Symptoms and treatment of gout. Gout: signs, treatment regimen. Symptoms and photos of gout Liver and gout connection

Residents of the Maori people from New Zealand rarely suffered from gout. Nowadays, gout is diagnosed in 10-15% of the population. A strange thing: seafood is considered one of the provocateurs of gout. But the Maori have been eating seafood for centuries.

What has changed?

The amount of consumption of one product has changed. Today Maori people consume 50 times more than a hundred years ago.

Recent studies have shown that fructose inhibits the excretion of uric acid. This provokes an increase in the level of circulating uric acid and the deposition of its crystals in the joints and surrounding tissues.

Only the liver can metabolize fructose in the body. With an excess of dietary fructose, the liver does not have time to absorb it and numerous by-products and toxins are formed, including a decent amount of uric acid.

The liver increases its production of uric acid when it becomes inflamed and under nutritional stress.

And what foods are the enemies of the liver?

First of all, it is fructose and cheap.

In this regard, it becomes clear why alcohol aggravates the course of gout. After all, alcohol is toxic to the liver.

Foods containing gluten protein often join the company of enemies of the liver: wheat, rye and barley. The latter compromise the integrity of the intestinal epithelium and ultimately lead to inflammation of the liver.

Plus, it's a missing link. I would even say a tragic link. After all, the knowledge of practitioners is only enough to limit purines. And the pathogenesis of gout is much more complicated than the direct causal relationship of gout with purines.

For example, toxic liver damage

Animal proteins such as poultry, pork, lamb, white fish, cheese and eggs contain less purines.

Representatives of plant foods also contain purines, although in smaller quantities. These include mushrooms, peanuts, asparagus (asparagus), cauliflower, soybeans, legumes (especially peanuts, which are also legumes), and foods that contain yeast.

The theory of a direct link between purines and gout is undermined by a study that did not find a significant increase in the risk of gout when eating purine-containing vegetables. It is believed that this is due to the lower bioavailability of vegetable purines, as well as the presence in vegetables of compounds that neutralize the harmful effect of purines.

Do not discount the alkalizing effect of vegetables. Alkalis are known to neutralize acids.

Fruit is another matter. An abundance of fruits should not be present in the diet of gout patients. Especially sweet fruits. Indeed, in the latter a lot of fructose. And juices from sweet fruits are generally a concentrated solution of fructose. Sorry, but it's time to say goodbye to your morning glass of (liver toxic) orange juice.

And about all kinds of sweet drinks, such as Coca-Cola and Pepsi-Cola, you should forget if your liver is dear to you. FRUCTOSE IN LIQUID FORM, REGARDLESS OF ITS ORIGIN, IMMEDIATELY INCREASES THE LEVEL OF URIC ACID!

If suddenly you find high fructose corn syrup in the list of ingredients on the product packaging, then be sure that the manufacturing company does not care about your health, but about its own profits.

On the other hand, low-fructose fruits such as avocado, lemon, lime, grapefruit, and berries are quite suitable for a gout patient.

The principal recommendation for gout is to limit the amount of fructose to 25 grams per day. It is even wiser to limit the amount of fructose to 15 grams. After all, not everyone is guaranteed to avoid hidden sources of fructose from drinks and industrial products.

SUGAR AND GRAIN PRODUCTS SHOULD BE LIMITED IN THE DIET OF PATIENTS WITH GOUT.

Their place should be taken by antioxidant-rich vegetables, as well as natural fats. Recommended sources of fat are butter, coconut products, avocados, extra virgin olive oil, nuts and seeds.

Raw vegetables (if you tolerate them) enhance the effect of the treatment. It is not bad to bring the share of raw vegetables up to 80%. Vary your diet with salads, vegetable juices, seed sprouts, and sprouted seed crackers. Thermally processed vegetable dishes should be saved for the evening meal.

Fermented foods (sauerkraut, kefir, pickles, kimchi, coconut kefir) will also benefit a compromised digestive system.

WARNING:

switch to low fructose / should be gradual.

In the initial phase, the amount of acidic metabolic products increases. The kidneys give priority to excretion of the latter, and uric acid is in the queue for excretion and therefore temporarily lingers in the body. This condition can trigger an attack of gout. To save from an attack at the beginning of a low-fructose diet, a radical restriction of animal flesh products will also help.

Before we move on to the non-drug treatment of gout and its attacks, I would like the readers to grasp the main point:

DIETARY CREDO FOR THE TREATMENT OF GOUT: LIMIT SWEET AND ANIMAL FLESH.

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Sincerely yours:

, candidate of medical sciences - doctor, specialist in natural medicine

In recent years, the number of patients with gout has increased dramatically. More often this disease affects people who are obese. The fact is that they often have a disorder in the regulation of the activity of the liver and kidneys, especially their enzymatic and metabolic functions, which causes the accumulation of a large number of intermediate metabolic products in the human body. As a result, beta-lipoproteins, cholesterol, uric acid salts and many other intermediate metabolic products accumulate. If the former contribute to the development of atherosclerosis of the coronary, cerebral and main vessels, then the accumulation of uric acid salts and their deposition in various tissues of the body contribute to the occurrence of an attack of gout.

How does this process develop and how does it manifest itself? The deep changes that occur in the body during an attack of gout are not clear enough and require further study at the subcellular and molecular level. Nevertheless, it is now possible to formulate certain views on the development of this complex process.

Clinical observations and special radiological studies show that in those suffering from gout, the absorption and excretory functions of hepatocytes (liver cells) are impaired. However, clinical signs of liver disease in gout could not be noted. There are also no clinical signs of kidney disease. Meanwhile, radioisotope methods make it possible to determine functional disorders both in the kidneys and in the liver. Curious, however, is the fact that gout sufferers in the family or in previous generations also had the disease.

How does a gouty attack occur? Observations show that such an attack usually appears a few hours after a hearty meal, when the patient has consumed a lot of proteins and fats, as well as alcoholic beverages. This plentiful dinner is, figuratively speaking, the last straw that overflowed the internal environment of the body with proteins. It is assumed that the overflow of liver cells with purines (protein breakdown products) leads to the accumulation of uric acid in the blood, which, due to a decrease in the excretory function of the kidneys, lingers in the body and turns into uric acid salts deposited in certain, so to speak, pantries of the human body. Such pantries are synovial membranes, primarily metatarsophalangeal joints of the big toes, elbow, ankle and knee joints, as well as tendon sheaths, auricles and coronary vessels.

Uric acid salts are converted into antigens, probably because these salts damage cellular structures and the resulting debris, in combination with the salts themselves, acquire these properties. Antigens, in turn, cause the formation of antibodies, their meeting is carried out at the microcirculatory level; as a result of these complex changes, an acute attack of an aseptic inflammatory process occurs in the joint. The resulting process is characterized by the sudden appearance of severe pain in the area of ​​the thumb, knee, ankle, elbow joint, the patient feels as if these joints are covered by a red-hot iron.

Gout pains are not comparable to pains of any other origin. Within a few hours, additional signs of acute inflammation appear one after another: redness of the skin, an increase in its temperature, swelling of soft tissues, dysfunction of the affected joint. The number of leukocytes in the blood also increases, the reaction of erythrocyte sedimentation is accelerated.

Such signs of inflammation can be observed in any other inflammatory processes, therefore, determining the content of uric acid in the blood serum is essential for clarifying the diagnosis. To conduct this study, the patient must first, within three days, exclude proteins from the diet. Then, using a special method, the amount of uric acid is determined. An increase in the level of this acid in the blood by two or even three times is an irrefutable confirmation of the gouty process.

Often with gout, an inflammatory process occurs in the mucous bag of the elbow joint. The bag, which is usually not palpable, takes on the size of a chicken egg; the tumor is painful, movements in the joint are significantly limited (Fig. 8).

Rice. 8. Deposition of uric acid salts in the area of ​​the elbow joints

Rice. 9. Deposition of uric acid salts in the auricle

The accumulation of uric acid salts and the development of the inflammatory process also occur in the area of ​​the foot. Sometimes this accumulation is so profuse that it causes the skin to break, and urate salts in the form of grains stand out on its surface. Moreover, it also happens that uric acid salts destroy the bones of the foot, specific osteomyelitis (inflammation of the bone marrow) develops and bone sequesters (dead parts of the bone) are released. The disease takes a chronic, prone to relapse course. It continues throughout life. Along with this, the gouty process can affect the auricle (Fig. 9), hands and other parts of the human body.

Once upon a time, only rich and noble people suffered from gout - the disease of kings. Indeed, the higher the standard of living of people, the more often it occurs.

It is known that during the war, in difficult economic conditions, this disease practically does not get sick.

Gout is 20 times more common in men than in women. The predominant age of the first diseased is 40-50 years. In children, gout is very rare, usually in cases of hereditary disorders of uric acid metabolism.

The disease was first described by Hippocrates, who called it a "foot trap" ("podos" - foot, "agro" - trap). The great healer believed that the causes of the disease lie in gluttony and alcohol abuse. Only in the nineteenth century, medicine established a connection between gout and high levels of uric acid in the blood, which is formed during the breakdown of proteins and is a white powder that is poorly soluble in water. If uric acid is formed more than normal or its excretion from the body is not enough, it begins to be deposited in the joints in the form of sodium monourate. The process of deposition of monourate in the tissues and causes an attack of gout. People who are prone to crystallization are especially susceptible to this.

gout classification

Clinically, there are three stages in the course of the disease:

• I - acute gouty arthritis;
• II - interictal gout;
• III - chronic tofus gout.

Acute attack of gout

As a rule, an exacerbation of gout begins suddenly at night, after a plentiful feast with the use of a large amount of meat and alcohol. The pay for a good time is truly terrible. The pain grows rapidly, the joint “fallen from the trap” turns red, swells, becomes hot to the touch. The patient does not find a place for himself, the slightest touch, even bed linen, to the affected joint is extremely painful ("a symptom of the sheet"). Body temperature may rise, chills occur. It seems to the unfortunate that a dog bites into his body with fangs and tears the tendons to pieces. An attack of gout can cover other joints, and after a few hours a person becomes almost immobilized. At first, such an attack can pass in a day or two, gout temporarily recedes only if a protein-free diet is followed and without any treatment, but after a while it will return again. Chronically proceeding, the disease affects the entire body, therefore, starting from the first metatarsophalangeal joint, gout gradually involves other joints with a similar pattern of inflammation in the process. For example, gout of the knee joint is characterized by redness, swelling, pain, severe limitation of movement, effusion in the joint. When puncturing the joint in the synovial fluid, sodium urate crystals are detected.

tophus gout

One of the characteristic symptoms of gout is the formation of tophi - gouty nodules, which are local accumulations of urate crystals in the subcutaneous tissue. Tophi are localized on the hands - in the area of ​​the elbow and metacarpal joints, forearms, on the legs - in the area of ​​the Achilles tendons, over the joints of the feet, on the extensor surface of the thighs and legs, on the forehead, in the area of ​​​​the auricles, as well as on the internal organs, including the kidneys, heart, pericardium and blood vessels.

As a rule, gouty nodes are painless. Soreness can occur if nearby tissues are involved in the inflammatory process.

Currently, much attention is paid to the treatment of patients in the period between attacks, despite the fact that they feel normal. This is the insidiousness of gout, that even in the absence of acute symptoms, the metabolism of uric acid remains impaired and, without proper treatment, microtophi continue to form in the tissues. The disease, like a clever hunter, freezes in anticipation that the victim will break the diet or, for example, get injured. And having waited, he slams his hellish trap on the next joint even more diligently. But if only this. Much more terrible consequences of the disease are damage to internal organs, including the heart and kidneys. Chronic kidney failure, for example, can be fatal.

