The first phase of gout occurs without symptoms; the level of urate in the body gradually increases, which can subsequently lead to gout. This stage lasts a very long time, up to 25 years or more.
In people with gout, diabetes mellitus begins early and atherosclerotic plaques form in the blood vessels because low-density lipoproteins are concentrated in the blood. Cholesterol in the blood of patients is higher than normal (see how to reduce cholesterol).
When diagnosing, the frequency of recurrent attacks is taken into account.
Treatment of gout comes down to relief of acute attacks, drug treatment, diet and prevention of repeated exacerbations.
To treat gout in the period between attacks at home, they eliminate hyperuricemia, relapses of gout attacks, prevent damage to internal organs, restore impaired joint function with the help of complex therapy, including medications, diet, physical influences and spa treatment.
Uricostatics inhibit the formation of uric acid, for example, Allopurinol: daily dose - 100-900 mg, which depends on the degree of hyperuricemia. For mild cases – 200-300 mg, for moderate cases – 300-400 mg, for severe cases – 600-900 mg/day. In two days you can reduce the level of uric acid by 2-3 times. The drug is used constantly because it does not have stability and duration of action. A break is taken in the summer for 1-2 months due to the appearance of a variety of plant-based products on the menu.
Usually, diet No. 6 is prescribed for gout, which has a full calorie content, it contains limited animal fats and salt, and a reduced amount of protein. The diet has many alkaline valences and requires increased fluid intake. The energy value of the diet is 3000 kcal. Diet No. 5 is also suitable.
Gout is manifested by the following complications:
Prolonged attacks may result in complete recovery. The prognosis is favorable and depends on the level of hyperuricemia and adequate treatment. People can remain able to work for many years and their quality of life does not suffer.
If, after reading the article, you suspect that you have symptoms characteristic of this disease, then you should seek advice from a rheumatologist.
Gout (gouty arthritis) is a disease of the joints, which is caused by the deposition of uric acid salts (urates) in them. It affects any joints: fingers, hands, feet, elbows, knees. Most often, gout affects the joints of the toes.
About one person in a thousand suffers from gout. Men get sick 20 times more often than women. The disease usually develops after age 40 in men and after menopause in women.
Heredity plays a role in the development of gout. Predisposing factors: excess nutrition, monotonous meat food, consumption of alcoholic beverages (especially beer and grape wines), sedentary lifestyle. Often the disease develops against the background of kidney failure and blood diseases.
Normally, uric acid, which is the end product of the metabolism of certain substances, enters the blood and is excreted by the kidneys. In some cases, the concentration of uric acid in the blood may increase significantly. This occurs as a result of insufficient excretion or increased production of uric acid. At the same time, its salts (urates) crystallize and are deposited in the joints, which causes inflammation and severe pain. In addition, urate can accumulate in the skin, forming nodules (tophi), and in the kidneys, forming calculi (stones).
As a rule, a gout attack develops against the background of drinking alcohol (especially beer) or overeating. The disease is manifested by sudden and intense pain, redness and “heat” in the joint. Gout attacks usually occur at night. The pain is so severe that many patients cannot even bear the weight of a sheet on the affected joint. A recurrent attack of gout is usually preceded by a tingling sensation in the affected joint. If gout is left untreated, attacks become more frequent and periods of exacerbation last longer. Arthritis affects more and more joints, often affecting the kidneys and urinary tract.
The diagnosis is established by a rheumatologist upon examination and questioning of the patient. As a rule, a biochemical blood test reveals an increased level of uric acid. In some cases, a puncture (puncture) of the joint with examination of the joint fluid or an x-ray is necessary.
Unfortunately, gout cannot be completely cured, but it can be controlled. To do this, first of all, it is necessary to change the nature of the diet - exclude foods such as beer, wine, meat of young animals, offal (liver, kidneys, etc.), legumes, mushrooms, sardines, fish roe.
