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Gouty arthritis

  This disease is a joint disease with diverse clinical manifestations caused by the deposition of calcium pyrophosphate dihydrate crystals, including intermittent acute arthritis; degenerative joint disease, sometimes severe, sometimes asymptomatic, X-ray examination can show the image of joint cartilage calcification in specific areas.

 

Table of Contents

1. What are the causes of gouty arthritis
2. What complications can gouty arthritis easily lead to
3. What are the typical symptoms of gouty arthritis
4. How to prevent gouty arthritis
5. What laboratory tests are needed for gouty arthritis
6. Dietary preferences and taboos for gouty arthritis patients
7. Conventional methods of Western medicine for the treatment of gouty arthritis

1. What are the causes of gouty arthritis

  The etiology of this disease is unknown and is often associated with trauma (including surgical procedures), amyloidosis, myxedema, hyperparathyroidism, gout, and hemosiderosis, suggesting that the deposition of calcium pyrophosphate dihydrate (PPD) crystals in cartilage is secondary to degenerative or metabolic changes in cartilage. Symptoms usually appear in patients over 60 years old, with an incidence of cartilage calcification of about 30% in those over 70, 50% in those close to 90, and the incidence is the same in both genders.

 

2. What complications can gouty arthritis easily lead to

  Fibrous cartilage and hyaline cartilage of the affected joint show punctate and strip-like calcification. Calcification can also be found in synovium, joint capsule, tendons, and intra-articular ligaments. Although the prognosis is generally good, severe destructive joint damage similar to neurogenic arthritis (Charcot joint) can also occur. Therefore, once diagnosed, active treatment should be initiated to prevent the occurrence of complications.

3. What are the typical symptoms of pseudo-gouty arthritis

  Resnick (1988) according to his report of a group of 192 cases, divided the clinical manifestations of the disease into the following 7 types:

  1, Type I Pseudo-gout:Similar to gout attacks but not gout, its characteristics are acute or subacute, self-limiting arthritis attacks, affecting one or several small joints, lasting from 1 day to several weeks, usually mild pain, this type is best involved in the knees, but hips, shoulders, elbows, wrists, ankles, and so on can be affected, accounting for about 10% to 20%.

  2, Type II Pseudo-rheumatoid Arthritis: It is characterized by persistent, acute exacerbation of arthritis, symptoms can last for 4 weeks to several months, with an increased ESR, accounting for about 2% to 6%.

  3, Type III Pseudo-osteoarthritis—(1): This type is the most common, accounting for about 35% to 60%, presenting as chronic progressive arthritis, and can be accompanied by occasional acute infection, symmetrically affecting large joints such as knees, hips, metacarpophalangeal joints, elbows, ankles, wrists, and shoulders. The characteristics are symmetric involvement and flexion contracture, especially in the knees and elbows.

  4, Type IV Pseudo-osteoarthritis—(2): It accounts for about 10% to 35%, and the clinical characteristics of this type are chronic progressive arthritis without acute exacerbation, like type III, its manifestations are similar to degenerative joint disease.

  5, Type V Asymptomatic Joint Disease: Although there are reports, asymptomatic patients with CPPD crystal deposition disease can account for 10% to 20%, and the incidence of this clinical type is quite high, but asymptomatic patients are rarely seen in clinical practice. In recent years, there have been reports that in elderly Jews, cartilage calcification can account for 27.6%, most of whom are asymptomatic, and even in some patients with joint symptoms, calcification occurs in joints without obvious symptoms. Aspiration of joints without symptoms, such as metatarsophalangeal joints, confirms the presence of CPPD crystal deposition, and these patients have or do not have radiological manifestations of pseudo-gout.

  6, Type VI Pseudo-neuroarthropathy: It accounts for about 0-2%, it is a rare clinical type of CPPD crystal deposition disease, and it is very similar to the manifestation of neuroarthropathy.

  7, Type VII Mixed Pattern (Miscellaneous Pattern): This is the least common type of the disease, accounting for about 0-1%, McCarty once emphasized that CPPD crystal deposition disease can produce symptoms similar to rheumatism and psychosomatic symptoms, and its clinical manifestations can also be similar to ankylosing spondylitis.

4. How to prevent pseudo-gouty arthritis

  For the prevention of this disease, particular attention should be paid to lifestyle habits:

  1. During holidays, avoid overeating and drinking, prevent overnutrition and obesity, maintain an ideal weight. Stay away from bad habits such as smoking and excessive drinking. Pay attention to the combination of work and rest. For those who work mentally, they should participate in physical activities every day to alternate between mental and physical activities and persist in this practice.

  2. Reasonable lifestyle arrangements. Life should be regular and moderate, while cultivating an optimistic spirit. Participate regularly in cultural and sports activities.

  3. Regular physical examinations. Physical examinations are very important for the prevention of gout, especially for those over 40 or overweight. A physical examination should be conducted every 1-2 years, including blood uric acid measurement, to detect hyperuricemia early and prevent the development of gout.