Diagnosis of gout

The diagnosis of gout is made in the presence of specific complaints and symptoms, laboratory data, radiography, positive dynamics in response to colchicine treatment. Unfortunately, in some cases, the patient's medical history may not describe arthritis characteristic of the disease, and gout is diagnosed at a late stage, when its consequences are identified: severe kidney damage and chronic renal failure.

Treatment

Treatment of gout should be comprehensive. First of all, it is a diet with the exclusion of foods that break down a large amount of uric acid: meat of young animals, fish, beans, peas, fish caviar, beer, etc. It is necessary to observe bed rest and take plenty of fluids to improve the excretion of urate from the body and prevent the formation of urate and oxalate kidney stones. In addition, the treatment of a patient diagnosed with gout involves the normalization of body weight, preferably under the supervision of a physician, in order to prevent rapid weight loss, which leads to excessive production of uric acid and gouty crises. Of the medications, the doctor may prescribe non-steroidal anti-inflammatory drugs, colchicine, in some cases glucocorticoids, and in the interictal period - allopurinol to maintain a normal level of uric acid in the blood.

In addition, much attention should be paid to changing the patient's lifestyle. This should be the focus of psychotherapy. It is quite difficult to work with such patients, because we are talking about changing habits and stereotypes of behavior. And the patient is ready to change only when he is in pain. The episodes of the acute manifestation of the disease are short enough to have time to rebuild your life and develop new habits, and even at the time of the attack, it’s not up to it. Therefore, only the joint work of the psychologist and the patient himself can bring results.

Diagnosis of gout

Currently, medicine has everything necessary for the diagnosis of gout. The diagnosis is made taking into account the patient's complaints, the history of the disease and life, visual examination data, laboratory diagnostics and other research methods.

Usually the patient complains of a sudden onset of acute pain in the joint, most often in the first metatarsophalangeal joint. As a rule, the strongest pain occurs at night, after a heavy feast and alcohol intake. The joint turns red, swells, becomes hot to the touch. The first attack is relatively quickly stopped. But over time, the effectiveness of anti-inflammatory drugs decreases, the interictal periods are reduced, other joints are involved in the process.

Seeing such a clinical picture, one can suspect that a person has an attack of gout, further diagnosis will confirm or exclude the diagnosis.

Tests for gout

In the general blood test during an attack, there will be an increase in the number of neutrophils with a shift to the left, an acceleration of ESR. Protein and oxalates may be present in the urine. A biochemical blood test will reveal an increase in the content of uric acid, seromucoid, sialic acids and some other indicators. Acicular crystals of uric acid salts are found in the synovial fluid.

Gout is characterized by a special x-ray picture: the formation of tophi in the tissues, the destruction of cartilage, the occurrence of marginal bone erosions. With gouty nephropathy, chronic renal failure can be detected. Not only for the treatment, but also for the diagnosis of gout, the drug colchicine can be used. The rapid effect of taking it in acute arthritis indicates the presence of this disease, because. the drug is very specific.

Diagnostic criteria

In 1961, the "Roman criteria" were adopted for diagnosis:

• History of an episode of sudden onset of acute arthritis, which passed in 1-2 days.
• The content of uric acid in the blood is above the level of 0.42 and 0.36 mmol / l, respectively, in men and women.
• The presence of tophi (gouty nodules).
• Detection of crystals of uric acid salts in tissues or synovial fluid.

The diagnosis of gout is made if the diagnosis revealed two or more of the above points.

The American Rheumatological Association has proposed 12 diagnostic criteria:

• Two or more acute attacks of arthritis in the past.
• Localization of inflammation in the first metatarsophalangeal joint.
• Unilateral lesion of the joints of the foot.
• Asymmetric swelling of the joint.
• Arthritis in one joint.
• Unilateral lesion of the first metatarsophalangeal joint.
• The peak of inflammation falls on the first day.
• Redness of the skin over the joint.
• The presence of tophi.
• Elevated levels of uric acid in the blood.
• The absence of any flora in the joint fluid.
• On radiographs, subcortical cysts without erosions.

The diagnosis is certain in the presence of six of the twelve signs, and/or in the presence of urate crystals in the synovial fluid and/or in the tophi.

Prevention of gout

Everyone knows that the disease is easier to prevent than to treat. Gout can be called a disease of eating behavior, so its prevention should first of all change the lifestyle of a person and his taste habits. First of all, it is necessary to limit the consumption of foods rich in protein (meat, fish, meat and fish broths, legumes, sorrel, cauliflower, etc.). You should also normalize body weight. This will help improve metabolism in general, and protein in particular, and will also significantly reduce the load on the joints of the legs during an attack of the disease. Rapid weight loss can cause an increase in uric acid in the blood and provoke an arthritic crisis. Therefore, weight loss should be gradual. Alcohol inhibits the excretion of uric acid from the body, thus increasing its content in the blood. It must be completely eliminated from use.

Preventive measures also include the following factors:

• increased motor activity;
• sufficient drinking regime;
• daily exposure to fresh air;
• limiting the use of coffee and tea;
• fight against nicotine addiction.

Prevention of gout should be directed not only to the patient himself, but also to close relatives, because it is quite difficult to change your own lifestyle if everything remains the same in the family.

The psychological status of the patient is of great importance. As a rule, people prone to gout have a cheerful, friendly and sociable temperament, high sexual activity, industriousness up to workaholism. An attack of gout puts a person to bed, and he suffers not only from pain, but also from forced inactivity, by any means trying to restore his working capacity as quickly as possible. He does not have time to change his lifestyle towards a healthy diet and the elimination of bad habits. Therefore, with gout, psychological methods of influence are used not only as a prevention, but also as a treatment. The patient's motivation for a healthy lifestyle comes to the fore.

Treatment of gout

Treatment of acute gouty arthritis and chronic gout different.

In gouty arthritis, mainly anti-inflammatory drugs are used.

Non-steroidal anti-inflammatory drugs (for example, indomethacin, naproxen, diclofenac, etc.) are prescribed until signs of acute inflammation in the joints are eliminated (usually for 1-2 weeks). Since an attack can happen at any time, a patient with gout should always have one of the drugs of this group with him. Non-steroidal anti-inflammatory drugs can cause stomach pain and heartburn, but these side effects usually do not occur with short-term use.

Glucocorticoids (hormones of the adrenal cortex and their synthetic analogues, such as prednisone) have a more powerful anti-inflammatory effect, so they are used for severe inflammation. If acute gouty arthritis has developed in one or two joints, glucocorticoids are injected directly into the joint. Usually one procedure is enough to effectively stop the attack. Intra-articular administration of drugs is carried out only by a rheumatologist. If more joints are affected, the doctor may prescribe glucocorticoid tablets for 7-10 days. They should only be taken as directed by a doctor. The use of these drugs in high doses for a long time can lead to brittle bones and cause other serious complications. When used correctly, glucocorticoids are safe and very effective.

During an attack, a painful joint needs rest. Ice can help relieve pain, which is applied for 5-6 minutes several times a day, wrapped in a cloth. Sometimes ice, on the contrary, increases pain (because it can increase the crystallization of uric acid salts). In this case, dry heat helps (for example, a warm shawl).

If attacks of gouty arthritis occur 2 times a year or more often, the doctor may decide to prescribe drugs that reduce the level of uric acid in the blood for an indefinitely long period. Properly selected treatment of the disease leads to a decrease in the frequency of arthritis attacks and the resorption of tophi. In addition, against the background of treatment, urolithiasis does not progress.

Like many centuries ago gout more often chooses a victim among people with a high standard of living. Here is a portrait of a typical "gouty": an active, pleasure-loving middle-aged man with a good income, often in a leadership position, very temperamental (usually choleric). Women get gout about 10 times less often.

Read more about the symptoms of gout.

Causes of gout

The "disease of kings" gout refers to metabolic diseases, its causes are a violation of the metabolism of purine bases: guanine and adenine - compounds that are part of the DNA and RNA of all living organisms, an increase in uric acid in the blood due to these disorders and a predisposition to crystal formation.

Uric acid is a white powder, poorly soluble in water. An increase in the concentration of uric acid in the blood leads to its deposition in the tissues in the form of salt - sodium monourate. The process of deposition of monourate crystals in tissues, including joints, causes an acute attack of the disease.

Other causes of gout include:

• hereditary predisposition;
• wrong way of life;
• other diseases (kidney disease, cancer, blood diseases);
• treatment with certain drugs (for example, diuretics, certain vitamins, chemotherapy for cancer);
• violations of other types of metabolism, in particular obesity;
• stress and more.

A visit to a sauna, a trip to hot countries (due to dehydration), a joint injury, and hypothermia can provoke an attack.

Improper lifestyle as a cause of gout includes:

• excessive irregular meals, with frequent feasts;
• eating foods rich in protein, especially meat;
• hypodynamia;
• alcohol abuse;
• workaholism.

It can even be said that, despite the hereditary factors and individual characteristics of the organism, gout is a disease of precisely the wrong lifestyle, the causes of which lie in the mind of a person, in his attitude both to himself and to the world around him. Therefore, an important component of the treatment of this disease is precisely the change in the habits and worldview of a person.

Diet for gout

One of the oldest and most effective treatments for gout is diet. Even Galen recommended people suffering from this disease, moderation in eating and limiting alcohol intake. Of course, with the help of a diet alone, it is unlikely that it will be possible to achieve normalization of protein metabolism, but even without following nutritional recommendations, it is difficult to count on the success of treatment.

It should be remembered that when cooking meat and fish, half of the purine bases contained in them pass into the broth. Therefore, meat and fish broths, jelly, sauces must be excluded from the diet.

Excess intake of proteins in the body leads to an increase in uric acid in the blood - the end product of their breakdown, which is an important link in the pathogenesis of this disease. Therefore, first of all, the menu for gout provides for the restriction of protein foods. The protein content should not exceed 1 g per 1 kg of the patient's body weight. The allowable amount of table salt is not more than 5-6 g per day. This means that you need to cook food without salt, and you can add a little salt already during the meal. The recommended amount of liquid is about 2-2.5 liters per day (if there are no contraindications from the heart and kidneys). Products for gout should contain a large amount of vitamins.

What not to eat with gout

• Offal (kidneys, liver, lungs, brains);
• meat of young animals (veal, lamb);
• fish: sprats, sardines, herring, pike;
• legumes, spinach, tomatoes, as well as foods rich in oxalic acid (sorrel, spinach, lettuce, eggplant, radish, rhubarb).

What can you eat with gout

• Dairy products (in limited quantities);
• eggs;
• bread;
• flour and sweet dishes in all forms;
• berries and fruits (especially lemons);
• greens and vegetables (except those included in the list of prohibited foods).

White fresh and sauerkraut has proven itself well. All kinds of salads, first and second courses are prepared from cabbage. Fresh leaves can be applied to swollen joints in the legs and arms as compresses to help reduce pain and inflammation. It is difficult for a person who is used to eating a large amount of meat to change his habits. Therefore, recipes for gout can be varied with soy products. "Steaks" and "entrecotes" from soy can satisfy the physiological craving for meat to some extent and at the same time replenish the protein reserves of the body.

For the treatment of gout, M.I. Pevzner proposed diet No. 6. Its chemical composition is as follows:

• Proteins - 79 g;
• fats - 79 g;
• carbohydrates - 409 g;
• energy value - 2739 calories.

