gout
Introduction
Introduction to gout 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 crystal deposition in joint synovial membrane, bursa, cartilage and other tissues. Recurrent inflammatory disease. 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 crystals, characteristic acute arthritis, tophi, interstitial nephritis caused by deposition, 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. basic knowledge The proportion of illness: 0.003%-2.84% (over 50 years old) Susceptible people: no specific population Mode of infection: non-infectious Complications: uremia acute renal failure kidney stones femoral head necrosis
Cause
Cause of gout
Drinking (25%):
Drinking alcohol is easy to cause gout, because alcohol in the liver tissue metabolism, a large amount of water, so that the blood concentration is strengthened, so that the uric acid that is already close to saturation, accelerate into the soft tissue to form crystallization, resulting in excessive reaction (sensitivity) of the body's immune system Inflammation, gout is known as the "King of the King", so the disease is good in the body of the nobles, such as Yuan Shizu Kublai in the old age because of excessive drinking and suffering from gout.
Diet (15%):
Gout can be caused by diet, weather changes such as sudden changes in temperature and pressure, and trauma. Some foods are metabolized, some of which can cause the uric acid crystals that were originally accumulated in the soft tissue to re-dissolve, which can induce and aggravate arthritis.
Long-term increase in uric acid (15%):
The long-term increase of uric acid in the blood is the key cause of gout. Human uric acid is mainly derived from two aspects: (1) nucleic acids and other terpenoids produced by protein catabolism in human cells, and endogenous uric acid is produced by some enzymes. . (2) The terpenoids, nucleic acids and nuclear protein components contained in foods are digested and absorbed, and then exogenous uric acid is produced by the action of some enzymes.
The formation of uric acid is a very complicated process and requires the participation of some enzymes. These enzymes can be roughly divided into two categories: enzymes that promote uric acid synthesis, mainly 5-phosphate nucleic acid-1-pyrophosphate synthase, adenine phosphate nucleoside Acid transferase, phosphoribosyl pyrophosphate amide transferase and xanthine oxidase; enzymes that inhibit uric acid synthesis, mainly hypoxanthine-guanosine transferase, gout is caused by various factors, such as the activity of these enzymes, such as It promotes the activity of uric acid synthase, inhibits the activity of uric acid synthase, etc., and leads to excessive production of uric acid, or the uric acid is blocked by various factors, causing uric acid to accumulate in the blood, resulting in hyperuricemia.
Hyperuricemia, such as long-term existence, uric acid will deposit in the form of urate in the joints, subcutaneous tissue and kidneys, causing arthritis, subcutaneous gout stones, kidney stones or gouty nephropathy and other clinical manifestations.
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.
Pathogenesis
Reduced uric acid breakdown as a mechanism leading to hyperuricemia has been ruled out, partially degraded into free sulfhydryl groups during the normal conversion of nucleic acids and nucleotides, mainly hypoxanthine and guanine, required for the synthesis of nucleotides. When the nucleic acid is excessive, it will rapidly degrade into hypoxanthine. The guanine will be deaminated to become jaundice under the action of guanine, and the hypoxanthine and astragalus will be oxidized to uric acid, purine nucleotides and gland by the action of xanthine oxidase. Purine 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 The guanine is converted into guanine nucleotides; the hypoxanthine is converted to hypoxanthine nucleotides; the adenine is converted to adenine nucleotides; or they can be resynthesized, the first step of sputum metabolism and its feedback inhibition site It is phosphoribosyl pyrophosphate (PRPP) + glutamine + H2O phosphoramidite + glutamic acid + pyrophosphate (PPI), which is catalyzed by phosphoribosyl pyrophosphate amide transferase (PRPPAT).
The possible mechanisms by which this reaction regulates uncontrolled and increased sputum synthesis are: PRPP, increased glutamine concentration; increased amount or activity of the enzyme; decreased sensitivity of the enzyme to feedback inhibition of purine nucleosides; Decreased acid or guanylic acid concentration leads to a decrease in inhibition of enzymes. In the absence of HPRT and overactive PRPP synthase, intracellular PRPP concentration is significantly increased, and sputum synthesis is 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, uric acid production increases, and others Including any process that causes the acceleration of adenosine decomposition in the cells, the uric acid production increases due to the accelerated degradation of sputum, causing hyperuricemia.
