Gout (gout) is a metabolic disease caused by an impairment of purine metabolism, where excessive uric acid production or poor uric acid excretion results in elevated uric acid in the blood and recurrent inflammatory disease caused by deposition of urate crystals in synovial membranes, bursae, cartilage and other tissues. The disease is characterized by bifocal monohydrate uric acid crystals found in joint fluid and gout stones.
It is most commonly seen in middle-aged and elderly men with obese bodies and postmenopausal women. With economic development and lifestyle changes, its prevalence is gradually increasing. Primary gout is mostly caused by congenital abnormalities of purine metabolism and often occurs in association with obesity, disorders of glycolipid metabolism, hypertension, atherosclerosis and coronary artery disease, while secondary gout is caused by certain systemic diseases or drugs.
More frequent in men over 40 (95%), women are generally common after menopause, hyperuricemia is not directly related to the occurrence of gout, only high uric acid has a higher possibility of gout, some people with hyperuricemia will not trigger gout in their lifetime, while some people will have their first gout within a week or a month after the discovery of hyperuricemia first gout, there is usually an interval of 1-2 years, and also 10 years interval (5%), during which active treatment is needed to prevent the formation of gout stones.
I. Causes of morbidity
1. Causes of high uric acid: endogenous purines from the oxidative decomposition of nucleic acids account for 80% of the total purines, and exogenous purines from food account for 20% of the total purines.
Eating food containing too much purine, and in the process of metabolism, purine is not further metabolized into excretion that can be excreted from the kidneys through urine. If the blood is saturated with uric acid, these substances eventually form crystals and accumulate in the soft tissues. If there is a trigger for the release of uric acid crystals deposited in soft tissues such as joint membranes or tendons, then the body’s immune system may become sensitized and inflammation may result.
If the concentration of uric acid in the blood is higher than this saturation point for a long time, it is called “hyperuricemia” in medical science.
2. Foods with high purine content.
(1) Animal offal such as brain, liver, kidney, heart and stomach. And dark-colored meat, Western-style thick meat soup, beef vegetarian, chicken essence, etc. Seafood; sardines, hamachi, herring (Herring), tooth scallops, multi-spring fish, scallops, sea cucumber, scallops, oysters, mussels, division catfish, shrimp, dried small fish, fish skin, fish eggs, etc. Goose meat, wild animals, etc.
(2) Hard-shelled fruits such as peanuts cashew nuts and the like, wine (in excess).
(3) Young sprouting parts of plants generally contain moderate ingredients, should not eat more, cauliflower type, bean seedlings, bamboo shoots, beans.
3. Causes of gout.
Gout can be triggered by diet, weather changes such as sudden changes in temperature and pressure, trauma and many other aspects.
Drinking alcohol can easily trigger gout, because when alcohol is metabolized in the liver tissue, a large amount of water is absorbed, which strengthens the blood concentration, making the original already close to saturation of uric acid, accelerating the formation of crystals into the soft tissues, resulting in the body’s immune system overreaction (sensitivity) and inflammation, gout is known as the “king’s disease”, so the disease occurs in the nobleman’s For example, Kublai, the founder of the Yuan Dynasty, suffered from gout in his later years due to excessive alcohol consumption.
Some foods are metabolized and some of the derivatives can trigger the re-dissolution of uric acid crystals that have accumulated in the soft tissues, which can then trigger and aggravate arthritis.
4, the reasons why men are prone to gout
Gout disease can occur at any age. However, the most common are middle-aged men over 40 years old. According to the latest statistics, the incidence ratio of men to women is 20:1. brain workers, fat people have a higher incidence.
The reason why gout prefers men is that estrogen in women promotes uric acid excretion and has the effect of inhibiting arthritis attacks. Men like to drink alcohol, go to banquets, and eat food rich in purines and proteins, which increases uric acid in the body and reduces its excretion. Some doctors statistics, feast constantly, the incidence of 30%, often eat hot pot incidence also more.
This is because the raw materials of hot pot are mainly animal offal, shrimp, shellfish, seafood, and then drink beer, which naturally adds fuel to the fire. Investigation proves: shabu shabu a hot pot than a meal purine intake 10 times higher, or even dozens of times. A bottle of beer can double the uric acid. Hypertensive patients are 10 times more likely to suffer from gout. Gout, like diabetes, is a lifelong disease. The key is to control your own diet, eat more alkaline foods containing low purine, such as fruits and vegetables, and less acidic foods such as meat and fish, so that the diet is light, low fat and low sugar, and drink more water to facilitate the excretion of uric acid in the body.
Caution gout patients: men should not drink alcohol, meat and fish do not overdo it. Once diagnosed with gout disease, meat, fish and seafood are among the restricted foods. Spicy, stimulating food is also not advisable to eat more, but also resolve to quit drinking!
