Introduction:
gout(gout) is caused by increased anabolic metabolism of sputum, excessive production of uric acid or elevated uric acid caused by poor uric acid excretion, and deposition of urate crystals in synovial membranes, bursae, 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 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.
Cause:
(1) Causes of the disease
Long-term increase in uric acid in the blood is a 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 produce endogenous uric acid 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.
(two) pathogenesis
The reduction in uric acid breakdown 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.
symptom:
There is no warning before the onset of 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. Here is an introduction to the American College of Rheumatology classification criteria for acute gouty arthritis (1977):
1. The specific urate crystals were found in the synovial fluid;
2. Gout stone is confirmed by chemical method or polarized light microscopy and contains sodium urate crystal;
3. Have the following clinical, laboratory and X-ray signs, including 6 of the 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) pain or swelling of the first ankle joint;
(6) unilateral seizure involving the first metatarsophalangeal joint;
(7) unilateral seizure involving the tibial joint;
(8) There is a suspicious tophi;
(9) hyperuricemia;
(10) X-ray shows joint asymmetry swelling;
(11) X-ray film shows that the subcortical cyst is not accompanied by qualitative erosion;
(12) The microbial culture of joint fluid was negative during the onset of joint inflammation.
If you have difficulty in confirming the diagnosis of acute arthritis, you can try it.ColchicineDiagnostic treatment, such as gout, rapid relief after taking colchicine, has 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 in the acute phase
1. There is a history of infection of group A hemolytic streptococcus before acute rheumatoid arthritis. The lesions mainly invade the heart and joints. The following characteristics can be identified: 1 more common in adolescents; 2 often hemolysis 1 to 4 weeks before onset Streptococcal infections such as pharyngeal and tonsillitis; 3 often invade knees, shoulders, elbows, ankles and other joints, and have migratory symmetry; 4 often accompanied by myocarditis, ring erythema and subcutaneous nodules; The hemolytic streptococcus antibody is elevated 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.
(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. 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 The disease is also more 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
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
Gouty arthritis is a disease that is misdiagnosed. In the acute phase, rheumatoid arthritis is the most misdiagnosed.Rheumatoid arthritisIt is common. In addition, surgeons often misdiagnose gout as erysipelas, cellulitis, septic arthritis, and traumatic arthritis.
For gout urinary urinary calculi combined with gout, because stone disease can be the first symptom of gout, it is easy to be misdiagnosed as simple urinary calculi, and missed gout. Gout nodules rupture and discharge white peony, which is misdiagnosed as osteomyelitis or tuberculous 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 and the like. In 1991, Wolfe et al. In 164 cases of newly diagnosed rheumatism outpatients, 164 (1.8%) non-gout patients were misdiagnosed as gout, including rheumatoid arthritis, pseudogout, fibrositis, psoriatic arthritis. Wait.
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 have elevated blood uric acid. However, in the intermittent or chronic phase, the blood uric acid content is often normal, so the blood uric acid should not be normal, and the gout diagnosis should be ruled out.
3. Carefully evaluate the therapeutic response of drugs that interfere with the inflammatory process. Various organic acid anti-inflammatory drugs, adrenocortical hormones, and phenylbutazone can alleviate the acute inflammation of gout, and also relieve the symptoms of non-goutic arthritis. 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 disease.
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. Emphasis on the characteristics of X-ray images The bone and joint X imaging of gout patients is characterized by a defect, which has a large characteristic. For patients suffering from several years, the positive rate is higher. According to this, it is possible to distinguish from the above-mentioned joint lesions to be identified.
6. Try to carry out the characteristic examination of urate as much as possible. The positive rate of joint sac fluid or gout nodule content for uric acid examination is extremely high. There are few domestic cases reported for this examination, which is worthy of vigorous promotion.
complication:
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 and malignant tumor. However, research in Japan in Asia has ranked first in uremia, followed by ischemic heart disease, cerebrovascular disease and malignant tumors. Regardless of the complication, these research statistics are worthy of our attention.