For some patients with gout, the direct pathological mechanism of hyperuricemia is the decrease of renal tubular clearance of urate. The excretion of urate by the kidney is filtered by glomerulus, but filtered urate. Almost completely absorbed by the proximal convoluted tubules (reabsorption before secretion), the urate fraction secreted by the renal tubules is also reabsorbed at the distal end of the proximal convoluted tubules, and a small amount is reabsorbed in Henry's and collecting ducts (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, the renal tubules are heavy to urate. Increased absorption or decreased renal tubular secretion of urate can cause a decrease in urate renal excretion, leading to hyperuricemia, when blood uric acid increases beyond supersaturated concentration, urate deposits in tissues, in gout patients It has been confirmed that the secretion of urate by the nephron is decreased.
Prevention
Gout prevention
In addition to applying appropriate drugs under the guidance of a doctor, gout patients should also pay attention to the following points in their daily lives:
(1) Diet: 1 pig, cow, lamb, ham, sausage, chicken, duck, goose, rabbit and various animal internal organs (liver, kidney, heart, brain), bone marrow and other high content, should try not to eat Fish, shrimp, spinach, beans, mushrooms, mushrooms, citron, peanuts, etc. also have a certain amount of cockroaches, eat less; most vegetables, all kinds of fruits, milk and dairy products, eggs, rice, sugar, etc. can be eaten.
2 more drinking water, to keep the daily urine volume above 2000ml, due to the occurrence of urinary calculi and urine uric acid concentration and the pH of the urine, if necessary, you can take alkaline drugs to prevent the occurrence of urinary calculi.
3 Avoid overeating or hunger.
4 alcohol and tobacco, especially alcohol.
5 Do not drink strong tea, coffee and other drinks.
(2) Properly treat the predisposing factors, disable or use less drugs that affect uric acid excretion: diuretics such as penicillin, tetracycline, high-dose thiazides and ampicillin, vitamins B1 and B2, insulin and low-dose aspirin (less than daily) 2g) and so on.
(3) Obese people should actively lose weight and lose weight, which is very important to prevent gout.
(4) Pay attention to the combination of work and rest, avoid overwork, mental stress, infection, surgery, generally do not advocate gout patients to participate in running and other strong physical exercise, or long-distance walking tour.
Complication
Gout complications Complications uremia acute renal failure kidney stones femoral head necrosis
According to the statistics of the causes of death in gout patients in Europe and America, the complications caused by gout are the most common with ischemic heart disease, followed by uremia, cerebrovascular disease, malignant tumors, etc., but the study in Japan in Asia With uremia at the top, followed by ischemic heart disease, cerebrovascular disease and malignant tumors, no matter what kind of complications, these research statistics are worthy of our attention.
1, uric acid nephrolithiasis
10% to 25% of patients with gout can develop uric acid nephrolithiasis, and some patients even see uric acid nephrolithia as the first symptom. Small sediment-like stones are easily discharged with urine, and patients can have no symptoms. Larger stones often cause renal colic and hematuria, and those with urinary tract infections may have urinary tract irritation or low back pain such as frequent urination, urgency, and dysuria.
2, gouty nephropathy
In the early stage, it is often characterized by intermittent proteinuria. The general course of disease progresses slowly. As the disease progresses, proteinuria gradually changes to persistence, kidney function is impaired, nocturia increases, isotonic urine, etc. Chronic renal insufficiency, manifested as edema, hypertension, blood urea nitrogen and creatinine, the final patient may die due to renal failure, a small number of patients with gouty nephropathy as the main clinical manifestations, and arthritis symptoms are not obvious, due to kidney When the filtration function is incomplete, the excretion of uric acid is reduced, which can cause the increase of blood uric acid level. Therefore, it is difficult to judge the causal relationship between hyperuricemia and renal disease in patients with chronic renal insufficiency and hyperuricemia.