5, pseudogout is a disease caused by the deposition of calcium pyrophosphate crystals in joint cartilage and its surrounding tissues to arthritis as the main manifestation, because the symptoms are similar to gout and named, also known as calcium pyrophosphate deposition disease or cartilage calcification disease. The incidence increases with age, and the ratio of men to women is 1.4:1.
Etiology: The etiology is unknown and may be related to genetics, trauma and metabolic disorders. The basic etiology is calcium pyrophosphate deposition.
Pathophysiology
When blood uric acid exceeds 7 mg/dl or 0.41 mmol/L plasma is saturated (at pH 7.4, temperature 37°C and normal serum sodium). At 30°C, the solubility of urate is 4mg/dl, so needle-shaped monosodium urate (MSU) is deposited in tissues with no blood supply (e.g. cartilage) or relatively little blood supply (e.g. tendons, ligaments), including distal peripheral joints and lower temperature tissues such as the ear. In patients with severe and prolonged disease, monosodium urate crystals may be deposited in large central joints and parenchymal organs such as the kidneys.
Gout stones are crystalline aggregates of MSU, initially large enough to appear as “chisel-like” lesions on radiographs of the joints, and later as subcutaneous nodules that can be seen with the naked eye or felt in the hand. Because of the acidic pH of urine, uric acid tends to form crystals and accumulate into stones, which can lead to obstructive urinary tract disease.
Persistent hyperuricemia is commonly due to decreased renal urate clearance, especially in patients receiving long-term diuretic therapy and in patients with primary kidney disease with decreased glomerular filtration rate. The higher the degree of hyperuricemia and the longer the duration of the disease, the greater the chance of crystal deposition and acute gout attacks. However, there are still many people with hyperuricemia who do not develop gout.
Increased purine synthesis can be due to an abnormal state of the primary disease or to accelerated nucleoprotein turnover due to blood disorders such as lymphoma, leukemia or hemolytic anemia, or to an increased rate of leukocyte proliferation and death due to psoriasis. The cause of increased uric acid synthesis in most gout patients is unclear, but in a few patients it is due to hypoxanthine-guanine phosphate ribosyltransferase deficiency or to elevated phosphoribosyl pyrophosphate synthase activity. Abnormalities of the former enzyme can cause renal calculi, nephropathy and severe gout in early childhood, while complete deficiency of this enzyme can cause neurological abnormalities, tardive dyskinesia, spasticity, mental retardation and compulsive self-harm (Lesch-Nyhan syndrome).
Uncontrolled consumption of purine-rich foods, especially in conjunction with alcohol, can significantly increase uric acid levels. Ethanol both promotes hepatic catabolism of nucleosides and inhibits renal tubular urate secretion, but a strict low purine diet can reduce blood uric acid by only about 1 mg/dl (0.06 mmol/L).
Serum urate reflects the volume of the extracellular pool of mixable urate, which normally turns over once every 24 hours; 1/3 of urate is excreted in the feces and 2/3 in the urine. Normal 24-hour uric acid excretion after a 3-day low purine diet is 300-600 mg,600-900 mg on a normal diet.Thus, intake of food sources of uric acid is about 450 mg per day.Hyperuricemia and gout are common complications in patients treated with cyclosporine after organ transplantation. Uric acid levels are 1mg/dl (0.6mmol/L) lower in premenopausal women than in men, but approach male levels after menopause.
Gout pathogenesis
The long-term increase of uric acid in the blood is the key reason for the occurrence of gout. Human uric acid mainly comes from two sources.
1, nucleic acid and other purine compounds produced by the decomposition and metabolism of proteins in human cells, through the action of some enzymes to produce endogenous uric acid.
2, food purine compounds, nucleic acid and nucleoprotein components, after digestion and absorption, through the action of some enzymes to produce exogenous uric acid.
The production of uric acid is a very complex 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-phosphoribosyl-1-pyrophosphate synthase, adenine phosphate nucleotidyl transferase, phosphoribosyl pyrophosphate amidotransferase and xanthine oxidase; and enzymes that inhibit uric acid synthesis, mainly hypoxanthine-guanine nucleotidyl transferase. Gout is caused by various factors that lead to abnormal activity of these enzymes, such as increased activity of enzymes that promote uric acid synthesis and decreased activity of enzymes that inhibit uric acid synthesis, resulting in excessive uric acid production. Or the kidneys may become impaired in excreting uric acid due to various factors, causing uric acid to accumulate in the blood and producing hyperuricemia.