 

5. What laboratory tests are needed for pseudogouty arthritis?

  This disease is mostly diagnosed using imaging methods, with the main manifestations in the following aspects:

  1. Cartilage calcification

  The most commonly affected areas are the knee, wrist, pubic symphysis, elbow, and hip, with affected cartilage including fibrous cartilage and hyaline cartilage.

  (1) Fibrous cartilage calcification: The most commonly affected are the menisci of the knee, the triangular fibrocartilage disk of the wrist, the pubic symphysis, the fibrous ring of the intervertebral disc, and the acetabular and scapular labrum. It can also affect the glenohumeral and sternoclavicular joint pads. The deposits of fibrous cartilage are manifested as thickening, roughness, and irregular dense areas, especially in the middle of the joint cavity.

  (2) Transparent cartilage calcification: It can occur in many locations, but is most common in the wrist, knee, elbow, and hip joints. These deposits are thin and linear, parallel to the subchondral bone adjacent to them.

  2. Synovial calcification

  Calcification within the synovium is a common sign of CPPD crystal deposition disease. This type of calcification often coexists with cartilage calcification, but it is often more prominent. Synovial calcification is most common in the wrist, especially around the radiocarpal joint, the ulnar collateral ligament, the knee, metacarpophalangeal, and metatarsophalangeal joints; it may also be seen in the humeral acetabulum, elbow, hip, and acromioclavicular joints. The deposits are cloudy, especially at the joint margins, and may also resemble idiopathic synovial osteochondromatosis. Fragments of calcified synovium may coexist with fragments of calcified cartilage.

  3. Joint capsule calcification

  CPPD crystals are deposited in joint capsules, most commonly in the elbow and metatarsophalangeal joints, also seen in the metacarpophalangeal and glenohumeral joints. These clusters of fine or irregular linear calcifications cross the joints and may also be associated with joint contracture, especially in the elbow joint.

  4. Calcification of tendons, bursae, and ligaments

  Patients with CPPD crystal deposition may have calcification of tendons and ligaments, commonly found in the Achilles tendon, triceps, quadriceps, supraspinatus tendons, and subacromial bursa; it may also be seen in the prepatellar bursa, where the calcification of tendons is thin and linear, extending from the edge of the bone to a considerable distance. Calcification of bursae with infection is common at the olecranon, shoulder tendons, and bursal calcification, which may sometimes be seen in shoulder rotator cuff injuries.

  5. Soft tissue and vascular calcification

  Some patients may show soft tissue and vascular calcification, manifested as unclear calcification deposits, with soft tissue calcification most common in the elbow, wrist, and pelvic area, and vascular calcification may be related to coexisting diseases such as diabetes.

6. Dietary preferences and taboos for patients with pseudogouty arthritis

  1. Abstain from alcohol, and drink less coffee, tea, and cocoa: Alcohol can induce gout attacks and worsen the condition, and alcohol should be absolutely prohibited for gout patients; in addition, gout patients should not drink too strong or too much coffee, tea, and cocoa.

  2. Reduce fat intake, as fat can reduce the excretion of uric acid. For patients with gout complicated with hyperlipidemia, fat intake should be controlled within 20% to 25% of total calories.

  3. Reducing salt intake is also one of the dietary taboos for pseudogouty arthritis. Patients should limit daily intake to 2 to 5 grams.

  4. Limit purine intake. Purines are a component of the nucleus of cells, and any food containing cells contains purines, and purines are more abundant in animal foods. Patients should avoid eating internal organs, bone marrow, seafood, fermented foods, and legumes.

7. Conventional methods of Western medicine for the treatment of pseudogouty arthritis

  1. Regarding the treatment of this disease, some scholars believe that general treatment for acute arthritis should be adopted during the acute stage, including joint immobilization, joint aspiration, but the most critical step is to repeatedly flush to reduce the concentration of pyrophosphate in the synovial fluid to prevent its deposition on the articular cartilage. After completing the above operations, it is appropriate to inject prednisolone (the best is Dexamethasone) into the joint to reduce the acute inflammatory reaction of the microcirculation and the permeability to calcium pyrophosphate. For patients with clearly calcified menisci and symptoms similar to meniscus locking, meniscectomy should be performed, and the joint cavity should be explored to remove osteophytes and remove loose bodies and other factors that hinder joint function, in order to avoid the formation of osteoarthritis as much as possible.

  2. The use of colchicine for the treatment of this disease is also effective. The method is intravenous injection of 1mg for more than 2 to 5 minutes (diluted to 20ml with 0.9% sodium chloride, if the pain persists, inject 1mg again within 12 hours). When there is effusion in the acute synovitis, it is necessary to completely remove the effusion. Examine the crystals in the effusion, then inject a suspension of adrenal cortical hormone microcrystals into the joint. Indomethacin 75 to 150mg/d or other NSAIDs can usually control acute attacks quickly. Comparative studies show that taking 0.5 to 1.5mg of colchicine daily can prevent acute attacks.

 

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