1. Uric acid nephrolithiasis can occur in 10% to 25% of gout patients with uric acid nephrolithiasis. Some patients even see uric acid nephrolithiasis as the first symptom. Small sediment-like stones are easy to excrete with urine, patients can have no symptoms, and larger stones often cause renal colic and hematuria. Patients with urinary tract infections may have urinary tract irritation or low back pain such as frequent urination, urgency, and dysuria.
2. Gouty kidney disease often manifests as intermittent proteinuria in the early stage. The general course of disease progresses slowly. With the development of the disease, proteinuria gradually changed into persistence, impaired renal function, increased nocturia, and isotonic urine. Chronic renal insufficiency can occur in the advanced stage, manifested as edema, hypertension, elevated blood urea nitrogen and creatinine, and eventually the patient may die from renal failure. A small number of patients with gouty nephropathy as the main clinical manifestations, and arthritis symptoms are not obvious. Due to renal insufficiency, uric acid excretion is reduced, which can cause an increase in blood uric acid levels. 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. Even caused 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 with angina And myocardial infarction, this is like a water pipe, due to dirt blocking, the water pipe diameter is getting smaller and smaller, and eventually 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. Currently, the American Heart Association lists gout as a risk factor for ischemic heart disease and arteriosclerosis. Promoting factor. Because gout is not well treated, persistent hyperuricemia causes excessive urate crystals to precipitate in the coronary arteries, and platelet aggregation is accelerated, which 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; because the more uric acid in the urine, the more acid and alkalin the acid, the more likely it is to have stones, so it is necessary to take more water and take small Soda to prevent the occurrence of kidney stones.
6. Obesity: Due to rapid economic growth and abundant food in China, there are more and more obese people. Obesity will not only make uric acid synthesis hyperactive, but also cause hyperuricemia, which will also hinder the excretion of uric acid, which may cause gout and high incidence. Blood lipids, diabetes, etc. The main reason is that they often overeating, so obese people should lose weight.
7. Hyperlipidemia: Gout is more common than overeating, and there are many obesity, so there are many hyperlipidemias, which is closely related to the occurrence of arteriosclerosis.
8. Diabetes: An oral glucose load test was performed on gout patients. It was found that 30-40% of patients had "mild non-insulin-dependent" diabetes; that is caused by obesity and overeating caused by low insulin sensitivity. With diet therapy and weight control, the susceptibility of insulin is quickly restored.
9. Hypertension: 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 drugs often use antihypertensive diuretics, it will inhibit uric acid excretion and increase uric acid value. This must be noted.
10. Avascular necrosis of the bone can occur in patients with femoral head necrosis, especially the femoral head. Mainly due to hyperlipoproteinemia type II and IV, there is fat embolism caused by bone necrosis. There are also cases associated with chronic alcoholism and/or the use of glucocorticoids. Most of these cases were confirmed to be gout at the time of surgery. When a patient with gout develops necrosis of the femoral head, it should be thought that gout may be the cause. Gout patients should be vigilant when they have 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. The literature reported that all cases underwent total hip replacement surgery.
Rheumatoid arthritis has been reported in domestic and foreign literatures, and gout is associated with connective tissue diseases such as rheumatoid arthritis, systemic lupus erythematosus and myofascial atherosclerosis. However, the epidemiological relationship and accompanying mechanisms associated with them are still to be further studied. Some people think that rheumatoid and gout are arthritis that restrict each other. This relationship may be related to immunity. In 30% of patients with chronic gout arthritis and 10% of acute gout, there is an increase in low titer of IgM rheumatoid factor. It is also believed that uric acid crystals can absorb IgG from the synovial membrane, stimulate macrophages, and increase them. In the process, the uric acid crystal containing the cell reaction substance interacts with the serum protein apo B, which has the effect of inhibiting the inflammatory process, thereby making the condition self-limiting; part of the IgG degraded by the crystal absorption can increase the titer of the rheumatoid factor.
treatment:
Western medicine treatment
The purpose of treatment is to:
(1) Terminating an acute attack with an anti-inflammatory drug;
(2) Prophylactic colchicine daily to prevent repeated acute attacks (if frequent episodes)
(3) Prevent the deposition of monosodium urate crystals and eliminate the existing tophi by reducing the concentration of urate in the body fluid. Preventive protective measures should address two aspects, namely prevention of bone and joint cartilage erosion and prevention of kidney damage. Special treatments should be selected according to the different periods of the disease and the severity of the disease. Hypertension, hyperlipidemia and obesity should be treated at the same time.