Drug treatment includes anti-inflammatory drugs and drugs that inhibit the formation and stimulate the excretion of uric acid.
Physiotherapy greatly improves your well-being. Surgical methods are also used to remove uric acid deposits in soft tissues.
Treatment includes correction of body weight and treatment of all metabolic diseases (atherosclerosis, diabetes) that accompany gout.
To prevent exacerbations of gout, it is recommended to follow a diet (see above). You need to drink plenty of fluids (at least three liters per day). Dehydration impairs kidney function and leads to increased plasma uric acid concentrations.
Gout is a chronic disease associated with a violation of uric acid metabolism - an increase in the level of uric acid in the blood and the deposition of crystals of 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 his book “Treatise on Gout.” It was later noted that in patients with gout the level of uric acid in the blood increases (hyperuricemia); 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 did experts establish 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 USA, in recent years, up to 2% of the adult population has suffered from 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, all countries have seen an increase in the incidence of gout. Thus, in Finland, according to N. Isorriaki II cont., the number of registered cases of gout has recently increased 10 times, in Germany - 20 times. However, information about the prevalence of gout is incomplete due to late diagnosis. Gout is diagnosed 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 in only 7% of patients.
The spread of gout in the most developed countries is associated with significant consumption of foods rich in purines (meat, fish) and alcoholic beverages. This is confirmed by the fact that there was a sharp decrease in the incidence of gout during the Second World War, when meat consumption was significantly reduced.
Gout affects mainly men. The first attack of gout can occur at any age, but in most cases after 40 years of age. In recent years, there has been a slight 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 with a renewal rate of 650 mg/day, i.e., 650 mg of uric acid is removed from the reserves every day and the same amount is replenished. Since uric acid is excreted from the body by the kidneys, it is important to know its clearance, i.e. the volume of blood that can be cleared of excess uric acid in the kidneys in a minute. Normally it is 9 ml/min.
The source of uric acid formation in the body is purine compounds, which come from food, and are also formed in the body during the metabolism of nucleotides.
The synthesis of purines begins in the body with the formation of phosphoribosylamine from the 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, inosinic acid, is formed, a significant part of which is converted into purine nucleotides of nucleic acids - adenylic and guanylic acids, which are mainly used for the construction of nucleic acids. However, part of the adenylic and guanylic acids is catabolized, turning into simple purines: guanine, xanthine and others, which, under the influence of the enzyme xanthine oxidase, are converted into uric acid, while most of them, with the participation of the enzyme hypoxanthine guanine phosphoribosyltransferase (GGPT), again form guanylic acid. Thus, the immediate precursors of uric acid are purines - guanine and xanthine.
In blood plasma, uric acid is found in the form of free sodium urate. The normal content of sodium urate in serum, determined using the calorimetric method, is 0.3 mmol/l for men and 0.24 mmol/l for women. The upper limit of normal for men is 0.42 mmol/l, for women 0.36 mmol/l. Uric acid levels above these numbers are considered hyperuricemia with a high risk of developing gout.
Over a long period of time, hyperuricemia may be asymptomatic, and only after a few years does the clinical picture of gout develop. When studying the daily dynamics of uricemia in healthy men, unstable asymptomatic hyperuricemia was found in 25.7% of cases, indicating the possibility of developing gout.
Normally, the processes of uric acid synthesis and its excretion are balanced, but if this process is disrupted in any way, an excess level 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, or a combination of these factors.
Increased formation of uric acid occurs with excessive intake of purines from food, increased endogenous synthesis of purines, increased catabolism of nucleotides, or 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. Insufficient 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 1/3 sufferers of gout, and 20% of family members of patients have hyperuricemia.