Dishes for gout are steamed, or the products are used in boiled form.

If the patient is obese, it is recommended to spend the so-called fasting days once a week. Normalization of body weight is one of the main tasks of diet therapy for this disease. The menu of such a fasting day may consist of:

• 1200-1500 kg of apples;
• 1500 kg of watermelon or melon;
• 400 g of cottage cheese and 500 ml of kefir;
• 1500 g fresh cucumbers, etc.

There may be many recipes. The main thing is that the one-day diet does not contain prohibited foods, but consists of 1-2 allowed ones.

Nutrition for gout during an attack should be even more strict. Abundant intake of fatty and meaty foods, flavored with alcohol, can lead to an gouty crisis. During the period of a vivid manifestation of the disease, the main principle of the diet is the maximum unloading - a hungry day. On such a day, the patient should receive a sufficient amount of liquid (mineral water, vegetable and fruit juices, especially lemon juice with water). You can’t eat anything during the day, and the next day a regular anti-gout diet with a high content of vitamins is prescribed (mainly dishes from vegetables and fruits).

Treatment of gout with folk remedies

Sometimes a gout attack occurs when it is not possible to immediately consult a doctor. You can try treatment with folk remedies, of which there are many.

Gout is successfully treated with bee products. A good effect is the introduction of bee venom into acupuncture points, as well as points corresponding to the meridian of the bladder along the spine from the side of the affected joint.

Folk recipes for the treatment of gout are aimed at freeing the body of excess uric acid, reducing inflammation in the affected joint and normalizing metabolism.

To reduce the concentration of uric acid in the blood, various herbs are used in the form of decoctions, infusions and juices:

• Cowberry;
• birch drooping;
• nettle nettle;
• lilac;
• tansy;
• sequence and others.

For the same purpose, you can use eggplant.

Herbal treatment is also used to relieve inflammation in the joints.

• Calendula flowers are crushed, poured with vinegar and iodine. The growths on the joints are lubricated with the bile of poultry, and then wiped with the resulting rubbing.
• 200 g of sage insist in one and a half liters of boiling water, used for bathing.
• 300 g of chamomile is poured with five liters of boiling water. Two hours later, the resulting solution is poured into a basin and the foot with the affected joint is lowered there for 20-30 minutes.

A known method of treatment with bees. A glass of dead bees (dead dried insects) is infused in a liter of vodka in a dark place for two weeks. Strain and rub sore spots.

Treatment of gout with honey

Honey is widely used to treat the disease.

• A couple of teaspoons of honey are added to a glass of decoction of lingonberry leaves and taken orally 3 times a day.
• Insist 600 ml of white wine, 300 g of onion gruel and half a glass of honey for 2 days. Use 1 tbsp. l. 3 r / d.
• Dried and powdered duckweed is mixed with honey and made into pills. Take one 3 times a day.
• 200 g of garlic, 500 g of cranberries, 300 g of onions insist for a day, add a kilogram of honey. The mixture is taken 3 r / d before meals for a teaspoon.

Treatment with honey is usually carried out within one to two months.

Gout recedes with the combined treatment of bee products with medicinal herbs.

Treatment of gout with iodine

Iodine has long been used to treat gout. Take a bottle with 10 ml of iodine and add 5 aspirin tablets there. The resulting solution, which becomes colorless, lubricates the affected areas before going to bed and put on warm socks or gloves at night.

You can try to cure gout at home with iodine foot baths. To do this, add 3 teaspoons of baking soda and 9 drops of iodine to three liters of water. Baths are taken at bedtime for one and a half to two weeks.

Gout has been known since ancient times, so traditional medicine has accumulated a lot of ways to deal with this scourge. Folk recipes for gout include treatment with cereal straw and activated charcoal, iodized salt and lard, onion soup and propolis. It is said that gout can be cured in two weeks by making fresh fish compresses at night. Also, diseased joints can be treated with the following ointment: butter warmed to foam is poured with alcohol in a 1: 1 ratio. Alcohol is set on fire, and when it burns out, the ointment is ready.

Since ancient times, gout and rheumatism have been treated at home with apple cider vinegar, which is taken in the morning mixed with honey and boiled water. Lemons and garlic passed through a meat grinder are also mixed. The mixture is poured for a day with boiled water and taken every morning for a quarter cup.

One of the popular methods is the treatment of gout with the help of millet, ground into flour, brewer's yeast and table salt. A mixture of these products is spread on a cloth and compresses are made on the legs, changing the dough after two hours. At the same time, be sure to stay warm.

Treatment of gout with folk methods does not cancel official medicine, diet, lifestyle changes. Only complex treatment can give positive results.

Complications of gout

Being an metabolic disease, gout can be very insidious and lead to serious complications. The most formidable of them is kidney damage. Unfortunately, sometimes it is gouty glomerulosclerosis and the presence of urate kidney stones that make it possible to diagnose royal disease. The severity of kidney damage determines the prognosis. In 20% of cases, renal failure developed against the background of the disease leads to death. Arterial hypertension of nephrogenic origin occurs in 40% of patients. Urolithiasis disease with the formation of X-ray negative urates in the kidneys occurs in about 20% of cases.

Complications of gout are also manifested by gradually developing osteoporosis, the appearance of tophi in various tissues. Tophi are local accumulations of sodium monourate. Most often they occur in the skin of the fingers, in the area of ​​the feet, knee and elbow joints, on the wings of the nose and auricles, as well as in the internal organs: the kidneys, on the heart valves, in the walls of blood vessels, in the pericardium.

Consequences of gout

If the first attacks of gout pass quickly and easily, then in the future, in the absence of adequate treatment, it becomes increasingly difficult to cope with them. One of the main points of treatment is to reduce the level of uric acid in the blood. If this is not achieved, then the joints, due to the deposition of urates, will become more and more deformed, other joints will become involved over time, a tophi form of gout will form, and arthritis will become chronic. At the same time, it must be remembered that tophi occur not only in the joints, but also in other tissues, which can lead to dysfunction of various organs and their systems. Therefore, one should not wait for the consequences of gout, it is necessary to be treated not only correctly, but also on time.

Gout is a disease that affects the human joints. This process occurs due to the deposition urates - salts of uric acid.

Gouty was first described in the seventeenth century in an English work called A Treatise on Gout. In it, pain in gout was compared with pain "when the limb is clamped with a press."

Gout mainly affects males. At the same time, the disease occurs in about three people per one thousand of the population. As a rule, gout manifests itself in people who are already forty years old. Women get gout in the period after. If a person develops gout, the symptoms of the disease are expressed by damage to any joints in the human body: these can be joints brushes , fingers , knees , elbows , feet . But most often the disease affects the joints of the toes.

Causes of gout

Factors leading to the development of gout are , . Gout often develops in people who have a hereditary predisposition to the disease, as well as in those who regularly eat improperly. Basically, a gout attack manifests itself after a person takes alcoholic beverages, severe overeating. Especially bad effect on the condition of patients prone to gout, beer. Gout attacks disturb patients mainly at night. With such an attack, a person feels a strong and sudden pain in the joints. His joints turn red. With a repeated attack of gout, a tingling sensation is initially felt in the affected joint. If gout is not treated, the symptoms described above become more common. At the same time, exacerbations become longer. Gradually, the disease affects new joints, sometimes the kidneys and urinary tract also suffer.

gout symptoms

The onset of intermittent gout is considered to be the first attack of arthritis. In this case, a person periodically alternates between remissions and acute attacks of the disease. During remission, the patient does not complain about the state of health at all. Sometimes after the first attack before repeated manifestations of the disease, years pass. However, most often such attacks recur once or twice a year. Gout progresses and its attacks recur more frequently.

In most cases, in a person suffering from gout, symptoms initially manifest as a lesion I metatarsophalangeal joint . At the same time, it develops spicy monoarthritis . The reason for the defeat of these joints is that in these joints, degenerative-dystrophic changes in the cartilage occur first. Therefore, urates are deposited in them earlier than in other joints. In more rare cases, other joints of the legs are affected first, and even more rarely, the joints of the hands. By the way, from the Greek language the word "gout" is translated as "foot trap".

Pain in the joint with gout develops abruptly, an attack can begin in the morning or at night, less often at other times of the day. A person suffers from very intense and sharp pain sensations. Sometimes the pain can be unbearable, and analgesics do not help get rid of it. The development of signs of local inflammation occurs very quickly, which manifests itself as much as possible after a few hours. In some cases, the patient's body temperature also increases - it can rise even up to forty degrees. Often, edema and hyperemia of the skin over the joint are expressed so strongly that they can resemble phlegmon . Due to such unpleasant sensations, the mobility of the joint is noticeably limited. After a few days (3–7–10 days), all symptoms of the disease completely disappear.

If the disease is not treated, then after a while it can provoke bone destructuring. And with more than four years of the disease, bumps appear over the patient's skin, which are quite dense to the touch. They accumulate uric acid crystals. Such tubercles occur over diseased joints. They are yellowish in color. Sometimes the bumps burst, and white crumbs come out of them. Some patients with gout also develop over time stones in the kidneys . At the same time, a person is disturbed by periodic attacks of increased , renal colic. Sometimes, quite rarely, gout also affects the heart muscle.

Diagnosis of gout

External manifestations of gout - swelling, swelling - the doctor detects already during the examination. During the survey, it is found out that the patient has signs of the disease.

The most accurate criterion for the diagnosis of gout is the detection by microscopic examination of sodium urate in tophus or synovial fluid. tofus - this is the deposition of crystals in the soft tissues of uric acid: they are deposited in the form of nodules. The elastic thick mass that fills the cavity of the joints is called synovial fluid .

There are other signs of gout that are very important in the diagnosis process. First of all, hyperuricemia in which the blood contains too high levels of uric acid. However, with this phenomenon, gout does not always occur, therefore, this phenomenon cannot be considered the main criterion in order to establish a diagnosis. In the process of diagnosing gout, the daily level of excretion of uric acid in the urine is determined. During an exacerbation of gout, the results of a blood test indicate the presence of an increase in ESR, an increased amount . X-ray examination is also one of the important points in the diagnosis of gout. However, in this case, the signs of the disease can be detected if it has been progressing for several years.

It is important to distinguish gout from other ailments with similar symptoms. So, sometimes gout is mistaken for rheumatoid or traumatic arthritis .

Treatment of gout

Treatment of gout involves the gradual implementation of several stages of therapy. First of all, it is very important to remove the acute manifestations of the disease. Further treatment is aimed at preventing an exacerbation of the disease in the future. Also, the attending physician takes measures to treat the complications of the disease and prevent further unpleasant manifestations of gout - for example, deposits of urate in the joints or in other tissues of the body. In addition, the treatment of gout involves the parallel therapy of a number of concomitant ailments - hanged man blood pressure , , diabetes and etc.

If a patient has an acute attack of gout, anti-inflammatory drugs are used in the first place to treat the disease. The drug is often used, and the doctor also prescribes other anti-inflammatory drugs, for example, , diclofenac sodium . If treatment with such drugs does not bring relief to a person, systemic or intra-articular use is used. glucocorticoids . It is important that a person strictly observes bed rest, and the affected limb is in an elevated state. You should adhere to certain rules of nutrition for gout.

