Gouty arthritis is caused by deposits of uric acid in the joint capsule, bursa, cartilage, bone and other tissues, resulting in lesions and inflammatory reactions. There are two types of gout: primary and secondary. The etiology is not well understood and is characterized by hyperuricemia and sodium urate crystal deposition in connective tissue structures (especially cartilage and synovium). There are many primary cases, but in a few patients, hyperuricemia due to metabolic diseases such as enzymehypox-anthineguanine and phosphoribosyl-transferase deficiency is called secondary gout.
1. Etiology and pathology
Gout is caused by a long-term disorder of purine metabolism and an increase in blood uric acid. If the concentration of uric acid in the blood is higher than this saturation point for a long time, it is medically called “hyperuricemia”. Gout can be triggered by diet, weather changes, trauma, etc. Alcohol consumption can also trigger gout. The body fails to metabolize purines further and excretes them in the urine after consuming foods that contain too much purine. If the concentration of uric acid in the blood reaches saturation solubility, these substances eventually form crystals and accumulate in the soft tissues. If there is a trigger for the release of uric acid crystals from soft tissues such as joint membranes or tendons, the body’s immune system may become sensitized and inflammation may result.
There is a family history of gout, and the pattern of inheritance is not known. Regarding the pathogenesis of gouty arthropathy, many scholars generally believe that it is related to polymorphonuclear white blood cells. In gout, sodium urate crystals released from synovial tissue and articular cartilage are engulfed by white blood cells in the joint fluid. The white blood cells in turn destroy and release proteases and inflammatory factors into the synovial fluid. The enzymes and inflammatory factors increase the number of white blood cells in the joint, so more white blood cells that have phagocytosed urate crystals break down releasing enzymes and inflammatory components, creating a vicious cycle that further leads to acute synovitis and destruction of articular cartilage. Gout stones are crystalline granulomas of different sizes surrounding urate crystals.
2.Clinical manifestations
(1) Asymptomatic phase: Longer period of time, only the blood uric acid is increased, about 1/3 of patients have joint symptoms later.
(2) Acute arthritis phase: Sudden onset at night with severe pain in the affected joints, the first joint often involves the bunion, followed by the ankle and knee. Redness, swelling, heat and pressure pain in the joints, general weakness, fever and headache. It can last from 3 to 11 days. Alcohol consumption, overeating, overwork and cold, surgical stimulation, and mental stress can be triggers for attacks.
(3) Intermittent period: For several months or years, with the repeated attacks of the disease interval becomes shorter, the disease period lengthens, the number of diseased joints increases, and gradually turns into chronic arthritis.
(4) Chronic arthritis phase: From acute onset to chronic arthritis phase for an average of about 11 years, the joints become stiff and deformed, and movement is limited. 30% of patients can see gout stones and kidney complications and ureteral stones. In the late stage, hypertension, renal cerebral arteriosclerosis, and cardiac infarction are present. A small number of patients die from renal failure and cardiovascular accidents. The course of secondary gout is similar, with a shorter interval secondary to hematologic and glycogen storage disease. Blood uric acid tests are elevated up to 20 mg% (normal: 7 mg% in men and 6 mg% in women). Polarized light microscopy reveals white blood cells that have engulfed urate crystals in the synovial fluid. In the acute phase, white blood cells are increased and blood sedimentation is accelerated. X-rays show penetrating chisel-like destruction of subchondral bone of the joint as well as localized osteoporosis, erosion or cortical fracture, joint space narrowing and marginal osteophytes. Gout stones may be calcified shadows.
3.Diagnosis
Clinical manifestations, laboratory tests, and x-ray examinations help in the diagnosis, but the complete diagnosis is subject to the detection of uric acid crystals by the synovial membrane or joint fluid, because psoriatic arthritis and rheumatoid arthritis sometimes have elevated uric acid levels.
In the clinical encounter with middle-aged and elderly male obese people, the sudden appearance of the first metatarsophalangeal joint or ankle joint, dorsal foot and other single joints red, swollen and severe pain, to colchicine treatment is effective, about 1 week symptom relief, with or without increased blood uric acid, can be diagnosed as acute gouty arthritis. At home and abroad, the diagnostic criteria developed by the American College of Rheumatology in 1977 are used.
(1) More than one episode of acute arthritis, with the peak of the attack within 1 day.