1. Generally, the protein intake is limited to about 1g/(kg·d). Do not enter sorghum food (animal heart, liver, kidney, sardines, etc.), strictly stop drinking, avoid induced factors. Encourage more water to make the urine volume above 2000ml/d. When the urine H concentration is 1000nmol/L (pH 6.0 or less), it is advisable to take a basic drug such as sodium bicarbonate 1~2g, 3 times/d to maintain the urine H concentration at 630.9~316.3nmol/L (pH value). 6.2 ~ 6.5) is appropriate. If the morning urine is acidic, add 250 mg of acetazolamide at night to keep the urine alkaline, increase the solubility of uric acid, and prevent the formation of stones. At the same time, drugs that inhibit uric acid excretion should not be used, such as hydrochlorothiazide (hydrochlorothiazide), furosemide, ethambutol, pyrazinamide, and niacin.
2. The treatment of acute arthritis should be absolutely rest in bed, raise the affected limb, avoid the weight of the affected joint, and continue to move until 72h after the joint pain is relieved. The following drugs should be used as soon as possible to control arthritis and relieve symptoms.
(1) colchicine: a significant effect on the control of gouty arthritis, as the first choice. Generally, the symptoms are relieved 6 to 12 hours after taking the drug, and about 90% of patients with 24 to 48 hours can be relieved. The usual dose is 0.5 mg per hour or 1 mg orally every 2 hours until the symptoms are relieved or gastrointestinal side effects such as diarrhea or if the maximum dose is 6 mg and the condition has not improved, it should be discontinued. Intravenous colchicine can work quickly and has fewer side effects in the gastrointestinal tract. Usage: 2mg of colchicine, dissolved in 10ml normal saline, slow injection (injection time is not shorter than 5min), if the condition requires, can be given 1mg after 6h, the general dose of 24h should be controlled within 3mg. However, it should be noted that if the drug solution leaks out during intravenous injection, it may cause tissue necrosis and should be strictly prevented. In addition, in addition to causing gastrointestinal reactions, colchicine can also cause bone marrow suppression, hepatocyte damage, hair loss, depression, ascending paralysis, respiratory depression and the like. Therefore, the original bone marrow suppression and the dose of patients with liver and kidney dysfunction should be halved and closely observed. Leukopenia is disabled.
(2) Non-steroidal anti-inflammatory analgesics: especially suitable for patients who cannot tolerate colchicine. The combination of these drugs with colchicine can enhance the analgesic effect, but should be taken after meals to reduce the gastrointestinal reaction. Commonly used drugs are indomethacin, piroxicam (inflammatory pain), naproxen, ibuprofen, phenylbutazone and hydroxybuzon. Among them, indomethacin is the most widely used. This class of drugs generally provides near-maximal doses at the start of treatment to maximize the control of acute symptoms and then gradually reduce the amount of symptoms as the symptoms are relieved.
1IndomethacinThe starting dose is 50mg, once every 6 hours, and the symptoms are gradually reduced to 25mg, 2~3 times/d. This medicine may have side effects such as gastrointestinal irritation, water and sodium retention, dizziness, rash, etc., and active peptic ulcer disease is prohibited.
2 ibuprofen: the usual dose is 0.2 ~ 0.4g, 2 ~ 3 times / d, usually 2 to 3 days can control the symptoms, the side effects of the drug is small, even can cause gastrointestinal reactions and elevated liver transaminase, should be note.
3 Baotaisong or hydroxybutan: the initial dose is 0.2-0.4g, and 0.1g every 4-6 hours later. After the symptoms improved, the score was reduced to 0.1g, 3 times / d. This medicine can cause gastritis and sodium retention, and occasionally white blood cells and thrombocytopenia. Those with active ulcer disease and cardiac dysfunction are hanged.
4 piroxicam (inflammatory pain Xikang): long time, 20mg / d, once served. Occasionally gastrointestinal reactions. Long-term medication should pay attention to the number of peripheral white blood cells and liver and kidney function.
5 naproxen: anti-inflammatory and analgesic effect is stronger, but the gastrointestinal reaction is lighter, oral 0.25g, 2 ~ 3 times / d.