If hyperuricemia persists for a long time, uric acid will be deposited in the form of urates 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 a recurrent acute or chronic arthritis of the peripheral joints, caused by the deposition of monosodium urate crystals in and around the joints, tendons, and other areas of the body with supersaturated hyperuricemia.
The main reason for the low incidence of gout in women is that estrogen in women can promote uric acid excretion and inhibit arthritis attacks.
In the case of hereditary gout patients, most of them have primary hypertension because of metabolic insufficiency.
V. Clinical manifestations
Due to the high concentration of uric acid in human blood, needle-like crystals are formed in soft tissues such as joint membranes or tendons, causing the body’s immune system to overreact (sensitivity) and resulting in painful inflammation. The usual sites of attack are the thumb joint, ankle joint, knee joint, etc. In chronic gout, there are cases of attacks in the finger joints and even in the soft tissue of the ear. Acute gout attacks are characterized by redness, swelling, heat, and severe pain, usually in the middle of the night, which can wake people from sleep. In the early stages of gout, attacks are mostly seen in the lower extremities. Gout can present with kidney damage. According to statistics, 20-25% of gout patients have uric acid nephropathy, and almost 100% of those with nephropathy are confirmed by autopsy. It includes gouty nephropathy, acute obstructive nephropathy and urinary tract stones.
Six, signs and symptoms
1, gouty nephropathy: persistent hyperuricemia, 20% have clinical manifestations of nephropathy, after several years or more can successively develop renal tubular and glomerular damage, a small number of development to uremic syndrome. The incidence of uric acid nephropathy is second only to gouty joint damage and is closely related to the course of the disease and its treatment. Studies have shown that urate nephropathy is independent of the severity of gouty arthritis, i.e., patients with mild arthritis can have nephropathy, whereas patients with severe arthritis do not necessarily have renal abnormalities. Mild unilateral or bilateral low back pain is present in the early stages, followed by mild swelling and moderately elevated blood pressure. The urine is acidic, with intermittent or persistent proteinuria, usually not exceeding +++ . There is almost always a decrease in tubular concentration, nocturia, polyuria, and low relative density of urine. About 5-10 years later, the nephropathy worsens and then develops into uremia, and about 17-25% die of renal failure.
Smaller stones are excreted with urine, but they are often not felt, and small brown grains of sand can be seen in the urine sediment; larger stones can obstruct the ureter and cause hematuria and renal colic, and become pyelonephritis due to secondary infection from poor urine flow. Large stones can cause deformation of the renal pelvis and pelvic effusion. When there is sodium urate and calcium salt, the stone shadow can be seen on the X-ray.
3. Acute obstructive nephropathy: It is seen when the blood uric acid and uric acid in the urine are significantly elevated, which is due to extensive obstruction of the renal tubules by a large number of uric acid crystals. Gout is often associated with hypertension, hyperlipidemia, atherosclerosis, coronary artery disease, and type 2 diabetes. Cardiovascular factors far outweigh renal insufficiency as a cause of death from gout in the elderly. However, there is no direct causal link between gout and cardiovascular disease, but both are related to obesity and dietary factors.
4. Gout stones: also known as gout nodules, are white crystals that precipitate in a part of the body due to excessive elevation of uric acid in the blood, exceeding its saturation level. Like a glass of salt water in the amount of salt exceeds a certain limit, the bottom of the glass will appear white deposits. The area where the crystals are deposited is called a gout stone. Gout stones can occur in almost all tissues of gout patients, except for the central nervous system. Gouty stones are most commonly found in the ear, the first metatarsophalangeal joint of the [toes, fingers, wrists, elbows, and knees, and in a few patients in the nasal cartilage, tongue, vocal cords, eyelids, aorta, heart valves, and heart muscle. It invades bone in the bones near the joints, creating skeletal deformities or causing bone destruction.
These gouty nodules can also be found in the bursal membrane, tendon sheaths and cartilage near the joints. Gout stones can vary in size from as small as a sesame seed to as large as an egg. These tiny crystals can trigger attacks of gouty arthritis and can cause destruction of joint cartilage and bone and fibrosis of the surrounding tissue, resulting in chronic joint swelling, pain, stiffness, deformity, and even fractures. Some gouty stones are deposited on the surface of the body, such as around the ear chakras and joints, and can be seen by our naked eye. Some gout stones are also deposited in the kidneys, causing kidney stones and inducing renal colic.
5, acute arthritis: mental stress, overexertion, eating a high purine diet, joint injury, surgery, infection, etc. are common triggers. Most patients wake up in the middle of the night with severe joint pain, accompanied by fever and other systemic symptoms. The early manifestation is monoarthritis, with the first metatarsal and k-toe joints being the most common, followed by the ankle, hand, wrist, knee, elbow and other joints of the foot. If the disease is recurrent, it may develop into polyarthritis, with redness, swelling, heat, pain and restricted movement in the affected joints.
