After drinking wine, I will feel sore and weak in my legs (knees) or arms (elbows) when I get home.

Friend, you may have eaten too much beer, red wine and seafood. I have the same symptom. I socialize a lot outside, which may be a symptom of high uric acid.

If uric acid is high, you must be careful not to eat foods with high protein content, such as bean products and eggs, including lean meat, and you should not drink alcohol. You should eat more vegetables, have a light diet and drink more water, which is beneficial to the excretion of uric acid. In addition, you should check what causes high uric acid. Some diseases can lead to high uric acid. When the primary symptoms are resolved, uric acid will automatically decrease. You should take medicine to lower uric acid.

People with high uric acid should pay attention to diet and avoid gout. Please log in.

Usually pay attention to several aspects: 1. Eat less high-protein food; 2. Try not to drink. 3. You can take some drugs that promote uric acid excretion, such as citric acid mixture. 4. Kosuya has a certain uric acid excretion effect. 5. If it can't be controlled by the above measures, you need to take allopurinol. At present, traditional Chinese medicine has not been found to reduce uric acid.

Clinical manifestations of gout

Gout used to be considered rare in China, but its incidence has been on the rise in recent years. 0.5 ~ 1% for western adults. 5% of arthritis patients are gout, and 5 ~ 20% are idiopathic hyperuricemia. More common in men, aged 30 ~ 40 years old, about 50% have a family history. Of the 40 cases reported in China Zhejiang Hospital, 39 cases (97.5%) occurred after the age of 50. More common in obese and mental workers. The onset seems to be related to drinking, big meals and allergies. Female gout only accounts for 5%, mostly occurring after menopause.

Gout is mainly divided into the following stages:

(1) asymptomatic period

This stage only shows hyperuricemia. The incidence of hyperuricemia is much higher than gout. American statistics are 13.2%. The upper limit of hyperuricemia is 417 μ mol l-1for men and 357 μ mol l-1for women. The average serum uric acid in childhood was 214 μ mol l-1,and it began to increase in men after puberty, while in women it increased mainly after menopause. In the asymptomatic period, there was only hyperuricemia, and there were no clinical manifestations such as arthritis, tophus and kidney calculi. In most cases, the onset time of acute gout is 20 ~ 40 years after persistent hyperuricemia. 10 ~ 40% of patients have had one or more episodes of renal colic before the first gout attack, and there may also be renal dysfunction such as proteinuria, hematuria and albuminuria under microscope. But the diagnosis of gout should include urate deposition and tissue inflammatory reaction, not just hyperuricemia and/or kidney calculi. Most patients are in hyperuricemia all their lives, and only a few have clinical gout. Without laboratory examination, the diagnosis is often missed.

(2) Acute phase

Acute arthritis is the main manifestation. The first attack occurred in the metatarsophalangeal joint of the big toe, accounting for 60%.

(1) Triggers 85% of patients can find triggers, such as diet, local trauma, excessive physical or mental work, cold and dampness, excessive excitement, infection, surgery and some drug applications (such as probenecid, diuretics, corticosteroids, mercurial, ergotamine tartrate).

(2) The first episode of prodromal symptoms is relatively sudden, and 70% of patients have prodromal symptoms in the subsequent episodes. Such as local discomfort, varicose veins of lower limbs, headache, insomnia, irritability, fatigue, fatigue, abdominal distension, belching, constipation or diarrhea, renal colic, etc.

