necessary to establish the diagnosis and rule out other similar diseases.
The key to diagnosing gout lies in confirming abnormal uric acid metabolism and the formation of monosodium urate crystals within the joints. The medical community has established clear diagnostic standards and processes, including the diagnostic criteria set forth by the American College of Rheumatology (ACR) in 1977, as well as new methods that incorporate imaging technologies. Through systematic evaluation, physicians can accurately differentiate gout from rheumatoid arthritis, infectious arthritis, and other diseases, thereby formulating personalized treatment plans.
Clinical evaluation is the first step in diagnosing gout, where physicians analyze the following aspects:
First, a detailed medical history inquiry is conducted, including the frequency of attacks, pain patterns, past medical history (such as hyperuricemia, kidney disease), and family history. Gout often presents as acute severe pain in a single joint, with the first metatarsophalangeal joint being the most commonly affected.
During the physical examination, physicians will observe the degree of redness and swelling in the affected joint, the range of motion limitations, and whether gouty tophi (gout nodules) are present. If the patient has a history of recurrent attacks, the extent of joint damage and the risk of chronic complications need to be assessed. Additionally, physicians will evaluate whether the patient has related factors such as metabolic syndrome symptoms (e.g., hypertension, obesity).
Blood tests primarily measure serum uric acid levels, but isolated blood uric acid values must be interpreted cautiously, as uric acid levels may temporarily decrease due to acute inflammation during gout attacks. Physicians typically combine blood uric acid results from the intercritical period to enhance diagnostic accuracy.
Joint aspiration to extract synovial fluid, followed by microscopic examination revealing birefringent monosodium urate crystals, is the gold standard for diagnosing gout. The crystals appear needle-shaped and must be confirmed for their positive birefringent characteristics using polarized light microscopy. Although this procedure is invasive, it can directly verify the diagnosis and avoid misdiagnosis.
X-ray examinations may appear normal during the acute phase, but in the chronic stage, bone destruction around the joint and gouty tophi can be observed. Ultrasound can detect intra-articular birefringent crystals or "gout stones" on the bone-cartilage surface, while dual-energy computed tomography (DECT) can non-invasively show uric acid deposits, becoming an emerging diagnostic tool.
Screening for gout should target high-risk groups, including those with a family history, hyperuricemia, kidney disease, or those on diuretic therapy. Physicians may use the 1977 ACR diagnostic criteria, which include a comprehensive assessment of symptom characteristics, laboratory data, and imaging findings.
Differential diagnosis is a critical step in the gout diagnostic process, requiring differentiation from the following diseases:
Rheumatoid arthritis: Typically affects symmetrical small joints, is positive for rheumatoid factor, and lacks uric acid crystals.
Infectious arthritis: Often accompanied by fever and a sharp increase in white blood cells, joint fluid cultures can confirm pathogens.
Pseudogout: Caused by calcium pyrophosphate crystals, X-rays show calcification, and the crystal morphology differs from monosodium urate.
During acute gout attacks, it is important to distinguish from gouty tophi infections and reactive arthritis, while in the chronic stage, it is necessary to assess for complications such as kidney stones or renal dysfunction. Physicians will make a comprehensive judgment based on the urgency of symptoms, the anatomical location of the affected joint, and the results of auxiliary examinations.
Early diagnosis can effectively prevent the progression of gout to chronic joint disease. Untreated patients may develop chronic gout within 5-10 years, leading to permanent joint destruction and kidney damage. Early use of urate-lowering therapy can reduce the frequency of acute attacks and decrease the cumulative effects of crystal deposition.
Early diagnosis also improves quality of life, as pain management during acute attacks should be initiated within 24 hours; delayed diagnosis may lead to symptom exacerbation. Studies show that the average time from symptom onset to diagnosis is 2-3 years, highlighting the importance of raising diagnostic awareness.
After diagnosis, a long-term follow-up mechanism should be established, monitoring blood uric acid levels and liver and kidney function every 3-6 months. Physicians will adjust treatment plans based on the patient's age, frequency of attacks, and complications to ensure blood uric acid levels are maintained at <6mg/dL to promote crystal dissolution.
During an acute gout attack, if symptoms of redness, swelling, and heat in the joints occur, and the severity of pain affects daily activities, it is recommended to seek medical attention promptly. If accompanied by fever or redness and ulcers on the skin around the joint, there may be a risk of infection, requiring immediate medical attention to rule out serious complications.
Why do physicians require fasting blood tests for uric acid measurement?Physicians request fasting blood tests to measure serum uric acid levels mainly to eliminate the temporary effects of diet on uric acid values, ensuring data accuracy. After consuming high-purine foods, uric acid levels may temporarily rise; fasting tests can more objectively reflect long-term metabolic status.
Why is regular monitoring of blood pressure and kidney function necessary during gout treatment?Hyperuricemia may share common pathophysiology with hypertension and renal dysfunction, and long-term use of urate-lowering medications may also affect kidney metabolism. Regular monitoring of these indicators can help detect drug side effects or metabolic complications early and adjust treatment strategies.
Which seemingly "low-purine" beverages might trigger gout in daily diet?High-sugar fruit juices and fructose in carbonated drinks may promote endogenous uric acid production, increasing the risk of gout attacks. Even if labeled as "low-purine," excessive intake of sugary beverages should be approached with caution, and it is recommended to replace them with plain water or unsweetened tea.
Why can't gout be diagnosed solely based on abnormal blood uric acid levels?Elevated blood uric acid levels may indicate metabolic abnormalities, but gout diagnosis requires a combination of clinical symptoms (such as sudden onset arthritis) and imaging studies (such as dual-energy CT). Some patients may have normal uric acid levels and still experience gout attacks, thus requiring a comprehensive assessment of multiple indicators.
%201.svg)
Copyright © 2025 MedFrontiers. All Rights Reserved.