It is accompanied by fever, with a temperature of 38-39°C. Sometimes there are symptoms such as chills, lethargy, anorexia and headache. Symptoms usually resolve over a period of 1 to 2 weeks. Arthritis subsides, activity is completely restored, and the local skin changes from red to brownish red and gradually disappears completely. Flaking and itching may sometimes occur, which are symptoms unique to this disease. Intermittent period can be months or years, some patients only once in a lifetime, but most patients relapse within 1 year, 1 attack or several attacks per year.
6. Renal lesions: mainly manifested in two aspects.
(1) Gouty nephropathy has an insidious onset, with only intermittent proteinuria in the early stage and persistent as the disease progresses, accompanied by increased nocturia when renal concentration function is impaired, and renal insufficiency may occur in the late stage, showing edema, hypertension, elevated blood urea nitrogen and creatinine, with a few showing acute renal failure with oliguria or anuria and increased uric acid excretion in the first 24 hours.
(2) Uric acid nephrolithiasis About 10% to 25% of gout patients have uric acid stones in the kidneys, which are muddy and often asymptomatic, while larger stones may cause renal colic and hematuria. When the kidney stones cause obstruction leads to hydronephrosis, pyelonephritis, pus accumulation in the kidney or perinephritis, infection section accelerates the growth of stones and renal parenchymal damage.
7.Symptoms in each clinical phase
(1) Gout symptoms in the acute attack phase: the attack time is usually the second half of the night. The symptoms of gout in this stage are pain, swelling and redness at the ankle joints or toes, arms and finger joints, accompanied by severe pain. Using a microscope, you will see pine-needle-shaped urate deposits in the affected tissue. It is the precipitation of urate that causes severe pain. Please note that the blood uric acid value in the onset of the disease is lower than the usual maximum value because precipitation has been produced.
(2) Intermittent gout symptoms: The main symptom of gout in this stage is high blood uric acid concentration. The so-called intermittent period refers to the interval between two attacks of gout, which is usually several months to a year. If uric acid-lowering methods are not used, the attacks will be frequent, the pain will increase and the duration of the disease will be prolonged.
(3) Gout symptoms in the chronic phase: Gout symptoms in this phase are mainly manifested by the presence of gout stones, chronic arthritis, uric acid stones and gouty nephritis and complications. At this time, gout attacks are frequent and gout stones begin to appear in body parts, which gradually become larger as time goes on.
VII. Laboratory tests
(1) Blood, urine routine and blood sedimentation.
During the acute attack, the peripheral blood leukocyte count increases, usually to (10-20)×109/L, rarely exceeding 20×109/L. Neutrophils increase accordingly. In those with decreased renal function, mild to moderate anemia may be present. Blood sedimentation is increased, usually less than 60mm/h.
If the kidneys are involved, there may be proteinuria, hematuria, pusuria, and occasionally tubular urine; if the kidney stones are complicated, obvious hematuria can be seen, and acidic urinary stones can also be seen.
(2) Blood uric acid determination: The majority of patients have elevated serum uric acid levels during acute attacks. It is generally considered to be of diagnostic value when measured by the uric acid enzyme method, >416μmol/L (7mg/dl) in men and >357μmol/L (6mg/dl) in women. Serum uric acid levels may not be high if uric acid elimination drugs or adrenocorticotropic hormones have been used. It can be normal during remission. Two to three percent of patients have a typical gout attack with a serum uric acid level less than the above.
(3) Measurement of uric acid level: In a normal male adult with no purine diet and no medication affecting uric acid excretion, the total 24h uric acid level does not exceed 3.54mmol/(600mg/24h). In primary gout, 90% of patients with uric acid excretion is less than 3.54mmol/24h. Therefore, normal uric acid excretion cannot exclude gout, while uric acid greater than 750mg/24h indicates excessive uric acid production, especially in non-nephrogenic secondary gout, where blood uric acid is elevated and uric acid is significantly elevated at the same time.
(4) Joint cavity aspiration examination
(1) Polarized light microscopy: when the synovial fluid is placed on a slide, a slow vibrating image of double refractive fine needle-like sodium urate crystals can be seen intracellularly or extracellularly. With the first-stage red compensation prism, the urate crystals are yellow when the direction is parallel to the mirror axis and blue when it is vertical.
②Ordinary microscopic examination: sodium urate crystals are rod-shaped needles, and the detection rate is only half of that of polarized light microscopy. If heparin is added to the slip solution, centrifuged and precipitated, and the precipitate is taken for microscopic examination, the detection rate can be improved.
