Gout (gout) is a recurrent inflammatory disease caused by increased purine biosynthesis, excessive uric acid production or poor uric acid excretion resulting in elevated uric acid in the blood and deposition of urate crystals in synovial membranes, bursae, cartilage and other tissues. The disease is characterized by the presence of bifocal monohydrate urate crystals in joint fluid and gout stones. The clinical features are: hyperuricemia and characteristic acute arthritis due to urate crystals and deposition, gout stones, interstitial nephritis, and in severe cases, joint deformity and dysfunction, often accompanied by uric acid urinary tract stones. It is mostly seen in middle-aged and elderly men and postmenopausal women who are obese. With economic development and lifestyle changes, its prevalence is gradually increasing.
Gout (gout) is a group of diseases caused by long-term purine metabolism disorders and increased uric acid in the blood leading to tissue damage. It is characterized by hyperuricemia, recurrent acute arthritis, gouty stone formation, chronic arthritis and joint deformity, as well as the development of renal uric acid stones and gouty renal parenchymal lesions later in the course of the disease.
It is called “gout” because of the severe pain in the joints of the lowest part of the body and the painful “pain”, which soon blows over like “wind” in 1-7 days. (95%), and is common in women after menopause because estrogen inhibits the formation of uric acid; however, the rate of attacks increases after menopause. There is no direct relationship between hyperuricemia and the development of gout, except that hyperuricemia has a higher likelihood of gout occurring. Some people with hyperuricemia will never have gout in their lifetime, while some people will have their first gout within a week or a month of finding out about hyperuricemia. There is usually a 1-2 year interval after the first gout, and also a 10 year interval (5%) during which active treatment is needed to prevent the formation of gout stones.
The main disease
Painful inflammation caused by high concentrations of uric acid in the body’s blood, which forms needle-like crystals in soft tissues such as joint membranes or tendons, causing the body’s immune system to overreact (sensitize). 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, and can wake people from sleep. In the early stages of gout, attacks are mostly seen in the lower extremities. Gout can cause kidney damage: Gout can cause 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.
1. Gouty nephropathy
Persistent hyperuricemia, 20% have clinical manifestations of nephropathy, and over several years or more, renal and glomerular damage can occur successively.
Tubular and glomerular damage can occur over several years or more, with a small proportion progressing to uremia. 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. The nephropathy worsens after about 5-10 years, and then develops into uremia, and about 17-25% die from renal failure.
2. Urinary stones
The urine of gout patients is acidic, so the concentration of uric acid in the urine increases. Smaller stones are excreted in the urine, but they are often not felt, and small brown grains of sand can be seen in the urine sediment. Large stones may 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
This 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 stone
Also known as gout nodules, they 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. As the amount of salt in a glass of salt water exceeds a certain limit, a white deposit will appear at the bottom of the glass. Gout stones can be formed in almost all tissues of gout patients except the central nervous system. Gouty stones are most commonly found in the ear chakra, but also in 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. The interval can be several months or years, and some patients have only one lifetime occurrence, but most patients have a relapse within one year, with one or several episodes per year.
6. Renal lesions
About 20% to 25% of patients with primary gout have kidney stones, of which about 85% belong to uric acid stones. When the stones are large, there may be renal colic and hematuria. Since uric acid stones can pass through X-rays, they are detected by pyelogram. About 20% to 40% of patients may have intermittent small amounts of proteinuria in the early stages. In late stages, interstitial nephritis or kidney stones often lead to renal insufficiency. In addition, patients with gout often have hypertension, obesity, atherosclerosis, and coronary atherosclerotic heart disease.
Symptoms of gout in various stages
1, acute attack of gout symptoms: the attack time is usually the second half of the night. The symptoms of gout at 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 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 episodes of gout, which is usually a few months to a year. If uric acid-lowering methods are not used, attacks will be frequent, pain will be aggravated and the duration of the disease will be prolonged. 3. Gout symptoms in the chronic phase: The main symptoms of gout in this phase are 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.
Classification of gout
The cause of gout is excessive blood uric acid (hyperuricemia), and according to the cause of hyperuricemia formation, gout can be divided into two categories: primary and secondary. On the basis of this, it can be further classified into excessive production and reduced excretion according to the production and metabolism of uric acid.