3. Acute renal failure
A large amount of urate crystals are blocked in the renal tubules, renal pelvis and ureter, causing urinary tract obstruction, resulting in sudden oliguria or even no urine. If not treated promptly, it can rapidly develop into acute renal failure and even cause death.
4. Ischemic heart disease
The so-called ischemic heart disease refers to the coronary artery hardening or obstruction that transports oxygen and nutrients to the heart muscle, so that the circulation of blood is hindered, thus causing chest pain and myocardial necrosis, mainly sciatic and myocardial infarction, which is like tap water. Like the tube, due to the fouling of the dirt, the water pipe diameter is getting smaller and smaller, and the water flow is reduced or completely unreasonable. Strictly speaking, this situation will happen to everyone. The difference is that some people will be accelerated by special factors. Now, the American Heart Association has listed gout as a risk factor for ischemic heart disease and a promoting factor for arteriosclerosis. If gout is not treated well, persistent hyperuricemia will cause excessive urate crystals. Precipitation in the coronary arteries, coupled with agglomeration of platelets, accelerates the progression of arteriosclerosis.
5, kidney stones
According to statistics, the incidence of kidney stones in gout patients is about one thousand times that of normal people; the more uric acid in the urine, the more acidic the acidity and alkalinity, the more likely it is to have stones, so you must take more water and take baking soda to prevent kidney stones. It happened.
6, obesity
Due to rapid economic growth and abundant food, there are more and more obese people in China. Obesity will not only make uric acid synthesis hyperthyroidism, but also cause hyperuricemia, which will also hinder the excretion of uric acid, easily cause gout, complicated with hyperlipidemia, diabetes, etc. The main reason is that they often overeating, so obese people should lose weight.
7, hyperlipidemia
People with gout are more likely to overeating and often have obesity, so there are many hyperlipidemias, which are closely related to the occurrence of arteriosclerosis.
8, diabetes
Oral glucose load test for gout patients, found that 30-40% of the combination of "mild non-insulin-dependent" diabetes; that is caused by obesity and overeating caused by low insulin sensitivity, if you can use diet therapy early, and Controlling body weight, insulin sensitivity can be restored quickly.
9, high blood pressure
About half of gout patients with hypertension, in addition to the above-mentioned renal hypertension caused by renal dysfunction, gout patients with obesity is also one of the reasons, because hypertension treatment drugs often use antihypertensive diuretics, will inhibit uric acid excretion, and It is necessary to pay attention to the increase in uric acid value.
10, femoral head necrosis
Patients with gout can develop ischemic necrosis of the bone, especially the femoral head, mainly due to hyperlipoproteinemia type II and IV, bone embolism caused by fat embolism, and some cases with chronic alcoholism and/or use Glucocorticoid-related, these cases are often confirmed by gout in the pathology of surgery, when gout patients with femoral head necrosis, it should be thought that gout may be the cause, gout patients should be vigilant when there is clinical symptoms of femoral head ischemia, In addition to routine treatment of gout, patients with surgical indications are still required to undergo femoral head replacement surgery. In the literature, individual cases have undergone total hip replacement surgery.
11, rheumatoid arthritis
Domestic and foreign literature reports that gout is associated with rheumatoid arthritis, connective tissue disease such as systemic lupus erythematosus and myofascial atherosclerosis, but their epidemiological relationship and its accompanying mechanisms, Further research is needed. Some people think that rheumatoid and gout are mutually restrictive arthritis. This relationship may be related to immunity. 30% of patients with chronic gout arthritis and 10% of acute gout have low titers of IgM rheumatoid factor. It is also believed that uric acid crystals can absorb IgG from the synovial membrane, stimulate macrophages, and increase it. In the process, uric acid crystals containing cell-reactive substances interact with serum protein apo B, which inhibits the inflammatory process, thereby The condition is self-limiting; part of the IgG degeneration of crystal absorption can increase the titer of rheumatoid factor, see Figure 1, 2 .