③ UV spectrophotometer determination: Using UV spectrophotometer, the most valuable method for determining sodium urate in gout is qualitative analysis of the contents of bursal fluid or suspected gout nodules. The method is to first measure the absorption spectrum of the specimen to be measured and then compare it with the absorption spectrum of known sodium urate. If they are the same, the measured substance is the known compound.
④ Purple uric acid amine (murexide) test: For specimens found to have sodium urate after ordinary light microscopy or polarized light microscopy, this test is feasible for further confirmation, and this method is simple and easy to perform. The principle is that sodium urate is heated with nitric acid to produce double alloxan, and then added to the ammonia solution to produce a purple-red ammonium urate.
⑤ urate dissolution test: in the synovial fluid with urate crystals, after adding uricase to keep warm, the urate crystals are degraded to allantoin and the crystals disappear.
(5) Gout nodule contents examination: for gout nodules to biopsy or puncture to aspirate their contents, or from the skin ulcer to take chalky mucous material smear, according to the above method, the positive rate of finding specific urate is very high.
(6) X-ray: Bone and joints are commonly involved in gout patients. There is also a large amount of calcium salts in the bone, which results in a high density and good contrast with the surrounding soft tissue. Therefore, the lesion is easily revealed by X-ray examination. Plain radiographs and digital radiographs (CR or DR) are simple and inexpensive, and can show the more obvious bone changes, joint space and bony joint surface abnormalities, and joint swelling in the bones and joints of the extremities.
X-rays include routine and special examinations. The routine examination should take a frontal and lateral view of the examined area, and the skeletal lesion should include an adjacent joint. Special examinations include magnification photography, body layer photography and soft tissue mammography. Magnification photography uses the principle that the x-ray beam with a small focal point expands from the focal point to the distance, so that the distance between the examination site and the film or x-ray induction plate is kept large, thus obtaining magnified images to better observe the fine structure of the bone. Body layer photography and soft tissue mammography are gradually being replaced by CT examinations and are now rarely used
(7) CT and MRI: Gout stones deposited in the joints appear as speckled images of varying grayness on CT scans, depending on their degree of graying. Gout stones appear as low to moderate density masses in both T1 and T2 images on MRI, and intravenous gadolinium injection enhances the density of gout stone shadows. The combination of the two tests can make an accurate diagnosis of most intra-articular gout stones.
Disease classification
The cause of gout is hyperuricemia, which can be classified as primary or secondary according to the cause of hyperuricemia. On this basis, according to the production and metabolism of uric acid, it can be further divided into excessive production type and excretion reduction type.
1. Excessive production of uric acid: It belongs to the high excretion type. It is mainly due to enhanced nucleic acid metabolism, i.e. various causes of excessive synthesis or degradation of purine bases and excessive purine metabolites, resulting in increased blood uric acid.
2.Decreased uric acid excretion type: There are four main methods to determine excessive uric acid production and decreased excretion as follows.
(1) Quantitative determination of uric acid in 24-hour urine normal urinary uric acid excretion <800mg/day (general diet) or <600mg/day (low purine diet) is poor excretion type. Normal urinary uric acid excretion <800mg/day (general diet) or >600mg/day (low purine diet) is overproduction type.
(2) uric acid clearance (Cua) is measured by accurately collecting urine for 60 minutes and leaving the urine in the middle segment. The normal range is 6.6-12.6 ml/min. Cua>12.6 ml/min is the overproduction type and <6.6 ml/min can be judged as reduced excretion type.
(3) The ratio of Cua to creatinine clearance (Ccr) was measured as Cua/Ccr×100％, if >10％ is overproduction type, <5％ is excretion reduction type. The random urine and the 24-hour urine Cua/Ccr are significantly and positively correlated, so the simple primary urine calculation method can be used in the outpatient clinic.
(4) Determination of uric acid/creatinine ratio in random urine is the easiest way to determine the ratio of uric acid/creatinine in random urine, if >1.O is overproduction type, <0.5 can be judged as excretion reduction type.
Nine, complications
1, renal dysfunction: If gout is not properly treated, long-term persistent hyperuricemia will cause excessive uric acid crystals to precipitate in the kidneys, resulting in gouty nephropathy, or renal dysfunction.
2, ischemic heart disease: ischemic heart disease refers to the hardening or blockage of the coronary arteries that carry oxygen and nutrients to the heart muscle, resulting in the obstruction of blood flow, thus causing chest pain and myocardial necrosis, mainly narrow heart disease and myocardial infarction, which is like a water pipe, due to dirt blockage, the caliber of the water pipe is getting smaller and smaller, resulting in reduced water flow or completely blocked.
