Introduction to gout

Description: Gout is a kind of uric acid that is caused by excessive anabolic metabolism, excessive uric acid production or poor uric acid excretion, and urate crystals deposited in synovial membranes, bursae, cartilage and other tissues. Recurrent inflammatory disease caused by it. The disease is characterized by the formation of birefringent sodium monohydrate sodium hydrate in joint fluid and tophi. Its clinical features are: hyperuricemia and urate crystal, characteristic acute arthritis caused by deposition, tophi, interstitial nephritis, severe joint deformity and dysfunction, often accompanied by urinary acid urinary tract stones. More common in middle-aged men and postmenopausal women with obesity. As the economy develops and lifestyle changes, its prevalence increases. Causes: (1) Causes of the disease Long-term increase of uric acid in the blood is the key cause of gout. Human uric acid mainly comes from two aspects: (1) Nucleic acids and other terpenoids produced by protein catabolism in human cells, and endogenous uric acid is produced by the action of some enzymes. (2) The terpenoids, nucleic acids and nuclear protein components contained in the food are digested and absorbed, and then exogenous uric acid is produced by the action of some enzymes. The production of uric acid is a very complicated process that requires the participation of some enzymes. These enzymes can be broadly classified into two categories: enzymes that promote uric acid synthesis, mainly 5-phosphate nucleic acid-1-pyrophosphate synthase, adenine phosphate nucleotide transferase, phosphoribosyl pyrophosphate amide transferase, and xanthine oxidase. An enzyme that inhibits uric acid synthesis, mainly hypoxanthine-guanine nucleoside transferase. Gout is caused by various factors leading to abnormal activities of these enzymes, such as promoting the activity of uric acid synthase, inhibiting the activity of uric acid synthase, and the like, resulting in excessive production of uric acid. Or due to various factors, the kidneys excrete uric acid, causing uric acid to accumulate in the blood, resulting in hyperuricemia. If hyperuricemia exists for a long time, uric acid will deposit in the form of urate in joints, subcutaneous tissues and kidneys, causing a series of clinical manifestations such as arthritis, subcutaneous gout stones, kidney stones or gouty nephropathy. The disease is recurrent acute or chronic arthritis of the peripheral joint, which is caused by deposition of monosodium urate crystals in the supersaturated hyperuricemia body fluid in and around the joints and tendons. (B) the pathogenesis of uric acid decomposition decreased as a mechanism leading to hyperuricemia has been ruled out. During the normal conversion of nucleic acids and nucleotides, some are degraded into free sulfhydryl groups, mainly hypoxanthine and guanine. When the nucleic acid required for synthesizing nucleotides is excessive, it will rapidly degrade into hypoxanthine. The guanine deaminated under the action of guanine to become jaundice. Hypoxanthine and Astragalus are oxidized to uric acid by the action of xanthine oxidase. Purine nucleotides, adenine nucleotides, hypoxanthine nucleotides and guanine nucleotides are terminal products of purine biosynthesis. The above three purine nucleotides can be synthesized by one of two pathways, directly synthesized from purine base, such as guanine to guanine nucleotide; hypoxanthine is converted to hypoxanthine nucleotide; adenine transformation Adenine nucleotides; or they can be resynthesized. The first step of sputum metabolism and its feedback inhibition are phosphoribosyl pyrophosphate (PRPP) + glutamine + H2O phosphoribosyl ribose + glutamate + pyrophosphate (PPI), which is composed of phosphoribosyl pyrophosphate amide transferase. (PRPPAT) catalysis. The possible mechanisms by which this reaction regulates uncontrolled and increased sputum synthesis are: increased PRPP, glutamine concentration; increased amount or activity of the enzyme; decreased sensitivity of the enzyme to feedback inhibition of purine nucleosides; A decrease in the concentration of acid or guanylate results in a decrease in the inhibition of the enzyme. When HPRT deficiency and PRPP synthetase were overactive, intracellular PRPP concentration increased significantly and sputum synthesis increased. In patients with increased uric acid production, the conversion of PRPP is accelerated. In addition, the cause of partial hyperuricemia is caused by the deficiency of hypoxanthine-guanine phosphoribosyltransferase (HGPRT). When the enzyme is abnormal, PRPP increases, sputum synthesis increases, and uric acid production increases. Others include any process that accelerates the breakdown of adenosine in the cell, which is accompanied by an increase in uric acid production due to accelerated degradation of the sputum, causing hyperuricemia. For some patients with gout, the direct pathological mechanism of hyperuricemia is a decrease in the clearance of urate from the renal tubules. The excretion of urate by the kidney is filtered by the glomerulus, but the filtered urate is almost completely absorbed by the proximal convoluted tubule (reabsorbed before secretion), and the urate fraction secreted by the renal tubule is far from the proximal convoluted tubule. The ends are also reabsorbed and a small amount is reabsorbed in Henry's and collecting tubes (reabsorbed after secretion). Therefore, urate excretion is almost secreted by the renal tubules, and eventually uric acid excretion from the kidney is 6% to 12% of glomerular filtration excess. When glomerular urate filtration is reduced, renal tubular reabsorption of urate is increased, or renal tubular secretion of urate is reduced, it can cause a decrease in urate renal excretion, leading to hyperuricemia. When blood uric acid increases above the supersaturated concentration, urate deposits in the tissue. In the study of gout patients, it has been confirmed that the secretion of urate by the nephron is decreased. Symptoms: There is no warning before acute gouty arthritis. Mild trauma, overeating