1. Excessive production of uric acid
It belongs to the high excretion type. It is mainly caused by enhanced nucleic acid metabolism, i.e., excessive synthesis or degradation of purine bases due to various reasons, and excessive purine metabolites, resulting in increased blood uric acid.
2.Decreased excretion type
There are four main methods to determine the excess production and reduced excretion of uric acid as follows
(1) Quantitative measurement of uric acid in 24-hour urine. Normal urinary uric acid excretion <800mg/day (general diet) or <600mg/day (low purine diet) is a poor excretion type. Normal urinary uric acid excretion <800mg/day (general diet) or >600mg/day (low purine diet) is considered overproduction.
(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 it is >10％, it is overproduction type and <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) Measurement of uric acid/creatinine ratio in random urine is the easiest way to determine the ratio of uric acid/creatinine in random urine.
Pathology
1. Causes of high uric acid
The oxidative decomposition of nucleic acid accounts for 80% of the endogenous purines, and exogenous purines such as food account for 20% of the total purines. The body fails to further metabolize purines into excretions that can be excreted in urine from the kidneys during the metabolic process by consuming foods that contain too much purine. 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. (1) Animal offal such as brain, liver, kidney, heart, belly, and dark meat, western-style thick broth, beef vegetarian, chicken essence, etc.; seafood: sardine, hamachi, herring (Herring), toothfish, multi-spring fish, scallops, sea cucumber, scallop, oyster, mussels, catfish, shrimp, dried 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 plant buds part generally contains 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 blown, so that the blood concentration is strengthened, so that the original uric acid, which is already close to saturation, accelerates into the soft tissues to form crystals, 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 their derivatives can trigger the redissolution of uric acid crystals that have accumulated in soft tissues, which can then trigger and aggravate arthritis.
Gout pathophysiology
Blood uric acid is saturated when it exceeds 7 mg/dl or 0.41 mmol/L plasma (at pH 7.4, temperature 37°C and normal serum sodium). At 30°C, the solubility of urate is 4 mg/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 cooler 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. Due to the acidic pH of urine, uric acid tends to form crystals and collect 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 kidney stones, nephropathy and severe gout in the early years, while complete deficiency of this enzyme can cause neurological abnormalities, tardive dyskinesia, spastic states, mental retardation and compulsive self-harm (Lesch-Nyhan syndrome), and purines in the diet also affect serum uric acid levels. Uncontrolled overeating of purine-rich foods, especially 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 only reduce blood uric acid by 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 is excreted 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 1 mg/dl (0.6 mmol/L) lower in premenopausal women than in men, but approach male levels after menopause.
Gout pathogenesis
A long-term increase in uric acid in the blood is the key cause of gout. Human uric acid is derived from two main sources.
(1) Nucleic acid and other purine compounds produced by protein breakdown and metabolism in human cells, which generate endogenous uric acid by the action of some enzymes.
(2) Purine compounds, nucleic acids and nucleoprotein components contained in food are digested and absorbed to produce exogenous uric acid by the action of some enzymes.
The production of uric acid is a very complex process that requires the participation of a number of 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 peripheral joints and is caused by the deposition of monosodium urate crystals from supersaturated hyperuricemic body fluids in and around joints, tendons.
The main reason for the low incidence of gout in women is that estrogen in women promotes uric acid excretion and has an inhibitory effect on arthritis attacks. In the case of hereditary gout patients, most of them have primary hypertension because of metabolic insufficiency.
New advances in gout treatment
In recent years, “natural treatment of gout” has been advocated and promoted by medical experts, and has gradually become the mainstream treatment of gout in medical practice. Chinese and foreign medical experts have found that “drinking polyphenol coffee can effectively prevent gout recurrence” and is very safe. Polyphenol coffee for gout prevention and treatment effect is mainly through the following three aspects to achieve.
1, anti-nutritional: polyphenol coffee is easy to combine with protein and purine in food, reducing the body’s absorption of exogenous purine.
2, antioxidant: polyphenol coffee can protect cells from acid oxidation and damage, reduce the conversion of endogenous purines into uric acid.
3, and metal ion chelation: polyphenol coffee in a number of neighboring hydroxyl groups can chelate with excessive sodium ions in the body, to avoid or reduce the combination of sodium ions and uric acid, the formation of sodium urate crystals, and thus reduce or stop the recurrence of gout.
