Pain wind is divided into primary and secondary types. The disease cause is not yet fully understood, with the prominent features being hyperuricemia and the deposition of sodium urate crystals in connective tissues (especially cartilage and synovial membrane). Primary cases are more common, while a minority of patients develop secondary pain wind due to metabolic diseases such as hypoxanthine-guanine phosphoribosyltransferase deficiency, which leads to hyperuricemia.

bubble_chart Etiology

The disease has a familial tendency, and the inheritance pattern is still unclear. Regarding the pathogenesis of gouty arthropathy, many scholars generally believe it is related to polymorphonuclear leukocytes. During gout, sodium urate crystals released by synovial tissue and articular cartilage are phagocytosed by leukocytes in the joint fluid. These leukocytes then rupture, releasing proteases and inflammatory factors into the synovial fluid. The enzymes and inflammatory factors increase the number of leukocytes in the joint, leading to more leukocytes phagocytosing urate crystals and subsequently rupturing, releasing enzymes and inflammatory components. This forms a vicious cycle, further causing acute synovitis and destruction of articular cartilage. Gouty tophi are granulomas of varying sizes that form around urate crystals.

bubble_chart Clinical Manifestations

The onset of the disease may involve two or three joints, including the first metatarsophalangeal joint. Lesions of the first metatarsophalangeal joint account for about 50% of pain wind patients, making it the most commonly affected joint. The ankle, tarsus, knee, elbow, and wrist joints may also be involved. In recent years, due to the development of anticancer treatments, secondary pain wind has shown an increasing trend. Primary pain wind is predominantly found in men over 40 years old, while it is less common in women, mostly occurring in postmenopausal women. It is typically divided into four stages:

(1) Asymptomatic Stage: This stage lasts for a long time, with only elevated hematuria acid levels. About one-third of patients later develop joint symptoms.

(2) Acute Arthritis Stage: The onset is often sudden at night, with severe pain in the affected joints. The first joint involved is usually the big toe joint, followed by the ankle, knee, etc. The joints become red, swollen, hot, and tender, accompanied by general weakness, fever, headache, etc. This stage can last 3 to 11 days. Triggers for an attack include alcohol consumption, overeating, overexertion, cold exposure, surgical stimulation, and mental stress.

(4) Chronic Arthritis Stage: The transition from acute onset to chronic arthritis takes an average of about 11 years. The joints become stiff and deformed, with limited movement. About 30% of patients develop pain wind stones and renal complications, such as ureteral stones. In the advanced stage, hypertension, renal and cerebral stirred pulse sclerosis, and myocardial infarction may occur. A few patients die from renal failure or heart blood vessel accidents. Secondary pain wind follows a similar course, but the intermittent stage is shorter when secondary to hematologic diseases or glycogen storage diseases.

Hematuria acid levels are elevated, with the highest reaching 20 mg% (normal: 7 mg% in men, 6 mg% in women). Polarized microscopy reveals white blood cells in the joint synovial fluid that have phagocytized urate crystals. During the acute stage, white blood cell counts increase, and the erythrocyte sedimentation rate accelerates.

X-ray examinations show punched-out erosions in the subchondral bone, localized osteoporosis, erosions, or cortical breaks, as well as joint space narrowing and marginal bone proliferation. Pain wind stones may appear as calcified shadows.

bubble_chart Diagnosis

Clinical manifestations, laboratory tests, and X-ray examinations aid in diagnosis, but definitive confirmation requires the identification of urate crystals in the synovial membrane or joint fluid, as psoriatic arthritis and rheumatoid arthritis can sometimes also exhibit elevated uric acid levels.

bubble_chart Treatment Measures

It includes both systemic and local aspects. Colchicine is commonly used as a medication, and other options include phenylbutazone or indomethacin. If serum uric acid levels remain elevated, probenecid can also be used, which works by inhibiting the reabsorption of urate in the renal tubules, making it one of the effective treatments. In cases of kidney disease, allopurinol is usually the preferred treatment. During the acute phase, intra-articular steroid injections, joint immobilization, and local cold compresses can significantly alleviate symptoms. Sometimes, for gouty arthritis, joint arthroplasty or artificial joint replacement may be chosen to relieve joint pain and restore joint function.