The reasons for the increase in uric acid levels during primary hyperuricemia can be different:
According to most authors, overeating and excessive alcohol consumption contribute to the occurrence of hyperuricemia and aggravate it. W. Curie, who studied 1077 cases of gout, found excess weight (10% or more) in 38.2% of patients. According to GP Rodnan, fatty foods and alcohol can block renal excretion of uric acid and cause hyperuricemia. Other risk factors for hyperuricemia include 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, by the deficiency of the enzyme involved in the resynthesis of nucleotides from purines. A decrease in the activity of this enzyme leads to insufficient use of purines in the body and thus increased formation of uric acid. This type of hyperuricemia is characteristic of 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 are still not entirely clear. The same can be said regarding the second main mechanism of primary hyperuricemia - impaired excretion of uric acid by the kidneys. It is known that sodium urate (urate) 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 tubules and only 10% is excreted in the urine (tubular secretion of urates increases progressively with increasing serum uric acid content ). 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 changes in the active excretion of urate by the kidneys is still unknown.
The most common cause of secondary hyperuricemia is renal failure, which results in decreased excretion of uric acid from the body (secondary renal hyperuricemia). Some blood diseases—essential polycythemia, chronic myeloid leukemia, chronic hemolytic anemia, pernicious anemia, myeloma—may be accompanied by hyperuricemia due to the breakdown of cell nuclei and increased catabolism of cellular nucleotides.
An increase in the level 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. People who have been suffering from hypertension, myxedema, hyperparathyroidism, diabetes, pregnancy toxicosis, and lead intoxication for a long time may develop hyperuricemia due to inhibition of tubular excretion and slower removal 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, believed to be due to a decrease in extracellular fluid volume. Salicylates in small doses (acetylsalicylic acid no more than 2 g/day) moderately increase the level of uric acid in the blood, and in large doses (4-5 g/day), on the contrary, they reduce it. The level 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 level of uric acid in the blood in the form of increased secretion of uric acid by the kidneys and deposition of urate in tissues. Urates (sodium uric acid) are 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 loss in the form of crystals with subsequent penetration into the cartilage and synovium, 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 bone substance, determined on radiographs, in the form of round bone defects (“piercers”).
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, bursae and under the skin leads to the formation of micro- and microtophus (round formations of various sizes containing sodium urate crystals).
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 cause of death in patients with gout.
Gouty nephropathy is 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. Canalicular 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 of gout is kidney damage - interstitial nephritis (due to widespread deposition of urates in the interstitial tissue of the kidneys).
E. Uehlinger associates renal vascular damage with a parallel disorder of protein metabolism and the formation of excess intermediate products (lipoproteins), which are deposited in the glomeruli and renal vessels. All this leads to sclerosis of the glomeruli and shrinkage of the kidneys with the development of hypertension and renal failure.
The pathological processes described above, associated with the deposition of urate in the tissues of the body, determine the main clinical manifestations of gout, of which the most striking is acute gouty arthritis.
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 impairment of the excretion of uric acid by the kidneys. Excessive drinking of alcohol and prolonged fasting have a similar effect.
The first leads to an increase in the concentration of uric acid in the body, which is formed during normal metabolism of alcohol, the second leads 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. Attacks can be triggered by injury or the use of medications that alter the normal excretion of uric acid by the kidneys, as well as heavy physical activity (due to increased production of lactic acid). Foods rich in purines and fats, according to the authors, are of less importance, but in persons prone to hyperuricemia, they can provoke an acute attack of gout.
D. McCarty and J. Hollander found that an acute attack of arthrosis develops due to the loss 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, clearly visible in polarized light, are constantly present in the synovial fluid (free 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 believed that it is associated either with a rapid increase in the urate content in the serum, which leads to the precipitation of crystals into the synovial fluid, which is already oversaturated with urates, or with a rapid decrease in their amount in the blood, which contributes to their mobilization from the depot. The dropped crystals are phagocytosed by neutrophils of the synovial fluid and synoviocytes, during which the release and activation of lysosomal enzymes occur, causing an inflammatory response. At the same time, 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 progresses, other components are also involved in the process, in particular coagulation factors, kinins, plasmin and complement components.