Technically speaking, this can happen to all people, but the difference is that some people will be affected by special factors and accelerate the process. If gout is not properly treated, persistent hyperuricemia will cause excessive uric acid crystals to precipitate in the coronary arteries, which, together with the hyperagglutination of platelets, will accelerate the progress of atherosclerosis.
3, kidney stones: According to statistics, the chance of kidney stones in gout patients is about a thousand times that of normal people; because the more uric acid in the urine, the more acidic the pH, the more likely to occur stones, so we must drink more water and take baking soda to prevent the occurrence of kidney stones.
4, obesity: China’s rapid economic growth, food, so more and more obese people; obesity will not only make the synthesis of hyperuric acid, resulting in hyperuricemia, will also impede the excretion of uric acid, easy to cause gout, combined with hyperlipidemia, diabetes, etc.. The main reason is often overeating, so obese people should lose weight.
5, hyperlipidemia: gout people more often binge drinking, and more obesity, so the combination of hyperlipidemia, which is very closely related to the occurrence of atherosclerosis.
6, diabetes: oral glucose load test for gout patients, the results found that 30-40% of the combination of mild non-insulin-dependent diabetes; that is obesity and overeating caused by low insulin sensitivity, such as the early use of diet therapy and weight control, insulin sensitivity can soon recover.
7, hypertension: about half of the gout patients combined with hypertension, in addition to the above renal dysfunction caused by renal hypertension, gout patients combined with obesity is also one of the reasons. Because hypertension treatment drugs often use antihypertensive diuretics, will inhibit uric acid excretion, and make uric acid value rise, this point must be noted.
X. Western medical diagnosis
Based on medical history and clinical manifestations. The diagnosis can be further clarified by testing the concentration of uric acid in blood.
Gout can be clinically divided into four stages: the first stage is the period of hyperuricemia, in addition to elevated blood uric acid, the patient does not appear the clinical symptoms of gout; the second stage is the early stage of gout, blood uric acid continues to increase, resulting in a sudden attack of acute gouty arthritis, most people are woken up in their sleep like a knife cut pain, the first site is often the big toe of the foot, the joint is red, swollen, burning and swollen, can not cover If the slightest breeze blows or touches the foot, the pain will immediately be as severe as if the toes were moving, but it will disappear within a few days or weeks.
The third stage is the middle stage of gout, from the initial onset of a toe joint, gouty arthritis repeated acute attacks, after several acute attacks, gradually spread to the joints of the fingers, toes, wrists, ankles, knees and other joints throughout the body, and then the surrounding soft tissues and bones. In turn, the surrounding soft tissues and bones are also damaged and dysfunctional to varying degrees, and uric acid crystals are deposited, slowly forming stones like “gout stones”, at this time, kidney function is normal or shows a mild decline;
In the fourth stage of gout, the deformity and dysfunction of the joints become more and more serious, and the gout stones increase in size and easily break down and flow out white urate crystals. Uric acid salt is deposited into the kidney, forming kidney stones, etc. Clinical swelling, oliguria, proteinuria, increased nocturia, hypertension, anemia, etc. indicate that kidney function is damaged and kidney function is significantly reduced. Further development of the disease, the kidney failure is not easily reversible and life-threatening.
Eleven, early diagnosis of gout:
1, clinical diagnosis of acute gout criteria: recurrent acute arthritis, accompanied by increased blood uric acid, colchicine treatment is effective, that is, within a few hours of the acute attack of arthritis, colchicine 0.5 to 1 mg every 1 to 2 hours, if it is acute gout, usually after taking the drug 2 to 3 times, the joints immediately do not hurt, from inching to walking.
2. Criteria proposed by the American Rheumatism Association: specific urate crystals in the joint fluid, or gout stones, and urate crystals confirmed by chemical methods or polarized light microscopic observation. The diagnosis is confirmed if one of the three above criteria is met. The diagnosis of gout can be confirmed if 6 of the following 12 clinical, laboratory tests and X-ray signs are present.
(1) More than 1 episode of acute arthritis.
(2) Inflammatory manifestations peaking within 1 day.
(3) A single episode of arthritis.
(4) Redness of the joint is observed.
(5) Pain or swelling of the first metatarsophalangeal joint.
(6) Unilateral attacks involving the first metatarsophalangeal joint.
(7) Unilateral attack involving the tarsal joint.
(8) Suspected gout stone.
(9) Hyperuricemia.
(10) Intra-articular asymmetric enlargement on x-ray.
(11) Subcortical cysts without bone erosion.
(12) Negative microbiological culture of joint fluid during an inflammatory episode of the joint.
(13) Typical gouty foot, i.e., first metatarsal phalangeal arthritis with periarticular soft tissue swelling.