(3) Glucocorticoid: It has a rapid alleviation effect on the onset of acute arthritis, but it is easy to relapse after stopping the drug, and long-term application is prone to complications such as diabetes and hypertension, so it is not suitable for long-term application. For those who are ineffective, insufficient or have contraindications for treatment with colchicine or non-steroidal anti-inflammatory drugs, short-term use may be considered. Usually use prednisone (prednisone) tablets 10mg, 3 times / d. After the symptoms are relieved, gradually reduce the amount to avoid recurrence.
(4) Aspiration of joints and fluids, followed by infusion of corticosteroids can also control acute exacerbations of gout. According to the size of the affected joint, 10~50mg of prednisolone tert-butyl ester was injected. ACTH80u single-dose intramuscular injection is a very effective treatment, just like intravenous colchicine, especially for patients with post-operative gout attacks. For multiple joint attacks, prednisone can also be applied for a short period of time, such as 20~30mg/d. Occasionally, several drugs need to be combined to treat acute gout attacks.
(5) In addition to special treatments, it is also necessary to pay attention to rest, ingest a large amount of liquid, prevent dehydration and reduce the deposition of urate in the kidney. Patients should enter soft food. In order to control pain, it is sometimes necessary to treat code 30~60mg. It is also helpful to fix the inflammation site on the splint. Drugs that lower serum urate concentration must be applied after acute symptoms are fully controlled.
3. Intermittent and chronic treatment Although the symptoms are still not suitable for control, repeated authors, can be maintained with small doses of colchicine, method: 0.5 ~ 1.0mg / d, should pay close attention to colchicine in the course of medication Possible inhibition of bone marrow and regular review of liver and kidney function. Rational use of drugs that inhibit uric acid synthesis and promote uric acid excretion, control hyperuricemia, maintain blood uric acid levels below 360 μmol / L (6mg / dl).
Both drugs have no anti-inflammatory and analgesic effects, and are usually selected according to the patient's renal function and 24h uric acid excretion. If the renal function is normal, 24h uric acid excretion is less than 3.75mmol, drugs that promote uric acid excretion may be used; if renal dysfunction, 24h uric acid excretion is greater than 3.75mmol, drugs that inhibit uric acid synthesis should be used.
(1) Drugs that inhibit uric acid synthesis: mainly allopurinol, which is a xanthine oxidase inhibitor, which inhibits xanthine oxidase and prevents hypoxanthine and xanthine from being oxidized to uric acid. Therefore, the blood uric acid concentration can be rapidly reduced, and the formation of tophi and uric acid stones can be reduced. If combined with drugs that promote uric acid excretion, it can accelerate the decline of blood uric acid levels, and mobilize urate deposited in tissues to dissolve tophi. The usual dose is 100mg, 2~4 times/d. The condition can be increased to 200mg, 3 times / d. After the blood uric acid concentration fell to 360 μmol/L (6 mg/dl), the amount was gradually reduced. In the early stage of medication, acute arthritis may be induced by increased blood uric acid metastasis. At this time, colchicine may be added. A small number of patients with this drug can develop allergic syndrome, which is characterized by fever, allergic rash, abdominal pain, diarrhea, white blood cells and thrombocytopenia. Should be vigilant, generally can be recovered after stopping the drug and symptomatic treatment. Individual patients may have severe epithelial tissue toxic necrolysis, acute vasculitis, severe liver and kidney dysfunction, and even a large area of liver necrosis, the condition is critical, should be actively rescued. Usually side effects are more common in patients with renal insufficiency. Therefore, in patients with impaired renal function, the dose should be reduced and closely observed as appropriate. In addition, elderly patients should be cautious when using this drug.
(2) drugs that promote uric acid excretion: These drugs mainly reduce blood uric acid levels by inhibiting renal tubular reabsorption of uric acid and increasing uric acid excretion. It is suitable for patients with normal renal function and low daily uric acid excretion. For 24h uric acid excretion greater than 3.57mmol (600mg) or existing uric acid stone formation, the application of such drugs may cause urinary infarction or promote the formation of uric acid stones, it should not be used. In order to avoid kidney damage and kidney stones caused by the rapid increase of urinary uric acid excretion after medication, it should be noted that starting from a small dose, oral sodium bicarbonate should be 3 ~ 6g / d, to alkalinize the urine; and drink more water, keep The urine volume is above 2000 ml/d. Certain drugs such as thiazide diuretics, furosemide, ethambutol, pyrazinamide, niacin, etc., can inhibit the excretion of uric acid and should be avoided.