Reasons why men are susceptible to gout disease
Gout disease can occur at any age. However, it is most common in middle-aged men over the age of 40. According to the latest statistics, the incidence ratio of men to women is 20:1, and the incidence is higher in brainy, fat people.
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, and also resolve to quit drinking!
Pseudogout and its causes
Pseudogout is a disease caused by the deposition of calcium pyrophosphate crystals in joint cartilage and its surrounding tissues, mainly due to arthritis, named because the symptoms are similar to gout, also known as calcium pyrophosphate deposition disease or cartilage calcification. The incidence increases with age, and the ratio of men to women is 1.4:1.
Etiology: The cause is unknown and may be related to genetics, trauma, and metabolic disorders. The underlying etiology is calcium pyrophosphate deposition.
Highly prevalent population
1, gender factors: men are more prone to gout than women, the ratio of male to female incidence is 20:1. Moreover, women suffer from gout almost always after menopause, which can be related to changes in ovarian function and changes in sex hormone secretion.
2, age factor: older people are more prone to gout than younger people, the age of onset is about 45 years old. However, due to the general improvement of people’s living standards, excess nutrition and reduced exercise in recent years, gout is developing at a younger age. Now around 30 years old gout patients are also very common.
3, weight factors: obese middle-aged men are prone to gout, especially those who do not like exercise, eat more meat and protein, and have excess nutrition are more prone to gout than those with average nutrition.
4, occupational factors: enterprises and institutions cadres, teachers, private business owners and other social entertainment and mental laborers are prone to gout.
5, dietary factors: people who eat a high purine diet are prone to gout, and people who crave meat are more prone to gout than vegetarians.
6, alcohol consumption factor: alcoholics are more likely to suffer from gout than non-drinkers.
Comorbidities
1, kidney dysfunction
If gout is not properly treated, long-term persistent hyperuricemia will cause excessive uric acid crystals to settle in the kidneys, resulting in gouty nephropathy or kidney dysfunction.
2. Ischemic heart disease
The so-called ischemic heart disease refers to the hardening or blockage of the coronary arteries that carry oxygen and nutrients to the heart muscles, resulting in the obstruction of blood flow, thus causing chest pain and myocardial necrosis, mainly sarcopenia and myocardial infarction, which is just like a water pipe, the caliber of which is getting smaller and smaller due to the blockage of dirt, resulting in the reduction of water flow or complete blockage. Strictly 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 settle in the coronary arteries, and platelet agglutination will accelerate the progression of atherosclerosis.
3. Kidney stone
According to statistics, the chance of kidney stone for gout patients is about a thousand times 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, take baking soda to prevent the occurrence of kidney stones.
4.Obesity
Our country because of the rapid economic growth, food enough, so more and more obese people; obesity will not only make the synthesis of uric acid hyperactive, resulting in hyperuricemia, but also will 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 overeating, and more obese phenomenon, so the combination of hyperlipidemia a lot, which has a very close relationship with the occurrence of atherosclerosis.
6.Diabetes
Oral glucose load test for gout patients, the results found that 30-40% of combined “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 be restored.
7. Hypertension
About half of the gout patients combined with hypertension, in addition to the above renal hypertension caused by renal dysfunction, gout patients combined with obesity is also one of the reasons. Because the hypertension treatment medicine often uses the hypotensive diuretic, will inhibit the uric acid excretion, and make the uric acid value rise, this point must pay attention to.
Clinical diagnosis
Based on the medical history and clinical presentation. The diagnosis can be further clarified by testing the concentration of uric acid contained in the blood. Gout can be clinically divided into four stages.
The first stage is the hyperuricemic stage, in which the patient does not show clinical symptoms of gout except for elevated blood uric acid.
The second stage is the early stage of gout, the 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, the joint is red, swollen, burning and swollen, can not cover the quilt, feet stretched out, if the slightest wind blowing or slightly touched, move the toes, immediately pain like a heart, but in a few days or a few weeks This phenomenon of “coming and going like the wind” is called “self-limiting”. After one painful episode, it seems that the inflammation in the joint is eliminated and the person is normal, but in fact, the uric acid crystals do not disappear and continue to act as a monster, and gradually the joint becomes swollen and stiff, and the flexion and extension are unfavorable.
