The friends of our coastal area pay attention to DDDD there is a kind of pain that comes and goes inexplicably DDDD it comes and goes like the wind, its name is gout!
To get rid of the “first pain of life”, reduce the pain, reduce the attack, and communication with friends, listen to the doctor’s advice, enjoy the “painless” life, please pay attention to Wendeng osteopathic foot and ankle, to help you solve the problem!
Gout is a recurrent inflammatory disease caused by increased purine biosynthesis, excessive production of uric acid or poor uric acid excretion resulting in elevated uric acid in the blood and deposition of urate crystals in the synovial membrane, bursa, bone, cartilage and other tissues. The disease is characterized by increased joint fluid and gout stone formation, and monohydrate uric acid crystals with double refractoriness can be found. Its prevalence is gradually increasing.
Second, the etiology: the main factors are.
1, drinking alcohol (25%): drinking alcohol is prone to gout, often to word liquor can drink less, are not correct, because alcohol in the liver tissue metabolism, a lot of blowing water, so that the blood concentration is strengthened, so that the original is close to saturation of uric acid, accelerated into the soft tissues to form crystals, resulting in the body’s immune system overreaction (sensitivity) and inflammation, whether liquor or beer will affect the metabolism of uric acid. Gout is known as the “King’s Disease”, and many friends in coastal areas are suffering from gout due to excessive alcohol consumption.
2. Diet (15%).
Gout can be triggered by diet, weather changes such as sudden changes in temperature and pressure, trauma and many other aspects. After metabolism of some foods, some of the derivatives can trigger the re-dissolution of uric acid crystals originally accumulated in soft tissues, which can trigger and aggravate arthritis.
3. Long-term increase in uric acid (15%).
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: nucleic acid and other purine analogues produced by protein breakdown and metabolism in human cells, which generate endogenous uric acid by the action of some enzymes. The 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 complex process that requires the participation of a number of enzymes, which can be broadly classified into two categories: enzymes that promote uric acid synthesis, mainly pyrophosphate 5 phosphate synthase, adenine phosphate nucleotidyl transferase, phosphoribosyl pyrophosphate amidotransferase and xanthine oxidase; enzymes that inhibit uric acid synthesis, mainly hypoxanthine-guanine nucleotidyl transferase, and gout is caused by various factors that lead to The activity of these enzymes is abnormal, for example, the activity of enzymes that promote uric acid synthesis is enhanced, and the activity of enzymes that inhibit uric acid synthesis is weakened, resulting in excessive production of uric acid, or the kidney excretes uric acid due to various factors, resulting in the accumulation of uric acid in the blood and hyperuricemia.
III. Pathogenesis
Reduced uric acid catabolism as a mechanism leading to hyperuricemia has been ruled out. During the normal conversion of nucleic acids and nucleotides, some are degraded into free purine groups, mainly hypoxanthine and guanine, which are rapidly degraded to hypoxanthine when there is an excess of nucleic acid needed for synthesis of nucleotides, guanine is deaminated to xanthine by the action of guanine enzyme, hypoxanthine and xanthine are oxidized by the action of xanthine oxidase to Uric acid, purine nucleotides, adenine nucleotides, hypoxanthine nucleotides and guanine nucleotides are the end products of purine biosynthesis, the above 3 purine nucleotides can be synthesized by 1 of 2 pathways, directly from purine bases, such as guanine into guanine nucleotides; hypoxanthine into hypoxanthine nucleotides; adenine into adenine nucleotides; or they can be resynthesized, purine metabolism The first step of the reaction and its site of feedback inhibition is ribose phosphate pyrophosphate (PRPP) + glutamine + H2O aminophosphate ribose + glutamate + pyrophosphate (PPI), which is catalyzed by ribose phosphate pyrophosphate amidotransferase (PRPPAT).
Possible mechanisms for the uncontrolled regulation of this reaction and increased purine synthesis are: increased concentration of PRPP, glutamine; increased amount or activity of the enzyme; decreased sensitivity of the enzyme to feedback inhibition of purine nucleosides; decreased concentration of adenosine or guanosine, which have a coordinating effect on enzyme activity, resulting in decreased inhibition of the enzyme, and significantly higher intracellular PRPP concentration in the absence of HPRT and overactive PRPP synthase , purine synthesis is increased, and in patients with increased uric acid production, the conversion of PRPP is accelerated, in addition, some of the causes of hyperuricemia are due to hypoxanthine-guanine phosphate ribose convertase (HGPRT) deficiency, and when this enzyme is abnormal, PRPP is increased, purine synthesis is increased, and uric acid production is increased, others include any process that leads to accelerated intracellular adenosine acid catabolism due to purine Degradation is accelerated and uric acid production is increased, causing hyperuricemia.