The first clinical manifestation of gout is an attack of acute arthritis, developing suddenly, as if in the midst of complete health, although some prodromal phenomena may be observed within 1-2 days: vague discomfort in the joint, general malaise, nervousness, dyspepsia, fever, insomnia, chills. The factor that provokes 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, tight shoes), mental or physical overload, infections (flu, sore throat).
The classic clinical picture of an acute gout attack is very characteristic. It consists of the sudden appearance (usually at night) of severe pain, most often in the first metatarsophalangeal joint, with its swelling, bright hyperemia of the skin and subsequent peeling. These phenomena quickly increase, reaching a maximum within a few hours and are accompanied by fever (sometimes reaching 40 ° C), chills, leukocytosis, and an increase in ESR. Excruciating pain, intensifying even when the affected joint comes into contact with a blanket, causes complete immobility of the affected limb. After 5-6 days, the signs of inflammation gradually subside and over the next 5-10 days completely disappear in most patients, the temperature and ESR return to normal, joint function is completely restored, and the patient feels completely healthy. Subsequently, acute attacks are repeated at various intervals, affecting an increasing number of joints of the legs and arms.
However, observations show that at present there are 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 subacute polyarthritis.
Our experience in studying gout in more than 300 patients shows that the classic picture of a gout attack at the onset of the disease involving the big toe is observed in only 60% of patients. In 40% of patients, the process either has an atypical localization without affecting the big toe, or occurs as polyarthritis. According to our observations, there are the following atypical forms of the first attack of gout:
The intensity and duration of the attack also vary from 3 days to 1.5 months. We observed a subacute and prolonged course of the first attack in 16% of patients. Such variability of clinical manifestations at the onset of the disease significantly complicates the early diagnosis of gout.
With a long course, the clinical picture of the disease consists of three syndromes: joint damage, tophi formation and damage to internal organs. The most striking clinical manifestation during this period of the disease remains articular syndrome.
In the first years of the disease (up to approximately 5 years from the onset of the disease), joint damage occurs as an acute intermittent arthritis with complete reverse development 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 almost obligatory damage to 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 one by one. At the same time, damage to the tendons is observed, most often pain and hardening of the heel tendon, as well as mucous bursae (usually the olecranon bursa).
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 periods between attacks become shorter and shorter. Gradually, persistent deformities and stiffness of the joints appear. caused by joint destruction by urates impregnating 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. Persistent swelling and deformation of the joints are noted, sometimes with large intra-articular effusion.
Joint deformation occurs due to the destruction of cartilage and articular surfaces, as well as the infiltration of periarticular tissues with urate with the formation of large tophi. In these cases, the skin covering the tophi may ulcerate, a fistula is formed, from which a pasty mass containing sodium urate crystals is released.
Destruction of the first metatarsophalangeal joint develops first, then other small joints of the feet, then the joints of the hands, elbows and knees. When the chronic destructive gouty process is localized in the small joints of the hands, in some cases a clinical picture resembling RA develops. Against the background of chronic gouty arthritis, frequent attacks of gout usually occur, less acute, but longer lasting than in the early period of the disease.
The most severe clinical picture develops in the presence of the so-called gouty status, when almost continuous intense attacks of arthritis in one or more joints are observed for several months 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 osteoarthritis in the affected joints, which significantly reduces the ability of patients to move and increases joint deformation. This process often involves the joints of the feet: deforming arthrosis develops in the area of the first metatarsophalangeal joint and metatarsal joints with the formation of osteophytes on the dorsum of the foot (tuberous gouty foot).
In 70-80% of patients, spondylosis deformans is also detected.
Patients with chronic gout can remain able to work 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, fairly clearly demarcated gouty nodes or tophi that rise above the surface of the skin. 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. They come in different sizes, from a pinhead to a small apple. Individual tophi merge to form large conglomerates; they are localized mainly on the ears, in the area of joints, most often elbows, as well as knees, on the feet (big toe, dorsum of the foot, heel), hands - around small joints and on the flesh of the fingers and , in addition, in the area of the calcaneal tendon, tendons of the dorsum of the hand, etc. and synovial bursae.
