The diagnosis of gout is a complex process that requires the integration of multiple assessment methods. Physicians typically begin with a detailed medical history inquiry and clinical observation to confirm whether the patient exhibits typical symptoms such as acute arthritis attacks, redness, swelling, heat, and pain in the joints. Further confirmation involves blood tests, joint fluid analysis, and imaging examinations to establish the diagnosis and exclude 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 procedures, including the 1977 American College of Rheumatology (ACR) diagnostic criteria and recent advancements incorporating imaging techniques. Through systematic evaluation, physicians can accurately differentiate gout from rheumatoid arthritis, infectious arthritis, and other conditions, thereby enabling personalized treatment plans.
Clinical assessment is the first step in diagnosing gout. Physicians analyze from the following perspectives:
First, a detailed medical history is taken, including the frequency of attacks, pain patterns, past medical history (such as hyperuricemia, kidney disease), and family history. Gout often presents as a sudden severe pain in a single joint, most commonly affecting the first metatarsophalangeal joint.
During physical examination, physicians observe the redness, swelling, and range of motion of the affected joint, and check for the presence of tophi (gout nodules). If the patient has a history of recurrent attacks, the extent of joint damage and risk of chronic complications are assessed. Additionally, physicians evaluate for associated metabolic syndrome factors such as hypertension and obesity.
Blood tests primarily measure serum uric acid levels. However, isolated serum uric acid values should be interpreted with caution, as uric acid may temporarily decrease during an acute gout attack due to inflammation. Physicians often combine blood uric acid results obtained during interictal periods to improve diagnostic accuracy.
Joint aspiration and analysis of synovial fluid under a microscope to observe negatively birefringent monosodium urate crystals is the gold standard for gout diagnosis. The crystals are needle-shaped and require confirmation with polarized light microscopy to verify their positive birefringence. Although this procedure is invasive, it provides direct evidence for diagnosis and helps prevent misdiagnosis.
X-ray may appear normal during the acute phase but can show joint erosions and tophi in chronic stages. Ultrasound can detect intra-articular double refraction crystals or tophi on the bone-cartilage surface, while dual-energy computed tomography (DECT) can non-invasively visualize urate deposits, emerging as a new diagnostic tool.
Screening for gout should target high-risk groups, including those with a family history, hyperuricemia, kidney disease, or on diuretic therapy. Physicians may use the 1977 ACR diagnostic criteria, which include a comprehensive assessment of symptoms, laboratory data, and imaging findings.
Differential diagnosis is a critical step in the gout diagnostic process, requiring differentiation from the following conditions:
Rheumatoid arthritis: Usually affects symmetrical small joints, with positive rheumatoid factor, and no urate crystals.
Infectious arthritis: Often accompanied by fever and a sharp increase in white blood cells; pathogen identification can be confirmed through joint fluid culture.
Pseudogout: Caused by calcium pyrophosphate dihydrate crystals, with calcification visible on X-ray, and crystal morphology different from urate crystals.
During acute gout attacks, differentiation from infected tophi or reactive arthritis is necessary. In chronic stages, evaluation for complications such as kidney stones or renal dysfunction is important. Physicians make comprehensive judgments based on symptom severity, affected joint location, and auxiliary test results.
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 renal damage. Early uric acid-lowering therapy can reduce attack frequency and decrease crystal deposition accumulation.
Early diagnosis also improves quality of life. Pain management during acute attacks should be initiated within 24 hours. Delayed diagnosis may worsen symptoms. Studies show that it takes an average of 2-3 years from symptom onset to diagnosis, highlighting the importance of improving diagnostic awareness.
After diagnosis, a long-term follow-up mechanism should be established, with monitoring of blood uric acid levels and renal and liver functions every 3-6 months. Physicians adjust treatment plans based on patient age, attack frequency, and complications, ensuring blood uric acid is maintained below 6 mg/dL to promote crystal dissolution.
During an acute gout attack, if redness, swelling, heat, and pain in the joint are severe enough to affect daily activities, prompt medical consultation is recommended. If accompanied by fever or redness and ulceration around the joint, which may indicate infection, immediate medical attention is necessary to exclude serious complications.
Why do doctors require fasting blood samples for uric acid testing?Fasting blood samples are requested to eliminate the influence of recent diet on uric acid levels, ensuring accurate results. After consuming high-purine foods, uric acid may temporarily increase; fasting provides a more objective reflection of long-term metabolic status.
During gout treatment, why is regular monitoring of blood pressure and kidney function necessary?Hyperuricemia may share pathogenic mechanisms with hypertension and renal dysfunction. Long-term use of uric acid-lowering drugs can also affect renal metabolism. Regular monitoring allows early detection of drug side effects or metabolic complications, enabling treatment adjustments.
Which seemingly "low-purine" beverages in daily diet may trigger gout?Fruit juices and carbonated drinks with high sugar content, especially fructose, can promote endogenous uric acid production, increasing the risk of gout attacks. Even if labeled as "low purine," excessive intake of sugary beverages should be cautious. It is recommended to replace them with plain water or unsweetened tea.
Why can't an elevated blood uric acid level alone diagnose gout?Elevated blood uric acid may indicate metabolic abnormality, but gout diagnosis requires clinical symptoms (such as sudden onset of arthritis) and imaging examinations (such as dual-energy CT). Some patients may experience gout attacks with normal uric acid levels; therefore, multiple indicators should be considered comprehensively.
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