1 probenecid (carboxybenzene sulfonamide): the initial dose was 0.25g, 2 times / d, gradually increased to 0.5g, 3 times / d after 2 weeks. The maximum dose should not exceed 2g/d. About 5% of patients may have side effects such as rash, fever, and gastrointestinal reactions.
2 sulfinpyrazone (benzenesulfazolone): a derivative of phenylbutazone. Its effect of promoting uric acid excretion is stronger than that of probenecid, and side effects are relatively small. It has a synergistic effect with propyl sulfonate. The initial dose is generally 50 mg, 2 times / d, increasing to 100 mg, 3 times / d, the maximum dose is 600 mg / d. The drug has a stimulating effect on the gastric mucosa and is used with caution in patients with ulcer disease.
3 benzbromarone: has a strong role in diuretic acid. The usual dose is 25 ~ 100mg, 1 time / d. The side effects are mild and there are few rashes, fever and gastrointestinal reactions.
(3) Adjunctive therapy: All patients with gout need to consume a large amount of fluid, at least 3L per day, especially in patients with chronic uric acid stones. Take sodium bicarbonate or trisodium citrate 5g three times a day to alkalinize the urine. Taking acetazolamide 50mg before going to sleep can effectively alkalinize morning urine. Care should be taken to avoid over-basing of urine as this may promote the deposition of calcium oxalate crystals. Because the drug is completely effective in reducing serum urate concentration, it is usually not necessary to strictly limit the amount of barium in the diet. In the quiescent period of gout, try to reduce the weight of obese patients. Giant tophi in the normal skin area can be surgically removed, and other tophi should be slowly resolved by appropriate reduction of blood uric acid treatment. In vitro ultrasonic lithotripsy may be considered for disintegration of kidney stones.
4. Treatment of acute renal failure caused by uric acid nephropathy, immediate administration of acetazolamide 500mg, followed by 250mg, 3 times / d. At the same time, add enough water to the vein, and inject a proper amount of 1.25% sodium bicarbonate solution. In order to increase the amount of urine, it can be intravenously injected with 40-100 mg of furosemide. In addition, allopurinol should be given as soon as possible, the initial dose is 8mg / (kg · d), 3 ~ 4 days reduced to 100 ~ 300mg / d. Blood urea nitrogen and creatinine increased significantly, feasible hemodialysis or peritoneal dialysis.
Urinary tract obstruction caused by renal pelvis or ureteric urinary stones can also cause acute renal failure. In addition to the use of allopurinol and alkalized urine, percutaneous nephrostomy can be performed to relieve urinary tract obstruction, and then removed after the condition is stable. Urinary tract stones.
5. Diet control reduces the source of exogenous sputum, avoid eating into glutinous diets such as animal viscera, fish and shrimp, meat, peas, etc.; to prevent obesity, generally do not advocate drinking, advocate drinking more water, keep daily urine volume in More than 2000ml.
Gout reference recipe: According to the sputum content, the food is divided into low-grade food (<25mg per 100g food), medium-sized food (25-150mg per 100g food), sorghum food (100mg per 100g food) ) 3 categories. However, this is only a principled estimate. In clinical practice, necessary adjustments should be made according to actual conditions.
(1) Low-lying foods that can be eaten:
1 staple foods: rice (rice, corn, millet, glutinous rice, etc.), wheat (barley, wheat, oats, buckwheat, cereal, etc.), noodle products (white powder, rich flour, noodles, cornmeal, taro, bread, biscuits, Cake), soda crackers, butter snacks, starch, sorghum, macaroni, potatoes (potatoes), sweet potatoes, hawthorn, winter flour, alfalfa, etc.
2 milk: fresh milk, condensed milk, cheese, yogurt, malted milk, milk powder, ice cream, etc.