In more rare cases, tophi are found on the eyelids, sclera, and wings of the nose. They are painless and, when small in size, are often detected only by a doctor.
With superficial deposits of urates, the contents of white tophi are visible through the skin covering them. Aspiration and microscopy of this content reveals typical needle-shaped crystals of sodium urate. When the tophi is ulcerated, 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 who have suffered from gout for more than 6 years or have 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 is observed (visceral gout). 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 renal failure). According to many authors, gouty nephropathy is the cause of death in 25-41% of patients with gout.
Kidney stones develop earlier and more often. 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 stages of the disease usually does not reveal renal pathology. Subsequently, 20-30% of patients experience leukocyturia, proteinuria, microhematuria, as well as signs of renal failure - decreased urine density, isohyposthenuria, especially in patients with 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 renal function is renal pathology detected.
According to our data, clinical and laboratory manifestations of kidney pathology are detected in 46.2% of patients. However, an in-depth study of renal function using radioisotope methods revealed impairment 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 people 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, authors described other manifestations of visceral gout - gouty phlebitis, pharyngitis, conjunctivitis, gastritis, colitis. Evidence of the gouty nature of these changes was considered to be that they occur during an exacerbation of gout and pass under the influence of colchicine. Most modern authors question this position and believe that humoral and neurovegetative disorders accompanying 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 blood vessels of the brain and heart in patients with gout remains debatable. Thus, W. Curie, having examined 1077 patients with gout in Great Britain, 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 experience myocardial infarction, and 13% suffered thrombosis of cerebral vessels. According to G. Heidelmann et al., the prevalence 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, the 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 lipid metabolism disorders accompanying gout. However, recently there has been evidence that in patients with gout, urate may also be deposited in the heart muscle.
The possibility of a combination of gout and obesity is a generally accepted fact. Obesity is observed in 66.7% of patients. Our observations show that 60% of patients have a disorder of fat metabolism (obesity, hypercholesterolemia, hyperlipoproteinemia and, more often, hypertriglyceridemia), especially in patients with severe gout, the presence of tophi and renal nephropathy. 2/3 of such patients have fatty liver, 10-15% have 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 of disturbance of uric acid, carbohydrate and fat metabolism in patients with gout.
X-rays of joints in the early stages of gout do not show any characteristic changes. With the development of chronic urate arthropathy, signs of osteochondral destruction appear on radiographs - narrowing of the joint space due to the destruction of cartilage, round, clearly defined defects of bone tissue in the epiphyses ("pierces") due to the formation of bone tophi in the subchondral bone, erosion of the articular surfaces as a result of opening of the tophi in side of the articular cavity. At the same time, on the x-ray one can see the compaction of soft periarticular tissues, which is formed as a result of chronic inflammation and infiltration of 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 area of the first metatarsophalangeal joint and small joints of the hands. Very large, clearly demarcated bone defects, sometimes with osteolysis of the epiphyses, are characteristic of tophi arthropathy.
There are several radiological stages of chronic gouty arthritis:
According to the authors, moderate radiological changes in joints occur on average after 9 years (stage I of the disease), and more significant ones after 10-15 years or more (stage II-III).
In the patients we observed, we identified radiological changes within 5 years from the onset of the disease.
The most important thing 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 uric acid clearance.
Our observations established that the average normal content of uric acid in the blood (as 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, for different types of hyperuricemia, these indicators are different (indicators of uric acid metabolism in patients with gout with different 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 level 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 good excretion in the urine and with normal clearance.
When studying the content of uric acid in the blood, you need to remember 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 release and slightly 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.