Treatment of gout involves the use of uricodepressants. These drugs help to suppress the production of uric acid. The most commonly used drug with such an effect is considered. Means that are used to treat gout, patients must take a long time - throughout the year. Then the doctor corrects the further method of using the drugs. Also, in addition to alopurinol, it is often prescribed uricosuric drugs stimulating the release of uric acid.

In the process of treatment with these drugs, it should be taken into account that with an intensive release of uric acid after the start of the use of such drugs, the risk of kidney stones greatly increases. Therefore, preventive measures are very important. In addition, when taking anti-gout drugs during the year, the risk of developing gout attacks may increase. Therefore, in parallel with such drugs, the drug colchicine or non-steroidal anti-inflammatory drugs should be taken.

Treatment of gout also includes physiotherapy, paraffin and mud applications, baths with radon and hydrogen sulfide. Such procedures should be carried out at the stage of remission. At the same time, UV irradiation is carried out on the area of ​​the affected joint and even in some cases helps to prevent an attack. Pain is relieved by potassium-lithium electrophoresis. Between exacerbations, for effective treatment of gout, it is necessary to do therapeutic exercises.

There are also some traditional medicine recipes that are used to treat gout. For everyday drinking, you can prepare a collection of calamus root, sage and bearberry leaves, St. John's wort. Another collection to drink as a tea includes a mixture of burdock and wheatgrass root, violet and veronica herbs. In addition, it is useful to periodically drink infusions of mint, nettle, chamomile, nine strength, lingonberry leaf, corn stigmas, and flax seeds. As a remedy that reduces pain in the joints, a decoction of oats is recommended.

For the treatment of gout, folk methods also prepare ointments for topical use. To do this, use dry , the powder of which should be rubbed in equal proportions with unsalted lard.

It is also fashionable to apply compresses from herbal decoctions to the affected joints (hops, elderberry, chamomile are used for this). You can also apply burdock, cabbage leaves to sore spots.

Taking baths with the addition of herbal decoctions can also be one of the treatments for gout. In this case, decoctions of horsetail, elderberry, oregano, burdock, nettle, juniper, etc. can be added to a warm bath.

The doctors

Medications

Prevention of gout

To avoid the manifestations of this unpleasant disease, you should avoid injuries to the joints, do not wear too narrow and uncomfortable shoes. An effective method of preventing gout is to maintain an active lifestyle, drinking plenty of fluids. You should not abuse foods that are rich in protein. It is important to control body weight, as obesity can be one of the provoking factors for the onset of gout. However, in this case, it is important to act gradually, as sudden weight loss can cause an increase in the level of uric acid in the blood.

Diet, food for gout

Patients must follow a special diet that will help significantly improve their condition. is designed so that all allowed foods are low in purines. In addition, the diet for gout contains few calories, so it helps to normalize a person's weight. In some cases, proper nutrition for gout can help normalize the production of uric acid. So, there is even evidence that during the period of famine, wars, the number of patients with gout decreases sharply due to limited nutrition.

Nutrition for gout involves the use of food of plant origin, as well as dairy products. Protein needs to be severely limited. The patient's diet should not include kidneys, brains, liver, chocolate, cocoa, coffee. Also, the diet for gout does not include the use of rich meat and fish broths. After all, during cooking, purines are released into the liquid. It is advisable to spend a fasting day about once every one and a half weeks. On such days, you can eat one of the following types of products: cottage cheese, kefir, vegetables, fruits. Also, patients with gout should not drink alcoholic beverages, since alcohol has a depressing effect on kidney function regarding the excretion of uric acid. Nutrition for gout involves minimizing the consumption of table salt, so food should at least be undersalted.

A diet for gout should include a large amount of fruits, various cereals, dairy products, and cheese. Increase the release of urates from the body will help the use of citrus fruits. It is advisable to include more raw vegetables and fruits in the diet. It is important to drink at least two liters of water every day, as this contributes to large amounts of urination. And to prevent the appearance of kidney stones, you should drink about half a liter of mineral alkaline water every day. You can use the liquid in the form of compotes, fruit drinks, weak tea.

Patients with gout should not starve, because complete fasting increases the amount of uric acid in the blood. Meals should be fractional: you should eat up to six times every day, while the portion should not be large.

List of sources

• Rheumatology: clinical. recommended / ed. E.L. Nasonov. - M., 2011;
• Maksudova A.N., Salikhov I.B., Khabirov R.A. Gout. - M., 2008;
• Ivashkin V.T., Sultanov V.K. Diseases of the joints: propaedeutics, differential diagnosis, treatment: A guide for physicians, for specialists. - M., Litterra, 2010;
• Benevolenskaya L.I., Brzhizovsky M.M. "Epidemiology of rheumatic diseases".// Moscow. "Medicine" - 1998.

Gout- a chronic disease associated with a violation of uric acid metabolism - an increase in the content of uric acid in the blood and the deposition of crystals of the sodium salt of uric acid (urates) in the tissues, which is clinically manifested by recurrent acute arthritis and the formation of gouty nodes (tophi). Gout has been known since ancient times, but the first and detailed description was made in 1685 by T. Sydenham in the book "A Treatise on Gout". Later, it was noted that in patients with gout, the content of uric acid in the blood (hyperuricemia) increased; in the 19th century, scientists discovered urate crystals in the joint fluid during an acute attack of gout. However, only in the middle of the 20th century, experts established the role of sodium salt crystals (urates) in the development of an acute attack of gout.

Gout is a fairly common disease. According to epidemiological studies conducted in Europe and the United States in recent years, up to 2% of the adult population fell ill with gout, and among men aged 55-64 years, the incidence of gout is 4.3-6.1%. In Europe and the USA, patients with gout make up 0.1-5.8% of all patients with RB.

In recent years, an increase in the incidence of gout has been observed in all countries. So, in Finland, according to N. Isorriaki ii cons., the number of registered cases of gout has recently increased 10 times, in Germany - 20 times. However, information on the distribution of gout is incomplete due to late diagnosis. The diagnosis of gout is established on average 4.8 years after the first attack. According to our data, during the 1st year of the disease, the diagnosis of gout was established only in 7% of patients.

The spread of gout in the most developed countries, it is associated with a significant consumption of foods rich in purines (meat, fish) and alcoholic beverages. This is confirmed by the fact of a sharp decrease in the incidence of gout during the Second World War, when meat consumption was significantly reduced.

Gout mainly affects men. The first attack of gout can be at any age, but in most cases after 40 years. In recent years, there has been some increase in cases of gout at a young age (20-30 years). In women, gout usually begins during menopause.

Normal uric acid metabolism. In the human body, uric acid is the end product of the breakdown of purines. The reserves of uric acid in the body are normally 1000 mg at a rate of renewal within 650 mg / day, that is, 650 mg of uric acid decreases daily from the reserves and the same amount is replenished. Since uric acid is excreted from the body by the kidneys, it is important to know its clearance, that is, the volume of blood that can be cleared in the kidneys of excess uric acid in a minute. Normally, it is 9 ml / min.

The source of the formation of uric acid in the body are purine compounds that come with food, and are also formed in the body during the exchange of nucleotides.

The synthesis of purines begins in the body with the formation of phosphoribosylamine from a molecule of phosphoribosyl pyrophosphate and glutamine under the influence of the enzyme aminotransferase. From this compound, after a series of reactions, the first purine nucleotide is formed - inosinic acid, a significant part of which is converted into purine nucleotides of nucleic acids - adenylic and guanylic acids, which are mainly used to build nucleic acids. However, part of the adenylic and guanylovone acids is catabolized, turning into simple purines: guanine, xanthine and others, which, under the influence of the xanthine oxidase enzyme, are converted into uric acid, while most of them, with the participation of the enzyme hypoxanthine guanine phosphoribosyltransferase (HHFT), form guanylic acid again. Thus, the immediate precursors of uric acid are purines - guanine and xanthine.

Uric acid is found in plasma as free sodium urate. The normal content of sodium urate in serum, determined using the calorimetric method, is 0.3 mmol / l for men, 0.24 mmol / l for women. The upper limit of normal for men is 0.42 mmol / l, for women 0.36 mmol / l. The content of uric acid above these figures is regarded as hyperuricemia with a high risk of developing gout.

For a long period, hyperuricemia may be asymptomatic, and only a few years later the clinical picture of gout develops. In a study of the daily dynamics of uricemia in healthy men, unstable asymptomatic hyperuricemia was found in 25.7% of cases, indicating the possibility of developing gout.

What provokes / Causes of Gout:

Normally, the processes of synthesis of uric acid and its excretion are balanced, but with any violation of this process, an excess of uric acid in the blood serum may occur - hyperuricemia. Thus, the cause of hyperuricemia can be: increased formation of uric acid, reduced excretion in the urine, a combination of these factors.

Increased formation of uric acid occurs with excessive intake of purines with food, increased endogenous synthesis of purines, increased catabolism of nucleotides, a combination of these mechanisms.

Increased synthesis of uric acid in a healthy person is accompanied by an increase in the content of uric acid in the urine. Inadequate excretion of uric acid by the kidneys may be associated with a decrease in glomerular filtration of urate or its secretion by the tubules, as well as a combination of these reasons.

Pathogenetic types of hyperuricemia. Primary hyperuricemia is the most common cause of primary gout. Most authors characterize it as constitutional dyspurinism, that is, as a family genetic anomaly of purine metabolism, apparently determined by several genes. In practice, this is confirmed by the fact that one third of those suffering from gout, and 20% of family members of patients, have hyperuricemia.

The reasons for the increase in the content of uric acid in primary hyperuricemia can be different:

• an increase in the synthesis of endogenous purines, the so-called metabolic type of hyperuricemia, characterized by high uricosuria and normal clearance of uric acid (the most common cause);
• impaired excretion of uric acid by the kidneys (renal type of hyperuricemia), due to low clearance of uric acid;
• a combination of both causes (a mixed type of primary hyperuricemia, the manifestation of which is normal or reduced uraturia with normal clearance of uric acid).

According to most authors, overeating and excessive alcohol consumption contribute to the occurrence of hyperuricemia and exacerbate it. W. Curie, who studied 1077 cases of gout, found overweight (by 10% or more) in 38.2% of patients. According to G. P. Rodnan, fatty foods and alcohol can block renal excretion of uric acid and cause hyperuricemia. Among other risk factors for hyperuricemia are also called hypertension, hyperglyceridemia, stressful situations, dehydration, etc.

The main role in the pathogenesis of primary hyperuricemia is played by genetically determined disorders in the enzyme system and, first of all, the deficiency of the enzyme involved in the resynthesis of nucleotides from purines. A decrease in the activity of this enzyme leads to an insufficient use of purines in the body and thus an increased production of uric acid. This type of hyperuricemia is characteristic of the Lesch-Nychen syndrome. Increased formation of purines can occur under the influence of high activity of the enzyme phosphoribosyl pyrophosphatase (PRPP), which is involved in the synthesis of the purine precursor.

According to most authors, the mechanisms responsible for the increased synthesis of uric acid in patients with primary gout are multifactorial and still not entirely clear. The same can be said about the second main mechanism of primary hyperuricemia - impaired excretion of uric acid by the kidneys. It is known that sodium urate (urates) is completely filtered in the renal glomeruli and completely reabsorbed in the proximal tubules, and then almost half of it is resecreted by the distal sections and only 10% is excreted in the urine (tubular secretion of urates progressively increases as the content of uric acid in serum increases). But in some patients with gout, hyperuricemia develops due to the inability of the kidneys to compensate for the urate load by increasing tubular excretion (renal type of primary hyperuricemia). However, the mechanism. which causes a change in the active excretion of urate by the kidneys, is still unknown.