In some patients with gout, the direct pathological mechanism of hyperuricemia is the decreased clearance of urate by the renal tubules. The renal excretion of urate is by glomerular filtration, but the filtered urate is almost completely absorbed by the proximal tubule (pre-secretory reabsorption), and some of the urate secreted by the renal tubules is also reabsorbed at the distal end of the proximal tubule, and a small amount is reabsorbed in the Henry’s loop and collecting duct (post-secretory reabsorption). Therefore, urate excretion is almost secreted by the renal tubules, and the final uric acid excretion from the kidney is 6-12% of the glomerular filtration. When glomerular urate filtration decreases, renal tubular reabsorption of urate increases or renal tubular secretion of urate decreases, all of which can cause a decrease in urate renal excretion, leading to hyperuricemia, and when blood uric acid increases beyond supersaturated concentrations, urate is deposited in the tissues, and in patients with gout The secretion of urate by the kidney unit has been confirmed to be decreased in studies of gout patients.
Clinical manifestations: acute gouty arthritis does not have any aura before the onset, mild trauma, overeating high purine food or excessive alcohol consumption, surgery, fatigue, emotional stress, medical emergencies (such as infection, vascular obstruction) can trigger an acute attack of gout, often at night, acute single joint or multi-joint pain is usually the first symptom, pain progressive aggravation, severe pain, signs similar to acute infection, with swelling Localized fever, redness and tenderness, localized skin tension, warmth, shine and dark red or purplish appearance are the most common sites of involvement.
The first few attacks usually involve only one joint and usually last only a few days, but later they can invade several joints simultaneously or successively, and if untreated can last for several weeks, and finally the local symptoms and signs subside and joint function is restored. In some cases, the joints of sacroiliac, thoracic clavicle or cervical vertebrae may also be involved.
1. Asymptomatic phase
Serum urate concentration increases with age, and there are gender differences. This stage is mainly characterized by a continuous or fluctuating increase in blood uric acid, and the time from the increase in blood uric acid to the appearance of symptoms can be years to decades.
2.Acute arthritis attack period
It is the most common first symptom of primary gout, and is most common in the joints of the lower limbs, with the bunions and the first metatarsal phalangeal joint being the most common, with inflammation of a single joint at first, and more joints being involved with repeated attacks.
3.Intermittent period
The gout attack lasts for several days to weeks and can be relieved naturally, leaving no sequelae and fully recovered, and then there is a symptom-free phase, called the acute attack interval, after which it can recur, about 60% of patients relapse within one year, and the interval can also last for more than 10 years.
4.Gout stone formation
In patients with untreated or poorly treated chronic arthritis, uric acid crystals are deposited in cartilage, tendons, bursal fluid and soft tissues, and gout stones are common in this stage, often occurring in the ears, forearms, toes, fingers, elbows, etc. The deposition of uric acid increases in the joints, and the inflammation repeatedly enters the chronic stage and does not disappear completely, causing bone erosion defects in the joints and fibrosis of the surrounding tissues, resulting in With repeated attacks of inflammation, the lesions become more and more aggravated and seriously affect the function of the joints.
V. Diagnosis
There is no unified standard for the diagnosis of gout in China, but generally the American Rheumatism Association standards, the American Holmes criteria and the Japanese revised standards are used.
1.Specific urate crystals are detected in the bursal fluid.
2. Gout stones are chemically or polarized light microscopically confirmed to contain sodium urate crystals.
3.With 6 out of 12 clinical, laboratory and X-ray signs as follows
(1) More than 1 episode of acute arthritis.
(2) Inflammatory manifestations peaking within 1d.
(3) Single episode of arthritis.
(4) The skin of the affected joint is dark red.
(5) Pain or swelling of the first metatarsal joint.
(6) Unilateral attacks involving the first metatarsophalangeal joint.
(7) Unilateral attacks involving the tarsal joints.
(8) Suspected gout stones.
(9) Hyperuricemia.
(10) X-rays show asymmetric swelling of the joint.
(11) Radiographs show subcortical cysts without mass erosion.
(12) Negative microbiological culture of joint fluid during the inflammatory episode of the joint.
If there is difficulty in confirming the diagnosis during the acute arthritis period, colchicine can be used as a diagnostic treatment. If it is gout, the symptoms are rapidly relieved after taking colchicine, which has diagnostic significance.