Symptom
Gout symptoms Common symptoms Uric acid in the joints... Toe gout fatigue joint local tingling rheumatoid nodule granuloma more drink white blood cells in joint fluid... refers to root pain
There is no aura before acute onset of gouty arthritis, mild trauma, overeating sorghum food or excessive drinking, surgery, fatigue, emotional stress, internal medicine emergency (such as infection, vascular obstruction) can induce acute gout attack, often at night The acute single or multiple joint pain is usually the first symptom, the pain is progressively aggravated, and it is severe pain. The signs are similar to acute infection, swelling, local fever, red and obvious tenderness, local skin tension, fever, and luster. The appearance is dark red or purple, the toe joint of the big toe involves the most common (foot gout), arch, ankle, knee, wrist and elbow joints are also common sites, body manifestations including fever, palpitations, chills , discomfort and leukocytosis.
At the beginning of a few episodes, usually only one joint is involved, usually only lasts for several days, but later it can invade multiple joints at the same time or in succession. If it is untreated for several weeks, the local symptoms and signs will disappear, the joint function will recover, and the symptoms will be asymptomatic. The length of the interval varies greatly. As the disease progresses, the disease progresses more and more. If it is not prevented, it will occur several times a year, chronic joint symptoms will occur, and permanent destructive joint deformity will occur. The hand and foot joints are often restricted in activity. In a small number of cases, joints such as sputum, chest lock or cervical vertebrae can also be affected. Urine deposits are common in the mucus wall and tendon sheath. The enlarged tophi is formed in the hands and feet, and the white urate crystal fragments are discharged. The gout caused by cyclosporin is often caused by central large joints, such as the hip and ankle joints, which can also be seen in the hands and even destroy the renal tubules.
1, asymptomatic period
Serum urate concentration increases with age, and there are gender differences. This stage is mainly characterized by persistent or fluctuating blood uric acid. The increase from blood uric acid to symptoms can last for several years to several decades. It is called gout when arthritis occurs.
2, acute arthritis episode
It is the most common first symptom of primary gout. It occurs in the lower extremity joints. It is more common in the big toe and the first metatarsophalangeal joint. It is a single joint inflammation at the initial onset, and the joint is increased after repeated attacks. The onset of gout indicates blood. The 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 period
Gout attacks last for several days to several weeks can be naturally relieved, completely recovered without leaving sequelae, and then appear asymptomatic stage, called acute exacerbation interval, after which it can be recurred, about 60% of patients relapse within 1 year, intermittent period also has a long time For more than 10 years.
4, tophi
And in patients with chronic arthritis without treatment or poor treatment, urate crystals are deposited in cartilage, tendon, bursal fluid and soft tissue. The common manifestations of tophi in this period often occur in the ear wheel, the forearm extension side, At the toe, fingers, elbows, etc., the deposition of urate in the joints increases, and 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 affected. Limit, with the repeated attacks of inflammation, the lesions are getting more and more serious, seriously affecting joint function, early prevention and treatment of hyperuricemia, patients can have no current performance.
Examine
Gout check
Laboratory tests are of great significance for the diagnosis of gout, especially the discovery of urate, which is the basis for diagnosis.
First, blood, urine routine and blood sedimentation
1, blood routine and erythrocyte sedimentation examination acute exacerbation, peripheral blood white blood cell count increased, usually (10 ~ 20) × 109 / L, rarely more than 20 × 109 / L, neutrophils increased, renal function decline , can have mild, moderate anemia, increased erythrocyte sedimentation rate, usually less than 60mm / h.
2, urine routine examination in the early stage of the disease generally no change, involving the kidneys, may have proteinuria, hematuria, pyuria, occasionally tubular urine; complicated with kidney stones, visible hematuria, also visible acidic urinary discharge.
Second, blood uric acid determination
The serum uric acid level is increased in most patients during acute attack. It is generally considered to be urinary enzymatic method, male 416mol/L (7mg/dl), female >357mol/L (6mg/dl), which has diagnostic value. Uric acid or adrenocortical hormone, serum uric acid content can not be high, normal period of remission can be normal, 2% to 3% of patients with typical gout attacks and serum uric acid content is less than the above level, there are three explanations: 1 central body temperature and peripheral joint temperature The gradient difference is large; 2 the body is in a state of stress, secreting more adrenocortical hormone, promoting serum uric acid excretion, while the content of sodium urate in the distal joint is still relatively high; 3 has been treated with uric acid or corticosteroids.