(3) The first attack of acute arthritis mostly started at 1 ~ 2 am, with single joint accounting for 94% and lower limbs accounting for 95 ~ 98%. Distal joint accounts for 90%, and more than half of the patients are extremely allergic when the medial surface of the metatarsophalangeal joint of the big toe is involved for the first time, so they can feel pain when covering the pad and often wake up suddenly at night. There are redness, swelling, pain, fever and varicose veins in the local area, which radiate to the lower limbs when touched, and can be complained of improvement during the day, but the local signs are aggravated. The pain intensified again in the early morning of the next day, and the local skin turned from red to purple-blue, with concave edema. Generally, it lasts for about 3 ~ 20 days, the symptoms are gradually relieved, the local signs are improved, and the skin is swollen, wrinkled and desquamated. The overall situation and local signs develop in parallel. Generally, the body temperature is normal or low, but it can be as high as 39℃ or above, accompanied by chills, general malaise, headache, irritability, tachycardia, abdominal pain, hepatomegaly and obvious polyuria, especially after acute attack. Uric acid decreased a few days before the attack, increased significantly at the end of the attack, increased further after the attack stopped, and then gradually returned to normal level. The erythrocyte sedimentation rate increased during the attack, generally 30 ~ 50 mm h- 1, and occasionally 50 ~ 100 mm h- 1 leukocytosis with neutropenia.

(4) If colchicine is given in time. 1 ~ 3 days complete remission, if allowed to develop naturally, the course of disease will be prolonged, but most of them can be completely recovered. Patients with110 may involve joints and leave discomfort.

(3) Intermittent period

That is, a period of rest between attacks. Most patients have repeated seizures many times in their lives, and some patients have never had an attack after one attack. Most patients have an interval of six months to one year. The interval between a few patients can be as long as 5 ~ 10 years. According to Gutman's report, 62% patients relapsed within the first year. 1 ~ 2 years recurrence rate is16%; The recurrence rate was about 1 1% in the second to fifth years, and about 4% in the fifth to fifth years. 7% patients were followed up 10 years, and no recurrence was found. In patients who did not receive anti-hyperuricemia drugs, the frequency of attacks became more and more frequent. The more advanced the course of the disease, the more joints are often involved. The more serious the disease is, the longer it lasts and the slower the relief is. It is difficult to diagnose hyperuricemia only based on medical history and intermittent period, but it is helpful to diagnose if urate crystals can be found in metatarsophalangeal joint fluid.

Chronic stage

The chronic stage is mainly characterized by tophi, chronic arthritis, urinary calculi and gouty nephritis.

(1) tophi gradually formed because uric acid was deposited in connective tissue. The process is insidious, the small ones can only be touched, and the big ones can be seen by the naked eye. The onset time of tophus is 3 ~ 42 years after onset. The average occurrence time is 10 year. It is rare that tophi is less than 5 years old. After 10 years, about 1/2 patients have tophi. After that, it gradually increased, and after 20 years, only 28% had no gout stones. The dysfunction of lower limbs reached 24%. Uric acid is deposited in and near joints, which is closely related to blood uric acid concentration. The frequency of occurrence is helix, hand, foot, elbow, knee, eyelid and nasolabial groove in turn. Less common parts are spinal joint, myocardium, mitral valve, cardiac conduction bundle and pharynx. The stones formed in the early stage are soft, with red skin and milky white liquid. Among them are sodium urate crystals. Within a few weeks, the acute symptoms disappeared, forming kidney hard tophi, which gradually increased, causing joint injury, joint stiffness, deformity and limited joint activity. Tophi can fester to form fistula, and fester is rare.

(2) Chronic joint diseases have evolved from10 to 20 years, involving multiple joints of upper and lower limbs. Due to the increase in the number of tophi, urate deposition in cartilage and connective tissue around the joint, fiber proliferation and bone destruction, joint stiffness and deformity may occur, and pseudo-rheumatoid arthritis-like joints may occur, resulting in complete loss of function.

(3) Kidney diseases The kidney diseases of gout can be divided into uric acid kidney diseases and uric acid kidney diseases. Their occurrence is related to long-term hyperuricemia.