(2) Acute arthritis is confined to individual joints. The entire joint is dark red in color. Swelling and pain in the first thumb joint.
(3) Acute attack of unilateral tarsal arthritis.
(4) There are gout stones.
(5) Hyperuricemia.
(6) Asymmetric joint swelling and pain.
(7) The attack can stop on its own.
The diagnosis can be confirmed if three or more of the above conditions are present and secondary gout can be excluded.
4.Treatment
The principles of gout treatment are: reasonable dietary control, restriction of high purine food. Adequate water intake, so that the daily urine volume is maintained above 2000 ml. Regular life system, pay attention to the combination of work and rest, avoid overwork and mental tension, and participate in physical exercise appropriately.
Treatment also includes both systemic and local aspects. Colchicine is the most commonly used medication, in addition to the use of POTUS or anti-inflammatory pain. Carbenoxolone can also be used to treat the persistent rise in serum uric acid by inhibiting the reabsorption of urate in the renal tubules, which is one of the effective treatment drugs. If renal disease is present, allopurin is usually used. In the acute phase, intra-articular steroid injections, joint braking and cold compresses can significantly reduce symptoms. Sometimes, gouty arthritis can be treated with arthroplasty, artificial joint replacement, etc. in order to reduce joint pain and restore joint function.
Precautions.
(1) In acute attacks, bed rest and cold compresses should be used locally.
(2) Do not eat foods with high purine content, such as liver, kidney and other internal organs and soy products. Drink more water. Avoid alcohol, especially beer.
(3) Prohibit vitamin B12 and sulfonamides.
(4) Take medication as prescribed by your doctor.
5.Gout recipes
The dietary treatment of gouty arthritis patients is a very important aspect of treatment. Controlling a high purine diet and reducing the production of uric acid can effectively control the disease. For example, in acute gout, the amount of purine should be controlled to less than 150 mg per day.
According to the purine content, foods are classified into three categories: low purine foods (<25 mg of purine per 100 g of food), moderate purine foods (25-150 mg of purine per 100 g of food) and high purine foods (150-1000 mg of purine per 100 g of food). However, this is only a principle estimate, and necessary adjustments should be made according to the actual situation in clinical practice.
Low purine foods that can be eaten (can be eaten without fear)
① Staple foods: rice, wheat, pasta products, soda crackers, starch, sorghum, macaroni, potatoes, sweet potatoes, yams, etc.
② Milk: fresh milk, condensed milk, cheese, yogurt, cream of wheat, milk powder, ice cream, etc.
③ Meat and eggs: eggs, duck eggs, skin eggs, pig blood, duck blood, chicken blood, goose blood, etc.
④ Vegetables: cabbage, cabbage, snow red, celery, leek, tomato, eggplant, melon, radish, gourd, green pepper, onion, onion, garlic ginger, fungus, squash, chili, kimchi, etc.
⑤ Fruits: apples, bananas, dates, pears, oranges, oranges, lemons, grapes, pomegranates, peaches, pineapples, peaches, plums, kumquats, watermelons, papayas, raisins.
⑥ Drinks: cola, soft drink, mineral water, fruit juice, cream of wheat, chocolate, cocoa, jelly, etc.
(7) Others: jam, soy sauce, honey, fats and oils, dried fruits, sugar, honey, jellyfish, seaweed.
Moderate purine foods (not to be consumed in acute pain, and to be consumed at a reduced discretion during normal times)
① Beans and their products: bean products, dried beans, bean seedlings, soybean teeth.
② Meat: chicken, pork, pork skin, beef, lamb and other meat.
③ Aquatic products: grass carp, carp flounder, sea bass, crab, eel, eel, abalone, fish ball, shark fin.
④ Vegetables: spinach, bamboo shoots, kelp, golden needle, silver fungus, mushrooms, cauliflower.
⑤ Oil and fat and others: peanuts, cashew nuts, sesame seeds, chestnuts, lotus seeds, almonds.
High purine foods (not edible).
① Legumes and vegetables: soybeans, lentils, purple cabbage, shiitake mushrooms.
② Meat: liver, intestines, heart, belly and other animal offal, thick gravy, meat pies, etc.
③ Aquatic products: fish, shellfish, shrimp, sea cucumber.
④ Others: yeast powder, various kinds of alcohol (especially beer)