Third, the determination of uric acid content
In the case of innocent diet and unaffected uric acid excretion drugs, the total male uric acid in normal males did not exceed 3.54mmol/(600mg/24h), and 90% of urinary uric acid in primary gout patients was less than 3.54mmol/24h. Therefore, uric acid excretion is normal, can not rule out gout, and uric acid is greater than 750mg / 24h, suggesting excessive production of uric acid, especially non-nephrogenic secondary gout, elevated blood uric acid, uric acid also increased significantly.
Fourth, joint cavity puncture examination
In the case of acute gouty arthritis, there may be effusion in the swollen joint cavity. The injection of the bursa fluid is very important for the diagnosis. The white blood cell count of the bursal fluid is generally (1~7)×109/L. Mainly for lobular granulocytes, whether in the treatment or not, most patients with intermittent period of joint bursal fluid examination, still visible sodium urate crystal.
(a) polarized light microscopy
The synovial fluid is placed on the slide, and a slow vibration image of the double-folded fine needle-like sodium urate crystal is observed in the cell or outside the cell, and the first-stage red compensation prism is used, and the urate crystal direction is yellow when parallel to the mirror axis. It is blue when it is vertical.
(two) ordinary microscopy
The sodium urate crystal is rod-shaped, and the detection rate is only half of that of the polarized light microscope. If heparin is added to the synovial fluid, the sediment is centrifuged and the sediment is taken for microscopic examination to improve the detection rate.
(3) Determination by ultraviolet spectrophotometer
Using UV spectrophotometer to qualitatively analyze the content of synovial fluid or suspected gout nodules to determine sodium urate is the most valuable method for gout. The method is to first determine the absorption spectrum of the specimen to be tested, and then known When the absorption spectra of sodium urate are compared, if the two are the same, the measured substance is a known compound.
(d) uric acid amine (murexide) test
For specimens found to have sodium urate by ordinary light microscopy or polarized light microscopy, this test is feasible for further confirmation. This method is simple and easy. The principle is that sodium urate plus nitric acid is heated to produce diuret, and then ammonia solution is added. That is, purple purple ammonium urate is produced.
(5) Urate dissolution test
In the synovial fluid with urate crystals, after the uricase was added, the urate crystals were degraded to the disappearance of allantoin crystals.
Five, gout nodule content inspection
For gout nodules, biopsy or puncture to absorb the contents, or take a white smear viscous smear from the skin ulcer, and check the above method to find that the positive rate of specific urate is extremely high.
Sixth, X-ray film inspection
Acute arthritis only manifests as swelling of soft tissue and normal joint development. As the disease progresses, the bone adjacent to the tophi may have irregular or lobulated defects, and the edge is warped; the articular cartilage edge is destroyed. Irregular articular surface, the joint space is narrowed after entering the chronic arthritis period, the subchondral bone has irregular or semi-circular piercing-like defects, the edge is sharp, and the defect edge bone may have a proliferative reaction. In addition, the dual energy can be utilized. The X-ray bone density measuring instrument can detect the bone mineral density of the affected joint at an early stage, and can be used as an evaluation index for the diagnosis and condition observation of gouty arthritis. The simple uric acid stone can pass X-ray, and the diagnosis depends on intravenous pyelography. Those who have mixed calcium salts can be found when examining abdominal plain films.
Seven, CT and MRI examination
The tophistone deposited in the joint showed a speckle-like image of gray scale in CT scan according to the degree of ashing. The tophi was a low to medium density block in the T1 and T2 images of the MRI examination. Shadow, intravenous injection of sputum can enhance the density of the tophi stone shadow, the two tests combined to make an accurate diagnosis of most intra-articular tophi.