Uric acid nephropathy: Chronic nephropathy is one of the most common manifestations of gout, accounting for about 20 ~ 40% of gout patients. There are two types of clinical manifestations: one is mainly glomerular disease, which is called gouty nephritis. The interstitial damage of these patients is relatively mild, and the average age of onset is 55 years old. Mostly after acute gout attack 15 ~ 25 years, but also before gout attack. The early manifestation is intermittent microalbuminuria. The decrease of concentration function is the early manifestation of renal function damage. 1/3 patients were accompanied by hypertension, which eventually led to azotemia's disease and renal failure. It is sometimes difficult to determine the causal relationship between gout and nephritis at the time of initial diagnosis. However, the past history of gouty arthritis can suggest that gout is primary. Chronic nephritis rarely causes gout, but it will aggravate the existing gout. Its mechanism is different from the traditional view. Recently, it is believed that the deposition of urate damages Henry's epithelium and its surrounding interstitial tissue, accompanied by vitreous degeneration of glomerular capillaries and proliferation of larger blood vessels. X- ray diffraction analysis confirmed that the crystals obtained from the matrix were urate crystals (not uric acid). It has been recognized that hyperuricemia in gout patients is harmful to the kidney, but it is not the only factor (not even the main factor) of renal damage. Other common diseases of gout patients (such as hypertension, chronic lead poisoning, ischemic heart disease, pre-existing occult renal lesions) may play a more important role in gouty nephritis than uric acid, especially in elderly gout patients; The second is because of interstitial nephropathy. This kind of glomerular damage is relatively light, with repeated urine sensation and leukocytosis, and the course of disease is relatively long, which may lead to renal failure, which may be related to urate blocking renal tubules.

② Uric acid nephropathy: It can be divided into competitive uric acid nephropathy and urinary calculi. The former is due to severe hyperuricemia. A large amount of uric acid is deposited in the collecting duct and ureter at one time, causing urinary closure and acute renal failure. This disease can be seen in gout patients with significantly increased purine metabolism, after strenuous exercise and major attack. But it is more common in leukemia and lymphoma patients. The patient's nucleic acid metabolism is accelerated, especially when chemotherapy (cytotoxic drugs) and radiotherapy are carried out at the same time, which accelerates cell destruction, increases the uric acid load of the kidney and increases uric acid excretion by 3 ~ 5 times. During chemotherapy, patients are dehydrated due to anorexia, nausea and vomiting, resulting in high urine concentration and low urine volume. At the same time, due to acidosis, uric acid is deposited in the collecting tube, blocking the lumen. The occurrence of this disease is related to the output of uric acid (not urate). Finally, it leads to proximal nephron dilatation and renal tubular epithelial cell degeneration. Animal experiments confirmed the above viewpoint. Clinical manifestations and diagnosis: in patients with hyperuricemia, the average serum urate is1190μ mol l-1(714 ~ 2140μ mol l-1), the highest record >. Have oliguria or anuria and azotemia. If there is urine, stones or a large number of uric acid crystals can be seen in the urine, and the ratio of uric acid to creatine in the urine is greater than 1. The renal failure caused by other reasons is less than 1. The latter stone is more common in gout patients. The incidence of urate stones in the general population is 0.0 1%, while in gout patients it is 10 ~ 25%. Than healthy people 1000 times. Among gout patients, the incidence of urinary calculi is 1% every year. Asymptomatic hyperuricemia was 0.2%. The incidence of urinary calculi is related to serum uric acid concentration and uric acid excretion. When the serum uric acid is greater than 774 μ mol L-1,the incidence of urinary calculi will reach 50%. 40% patients with urinary calculi appear before gout. A few patients had stones before gout 10 years. Chemical analysis confirmed that 70 ~ 80% of the stones were pure uric acid stones, and the rest were mixed stones of urate and oxalate, pure calcium oxalate or calcium phosphate stones. The average age of stones is 44 years old, which is 2 years later than the first gout attack. The incidence of urinary calculi in secondary gout is high, such as 42% in myeloproliferative diseases. On the contrary, urinary calculi in patients with lead poisoning gout are rare. The mechanism is that there are factors that promote the formation of uric acid crystals. The solubility of uric acid can be affected by the increase of uric acid content, low pH value, urine concentration and the change of urine quality and quantity. Uric acid is a weak acid, (pK5.75). When the urine pH is pH6.75, 9 1% exists in the form of urate. When the urine pH is pH4.75, 9 1% exists in the form of uric acid. The solubility of uric acid is lower than that of urate (at pH6.82, the solubility of urate is 10 times that of uric acid). When the pH value decreases and a large amount of uric acid exists, uric acid supersaturation will occur. When nuclei with high organic matter content exist, stones can be formed. When the pH of urine is less than 5.5 ~ 5.7, uric acid in urine is always supersaturated, especially when uric acid excretion promoting drugs are used, uric acid in urine can be increased, which leads to the formation of urinary calculi. About 65438 06% of the stones occurred after the application of uric acid excretion promoting drugs. Stones are produced in the early stage of medication, so preventive measures should be taken, such as adding drugs to alkalize urine (such as sodium bicarbonate) and increasing drinking water.