In short, acute gout is not difficult to diagnose based on typical clinical manifestations, laboratory tests and treatment response, while the diagnosis of chronic gouty arthritis requires careful differentiation and should be based on urate crystals as much as possible.
Differential diagnosis of gout
Differential diagnosis of acute phase: 1. Pseudogout is caused by the deposition of calcium pyrophosphate in joint cartilage, especially in acute type A attacks, the performance is similar to gout, but has the following characteristics.
(1) the elderly are more common;
(2) The lesions mainly affect large joints such as 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.
The serum uric acid level is often normal.
⑤Calcium pyrophosphate monoclinic or triclinic crystals can be found in the synovial fluid.
⑥Colchicine treatment is less effective.
2, septic arthritis Mainly due to Staphylococcus aureus, the main points of differentiation are.
① Primary infection or septic lesions can be found;
②More occur at the age of major joints such as hip, knee, and accompanied by high fever, chills and other symptoms.
③ joint cavity puncture fluid is purulent exudate, smear microscopy can be seen gram-positive staphylococcus and culture of Staphylococcus aureus.
④No urate crystals in the synovial fluid.
⑤ Anti-anterior wind drug treatment is ineffective.
3.Traumatic arthritis
①History of joint trauma.
②The involved joint is fixed and not wandering.
③No urate crystals in synovial fluid.
④Serum uric acid is not high.
VII. Laboratory tests, which are important for the diagnosis of gout, especially the finding of urate, are the basis for confirming the diagnosis.
(a) Blood, urine routine and blood sedimentation
1.Blood routine and sedimentation examination During acute attack, the peripheral blood leukocyte count is elevated, usually (10-20)×109/L, rarely exceeding 20×109/L, and the neutral leukocyte is correspondingly elevated, and those with decreased renal function may have mild or moderate anemia, and the blood sedimentation is increased rapidly, 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, obvious hematuria can be seen, and acidic urinary stone discharge can also be seen.
(B) Blood uric acid measurement
The majority of patients with acute attacks have elevated serum uric acid levels, 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, if uric acid excreting drugs or adrenocorticotropic hormones have been used, the serum uric acid level may not be high and may be normal during remission, with 2% to 3% of patients showing typical gout attacks. Gout attack and serum uric acid content is less than the above level, there are three explanations: ① central body temperature and peripheral joint temperature gradient difference is large; ② the body is in a state of stress, secrete more adrenocorticotropic hormone, promote the excretion of serum uric acid, while the distal joint sodium urate content is still relatively high; ③ has been used to uric acid detoxification drugs or the influence of corticosteroid treatment.
(C) Joint cavity aspiration examination
In acute gouty arthritis, fluid may accumulate in the swollen joint cavity. Bursal fluid examination by injection needle is of great diagnostic importance, and the white blood cell count of bursal fluid is usually in the range of (1-7) × 109/L, mainly fractionated nuclear granulocytes.
(iv) X-ray radiographs
In acute arthritis, only swelling of soft tissues and normal joint imaging are seen. As the disease progresses, irregular or lobulated defects with warped edges may appear in the bone adjacent to the gout stone; the cartilage edge of the joint is destroyed and the joint surface is irregular. In addition, the use of dual-energy X-ray bone densitometry can be early detection of bone density changes in the affected joints, and can be used as an evaluation indicator for the diagnosis of gouty arthritis and disease observation, simple uric acid stones can be X-rayed, and their diagnosis depends on intravenous pyelography, mixed with calcium salts can be detected during abdominal plain film examination.
(v) CT and MRI examination
Gout stones deposited in the joints may appear as speckled images of varying grayness in CT scans depending on the degree of graying, and gout stones may appear as low to medium density masses in T1 and T2 images in MRI examinations.
VIII. Treatment
Treatment is aimed at.
(1) Terminate acute attacks with anti-inflammatory drugs.
(2) Prophylactic application of colchicine daily to prevent recurrent acute attacks (if they are frequent).
(3) Prevention of further deposition of monosodium urate crystals and elimination of existing gout stones by reducing urate concentration in body fluids. Prophylactic protection should be directed at two aspects, namely prevention of disability caused by erosion of bone and joint cartilage and prevention of kidney damage.
The drug treatment of gout is complicated, so please consult a professional physician in order to get good treatment.
Nine: attention to diet is an indispensable part of the control of gout attacks
1, safflower and hemlock drink: safflower, hemlock, add the right amount of water, decoction for twenty minutes, remove the slag and take the juice with the right amount of sugar to taste, 3 times a day in warm before eating. Suitable for swollen joints, subcutaneous nodules.