In short, laboratory tests are an indispensable method for the diagnosis of gout and observation of disease progression, especially the discovery of urate crystallization, which is the key to improving the quality of gout diagnosis.
Diagnosis
Gout diagnosis
diagnosis
There is no uniform standard for gout diagnosis in China. Generally, the American College of Rheumatology standards, the US Holmes standard and the Japanese revised standards are used. The American College of Rheumatology classification criteria for acute gouty arthritis (1977) is introduced:
1. The specific urate crystals were found in the synovial fluid.
2, gout stone by chemical methods or polarized light microscopy, confirmed to contain sodium urate crystals.
3. With the following clinical, laboratory and X-ray signs, 6 of 12 items.
(1) More than one episode of acute arthritis.
(2) Inflammation showed a peak within 1d.
(3) Single arthritis episodes.
(4) The skin of the affected joint is dark red.
(5) The first ankle joint is painful or swollen.
(6) Unilateral seizures involve the first metatarsophalangeal joint.
(7) Unilateral seizures involve the tibial joints.
(8) There are suspicious tophi.
(9) hyperuricemia.
(10) X-ray shows joint asymmetry swelling.
(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 short, acute gout is not difficult to diagnose according to typical clinical manifestations, laboratory tests and treatment response. The diagnosis of chronic gouty arthritis needs to be carefully identified, and urate crystals should be obtained as much as possible.
Differential diagnosis of gout
(1) Differential diagnosis in the acute phase
1. There is a history of infection of group A hemolytic streptococcus before acute rheumatoid arthritis. The lesion mainly invades the heart and joints. The following characteristics can be identified:
1 more common in teenagers.
2 1 to 4 weeks before the onset of hemolytic streptococcal infections such as pharynx, tonsillitis history.
3 often invade the knees, shoulders, elbows, ankles and other joints, and has a migratory symmetry.
4 often accompanied by myocarditis, ring erythema and subcutaneous nodules.
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 caused by calcium pyrophosphate deposition in articular cartilage, especially in type A acute sexual assault, the performance is similar to gout, but has the following characteristics:
1 more common in the elderly;
2 lesions mainly invade knees, shoulders, hips and other large joints.
On the 3X line, the joint space was narrowed and the cartilage calcification was densely dotted or linear, with no bone destruction.
4 serum uric acid content is often normal.
5 Sodium pyrophosphate monoclinic or slant crystal can be found in the synovial fluid.
6 colchicine treatment effect is poor.
3, septic arthritis is mainly caused by Staphylococcus aureus, the identification points are:
1 can find primary infection or suppurative lesions;
More than 2 years old major joints such as the hips, knee joints, accompanied by high fever, chills and other symptoms.
3 joint cavity puncture fluid is purulent exudate, smear microscopic examination showed Gram-positive staphylococci and cultured Staphylococcus aureus.
4 There is no urate crystal in the synovial fluid.
5 anti-foreign drug treatment is invalid.
4. Traumatic arthritis
1 has a history of joint trauma.
2 affected joints are fixed, no migration.
3 There is no urate crystal in the synovial fluid.
4 serum uric acid is not high.
5. The acute attack of gonorrhea is similar to that of gout, but it has the following characteristics:
1 has a history of smelting or gonorrhea;
2 In the synovial fluid, the gonorrhea can be found to be positive for culture of the bacterium, and there is no uric acid crystal.
3 penicillin G and ciprofloxacin are effective and can be identified.
(2) Differential diagnosis of chronic phase
1, chronic rheumatoid arthritis This disease is often chronic, about 10% of cases have subcutaneous nodules near the joints, easy to be confused with atypical gout, but this disease:
1 finger toe facet joints often have symmetric prismatic swelling, which is completely different from unilateral asymmetrical gout arthritis.
2X-ray film showed that the articular surface was rough, the joint space was narrowed, and sometimes some of the articular surface was fused, and the bone was generally loose, but no osteocortical defect was changed.
3 active rheumatoid factor positive, no urate crystals in joint fluid.