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 fingers, toes, wrists, ankles, knees and other joints throughout the body, and then the surrounding soft tissues and bones are also damaged to varying degrees and dysfunction, uric acid crystals continue to deposit, slowly forming a stone like ” gout stones”, at which time, the kidney function is normal or shows a mild decrease.
The fourth stage is the late stage of gout, in which the joint deformity and dysfunction of the patient become more and more serious, and the gout stones increase in size and easily break down and flow out white urate crystals, which affects the daily study, work and life due to the permanent deformity of the joints and brings great physical and mental pain to the patient. 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. If the disease develops further, the renal failure which is not easily reversible will be life-threatening.
1.X-ray examination of gout
Bone and joint are the common parts of gout patients. There is also a large amount of calcium salts in the bones, so the density is high and forms a good contrast with the surrounding soft tissues. 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 more obvious bone changes, joint space and bony joint surface abnormalities, and joint swelling in the bones and joints of the extremities, and radiographs are usually the imaging method of choice for understanding the presence or absence of bone and joint involvement in gout patients. 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 examination, and are now rarely used
2.Early diagnosis of gout
1.Criteria for clinical diagnosis of acute gout: recurrent acute arthritis with increased blood uric acid, effective treatment with colchicine and gout clear, that is, colchicine 0.5~1mg every 1~2 hours within a few hours of an acute attack of arthritis, and if it is acute gout, usually after taking the drug 2~3 times, the joints are immediately painless, and it is possible to walk from inch to inch.
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 and 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 attack involving the first metatarsophalangeal joint.
(7) Unilateral attack involving the tarsal joint.
(8) Suspected gout stone.
(9) Hyperuricemia.
(10) Asymmetric intra-articular enlargement on X-ray.
(11) Subcortical cysts without bone erosion.
(12) Negative microbiological culture of joint fluid during an inflammatory joint episode.
(13) Typical gouty foot, i.e., first metatarsal toe 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.
Examination and laboratory tests
1.Blood, urine routine and blood sedimentation
During acute attack, the peripheral blood leukocyte count increases, usually (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 kidney is involved, there may be proteinuria, hematuria, pusuria, and occasionally tubular urine; if the kidney stone is complicated, there may be obvious hematuria and acidic urinary stone discharge.
3.Blood uric acid measurement
The majority of patients have elevated serum uric acid level during acute attack. It is generally considered to be of diagnostic value when measured by 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 adrenocorticosteroids have been used. It can be normal during remission. There are 2-3% of patients with typical gout attack and the serum uric acid level is less than the above level.
4.Uric acid level measurement
In the case of purine-free diet and no drugs affecting uric acid excretion, the total 24h uric acid level in normal male adults does not exceed 3.54mmol/(600mg/24h). In 90% of primary gout patients, uric acid excretion is less than 3.54 mmol/24 h. Therefore, normal uric acid excretion cannot exclude gout, while uric acid greater than 750 mg/24 h indicates excessive uric acid production, especially in non-nephrogenic secondary gout, where blood uric acid is elevated and uric acid is also significantly elevated.
Articular cavity aspiration examination
(i) 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 appear yellow when the direction is parallel to the mirror axis and blue when it is perpendicular.
(B) Ordinary 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.
(C) UV spectrophotometer determination
Using UV spectrophotometer, qualitative analysis of the contents of bursal fluid or suspected gout nodules to determine sodium urate is the most valuable method for gout. 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 the two are the same, the measured substance is the known compound.
(iv) 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 in order to further confirm the presence of 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. (E) uric acid salt 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 are seen to disappear.
Gout nodule contents examination
Gout nodules are examined by biopsy or aspiration of their contents by puncture, or by smear of chalky mucous material from skin ulcers, and the positive rate of finding specific urates is very high.
X-ray radiography, CT and MRI examination
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 on both T1 and T2 images on MRI, and intravenous gadolinium can enhance the density of gout stone shadows. The combination of the two tests provides an accurate diagnosis of most intra-articular gout stones.
Differential diagnosis
Differential diagnosis of acute phase
1. Acute rheumatoid arthritis with a history of Group A Streptococcus haemolyticus infection prior to the disease lesions mainly invade the heart and joints The following features can be distinguished.
(1) Prevalence in adolescents.