3 meat and eggs: eggs, duck eggs, preserved eggs, pig blood, duck blood, chicken blood, goose blood and so on.
4 vegetables: cabbage, cabbage, lettuce (lettuce), leeks, scallions, sage, celery, mustard leaves, water leek, leeks, sorghum, tomato, eggplant, melons (cucumber, melon, loofah, pumpkin, courgette, bitter gourd Etc.), radish (including carrots, dried radishes, etc.), kale, kale, gourd, green pepper, onion, onion, garlic, ginger, fungus, mustard, pepper, kimchi, pickles, etc.
5 fruits: apples, bananas, red dates, black dates, pears, mangoes, oranges, oranges, lemons, grapes, pomegranates, alfalfa, pineapples, peaches, plums, kumquats, watermelons, papayas, raisins, dried longan.
6 drinks: soda, cola, soda, mineral water, tea, juice, coffee, chocolate, cocoa, jelly, etc.
7 Others: tomato sauce, peanut butter, jam, soy sauce, melon sugar, honey. Desserts and condiments made from oils and fats (melon seeds, vegetable oil, butter, butter, almonds, walnuts, hazelnuts), coix seed, dried fruit, sugar, honey, sea bream, seaweed, animal glue or agar.
(2) A limited amount of medium-sized food:
1 Beans and their products: soy products (tofu, dried bean curd, milk tofu, soy milk, soy milk), dried beans (mung beans, red beans, black beans, broad beans), bean sprouts, bean sprouts.
2 Meat: chicken, pheasant, turkey, pheasant, stone chicken, duck, goose, pigeon, sorghum, pork, pig skin, beef, lamb, dog, venison, rabbit.
3 aquatic products: grass carp, squid, squid, flounder, squid, barracuda, swordfish, crab, squid, squid, snail, red painted, abalone, fish balls, shark fin.
4 vegetables: spinach, bamboo shoots (winter bamboo shoots, asparagus, dried bamboo shoots), beans (green beans, green beans, kidney beans, kidney beans, peas), kelp, golden needles, white fungus, mushrooms, cauliflower, asparagus.
5 oils and other: peanuts, cashews, sesame seeds, chestnuts, lotus seeds, almonds.
(3) Taboo sorghum food:
1 Beans and vegetables: soybeans, lentils, seaweed, mushrooms.
2 meat: liver (porcine liver, beef liver, chicken liver, duck liver, foie gras), intestine (pork intestine, bovine intestine, chicken intestine, duck intestine, goose intestine), heart (pig heart, beef heart, chicken heart, Duck heart, goose heart), belly and stomach (pig liver, beef liver, chicken stomach, duck stomach, goose stomach), kidney (porcine kidney, beef kidney), lung brain, pancreas, meat emulsion, thick gravy, meat filling, etc. .
3 aquatic products: fish (fish skin, fish eggs, dried fish, sardines, anchovies, squid, squid, mullet, shark, octopus, kiss larva, sea bream, dried squid, squid), shellfish (蛤蜊, oysters, oysters, clams, mussels, scallops), shrimps (grass shrimp, golden hook shrimp, shrimp, shrimp), sea cucumber.
4 Others: yeast powder, various alcohols (especially beer).
(two) prognosis
Gout is a lifelong disease. Those who have no renal dysfunction or joint deformity can maintain normal life and work after effective treatment, and will not affect their longevity. However, if the treatment is not appropriate, repeated episodes of acute arthritis can cause greater pain. The quality of life of people with abnormalities and kidney stones will be affected. Patients with severe renal impairment have a poor prognosis.
All treatments are currently symptomatic. Untreated gouty arthritis varies greatly in severity and speed of development. Some patients have only a few episodes in their lifetime, but most of them, if left untreated, progressively worsen with the repetition, frequency, and extent of seizures. Some people have reported that the life expectancy of patients with gout is 5 years shorter than that of ordinary people, but this is completely related to the individual's condition and the effect of treatment. When articular cartilage disappears, subchondral bone erosion and tissue infiltration around the joint cause progressive disability, a small number of critically ill patients can produce huge tophi and severe joint damage within a few years. Affect the life of most patients is the presence or absence of complications. These factors are summarized as follows:
1. The younger the age of onset, the more severe the condition.
2. Those with a positive family history have a serious condition.
3. The longer the course of the disease, the heavier the progressive damage.
4. The frequency of recurrence is high, and the disease progresses rapidly.
5. The prognosis of patients with faster gout nodules is poor.
6. Gout complicated by hypertension, coronary heart disease and kidney disease, the condition is heavier.
7. Diet control or not, especially during the interval.
8. Treatment measures, how is the disease control? In particular, whether the acute phase control is rapid, whether the treatment is consistent with the prognosis in the intermittent period is closely related.