2, psoriatic arthritis This disease is also more common in men, often asymmetrically invade the distal toe joint, and 0.5 patients with elevated blood uric acid content, it needs to be identified with gout, the main points are:
1 Most patients with joint disease occur after psoriasis.
2 lesions infringe the distal end of the toe joint, more than half of the patients with nail thickening and depression into a ridge-shaped bulge.
The 3X line image showed severe joint destruction, the joint space was widened, and the bone end of the fingertips was shortened and the knife was cut.
4 joint symptoms with the improvement of skin lesions to reduce or worsen with the deterioration of skin lesions.
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 have active tuberculosis lesions;
3 may have a history of acute arthritis; can also be only manifested as chronic joint pain, but no joint stiffness.
4 The skin around the joints often has nodular erythema.
5X-ray showed osteoporosis, no cortical defect changes; 6 synovial fluid showed more mononuclear cells, but no urate crystals.
7 tuberculin test is strongly positive, anti-caries treatment is effective.
(3) Misdiagnosis
Gout is more likely to be misdiagnosed. In Europe and the United States, gout is more common, so doctors sometimes diagnose non-gout diseases as gout. In China, because gout is relatively rare, it is often easy to treat gout as non-gout disease. The author believes that the main There are two reasons: First, the diagnosis of lack of awareness of gout; second, gout is not typical.
1, missed diagnosis of gout
Gouty arthritis is a disease that is misdiagnosed. In the acute phase, rheumatoid arthritis is the most common. Rheumatoid arthritis is common in the interictal period. In addition, surgeons often misdiagnose gout as erysipelas, cellulitis, and suppuration. Arthritis, traumatic arthritis, etc.
For gout urinary urinary calculi combined with gout, because calculus can be the first symptom of gout, it is easy to be misdiagnosed as simple urinary calculi, and missed out of gout, gout nodule rupture and vaginal discharge, misdiagnosed as osteomyelitis or tuberculosis Sexual abscess.
2. Diseases that are misdiagnosed as gout
On the other hand, in areas with frequent gout, some other diseases with joint manifestations are often misdiagnosed as gout. These diseases include: joint pain caused by osteoporosis or osteoporosis in the elderly, hyperuricemia combined with neurogout or Joint pain syndrome, etc. In 1991, Wolfe et al., in 9108 cases of rheumatism outpatients, 164 (1.8%) non-gout patients were misdiagnosed as gout, including rheumatoid arthritis, pseudogout, fibrositis, Psoriatic arthritis, etc.
3. Experience worth learning
In the past ten years, the incidence of gout in China has increased. In order to prevent missed diagnosis, the following experiences are available for reference:
1. Familiar with the clinical features of gout The clinical manifestations of gout do have many characteristics. Familiarity with these characteristics is a prerequisite for preventing missed diagnosis.
2, understand the evolution of hyperuricemia before the onset or onset of gout, the majority of patients with elevated blood uric acid, but in the intermittent or chronic phase, the blood uric acid content is often normal, it should not be normal, blood uric acid, rash Eliminate gout diagnosis.
3, careful evaluation of the treatment of drugs that interfere with the inflammatory process, a variety of organic acid anti-inflammatory drugs, adrenal cortex hormones, phenylbutazone and other drugs, can relieve the acute inflammation of gout, but also can relieve the symptoms of non-gout arthritis, it should not As a basis for the diagnosis of gout, it should not be used as a basis for the diagnosis of rheumatic, rheumatoid arthritis and other connective tissue diseases with joint lesions.
4, for patients with urinary calculi should exclude the possibility of frequent or recurrent urinary calculi, may be the first symptom of gout, pay attention to review blood uric acid, if necessary, 24-hour urine uric acid quantification to prevent gout out of diagnosis.
5, pay attention to the characteristics of X-ray image of the gout patients have bone, joint X imaging is a defect change, has a large characteristic, for patients suffering from several years, the positive rate is higher, according to which can be combined with the above identified joints The lesion was identified.
6, as far as possible to carry out characteristic examination of urate joint joint bursal fluid or gout nodule content for uric acid test positive rate is very high, domestic cases reported as the examiner is less, it is worth promoting.