In conclusion, acute gout is not difficult to diagnose based on the typical clinical presentation, laboratory tests and response to treatment.
The diagnosis of chronic gouty arthritis requires careful differentiation, and urate crystals should be obtained as much as possible as a basis.
Chinese medicine diagnosis
Chinese medicine also has the name of “gout”, and has been discussed by doctors for many generations. Yuan Danxi Zhu “Ge Zhi Yu Lun” has listed a special section on gout, cloud: “Gout, most of the blood has been boiling since the heat, after or wading in the water or standing in the wetlands …… cold outside the fight, hot blood to get cold, sweat turbid stagnation, so pain, night is pain, line in Yang.” Ming Jing Yue Zhang “Jing Yue Quanshu” in the view that outside is Yin cold water dampness, now the dampness of the evil attack on the skin and flesh and tendons; internal by the plain fat and sweet excessive, dampness congestion of the lower jiao; cold and dampness of the evil conjunctive depression and heat, stay in the skin …… lesion parts redness and swelling hot flashes, long then bone erosion. Qing・Lin Peiqin, “the treatment of the class of symptoms”: “gout, pain paralysis one of the symptoms, …… at first because of wind, cold and damp paralysis of the yin part, a long time will turn into heat to cause pain, to the night more dramatic.” The modern medical term gout is also equivalent to the Chinese medical term “painful paralysis”, “joint”, “foot gas” and other diseases.
Early diagnosis of gout in Chinese medicine.
1. Damp-heat paralysis: sudden redness, swelling, heat and pain in the small joints of the lower extremities, refusal to press, localized burning when touched, relieved when cooled, accompanied by fever and thirst, restlessness, yellow urination, red tongue with yellow coating and slippery pulse.
2, internal stasis and heat: red, swollen and stinging joints, local swelling and deformation, unfavorable flexion and extension, purple and clear skin, slightly hard when pressed, scrofula” hard nodes around the lesion, purple and dark tongue or petechiae, thin yellow moss, thin and astringent pulse or sunken string.
3.Phlegm-damp obstruction: swollen joints, or even diffuse swelling around the joints, localized soreness and pain, or “scrofula” hard nodes without redness, accompanied by dizziness, swollen face and feet, stuffiness in the chest and epigastrium, fat tongue with dull texture, white greasy moss, slow or smooth pulse.
4.Yin deficiency of liver and kidney: the disease occurs repeatedly for a long time, with joint pains like a cane, local joint deformation, light day and heavy night, numbness of skin, difficulty in walking, constriction of tendons and veins, unfavorable flexion and extension, dizziness and tinnitus, red cheek and dry mouth, red tongue with little moss, and thin or fine pulse.
Analysis of the symptoms: Wind, cold and dampness attack the body, paralyze the meridians and channels, and cause pain in the limbs and joints. If the wind is superior, the joints will be wandering pain; if the cold is superior, the joints will be in severe pain, and the pain will be fixed;
1, damp-heat blocking paralysis: the small joints of the lower extremities suddenly become red, swollen, hot and painful, refusing to be pressed, localized burning when touched, relieved by cooling, accompanied by fever and thirst, disturbed and restless, yellow urination, red tongue with yellow coating, slippery pulse.
2, internal stasis and heat: red, swollen and stinging joints, local swelling and deformation, unfavorable flexion and extension, purple and clear skin, slightly hard when pressed, scrofula” hard nodes around the lesion, purple and dark tongue or petechiae, thin yellow moss, thin and astringent pulse or sunken string.
3.Phlegm-damp obstruction: swollen joints, or even diffuse swelling around the joints, localized soreness and pain, or “scrofula” hard nodes without redness, accompanied by dizziness, swollen face and feet, stuffiness in the chest and epigastrium, fat tongue with dull texture, white greasy moss, slow or smooth pulse.
4.Yin deficiency of liver and kidney: the disease occurs repeatedly for a long time, with joint pains like a cane, local joint deformation, light day and heavy night, numbness of skin, difficulty in walking, constriction of tendons and veins, unfavorable flexion and extension, dizziness and tinnitus, red cheek and dry mouth, red tongue with little moss, and thin or fine pulse.
Analysis of the symptoms: Wind, cold and dampness attack the body, paralyze the meridians and channels, and cause pain in the limbs and joints. In the case of wind, the joints are wandering pain; in the case of cold, the joints are in severe pain, and the pain is fixed;
Differential diagnosis
Differentiation of acute phase
1, acute rheumatoid arthritis has a history of Group A hemolytic streptococcal infection before the disease lesions mainly invade the heart and joints the following characteristics can be distinguished.