The most common cause of secondary hyperuricemia is kidney failure, which reduces the excretion of uric acid from the body (secondary renal hyperuricemia). Some blood diseases - essential polycythemia, chronic myeloid leukemia, chronic hemolytic anemia, pernicious anemia, multiple myeloma - may be accompanied by hyperuricemia due to the breakdown of cell nuclei and increased catabolism of cell nucleotides.

An increase in the content of uric acid in the blood can be observed with extensive psoriasis due to the renewal of epidermal skin cells and increased formation of purines from cell nuclei. Persons suffering from hypertension for a long time, myxedema, hyperparathyroidism, diabetes, pregnancy toxicosis, lead intoxication may develop hyperuricemia due to inhibition of tubular excretion and slowing down the excretion of uric acid from the body.

Drug-induced hyperuricemia occurs with the use of a number of drugs. Diuretics increase uric acid levels by inhibiting tubular excretion, thought to be due to a decrease in extracellular fluid volume. Salicylates in small doses (acetylsalicylic acid not more than 2 g / day) moderately increase the content of uric acid in the blood, and in large doses (4-5 g / day), on the contrary, they reduce it. The content of uric acid in the blood serum decreases when taking thiazine drugs.

The main mechanism for the development of gout is long-term hyperuricemia, in response to which a number of adaptive reactions occur in the body, aimed at reducing the content of uric acid in the blood in the form of an increase in the excretion of uric acid by the kidneys and the deposition of urate in tissues. Urate (uric acid sodium) is deposited selectively in the joints, their vaginas, bursae, skin, kidneys, causing morphological changes in these tissues, described by Uehlinger E. Hyperuricemia leads to an increase in the content of uric acid in the synovial fluid, its precipitation in the form of crystals, followed by their penetration into the cartilage and synovial membrane, where they are deposited in the form of needle-shaped crystals of sodium urate. Through cartilage defects, uric acid penetrates to the subchondral bone, where, forming tophi, it causes the destruction of the bone substance, which is determined on radiographs, in the form of rounded bone defects (“punches”).

At the same time, synovitis occurs in the synovial membrane with hyperemia, proliferation of synoviocytes and lymphoid infiltration.

The deposition of microcrystals of sodium urate in tendons, vaginas, bags and under the skin leads to the formation of micro and microtophi (rounded formations of various sizes containing crystals of sodium urate).

Of particular importance is the deposition of uric acid in the kidneys (gouty kidney or renal nephropathy), since this pathology often determines the fate of the patient. Uremia, as well as heart failure and strokes associated with nephrogenic hypertension, are the most common causes of death in gout patients.

Gouty nephropathy- a collective concept that includes all renal pathology observed in gout: tophi in the kidney parenchyma, urate stones, interstitial nephritis, glomerulosclerosis and arteriolosclerosis with the development of nephrosclerosis. Tubal tophi are formed in 50%, and urate stones in the pelvis in 10-25% of patients. Both processes create conditions for urinary tract infection. A distinctive feature in gout is kidney damage - interstitial nephritis (due to the widespread deposition of urates in the interstitial tissue of the kidneys).

E. Uehlinger associates damage to the vessels of the kidneys with a parallel violation of protein metabolism and the formation of an excess of intermediate products (lipoproteins), which are deposited in the glomeruli and vessels of the kidneys. All this leads to sclerosis of the glomeruli and wrinkling of the kidneys with the development of hypertension and renal failure.

The pathological processes described above, associated with the deposition of urates in the tissues of the body, determine the main clinical manifestations of gout, of which the most striking is acute gouty arthritis.

Pathogenesis (what happens?) during Gout:

The pathogenesis of an acute attack of gout. An acute attack of gout usually develops after persistent and long-term hyperuricemia. Its occurrence is associated with a number of provoking factors, leading mainly to a significant violation of the excretion of uric acid by the kidneys. Excessive consumption of alcohol and prolonged fasting work in a similar way.

The first leads to an increase in the concentration of uric acid in the body, which is formed during the normal metabolism of alcohol, the second - to an increase in the content of ketone acids. All these substances disrupt the normal secretion of uric acid by the tubules and lead to a sharp increase in its content in the blood. Seizures can be triggered by trauma or drugs that change the normal excretion of uric acid by the kidneys, as well as by heavy physical exertion (due to increased production of lactic acid). Foods rich in purines and fats, according to the authors, are of lesser importance, but in individuals with a tendency to hyperuricemia, they can provoke an acute attack of gout.

D. McCarty and J. Hollander found that an acute attack of sprt!; ts develops as a result of the precipitation of sodium urate microcrystals into the joint cavity, which causes an acute inflammatory reaction of the synovial membrane. Needle-shaped birefringent crystals of sodium urate, well seen in polarized light, are constantly present in the synovial fluid (freely or in the cytoplasm of leukocytes) in patients during an acute attack of gout.

The immediate mechanism for the sudden precipitation of sodium urate crystals is unknown. It is assumed that it is associated either with a rapid increase in the content of urates in the serum, which leads to the precipitation of crystals into the synovial fluid already oversaturated with urates, or with a rapid decrease in their amount in the blood, which contributes to their mobilization from the depot. The precipitated crystals are phagocytosed by synovial fluid neutrophils and synoviocytes, during which the release and activation of lysosomal enzymes that cause an inflammatory reaction occur. Simultaneously, as a result of the metabolic activity of neutrophils in the synovial fluid, a decrease in pH occurs, which, as McCarty suggests, leads to further precipitation of urate crystals, thus creating a vicious circle.

As inflammation develops, other components are also involved in the process, in particular coagulation factors, kinins, plasmin, and complement components.

Symptoms of Gout:

First clinical manifestation of gout is an attack of acute arthritis that develops suddenly, as if in the midst of complete health, although some prodromal phenomena may be observed in 1-2 days: vague discomfort in the joint, general malaise, nervousness, dyspepsia, fever, insomnia, chills. The factor provoking an acute attack of gout is most often a violation of the diet - overeating, especially eating foods rich in purines (meat soups, fried meat, game, etc.), or alcohol abuse.

Quite often, provoking factors are injuries and microtraumas (long walking, narrow shoes), mental or physical overload, infections (flu, tonsillitis).

Classical clinical picture acute gouty attack is very characteristic. It consists in the sudden appearance (usually at night) of the sharpest pains, most often in the I metatarsophalangeal joint, with its swelling, bright hyperemia of the skin and subsequent peeling. These phenomena increase rapidly, reaching a maximum in a few hours and are accompanied by fever (sometimes reaching 40 ° C), chills, leukocytosis, and an increase in ESR. Excruciating pains, aggravated even when the diseased joint comes into contact with the blanket, cause the complete immobility of the diseased limb. After 5-6 days, the signs of inflammation gradually subside and over the next 5-10 days in most patients completely disappear, the temperature and ESR return to normal, the function of the joint is fully restored, and the patient feels completely healthy. Subsequently, acute attacks are repeated at various intervals, capturing an increasing number of joints of the legs and arms.

However, observations show that there are currently some features of the clinical course of gout and, in particular, the first attack. They consist both in the atypical localization of arthritis (small joints of the hands, elbow or knee joints), and in the nature of the course in the form of acute or sub-acute polyarthritis.

Our experience of studying gout in more than 300 patients shows that the classic picture of a gouty attack at the onset of the disease involving the big toe is observed only in 60% of patients. In 40% of patients, the process has either atypical localization without damage to the big toe, or proceeds according to the type of polyarthritis. According to our observations, there are the following atypical forms of the first attack of gout:

• rheumatoid-like form with a protracted course of an attack and localization of the process in the joints of the hands or in 1-2 large or medium joints;
• pseudophlegmonous form - monoarthritis of a large or medium joint with severe local and general reactions (sharp swelling and hyperemia of the skin, extending beyond the affected joint, high fever, significantly increased ESR, hyperleukocytosis;
• polyarthritis resembling rheumatic or allergic (migratory), with rapid regression;
• subacute form with typical localization in the joints of the big toe, but with small subacute phenomena;
• asthenic form - slight pain in the joints without swelling, sometimes with slight flushing of the skin;
• periarthritic form with localization of the process in the tendons and bursae (most often in the calcaneal tendon with its compaction and thickening) with intact joints.

The intensity and duration of the attack also vary from 3 days to 1.5 months. We observed subacute and protracted course of the first attack in 16% of patients. Such variability of clinical manifestations at the onset of the disease greatly complicates the early diagnosis of gout.

With a long course, the clinical picture of the disease consists of three syndromes: joint damage, formation of tophi and damage to internal organs. Articular syndrome remains the most striking clinical manifestation during this period of the disease.

In the first years of the disease (up to about 5 years from the onset of the disease), joint damage proceeds according to the type of acute intermittent arthritis with complete regression of all articular manifestations and restoration of joint function in the interictal period.

With each new attack, more and more joints are involved in the pathological process, i.e., there is a gradual generalization of the articular process with an almost obligatory lesion of the joints of the big toes. In most patients, intermittent gouty arthritis is detected in the joints of the legs (usually no more than 4 joints), but with severe course and duration of the disease, all joints of the limbs and even (very rarely) the spine can be affected. The hip joints almost always remain intact. During an acute attack, many joints can be simultaneously involved in the process, but more often they are affected alternately. At the same time, there is a lesion of the tendons, most often soreness and compaction of the calcaneal tendon, as well as mucous bags (often the bursa of the olecranon).

Thus, with a long course of gout, the number of affected joints and the localization of the process change.

Attacks of gouty arthritis can recur at different intervals - after several months or even years. Between attacks the patient usually feels well and does not show any complaints. But over time, the interictal periods become shorter and shorter. Gradually, persistent deformities and stiffness of the joints appear. caused by the destruction of the joint by urates impregnating the articular tissues, and the development of secondary osteoarthritis.

Infiltration of articular tissues with urates is accompanied by a constant inflammatory reaction of the tissues surrounding the joint, with the development of chronic tophi arthritis or urate arthropathy.

During this period, which occurs 5-6 years after the first attack, patients complain of constant pain and limited movement in the joints. There is persistent swelling and deformity of the joints, sometimes with a large intra-articular effusion.

Joint deformity occurs due to the destruction of cartilage and articular surfaces, as well as infiltration of periarticular tissues with urates with the formation of large tophi. In these cases, the skin covering the tophi may ulcerate, a fistula is formed, from which a mushy mass containing sodium urate crystals is released.

First of all, destruction of the I metatarsophalangeal joint develops, then other small joints of the feet, then the joints of the hands, elbows and knees. With the localization of a chronic destructive gouty process in the small joints of the hands, in some cases a clinical picture resembling RA develops. Against the background of chronic gouty arthritis, frequent gout attacks usually occur, less acute, but longer than in the early period of the disease.

The most severe clinical picture develops in the presence of the so-called gouty status, when for several months there are almost continuous intense attacks of arthritis in one or more joints against the background of constant moderate inflammation.

One of the consequences of the destruction of articular tissues in chronic arthritis is the development of secondary osteoarthrosis in the affected joints, which significantly reduces the ability of patients to move and increases joint deformity. This process often captures the joints of the feet: deforming arthrosis develops in the region of the I metatarsophalangeal joint and metatarsal joints with the formation of osteophytes on the back of the foot (lumpy gouty foot).

In 70-80% of patients, deforming spondylosis is also detected.