2, papaya psyllium coix rice drink: papaya, fresh psyllium (dried psyllium with 30 grams), coix seeds, add water for 20 minutes, decoction, remove the dregs to take juice, drink as tea at any time in the joint swelling and pain, urine yellow heat.
3, Job’s tear porridge: Job’s tear with rice, add the right amount of water to cook the porridge. Take 1 time in the morning and 1 time in the evening, 10 days as a course of treatment. Suitable for people with high blood uric acid and no obvious symptoms.
Food therapy is recommended
(1) Low purine foods that can be eaten.
(1) Staple foods: rice (rice, corn, millet, glutinous rice, etc.), wheat (barley, wheat, oats, buckwheat, cereals, etc.), flour products (refined white flour, rich flour, noodles, cornmeal, steamed buns, bread, cookies, cakes), soda crackers, butter snacks, starch, sorghum, macaroni, potatoes (potatoes), sweet potatoes, yams, winter flour, water chestnuts, etc.
② Milk: fresh milk, condensed milk, cheese, yogurt, cream of wheat, milk powder, ice cream, etc.
③Meat: pig blood, duck blood, chicken blood, goose blood, etc.
④Vegetables: cabbage, cabbage, lettuce (lettuce), amaranth, potherb mustard, chrysanthemum, celery, mustard leaves, water jar greens, leeks, chives, tomatoes, eggplant, melons (cucumber, winter melon, loofah, pumpkin, carrot, bitter melon, etc.), radish (including carrot, dried radish, etc.), kale, collard greens, gourd, green pepper, onion, onion, garlic, ginger, fungus, squash, chili, kimchi, pickles, etc.
⑤ Fruits: apples, bananas, red dates, black dates, pears, mangoes, oranges, oranges, lemons, grapes, pomegranates, loquats, pineapples, peaches, plums, kumquats, watermelons, papayas, raisins, dried longan.
(6) Drinks: soda, cola, soft drink, mineral water, tea, juice, coffee, chocolate, cocoa, jelly, etc.
(7) Others: tomato paste, peanut butter, jam, soy sauce, winter melon candy, honey. Oils and fats (melon seeds, vegetable oil, butter, cream, almonds, walnuts, hazelnuts), coix seeds, dried fruits, sugar, honey, jellyfish, seaweed, snacks and condiments made of animal glue or agar.
(2) The appropriate limited amount of medium purine food.
①Beans and their products: soy products (tofu, dried tofu, dairy tofu, soy milk, soy milk), dried beans (mung beans, red beans, black beans, broad beans), bean sprouts, soy bean sprouts.
②Meat: chicken, pheasant, turkey, spotted chicken, stone chicken, duck, goose, pigeon, quail, pork, pork skin, beef, lamb, dog, venison, rabbit.
③ Aquatic products: grass carp, carp, cod, flounder, perch, pike, swordfish, crab, eel, eel, snail, red paint, abalone, fish ball, shark fin.
④Vegetables: spinach, bamboo shoots (asparagus, asparagus, dried bamboo shoots), beans (string beans, green beans, kidney beans, cowpeas, peas), kelp, golden needles, silver fungus, mushrooms, cauliflower, lobster.
⑤ Fats and oils and others: peanuts, cashew nuts, sesame seeds, chestnuts, lotus seeds, almonds.
Avoid
Contraindicated high purine foods.
① Legumes and vegetables: soybeans, lentils, nori, shiitake mushrooms.
Meat: liver (pig liver, beef liver, chicken liver, duck liver, goose liver), intestine (pig intestine, beef 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 (pig kidney, beef kidney), lung and brain, pancreas, dried meat, thick gravy, minced meat, etc.
③Aquatic products: fish (fish skin, fish eggs, dried fish, sardines, anchovies, mackerel, silver carp, eel, shark, striped bass, kissing fish, sea eel, dried bream, pomfret), shellfish (clams, oysters, clams, oysters, tamari, dried shellfish), shrimp (grass shrimp, golden hook shrimp, small shrimp, shrimp rice), sea cucumber.
④Other: yeast powder, various kinds of alcohol (especially beer).
(The information provided above and its contents are for reference only, and you need to consult a professional doctor for details.)
Have you seen this kind of gout?
Have you ever seen this kind of gout?
Look at the picture and talk!
Gout case sharing.
Pre-operative appearance
Intraoperative appearance of the left foot
Post-operative appearance of the left foot
Intraoperative appearance of the right foot
Right foot intraoperative appearance
This is what a gout stone looks like!