Today, gout has spread all over the world, which is closely related to the development of society, economic progress, and education. But it cannot be ignored because gout is an ancient disease. The more advanced countries are now, the higher the incidence rate, especially in countries and regions with economic prosperity. Therefore, the prevention and prognosis of gout is also related to the degree of attention.
prevention:
How to distribute the three major nutrients of gout patients?
Under the premise of limiting total calories, the three major nutrient distribution principles are: high carbohydrate, medium protein and low fat. 1 Carbohydrate: Rice noodles, including vegetables and fruits, should account for 55% to 60% of total calories. This is also in line with the eating habits of the Chinese people. In this way, it can reduce the decomposition of fat to produce ketone bodies, which is beneficial to urate excretion. However, you should try to eat less sugar or sugar beets. 2 protein: protein should account for 11% to 15% of total calories, usually 0.8 to 1.0 g / kg body weight per day. 3 fat: the rest of the total calories, supplemented with lipids, usually 40 ~ 50g / day. Since fat oxidation produces heat, about twice as much as carbohydrate or protein, it should undoubtedly limit the weight of the patient.
It is best for gout patients to eat less chicken:
Chicken essence is a compound seasoning. Its basic ingredient is 40% MSG. It is processed with raw materials such as preservative, salt, sugar, chicken powder, spice and chicken flavor. It contains a variety of amino acids. Chicken essence has both the savory taste and the flavor of the chicken. It achieves two-in-one flavoring and freshening seasoning; the freshness is 1.5-2 times that of MSG, and it is also a healthy food with higher nutrition.
Chicken essence is non-toxic and harmless to the human body, so in the cooking process, the use conditions are much looser than the MSG. However, not all dishes are suitable for adding chicken essence, stewed beef, pork ribs and other foods with their own flavor. Adding chicken essence will make the food taste and affect the taste of the vegetables. At this time, you can use ordinary MSG, beef extract, mushroom essence and other seasonings instead. Another point to note is that chicken essence contains nucleotides, and its metabolite is uric acid, so it is best for gout patients to cook less chicken.
How should gout be prevented?
Prevent gout diet
Holidays must be moderated, especially if you don’t eat too much food such as aquatic products. In the past, when you were full of fish and shrimp, you felt knee and knee pain. When you check the blood in the hospital, the uric acid content increased significantly. Was diagnosed with gout.
In order to prevent and treat gout diet, it should be done more than three or three:
l) Drink more water, drink more soup, blood uric acid and gout patients should drink more boiled water, drink less broth soup, chicken soup hot pot soup. The osmotic pressure of boiled water is most beneficial to dissolve various harmful substances in the body. Drinking boiled water can dilute uric acid and accelerate excretion, so that the level of uric acid is lowered. The soup contains a lot of bismuth ingredients. After drinking, not only can uric acid be diluted, but uric acid is increased.
2) Eat more alkaline foods and eat less acidic foods. Patients with gout have abnormal uric acid metabolism. If too much acid food will aggravate the condition, it is not conducive to rehabilitation. Eating more alkaline food can help supplement potassium and sodium chloride ions. pH balance.
3) Eat more vegetables, eat less and eat more vegetables is conducive to reducing the intake of sputum, increase vitamin C, increase fiber, eat less is beneficial to control calorie intake, limit weight loss and reduce fat.
Patients with acute gouty arthritis should not eat sorghum foods such as yeast, pancreas, concentrated gravy, meat sardines, anchovies, animal hearts, etc.; grapes, oranges, hawthorn, tomatoes, apples, coffee, Tea, milk, eggs, seaweed and other low-lying alkaline foods should not drink beer.
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