Patients with chronic gout can remain able-bodied for quite a long time. In the presence of urate arthropathy with significant destruction of the joint and severe secondary arthrosis, the patients' ability to work is partially or even completely lost.

The second characteristic manifestation of gout is the deposition of urates under the skin with the formation of dense, rather clearly delimited and rising above the surface of the skin, gouty nodes or tophi. They develop on average 6 years after the first attack, but in some patients earlier - after 2-3 years. In some cases, tophi may be absent. Their sizes are different - from a pinhead to a small apple. Separate tophi merge, forming large conglomerates, they are localized mainly on the auricles, in the area of ​​\u200b\u200bjoints, most often elbows, as well as knees, on the feet (thumb, rear of the foot, heel), hands - around small joints and on the pulp of the fingers and, in addition, in the area of ​​​​the calcaneal tendon, tendons of the back of the hand, etc. and synovial bags.

In more rare cases, tophi are found on the eyelids, sclera, wings of the nose. They are painless and, when small, are often detected only by a doctor.

With superficial deposits of urates, the content of white tophi shines through the skin covering them. Aspiration and microscopy of this content reveals typical needle-like crystals of sodium urate. With ulceration of tofus, fistulas are formed. In this case, the addition of a secondary infection is often observed.

The presence and nature of tophi determine the duration and severity of the disease, as well as the level of hyperuricemia. Multiple and large tophi develop, according to our data, in patients suffering from gout for more than 6 years or with a high degree of hyperuricemia - over 0.09 g / l; in this case, they may appear in 2-3 years. Almost always, urate arthropathy occurs.

Thus, tophi are an indicator of the duration and severity of uric acid metabolism disorders. In the clinical picture of gout, damage to other organs and systems (visceral gout) is also observed. The most severe of them is gouty nephropathy (gouty kidney), which often determines the fate of the patient. The development of gouty nephropathy is associated with the formation of tophi in the tubules, urate stones in the pelvis, which creates conditions for the development of interstitial nephritis and infection of the urinary tract. At the same time, blood vessels and kidneys are affected (glomerulosclerosis and nephrosclerosis with the development of hypertension and insufficiency of kidney function). According to many authors, gouty nephropathy is the cause of death in 25-41% of patients with gout.

The earliest and most common is nephrolithiasis. Often the first symptoms of this disease appear before the first attack of gout due to prolonged asymptomatic hyperuricemia. All other types of gouty nephropathy - interstitial nephritis, pyelitis, nephrosclerosis - appear later. Clinical examination of patients in the early stage of the disease usually does not reveal renal pathology. In the future, 20-30% of patients have leukocyturia, proteinuria, microhematuria, as well as signs of renal failure - a decrease in urine density, isohyposthenuria, especially in patients with the presence of tophi. Sometimes arterial hypertension develops. It should be remembered that gouty interstitial nephritis in most cases proceeds and progresses slowly, almost asymptomatically, and only with a special study of kidney function is renal pathology detected.

According to our data, clinical and laboratory manifestations of kidney pathology are found in 46.2% of patients. However, an in-depth study of kidney function using radioisotope methods revealed a violation of glomerular filtration, renal blood flow and tubular reabsorption in 93.6% of patients. The development of these changes at the height of the gouty process and in the presence of severe hyperuricemia allows us to regard them as a manifestation of visceral gout.

According to G. Schroder, pathological changes in urine with impaired renal function are observed in 54% of individuals with asymptomatic hyperuricemia.

Gouty nephropathy should be distinguished from the so-called secondary renal gout, when hyperuricemia and the clinical picture of gout develop as a result of primary kidney damage (chronic nephritis with renal failure).

In the past, the authors described other manifestations of visceral gout - gouty phlebitis, pharyngitis, conjunctivitis, gastritis, colitis. The evidence of the gouty nature of these changes was considered to be that they occur during the period of exacerbation of gout and pass under the influence of colchicine. Most modern authors question this position and believe that humoral and neurovegetative disorders that accompany an acute attack of gout favor the development of these processes. The question of the mechanisms of earlier and more frequent development of coronary disease and atherosclerosis of the vessels of the brain and heart in patients with gout remains debatable. So, W. Curie, examining 1077 patients with gout in the UK, found hypertension in 27.8%. Atherosclerosis was detected in men suffering from gout, 2 times more often than in healthy men. According to G. Bluhm, G. Riddle, 10% of patients have myocardial infarctions, and 13% suffered cerebral thrombosis. According to G. Heidelmann et al., the spread of atherosclerosis in patients with gout is 10 times higher than in the general population.

We found hypertension, coronary heart disease and cerebral sclerosis in 42.4% of patients. However, there is no reliable data on the correlation between cardiovascular pathology, the severity of hyperuricemia and the severity of gout, but there is a certain relationship between the state of the cardiovascular system, age, severity of cholesterolemia and obesity in these patients. Thus, we can confirm the opinion of G. Currie et al., who believe that cardiovascular diseases in patients with gout develop not as a result of the effect of urates on the vascular wall, but as a result of a lipid metabolism disorder associated with gout. However, recently there has been evidence that in patients with gout, deposition of urates in the heart muscle is also possible.

The possibility of a combination of gout with obesity is a generally recognized fact. Obesity is observed in 66.7% of patients. Our observations show that 60% of patients have a violation of fat metabolism (obesity, hypercholesterolemia, hyperlipoproteinemia and more often hypertriglyceridemia), especially in patients with severe gout, the presence of tophi and renal nephropathy. In 2/3 of such patients, fatty degeneration of the liver is observed, in 10-15% - diabetes mellitus, and, according to the authors, disorders of uric acid and carbohydrate metabolism are mutually potentiated. These facts force us to agree with the assumption that there are some common mechanisms for the disturbance of uric acid, carbohydrate and fat metabolism in patients with gout.

Diagnosis of Gout:

• Radiography

X-ray of the joints in the early stage of gout does not show any characteristic changes. With the development of chronic urate arthropathies, signs of osteochondral destruction appear on radiographs - narrowing of the joint space due to cartilage destruction, rounded, clearly defined bone tissue defects in the epiphyses ("punches") due to the formation of bone tophi in the subchondral bone, erosion of the articular surfaces as a result of opening the tophi towards the articular cavity. At the same time, on the radiograph, one can see the compaction of the soft periarticular tissues, which is formed as a result of chronic inflammation and infiltration with urates. With the development of secondary osteoarthritis, more or less pronounced marginal osteophytosis is added to these signs. Of all the signs, the most typical for gout and having diagnostic value are "punches", which are most often found in the region of the I metatarsophalangeal joint and small joints of the hands. Very large, well-defined bone defects, sometimes with epiphyseal osteolysis, are characteristic of tophi arthropathies.

There are several radiographic stages of chronic gouty arthritis:

• I - large cysts (tophi) in the subchondral bone and in deeper layers, sometimes hardening of soft tissues;
• II - large cysts near the joint and small erosions on the articular surfaces; constant compaction of the periarticular soft tissues, sometimes with calcifications; I
• II - large erosion of at least 1/3 of the articular surface; osteolysis of the epiphysis, significant compaction of soft tissues with lime deposition.

In the patients we observed, we revealed radiographic changes already 5 years after the onset of the disease.

• Laboratory research

The most important for the diagnosis and treatment of gout is the study of uric acid metabolism: the content of uric acid in the blood serum, in daily urine and the determination of the clearance of uric acid.

In our observations, it was found that the average normal content of uric acid in the blood (when determined by the Grossman method) is about 0.3 mmol/l, in daily urine 3.8 mmol/day, the average normal clearance of uric acid is 9.1 ml/min. However, with different types of hyperuricemia, these indicators are different (indicators of uric acid metabolism in patients with gout with various types of hyperuricemia are presented in Table 17); in the presence of an acute attack of gout or chronic gouty arthropathy, the amount of uric acid in the blood usually increases. In severe cases, the content of uric acid in the blood reaches 0.84-0.9 mmol / l.

Most often, according to our data, the metabolic type of hyperuricemia is detected: the highest content of uric acid in the blood with its good excretion with urine and with normal clearance.

When examining the content of uric acid in the blood, one must be aware of the possibility of its daily fluctuations. According to T.K. Loginova et al., the maximum content of uric acid is observed at 11 o'clock in the afternoon.

In second place in frequency is the mixed type of hyperuricemia, in which the same or slightly lower content of uric acid is observed, but with less excretion and somewhat reduced clearance. In the renal type, the amount of uric acid is less than in other types, but there is a significant decrease in its excretion in the urine and the lowest clearance.

On our material, the most severe course of gout was observed in patients with a mixed type of hyperuricemia, when both the synthesis of uric acid and its excretion were impaired.

During an attack in patients with gout, ESR increases (usually 25-40 mm / h), moderate leukocytosis, a positive reaction to C-reactive protein and other indicators of the acute phase of inflammation can be observed. In the interictal period, these indicators are normal, but in the presence of urate arthropathy, they can be weakly positive.

In urine tests, with the involvement of the kidneys in the pathological process, there is a decrease in urine density, slight albuminuria, leukocyturia and microhematuria. The indicators of the Zimnitsky test are very important, since the deterioration in the concentration ability of the kidneys indicates the presence of asymptomatic chronic interstitial nephritis in the patient with the gradual development of nephrosclerosis. For the same purpose, a periodic blood test for the content of residual nitrogen is necessary. In patients with gout, hypercholesterolemia and an increase in blood triglycerides are often found, which indicates a simultaneous violation of lipid metabolism.

In the study of synovial fluid taken during a puncture of the knee joint, during an acute attack of gout, low viscosity is found, high cytosis (more than 10103 ml of cells), mainly due to multinucleated leukocytes. When microscopically examined using a polarizing microscope, numerous birefringent long needle-like crystals of sodium urate are easily determined.

Morphological examination of the biopsied synovial membrane during an acute attack reveals its hyperemia, edema, cellular infiltration predominantly by polynuclear neutrophils, which often contain sodium urate crystals.

In chronic gouty arthritis, proliferation of synovial villi, hypervascularization and perivascular lymphocytic and plasma cell infiltration, giant cells, i.e. chronic proliferative synovitis, which is a consequence of synovial membrane inlay with urates, are detected. Similar depots of losses can be in articular cartilage, epiphyses of bones, tendons, synovial bags.

Of great diagnostic importance is the morphological study of subcutaneous tofus. In its center, against the background of dystrophic and necrotic tissue changes, a whitish mass of sodium urate crystals is revealed, around which there is an inflammatory reaction zone with proliferation of histiocytes, giant cells and fibroblasts; the subcutaneous tophi is surrounded by dense fibrous connective tissue.

The course of gout is variable. In some patients, the disease has a relatively benign course for a long time with rare attacks of acute intermittent arthritis, without tophi and severe osteochondral destruction, and in most cases does not cause disability. In other cases, attacks are repeated very often, chronic gouty arthritis, tophi, and kidney damage develop rapidly. Long-term observation of patients with gout allows us to distinguish three variants of the course of the disease:

• lung, when attacks of arthritis recur only 1-2 times a year and capture no more than two joints; there are no signs of articular destruction on the radiograph, no damage to the kidneys is noted, there are no tophi or there are single, small ones;
• moderate with a frequency of attacks 3-5 times a year, damage to two to four joints, moderately pronounced osteoarticular destruction, multiple small tophi and the presence of nephrolithiasis;
• severe with a frequency of attacks more than 5 per year, multiple lesions of the joints, with pronounced osteoarticular destruction, multiple large tophi and the presence of severe nephropathy.