Clinical manifestations of secondary gout;

It is mainly hyperuricemia, and the clinical symptoms of gout are atypical, which are often covered by the primary disease, mostly secondary to kidney disease, hypertension and myeloproliferative diseases. Especially leukemia and lymphoma. Because of the short course of disease, the clinical manifestations of gout are not obvious. Blood uric acid is often higher than primary gout because of strong nucleic acid metabolism or blocked excretion.

Complications of gout:

(1) The average common weight of obesity exceeds 10 ~ 30% of the standard weight.

(2) 2 ~ 50% of diabetic hyperuricemia has diabetes, 7 ~ 74% of gout patients have abnormal glucose tolerance, and those with clinical manifestations of diabetes are generally type II diabetes.

(3) Hypertriglyceridemia in patients with hyperlipidemia and gout is 75 ~ 84%. In hypertriglyceridemia patients, hyperuricemia reached 82%.

(4) Hypertension Among untreated hypertensive patients, 22-38% have hyperuricemia, which is significantly higher than the incidence of hyperuricemia in the general population. In patients with hypertension, the incidence of gout is 2 ~ 12%, and serum urate concentration is inversely proportional to renal blood flow and urate clearance rate. Therefore, hypertension complicated with hypertensive uric acid may be related to the decrease of renal blood flow in patients with hypertension.

(5) The incidence of hyperuricemia in patients with arteriosclerosis increased significantly, and hyperuricemia was regarded as a risk factor of coronary heart disease.

From the above statistics, gout seems to be related to obesity, diabetes, hyperlipidemia, hypertension and arteriosclerosis, but there is no obvious correlation between them after correction according to gender, age and weight. It seems that in patients with hyperuricemia, hypertension, diabetes, hyperlipidemia, obesity and other factors work together, leading to hyperuricemia and arteriosclerosis.

Diagnosis of gout

Typical gout is easy to diagnose. Gouty, a family history, is common on the inner side of the metatarsophalangeal owl at the distal end of the lower limb. It starts in the middle of the night and has severe pain, which improves during the day. Colchicine has special effects. History of urinary calculi, hyperuricemia and hyperuricemia. The diagnosis of chronic gout is based on medical history and tophi, but few gout patients have the above symptoms. The following diagnostic criteria can be used:

(1) male serum uric acid > 417 μ mol l-1; Female > 357 μ mol l- 1.

(2) There are tophi.

(3) Sodium urate crystals were found in joints or sodium urate deposits were found in tissues.

(4) Have more than two attacks.

(5) There is a typical attack, with sudden onset, night drama and slow day, which is limited to the distal end of lower limbs.

(6) Remission within 48 hours after colchicine treatment. If the above two criteria are met, gout can be diagnosed.

High uric acid and diet

In the physical examination, one item in the blood test report is uric acid, and the normal reference value range is:150-440 umol/L.

The clinical research results in the medical field confirm that patients with hypertension have too much uric acid and the higher the probability of stroke.

