Chronic gout

Introduction 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 are deposited in synovial membranes, bursae, cartilage and other tissues. Recurrent inflammatory disease caused. The disease can be found in the joint fluid and tophi, there are birefringence of sodium sulphate crystal as its characteristic cause (a) the cause of the disease Long-term increase in 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 Subcutaneous tophi and chronic tophus arthritis are long-term significant hyperuricemia, a large number of monosodium urate crystals deposited in the subcutaneous, synovial, cartilage, bone and soft tissues around the joints. The typical site of subcutaneous tophi is the auricle, which is also common around recurrent joints and olecranon, Achilles tendon and sacral bursa. The appearance is a yellow-white scorpion creature of different sizes under the skin, and the surface of the skin is meager. After rupturing, the white powder or paste is discharged, and the skin is not cured for a long time. Subcutaneous tophi is often associated with chronic tophus arthritis. A large amount of tophis deposited in the joints can cause joint bone destruction, tissue fibrosis around the joints, and secondary degeneration. The clinical manifestations are persistent joint swelling, pain, deformity and dysfunction. The symptoms in the chronic phase are relatively mild, but there may be an acute attack. There is no uniform standard for diagnosis of gout diagnosis 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. Pseudogout is caused by the deposition of calcium pyrophosphate on articular cartilage, especially in type A acute sexual assault, which is similar to gout. However, it has the following characteristics: 1 The elderly are more common; 2 The lesion mainly invades the large joints such as the knee, shoulder and hip; the 3X line shows the narrowing of the joint space and the cartilage calcification is densely dotted or linear, without bone destruction. Change; 4 serum uric acid content is often normal; 5 can be found in the synovial fluid calcium monoclinic or triclinic crystal; 6 colchicine treatment effect is poor. 3. Suppurative arthritis is mainly caused by Staphylococcus aureus. The main points of identification are: 1 primary infection or suppurative lesions can be found; 2 major joints such as hips and knee joints with high fever and chills are involved; 3 joint cavity puncture fluid for purulent exudate, smear microscopic examination showed Gram-positive staphylococci and cultured Staphylococcus aureus; 4 no urate crystals in synovial fluid; 5 anti-foreign drug treatment was ineffective. 4. Traumatic arthritis 1 has a history of joint trauma; 2 affected joints are fixed, no migratory; 3 no urate crystals in synovial fluid; 4 serum uric acid is not high. 5. Acute attack of gonorrhea is similar to gout, but it has the following characteristics: 1 history of smelting or gonorrhea; 2 sputum can be found in gonorrhea or bacterial culture positive, no uric acid crystal; 3 penicillin G and ciprofloxacin are effective and can be identified. (B) differential diagnosis of chronic phase 1. Chronic rheumatoid arthritis This disease is often chronic, about 10% of cases have subcutaneous nodules near the joint, easy to be confused with atypical gout. However, the disease: 1 finger toe small joints often have symmetric prismatic swelling, which is completely different from unilateral asymmetrical gout arthritis; 2X line shows coarse joint surface, narrow joint space, sometimes partial articular surface fusion, bone The quality is generally loose, but no cortical defect changes; 3 active rheumatoid factor positive, joint fluid without urate crystallography. 2. Psoriatic arthritis This disease is also common in men, often asymmetrically invading the distal toe joint, and 0.5 patients with elevated blood uric acid content, it is necessary to identify with gout. The main points are as follows: (1) Most patients with joint lesions occur after psoriasis; 2 lesions often invade the distal end of the toe joint, more than half of the patients with nail thickening and depression into ridge-shaped bulge; 3X line image can be seen severe joint destruction, joints The gap is widened, and the bone absorption at the end of the toe is shortened and the knife is cut; the symptoms of the joints are alleviated as the skin lesions improve or worsen as the lesions deteriorate. 3. Tuberculosis allergic arthritis is caused by allergic reaction caused by Mycobacterium tuberculosis infection. 1 often involves the small joints, gradually affecting the large joints, and has multiple, migratory features; 2 patients with active tuberculosis; 3 may have a history of acute arthritis; can also only show chronic joint pain, but from No joint ankylosis; 4 joints around the joint often have nodular erythema; 5X line shows osteoporosis, no cortical defect changes; 6 synovial fluid showed more mononuclear cells, but no urate crystals; 7 tuberculosis The bacteriocin test is strongly positive and the anti-caries treatment is effective. (3) Misdiagnosis of gout is easier to misdiagnose. In countries such as Europe and the United States, because gout is more common, doctors sometimes diagnose non-gout diseases as gout. In China, because gout is relatively rare, it is often easy to treat gout as a non-gout disease. The author believes that there are two main reasons: First, the diagnosis of lack of awareness of gout; second, gout is not typical. 1. Missed diagnosis of gout Read more...