Observations show that the severe variant occurs mainly with the development of the disease at a young age or with a long course of the disease and high hyperuricemia.

Determining the severity of the course of gout is necessary when choosing doses of drugs for adequate therapy.

• Diagnostic criteria

In the presence of a classic picture of gout with a typical localization of the process in the I metatarsophalangeal joint, a rapid increase in the symptoms of acute arthritis and its complete reverse development after a few days, the suspicion of the possibility of developing this disease (especially in men) may arise already in the early period of the disease after 1-2 attacks. The diagnosis is confirmed by the detection of hyperuricemia, rapid relief of the attack with colchicine, especially the detection of sodium urate crystals in the synovial fluid.

With a long course of gout, when, in addition to recurring attacks of arthritis, there are already such signs characteristic of gout as the development of tophi, the presence of "punches" on radiographs of the hands and feet, hyperuricemia, the diagnosis of gout is usually not difficult. Difficulties arise with an atypical picture of the first gouty attacks (damage to the small joints of the hands or periarticular tissues), with their protracted course or low intensity, as well as in the presence of polyarthritis. In these cases, it should be borne in mind that, despite the atypical localization of the process, the intensity or duration of the gouty attack, it retains the basic patterns inherent in gout (sudden onset, rapid increase in symptoms and their complete reversibility in the early period of the disease).

At the International Symposium on the Diagnosis of RB in Rome, criteria for the diagnosis of gout were developed:

• an increase in the content of uric acid in the blood serum (more than 0.42 mmol / l in men and 0.36 mmol / l in women);
• tophi;
• crystals of sodium urate in the synovial fluid or in tissues, identified by microscopic or chemical examination;
• acute attacks of arthritis that occur suddenly, with complete clinical remission within 1-2 weeks.

The diagnosis of gout is established by the presence of two criteria.

Not all of these features are pathognomonic for primary gout. So, the first sign - hyperuricemia can be in people who do not suffer from gout, but occur, for example, under the influence of various drugs taken by patients to treat arthritis (for example, small doses of salicylates). However, in patients with gout, the level of uric acid in the blood may be normal if he took large doses of salicylates, pyrazolone drugs, or corticosteroids to treat arthritis. The fourth sign - acute attacks of arthritis with rapid reversibility of articular manifestations can occur with allergies, pyrophosphate arthropathy, in the early stage of RA with palindromic "rheumatism", etc.

The second sign - tophi, - very characteristic of gout, may be absent in the first 5 years of the disease.

The third sign has the greatest diagnostic value - the presence of microcrystals of sodium urate in the synovial fluid or in tissues (if joint puncture, tissue biopsy and microscopy are available research methods in this medical institution).

The lack of information content of these criteria and the criteria of the American Rheumatic Association, especially in the early stage of gout, was the reason for the development of new criteria for the presumptive diagnosis of gout, which can be used in patients in the early stage of the disease even before the formation of tofusev:

• more than one attack of acute arthritis;
• inflammation of the joint reaches a maximum on the 1st day of illness;
• monoarticular nature of arthritis;
• redness of the skin over the joint during an attack;
• swelling and pain in the I metatarsophalangeal joint;
• unilateral lesion of the 1st metatarsophalangeal joint;
• unilateral damage to the joints of the foot;
• suspicion of tophi;
• hyperuricemia;
• asymmetric changes in the joints on the radiograph;
• subcortical brushes without erosions on the radiograph;
• lack of flora when synovial fluid was cultured.

According to the authors, five signs or more occur in 95.5% of patients with gout in the early stages of the disease and much less frequently in patients with other arthritis (6-7%). However, with chondrocalcinosis (pseudogout), a combination of 5 or more symptoms occurs in 27.3% of patients.

Despite these defects, both criteria can provide some help in the diagnosis of gout. A particularly important sign, according to modern authors, are tophi and sodium urate microcrystals in the synovial fluid, which is detected in 84.4% of patients.

• Differential Diagnosis

In the early period of the disease, acute gouty monoarthritis, especially if it occurs without damage to the big toe, should first of all be differentiated from acute infectious arthritis, which can give an identical clinical picture: sudden onset, sharp pain, rapid increase in exudate, fever. In these cases, a carefully collected anamnesis helps - indications of recurrent similar attacks that pass without any residual effects (with gout), and the presence of any infection or injury in the past or present, a protracted course of arthritis, the detection of lymphangitis, a good effect of antibiotics (in acute infectious arthritis).

If an acute gouty attack proceeds like polyarthritis, especially with damage to the joints of the hands, it sometimes has to be differentiated from the early stage of RA, rheumatic or reactive allergic polyarthritis. In these cases, one should take into account the absence of indications of an infectious allergy, the absence of signs of heart damage. The very rapid development of a gouty attack with very sharp pains, bright hyperemia of the skin over the affected joint, followed by its cyanosis and flaking, which is usually absent in the above diseases, is also important.

Suspicion of RA may also arise in subacute gouty arthritis of one or two large joints, since RA, especially in young people, can begin as mono or oligoarthritis. However, there is a protracted course of arthritis with the gradual formation of defiguration, and sometimes contractures of the joint. In acute gouty arthritis with severe pain, fever, significant swelling and flushing of the skin around the joint, erysipelas may be suspected. But at the same time, there is no ridge-like infiltrate characteristic of erysipelas along the periphery, which sharply limits the area of ​​the lesion, as well as bullous elements against the background of hyperemic skin. An acute attack of gout is extremely difficult to distinguish from an attack of acute arthritis in chondrocalcinosis (pseudogout), which gives an identical clinical picture. However, this disease lacks hyperuricemia, tophi, and urate crystals in the synovial fluid.

Chronic gouty arthritis (polyarthritis) is also sometimes confused with chronic RA, since in both cases there is a long course with periodic exacerbations, and tophi in the elbow joints are mistaken for rheumatoid nodules. The difference is that with gout, the flare-ups of arthritis are sharper and shorter. The deformation of the joints is not explained by proliferative phenomena in the periarticular tissues, but by the infiltration of the articular and periarticular tissues with urates with the destruction of these tissues and bone growths around the articular surfaces (secondary osteoarthritis).

On the x-ray of the joints with gout, there are characteristic bone defects - “punches”. Gouty nodules (tophi) are firmer and more irregular than rheumatoid nodules and can sometimes be very large (the size of a hen's egg or more). The skin over large tophi is thinned, and a whitish content shines through it, and sometimes there is a fistula with the release of a mushy mass of urates. Histological examination makes it possible to clearly differentiate tofus from a rheumatoid nodule.

In some cases, when a patient with chronic gout clinically and radiologically has signs of secondary deforming arthrosis, they mistakenly diagnose primary osteoarthritis, and gouty attacks (especially if they are subacute) are mistaken for recurrent reactive synovitis. However, in primary deforming arthrosis, pain in the joints is predominantly mechanical in nature (occurs when the joint is loaded, more in the evenings), exacerbations of synovitis proceed much milder than with gout, without significant edema and without skin hyperemia, quickly subside at rest, while there are no tophi, and on radiographs there are no “punch holes” characteristic of gout.

When establishing the diagnosis of gout, the question of whether gout is secondary is very important. It is resolved with the help of a thorough questioning and examination of the patient for the presence of factors that can cause the development of secondary gout - blood diseases, malignant tumors, long-term use of diuretics, etc.

In addition, it is necessary to take into account the clinical features of secondary gout, the older average age of patients, the greater incidence of women, the absence of family cases of the disease, higher rates of hyperuricemia and uricosuria with a very frequent formation of stones in the urinary tract.

Gout treatment:

Treatment of gout should be aimed at preventing and stopping an acute attack and deposition of urates in tissues, as well as their resorption.

With the help of modern therapeutic drugs, it is possible both to quickly stop an acute attack of gout and to normalize the content of uric acid in the serum in most patients (provided that appropriate drugs are used throughout life).

Asymptomatic hyperuricemia requires treatment only if the serum uric acid content is high enough - consistently above 0.54 mmol / l - and, therefore, there is a high risk of developing an acute attack or the formation of urate stones. With hyperuricemia below 0.54 mmol / l, not accompanied by clinical symptoms of gout, treatment is not required.

Treatment of an acute attack of gout. Colchicine is the most powerful drug that suppresses acute gouty arthritis. According to modern views, the mechanism of action of colchicine lies mainly in its overwhelming effect on the functions of polymorphonuclear leukocytes - the migration and phagocytosis of urate crystals. In addition, colchicine affects the excretion of urates and their solubility in tissue.

Colchicine is used from the very beginning of the attack, preferably before its development, with the onset of prodromal phenomena (severity and vague discomfort in the joint). The dose of colchicine is 1 mg every 2 hours or 0.5 mg every hour, but not more than 4 mg on the first day of treatment, followed by a gradual dose reduction. On the 2nd and 3rd day, the dose is reduced by 1 and 1.5 mg/day, on the 4th and 5th day - by 2 and 2.5 mg/day, respectively. After the cessation of the attack, colchicine therapy is continued for 3-4 days. Colchicine causes toxic effects on the part of the gastrointestinal tract (diarrhea, nausea, vomiting), as a result of which it is sometimes necessary to quickly reduce the dose or even stop the drug before the end of the attack. A few days after the abolition of colchicine, its toxic effect disappears.

Under the influence of colchicine after 24-48 hours in 60-75% of patients pain and swelling of the joint are sharply reduced. In the remaining 40-25% of patients, colchicine may be ineffective due to significant side effects that do not allow reaching the required dosage, or improper treatment when colchicine is prescribed late - a few days after the onset of the attack or at too low doses.

The effect of colchicine on acute gouty arthritis is so specific (it does not have a similar effect on any other arthritis) that the effect of colchicine is a generally accepted diagnostic test confirming the presence of gout.

Pyrazolone and indole preparations are also effective treatments for acute gout. Pyrazolone preparations - butadione, reopyrin, ketazon, phenylbutazone - are quite effective and less toxic than colchicine. They have a pronounced anti-inflammatory effect and, in addition, increase the excretion of urates from the body. They are prescribed at a dose of at least 200 mg in the first few days, followed by a decrease.

Preparations of the indole series - indocid, indomethacin, metindol - give a good therapeutic effect, although less pronounced than pyrazolone derivatives. Drugs on the 1st day are taken at 100-150 mg / day, then the dose is reduced. Indomethacin in a high dose can cause headache, dizziness, nausea, therefore, in case of hypertension and dysfunction of the gastrointestinal tract, it should be used carefully, preferably in the form of 100 mg suppositories.

Corticosteroid drugs due to a distinct anti-inflammatory effect can be prescribed for acute attacks of gout, especially in patients in whom all of the above drugs had no effect or caused a drug reaction. However, corticosteroids do not give a lasting effect, and after their withdrawal, signs of arthritis may resume. In view of this, there is a danger of long-term corticosteroid therapy and corticodependence, which forces many authors to have a negative attitude towards their use in gout. We believe that with resistance to other drugs, prednisolone can be used for several days (20-30 mg / day, followed by a dose reduction), but always against the background of low doses of butadion or indocide tolerated by patients. After the end of the attack and the abolition of prednisolone, these drugs are continued for another week or 10 days.

In the case of severe joint pain in the first 1-2 days of an attack, when the effect of the drugs used has not yet manifested itself, a rapid analgesic and anti-inflammatory effect can be obtained with intra-articular administration of 50-100 mg of prednisolone in a large or medium joint and 25 mg in a small joint. After that, pain and exudation in the joint are sharply reduced after a few hours.