sorghum food or excessive drinking, surgery, fatigue, emotional stress, medical emergency (such as infection, vascular obstruction) can induce acute gout attacks. Acute single or multiple joint pain, often occurring at night, is usually the first symptom. The pain progressed progressively and it was severe pain. Signs are similar to acute infections, swelling, local fever, red and obvious tenderness. Local skin is tense, hot, shiny, and the appearance is dark red or purple. The metatarsophalangeal joint of the big toe involves the most common (foot gout), and the arch of the foot, ankle, knee, wrist and elbow are also common sites. Whole body performance includes fever, palpitations, chills, discomfort and leukocytosis. The first few episodes usually involve only one joint, usually lasting only a few days, but later multiple or more joints can be violated at the same time or in succession. If left untreated for several weeks. Finally, local symptoms and signs subsided and joint function recovered. The length of the asymptomatic interval varies greatly, and the disease progresses more and more. If not prevented, it will occur several times a year, chronic joint symptoms, permanent destructive joint deformity, and limited hand and foot joints. In a few cases, joints such as tendons, chest locks or cervical vertebrae can also be affected. Urate deposits are common in the mucus wall and tendon sheath. Hands, feet can appear enlarged tophi and discharge white urate-like urate crystal fragments. The gout caused by cyclosporin is often caused by central large joints, such as the hip and ankle joints, which are also found in the hands and even destroy the renal tubules. 1. Asymptomatic serum urate concentration increases with age, and there are gender differences. This stage is mainly characterized by sustained or fluctuating blood uric acid, which can be as long as several months to decades from the increase of blood uric acid to symptoms. It is called gout only when arthritis occurs. 2. Acute arthritis is the most common first symptom of primary gout. It occurs in the lower extremity joints, and the hallux and first metatarsophalangeal joints are more common. At the initial onset, it is a single joint inflammation, and repeated attacks increase the number of affected joints. The onset of gout indicates that the blood uric acid concentration is supersaturated over a long period of time resulting in the deposition of large amounts of urate in the tissue. 3. Intermittent gout episodes lasting for several days to several weeks can be naturally relieved, completely recovered without leaving sequelae, and then appear asymptomatic phase, called acute episode intermittent. After that, it can be re-issued, about 60% of patients relapse within 1 year, and there are also more than 10 years in the intermittent period. 4. In patients with untreated or poorly treated arthritis and chronic arthritis, urate crystals are deposited in cartilage, tendons, synovial fluid, and soft tissues. Common manifestations of tophi in this period, often occur in the ear wheel, forearm extension, metatarsophalangeal, finger, elbow and so on. The deposition of urate in the joints increases, the recurrent inflammation enters the chronic stage and cannot completely disappear, causing the joint bone erosion defect and the surrounding tissue fibrosis, causing the joint to be stiff and deformed, and the activity is limited. With the repeated attacks of inflammation, The lesions are getting worse and worse, which seriously affects joint function. Early prevention and treatment of hyperuricemia, patients can not have the performance of this period. Diagnosis: There is no uniform standard for the diagnosis of gout in China. The American College of Rheumatology standards, the US Holmes standard, and the Japanese revised standard are generally used. Introduced the American College of Rheumatology classification criteria for acute gouty arthritis (1977): 1. The specific urate crystals were found in the synovial fluid; 2. The goutstone was confirmed by chemical methods or polarized light microscopy. Sodium crystallization; 3. With the following clinical, laboratory and X-ray signs, 6 of 12 items. (1) more than one episode of acute arthritis; (2) the peak of inflammation within 1d; (3) the onset of single arthritis; (4) the skin of the affected joint is dark red; (5) the pain of the first ankle joint Or swelling; (6) unilateral seizure involving the first metatarsophalangeal joint; (7) unilateral seizure involving the tibial joint; (8) suspicious tophi; (9) hyperuricemia; (10) X-ray display Asymmetric swelling of the joint; (11) X-ray showed that the subcortical cyst was not accompanied by qualitative erosion; (12) The microbial culture of joint fluid was negative during the onset of joint inflammation. When the diagnosis of acute arthritis is difficult, you can try colchicine for diagnostic treatment. If it is gout, the symptoms will be relieved quickly after taking colchicine, which is of diagnostic significance. In conclusion, acute gout is not difficult to diagnose based on typical clinical manifestations, laboratory tests and treatment responses. The diagnosis of chronic gouty arthritis needs to be carefully identified, and urate crystals should be obtained as much as possible. Identification (1) Differential diagnosis of acute phase 1. Before acute rheumatoid arthritis, there is a history of infection of group A hemolytic streptococcus. The lesion mainly invades the heart and joints. The following characteristics can be identified: 1 more common in adolescents; 1 to 4 weeks before the disease often have hemolytic streptococcal infection such as pharynx, tonsillitis history; 3 often invade the knee, shoulder, elbow, ankle and other joints, and have migratory symmetry; 4 often accompanied by myocarditis, ring erythema And subcutaneous nodules and other manifestations; 5 anti-hemolytic streptococcus antibodies such as ASO> 500U, anti-streptokinase > 80U, anti-hyaluronidase > 128U; 6 salicylic acid preparation is effective; 7 blood uric acid content is normal. 2. Pseudo gout Read more...