① Adolescents are more common;
② 1-4 weeks before the onset of the disease often have a history of hemolytic streptococcal infections such as pharyngeal tonsillitis;
(3) It often affects the knee, shoulder, elbow, ankle and other joints and has a wandering symmetry;
④ There is often myocarditis with erythema annulare and subcutaneous nodules;
⑤ Elevated anti-streptococcal antibodies such as ASO>500U, anti-streptococcal kinase>80U, anti-hyaluronidase>128U;
⑥ Salicylic acid preparations are effective in treatment;
(7) Normal blood uric acid level
2. Pseudogout is caused by the deposition of calcium pyrophosphate in the cartilage of the joints, especially in acute attacks of type A. It is similar to gout but has the following characteristics.
(1) It is more common in the elderly;
② Lesions mainly invade the knee, shoulder, hip and other large joints;
③ Radiographs show narrowing of the joint space and foci of cartilage calcification in the form of dense dots or lines without bone destruction;
④ Serum uric acid level is often normal;
⑤ Calcium pyrophosphate monoclinic or triclinic crystals can be found in the synovial fluid;
(6) Colchicine treatment is less effective
3, septic arthritis is mainly due to Staphylococcus aureus The main points of differentiation are.
① Primary infection or septic lesions can be found;
② Most of the major joints such as hip and knee joints with symptoms such as high fever and chills;
③ The joint cavity puncture fluid is purulent exudate smear microscopy can be found gram-positive staphylococcus and culture of Staphylococcus aureus;
④ No urate crystals in the synovial fluid;
⑤ Anti-anterior wind drug treatment is ineffective
4.Traumatic arthritis
① History of joint trauma;
② No wandering of the involved joint;
③ No uric acid crystals in synovial fluid;
④ Serum uric acid is not high
5. Acute attacks of gonorrheal arthritis are similar to gout but have the following characteristics.
① history of travel or gonorrhea;
(2) The presence of gonorrhea bacilli in the synovial fluid or positive bacterial culture without uric acid crystals;
(3) Penicillin G and ciprofloxacin are effective for differentiation.
Chronic phase differentiation
1, chronic rheumatoid arthritis this disease is often chronic about 10% of cases in the joint near the subcutaneous nodules easily confused with atypical gout, but the disease.
① The small joints of the fingers and toes are often symmetrical prismatic swelling and unilateral asymmetric gouty arthritis is very different;
② X-ray shows rough joint surfaces, narrowing of joint spaces, and sometimes partial fusion of joint surfaces with generalized osteoporosis but no cortical defects;
③ active rheumatoid factor positive joint fluid without uric acid crystals can be detected
2, psoriatic arthritis is also common in males, often asymmetrically invading the distal phalangeal joints and with elevated uric acid levels in 0.5 patients, so it needs to be differentiated from gout.
① Most patients have arthritic lesions after psoriasis;
More than half of the patients have thickened and depressed nails with ridge-shaped bulges;
③ X-ray image shows severe joint destruction, widening of joint space, shortening of bone resorption at the end of the finger and toe bones, and a knife-sharp appearance;
④ Joint symptoms are reduced with the improvement of skin lesions or aggravated with the deterioration of skin lesions.
3. Tuberculosis metaplastic arthritis is caused by a metaplastic reaction to Mycobacterium tuberculosis infection.
(1) The small joints are often involved first and gradually spread to the large joints and have multiple wandering characteristics;
② The patient has active tuberculosis foci in the body;
(3) There may be a history of acute arthritis or chronic arthralgia without joint ankylosis;
④ The skin around the joint often has nodular erythema;
⑤ Radiographs show osteoporosis without cortical defects;
(6) Synovial fluid shows more mononuclear cells but no urate crystals;
(vii) Strongly positive tuberculin test and effective anti-TB treatment.
XIV. Early detection
In the absence of conditions for mass blood uric acid testing, routine testing of blood uric acid should be performed at least in the following individuals.
1. Elderly people over 60 years of age, regardless of male or female and whether they are obese or not.
2, obese middle-aged men and post-menopausal women.
3.Patients with hypertension, atherosclerosis, coronary heart disease, cerebrovascular disease (such as cerebral infarction, cerebral hemorrhage).
4.Diabetes mellitus (mainly type II diabetes).
5.Arthritis of unknown cause, especially in middle-aged or older patients, characterized by the onset of monoarthritis.
6, kidney stones, especially patients with multiple kidney stones and bilateral kidney stones.
7, members with a family history of gout.
8.People of middle age or older who have a long-term taste for meat and have a habit of drinking alcohol. Anyone who belongs to any of the above listed conditions should take the initiative to go to the hospital to do laboratory tests on gout, so as to detect hyperuricemia and gout as early as possible, and not to wait until there is a canon.