In addition to the use of drugs, during an acute attack of gout, complete rest, a low-calorie diet and a plentiful alkaline drink up to 2.5 l / day are necessary.

Long-term treatment of gout. The most important component of gout therapy is a special anti-gout diet, poor in purines, proteins and lipids. All foods rich in purines should be excluded from the diet: meat soups and extracts, kidneys, liver, lungs, brains, game, crayfish, fatty fish, fried meat, meat of young animals (young veal) green peas, cauliflower. Meat or fish is consumed only boiled 23 times a week. Of the meat products, chicken and ham are recommended, as they are relatively poor in purines. The amount of proteins should not exceed 1 g/kg. Since an excess of dietary lipids prevents the excretion of uric acid at night and provokes an acute attack of gout, foods rich in fats should be excluded: eggs, sausages, fatty milk and dairy products. The food of a patient with gout should contain no more than 1 g of fat per 1 kg of the patient's body weight. With excess weight, a hypocaloric diet, unloading (vegetable or fruit) days are recommended once a week or 10 days. Alcoholic beverages, strong tea and strong coffee are prohibited. It has long been noted that the use of these substances can provoke gouty attacks.

The study of the mechanism of the hyperuricemic action of alcohol showed that lactic acid, which is formed during the metabolism of ethyl alcohol, is able to temporarily inhibit the renal excretion of uric acid. With a load of alcohol and food rich in purines, the content of uric acid can increase by 26.1% against the initial one, which leads to a change in the concentration of uric acid in the synovial fluid, the release of sodium urate microcrystals from the intraarticular cartilage of tophi and the development of acute arthritis. Since an attack of gout can be triggered not only by a rapid increase in the content of uric acid in the blood, but also by a rapid decrease, fasting is not recommended for patients with gout. For sufficient excretion of uric acid, patients must have good diuresis (at least 1.5 l / day), therefore, it is recommended to drink plenty of water up to 2-2.5 liters per day (if there are no contraindications from the cardiovascular system and kidneys). Alkaline drinking is recommended (soda water, mineral waters such as Borjomi), since alkalinization of urine reduces the conversion of sodium urate to less soluble uric acid. Such a diet improves the course of gout, reduces the frequency and intensity of attacks, but does not cure the disease and does not lead to a complete normalization of the uric acid content when it is significantly increased. The decrease in the content of uric acid only with a diet is small.

The basic therapy for gout is the long-term use of drugs that normalize the content of uric acid in the blood. The issue of indications for the use of antigout drugs remains debatable. In patients with rare attacks (without tophi and chronic arthritis), with a uric acid content in the blood below 0.4-7 mmol / l, you can limit yourself to a diet only. However, according to W. N. Kelley, antigout drugs are indicated in the tissues and the development of gouty nephropathy.

The basic principle of the basic therapy of gout is the long-term and almost continuous use of anti-gout drugs throughout the patient's life, since after their cancellation, the uric acid content again reaches the previous figures and gout attacks resume.

All anti-gout drugs used for long-term treatment of gout:

• drugs that reduce the synthesis of uric acid by inhibiting the enzyme xanthine oxidase, which converts hypoxanthine to xanthine, xanthine to uric acid (uricodepressive drugs);
• drugs that increase the excretion of uric acid by reabsorption of urates by the renal tubules (uricosuric drugs).

Curicodepressive drugs include allopurinol and its analogues milurit, thiopurinol, as well as hepatocatalase, orotic acid. The most effective of these agents is allopurinol (hydroxypyrazolopyrimidine). The mechanism of suppression of uricosynthesis by allopurinol consists not only in inhibition of the xanthine oxidase enzyme, but also in a decrease in the synthesis of new purines, due to the inhibitory effect of the allopurinol nucleotide on the first reaction of this synthesis. The decrease in uricemia under the influence of allopurinol is accompanied by a decrease in uricosuria and, thus, is not associated with the risk of formation of urate stones in the urinary tract. Therefore, allopurinol can be used in the presence of renal pathology (however, without severe renal failure). The use of allopurinol at a dose of 200-400 mg / day (depending on the level of uric acid in the blood) causes a gradual decrease in the content of uric acid in the blood to normal within a few days 2-3 weeks. As hyperuricemia decreases, the dosage of allopurinol also decreases, complete and stable normalization of uricemia usually occurs after 4-6 months, after which a maintenance dose of 100 mg / day is prescribed.

A significant improvement in the reduction and decrease in the intensity of attacks, softening and resorption of tophi is observed in most patients after 6-12 months of continuous use of allonurinol. However, the drug does not have a noticeable effect on gouty nephropathy. Allopurinol can also be successfully used in secondary gout caused by diuretins or blood diseases when treated with cytostatics, when, under the influence of the use of these drugs, a rapid breakdown of cell nucleic acids occurs. In these cases, the dose of cytostatics should be reduced by 25% to avoid toxic reactions. The use of allopurinol can continue for many years with short breaks of 2-4 weeks (with a normal level of uric acid in the blood). Tolerability of the drug is good. Only occasionally allergic reactions (itching, skin rash, allergic Quincke's edema) are noted.

All of the above also applies to the analogue of allopurinol, the Hungarian drug milurit. Thiopurinol (mercaptopyrazolopyramidine) reduces uricemia as effectively as allopurinol, but is much better tolerated by patients. The mechanism of its action is mainly in the inhibition of the synthesis of new purines due to inhibition of the enzyme aminotransferase. It is used at a dose of 300-100 mg / day.

Orotic acid is a less active drug that reduces the synthesis of uric acid at the very beginning of the purine cycle by binding phosphoribozol pyrophosphate (usually not more than 0.1-2 mmol / l). At the same time, it enhances uricuria. The drug is well tolerated by patients at a dose of 25 mg / day. Treatment is carried out in courses of 1 month with a break of 1-2 weeks.

The preparation of beef liver hepatocatalase not only reduces the synthesis of endogenous uric acid, but also increases its breakdown. Like orotic acid, this drug is inferior in its effectiveness to allo and thiopurinol. It is administered intramuscularly 2-3 times a week for 10,000-25,000 units.

The group of uricosuric drugs includes drugs such as Anturan, Ketazon, Probenecid (Benemid), Etamide, acetylsalicylic acid. Their common mechanism of action is to reduce tubular reabsorption of urate. resulting in increased excretion of uric acid by the kidneys. However, it has been found that their mechanism of action is more complex. Thus, ketazone, probenecid and anturan appear to reduce the binding of urate to plasma proteins and therefore increase their glomerular filtration.

The disadvantage of all uricosuric drugs is that with an increase in the excretion of uric acid by the kidneys, they thereby contribute to its deposition in the urinary tract, causing attacks of renal colic, mainly in patients suffering from urolithiasis. Therefore, uricosurics are not indicated for such patients. Many authors believe that it is better to avoid the use of uricosuric agents with a high content of uric acid in the urine (over 3.5-6 mmol / day), and it is better to prescribe uricosuric drugs to these patients.

The use of uricosuric drugs must be combined with abundant alkaline drinking (up to 2 l / day), which is the prevention of renal colic. In some cases, these drugs can increase the symptoms of kidney failure if the patient has a "gouty kidney."

Probenecid (benemide) is a derivative of benzoic acid, the most studied and widely used remedy for gout. The drug is prescribed in a dose of 0.5 g (no more than 4 tablets per day). The daily dose of this drug has a rapid uricosuric effect within 24 hours. Benemide is fairly well tolerated, but in some cases it can cause disturbances (skin rashes, itching, fever, etc.).

While taking probenecid, patients should not be given acetylsalicylic acid, which interferes with the uricosuric action.

Anturan (sulfinpyrazone) is an analogue of phenylbutazone. It has been used as a uricosuric agent since 1958. It is used in tablets but 100 mg (no more than 600 mg / day). Its uricosuric effect is longer than that of benecid, about 8 hours. In some cases, it has an effect in patients resistant to probenecid. It is well tolerated and only in some cases can cause stomach pain, nausea, leukopenia. Acetylsalicylic acid is also an antagonist of the uricosuric action of anturan.

Probenecid and Anturan are contraindicated in renal failure, urolithiasis, gastritis, gastric and duodenal ulcers, hepatitis, leukopenia.

Etamidsovetsky drug has a weaker uricosuric effect than previous drugs. It is used in tablets of 0.7 g 3-4 times a day, in cycles of 7-10 days (2 cycles with a week break). Treatment is repeated 3-4 times a year. Tolerability is good. Occasionally, skin itching, small dyspeptic and dysuric phenomena are observed.

Acetylsalicylic acid at a dose of 3 g / day can have a uricosuric effect, however, given its toxic effect on the stomach, it can hardly be recommended for the long-term treatment of gout.

All uricosuric agents are less effective at reducing hyperuricemia than uricosuric agents. With their use, the level of uric acid in the blood rarely drops below 0.36 mmol / l.

With prolonged use of anti-gout medications against the background of an anti-gout diet, a decrease in the content of uric acid in the blood, a decrease in attacks or even their complete disappearance, and a decrease in the manifestations of chronic arthritis are achieved. Due to the decrease in tissue infiltration with urates, “punch holes” on the radiograph may decrease or even disappear. There is softening and a decrease in the size of tophi. However, it should be borne in mind that with a decrease in uricemia under the influence of anti-gout medications in the first months of treatment, gout attacks, especially in patients with tophi, may become more frequent and more intense due to the breakdown of urate deposits and their mobilization from the depot.

To prevent this, when using anti-gout medications, it is necessary to simultaneously prescribe to patients in the first months of treatment continuous colchicine therapy in small doses (1 mg / day).

The choice of drugs for long-term treatment. When developing a treatment regimen and choosing medications, one should take into account: the severity of the course, the height and type of hyperuricemia, the condition of internal organs, the presence of allergies, and the individual reactivity of the patient.

For mild illness(rare recurrences, absence of tophi and nephropathy) and slight hyperuricemia (not higher than 0.47-0.5 mmol / l), you can get by with a diet and periodic courses of less active drugs such as orotic acid, etamide, which are well tolerated by patients. In moderate and severe cases and higher numbers of hyperuricemia, it is necessary to continuously take active therapeutic agents. The correct choice of a specific therapeutic drug can be made only after a thorough clinical and laboratory examination of the patient with the determination of not only the level of uric acid in the blood, but also its daily excretion in the urine and its clearance.

With metabolic type hyperuricemia with a high level of uric acid in the blood with good excretion and good clearance (uricuria over 3.5-6 mmol / day, clearance 6-7 ml / min), a patient with long-term treatment should be prescribed drugs that reduce the synthesis of uric acid, i.e. allopurinol, milurite or thiopurinol. Anturan, probenecid and other uricosuric drugs are not indicated in these cases. They must be prescribed for insufficient excretion of uric acid in the urine - less than 3.5-6 mmol / day (renal type of hyperuricemia), but only for patients who do not have renal failure and nephrolithiasis, liver and gastrointestinal tract diseases. In the presence of this pathology, only uricodepressive agents (allopurinol, etc.) are used. If a patient with high hyperuricemia has a reduced excretion of uric acid by the kidneys (less than 3.5-6 mmol / day), which is observed with a mixed type of hyperuricemia, then in the absence of a contraindication, a combined method of treatment with both uricodepressive and uricosuric drugs can be used, the doses of which are selected depending on the content of uric acid in the blood and in daily urine. The use of antigout drugs is continued for a year, after which you can take a break for 2 months (with a normal uric acid content) or prescribe another drug.