A report on "Life Research" recently published by The Lancet, an authoritative British medical academic journal, shows that researchers compared two antihypertensive drugs-losartan, angiotensin Ⅱ, and atenolol, a traditional antihypertensive drug (β-blocker), to test their effects on blood pressure and cardiovascular diseases.

Studies have shown that losartan and atenolol have similar curative effects, and both can effectively control blood pressure and keep it normal. However, the incidence of stroke in patients taking losartan was 25.8% lower than that in patients taking atenolol, and the overall risk of stroke, cardiovascular necrosis and myocardial infarction was also reduced by 65,438+03%.

Uric acid is associated with stroke

In addition, the incidence of stroke, cardiovascular necrosis and heart disease in the 25% patients with the highest uric acid content in blood is higher than that in the 25% patients with the lowest uric acid content.

The study was conducted in 945 medical centers in 7 countries and regions, involving 9 193 hypertensive patients with left ventricular hypertrophy, and the results were obtained about 5 years later.

Hypertensive people are prone to stroke, 90% of them will have a stroke because of blood vessel obstruction, and about half of them have the problem of high uric acid, but many hypertensive people often ignore the problem of uric acid.

Uric acid is a metabolite of purine.

Uric acid refers to the final product of purine metabolism in human body. Will accumulate too much uric acid in the body, causing metabolic disorders.

Usually, purine becomes uric acid after oxidation and metabolism in the liver, and then it is excreted from the kidney and intestine. Basically, the production and excretion of purine are roughly equal.

One third of purine production comes from food, and the rest is self-synthesized in the body; One-third of the excretion comes from the intestine and two-thirds from the kidney. If it is produced too much or cannot be excreted, uric acid will accumulate in the body, leading to an increase in uric acid value in the blood.

Uric acid is too high is usually associated with metabolic diseases such as eating red meat and animal viscera, old age, obesity, excessive drinking and diabetes.

Consideration of antihypertensive drugs.

Uric acid can affect endothelial cells, hinder the balance of nitric oxide in narrow blood vessels, lead to cell blockage in the inner wall of blood vessels, and lead to stroke. In daily life, patients should take low purine food as the standard.

The above study found that the more hypertensive patients can reduce uric acid, the lower the probability of stroke, so when choosing drugs, besides lowering blood pressure, other effects must be considered.

Losartan has the effect of lowering uric acid besides anti-blood pressure and protecting kidney, but atenolol lacks this advantage. In the kidney, losartan can prevent the blood from absorbing uric acid and directly excrete uric acid; Taking diuretics will lead to the increase of uric acid, because it will hinder the process of blood secretion of uric acid, so that uric acid can not be excreted.

Uric acid is too high can also cause other diseases, such as urate deposition in joints, leading to joint inflammation and gout.

Purine content index in food

* Trace purine content (0-25g purine per100g)

Milk, cheese, cheese, eggs, most vegetables, fruits, rice, flour, bread, fat, oil, tea, coffee, etc.

* Medium purine content (25-100g purine)

Lean meat, pork, mutton, poultry, fish, shrimp, lobster, tofu, soybean milk, spinach, mung bean, cauliflower, asparagus, mushrooms, laver, etc.

* High purine content (per100g purine150-1000g)

Goose, animal viscera (liver, kidney, intestine, heart and brain), eel, herring, fish eggs, fish skin, shrimp skin, seafood, scallops, oysters and other shellfish, baking powder, etc.

Guidelines for food treatment of hyperuricemia

① Choose foods with slight purine content.

(2) Take protein in moderation, and you can only take 0.8 grams of protein per kilogram of body weight. For example, a person of 60 kilograms can take up to 50 grams of protein every day.

③ Limit the intake of fat, and the fat content in total calories is less than 30%.

④ Increase fluid intake, at least 2 liters per day (about 8 to 10 cups) to increase urine output.

⑤ Maintain normal weight and avoid drastic weight loss, because this will destroy muscle tissue and temporarily increase uric acid.

⑥ Avoid or reduce alcohol intake.