② often have a history of hemolytic streptococcal infections such as pharyngeal tonsillitis 1 to 4 weeks before the onset of the disease.
(3) It often affects the knee, shoulder, elbow, ankle and other joints and has a wandering symmetry.
(iv) Often accompanied by myocarditis with erythema annulare and subcutaneous nodules.
(5) Elevated anti-streptococcal antibodies such as ASO>500U, anti-streptococcal kinase>80U, anti-hyaluronidase>128U;
(vi) Salicylic acid preparations are effective in treatment.
(vii) normal blood uric acid level
Pseudogout is caused by calcium pyrophosphate deposited 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) The lesions mainly affect large joints such as the knee, shoulder and hip.
(3) X-rays show narrowing of the joint space and foci of cartilage calcification in the form of dense dots or lines without bone destruction.
④Serum 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
Septic arthritis is mainly due to Staphylococcus aureus The main points of differentiation are.
① primary infection or septic lesions can be found.
②Most 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 seen gram-positive staphylococcus and culture of Staphylococcus aureus.
(iv) No urate crystals in the synovial fluid.
⑤ anti-prowind drug treatment is ineffective
Traumatic arthritis
① history of joint trauma.
② no wandering of the involved joint fixation
③ no uric acid crystals in synovial fluid
④Serum uric acid is not high
The acute attack of gonorrheal arthritis is similar to gout but has the following characteristics.
(1) a history of travel or gonorrhea.
(ii) gonococcus gonorrhoeae can be detected in synovial fluid or positive bacterial culture without uric acid crystals.
(3) Penicillin G and ciprofloxacin are effective for differentiation.
Differential diagnosis of chronic phase
1, chronic rheumatoid arthritis this disease is often chronic about 10% of cases have subcutaneous nodules near the joints easily confused with atypical gout but the disease.
① small joints of the fingers and toes are often symmetrical prismatic swelling and unilateral asymmetric gouty arthritis is very different.
(ii) Radiographs show rough joint surfaces narrowing of joint spaces and sometimes partial joint surface fusion with generalized osteoporosis but no cortical deficient changes.
③ active rheumatoid factor-positive joint fluid without urate crystals are detected
2, psoriatic arthritis is also common in men, often asymmetrically invading the distal phalangeal joints and 0.5 patients with elevated blood uric acid levels, so it needs to be differentiated from gout.
(i) Most patients have arthritic lesions after psoriasis.
More than half of the patients have thickened and depressed nails with ridge-shaped elevations.
③X-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.
④Joint symptoms decrease with improvement of skin lesions or worsen with deterioration of skin lesions
Tuberculous 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 with multiple wandering characteristics.
(ii) The patient has active tuberculosis foci in the body.
③There may be a history of acute arthritis or chronic arthralgia without joint deformity.
(iv) The skin around the joint often has nodular erythema.
⑤ X-ray shows osteoporosis without cortical deficiency changes.
(6) Synovial fluid shows more mononuclear cells but no urate crystals.
(7) Strongly positive tuberculin test with effective anti-TB treatment
Early diagnosis of gout in Chinese medicine.
1. Dampness and heat blocking paralysis
The small joints of the lower extremities are suddenly red, swollen, hot and painful, refusing to be pressed, burning when touched, relieved when cooled, accompanied by fever and thirst, restlessness, yellow urine, red tongue with yellowish coating and slippery pulse.
2.Heat stasis and internal stagnation
Red, swollen and stinging joints, local swelling and deformation, unfavorable flexion and extension, purple and clear skin color, slightly hard when pressed, or scrofula” hard knots 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 pain and soreness, or “lumpy scrofula” hard nodes without redness, accompanied by dizziness, swollen face and feet, stuffiness in the chest and epigastrium, fat and dull tongue, white greasy moss, slow or smooth pulse.
4.Yin deficiency of liver and kidney
The disease occurs repeatedly for a long time, with joint pain like a cane, local joint deformation, light day and heavy night, numbness of the 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, thin or fine pulse.
5.Wind-cold damp paralysis type
Pain in the limbs and joints, or wandering pain, or severe pain in the joints that does not move, or heavy swelling and pain in the joints of the limbs and numbness of the skin. It is aggravated on rainy days, with thin white tongue coating and tight or moist pulse.
Analysis of the symptoms: Wind, cold and dampness attack the organism and paralyze the meridians.