In 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 CRP and other indicators of the acute phase of inflammation may 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, when the kidneys are involved in the pathological process, a decrease in urine density, slight albuminuria, leukocyturia and microhematuria are noted. The indicators of the Zimnitsky test are very important, since a deterioration in the concentrating 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, periodic blood testing for residual nitrogen content is necessary. In patients with gout, hypercholesterolemia and increased blood triglycerides are often detected, which indicates a simultaneous disorder of lipid metabolism.
When examining synovial fluid taken during puncture of the knee joint, low viscosity and high cytosis (more than 10-103 ml of cells), mainly due to multinucleated leukocytes, are found during an acute attack of gout. When examined microscopically using a polarizing microscope, numerous birefringent long needle-shaped crystals of sodium urate are easily identified.
A morphological examination of the biopsied synovial membrane during an acute attack reveals its hyperemia, edema, and cellular infiltration of predominantly 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 are detected, i.e., proliferative chronic synovitis, which is a consequence of encrustation of the synovial membrane with urates. Similar depots of losses can be in articular cartilage, epiphyses of bones, tendons, and synovial bursae.
Morphological examination of subcutaneous tophi is of great diagnostic importance. In its center, against the background of dystrophic and necrotic changes in tissue, a whitish mass of sodium urate crystals is revealed, around which there is a zone of inflammatory reaction 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 proceeds for a long time in a relatively benign manner 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 quickly develop. Long-term observation of patients with gout allows us to distinguish three variants of the course of the disease:
Observations show that the severe variant occurs mainly when the disease develops at a young age or with a long course of the disease and high hyperuricemia.
Determining the severity of gout is necessary when choosing doses of medications for adequate therapy.
In the presence of a classic picture of gout with a typical localization of the process in the first metatarsophalangeal joint, a rapid increase in the symptoms of acute arthritis and its complete reverse development after a few days, 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 by the detection of sodium urate crystals in the synovial fluid.
With a long course of gout, when, in addition to periodically recurring attacks of arthritis, there are already signs characteristic of gout, such 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 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, intensity or duration of a gout attack, it retains the basic patterns characteristic of 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 Gout in Rome, criteria for the diagnosis of gout were developed:
The diagnosis of gout is made when two criteria are met.
Not all of the listed signs are pathognomonic for primary gout. Thus, the first sign - hyperuricemia can occur in people who do not suffer from gout, but may arise, for example, under the influence of various medications 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 they took large doses of salicylates, pyrazolone drugs or corticosteroids to treat arthritis. The fourth sign is that acute attacks of arthritis with rapid reversibility of articular manifestations can occur with allergies, pyrophosphate arthropathy, in the early stages of RA with palindromic “rheumatism,” etc.
The second sign - tophi - is very characteristic of gout, but 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 a given medical institution).
The insufficient 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 tofus:
According to the authors, five or more signs occur in 95.5% of patients with gout in the early stages of the disease and much less often in patients with other arthritis (6-7%). However, with chondrocalcinosis (pseudogout), a combination of 5 or more signs occurs in 27.3% of patients.
Despite these defects, both criteria can provide some assistance in the diagnosis of gout. A particularly important sign, according to modern authors, is tophi and microcrystals of sodium urate in the synovial fluid, which is detected in 84.4% of patients.
In the early period of the disease, acute gouty monoarthritis, especially if it occurs without affecting 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 periodically recurring similar attacks that pass without any residual effects (with gout), and the presence in the past or present of any infection or injury, prolonged course of arthritis, identification of lymphangitis, good effect of antibiotics (with acute infectious arthritis).
If an acute gouty attack occurs as a 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 infectious allergies and the absence of signs of heart damage. The very rapid development of a gouty attack with very acute pain, bright hyperemia of the skin over the affected joint, followed by cyanosis and peeling, which is usually absent in the above diseases, is also important.
Suspicion of RA may also arise in case of subacute gouty arthritis of one or two large joints, since RA, especially in young people, can begin as mono or oligoarthritis. However, in this case, a protracted course of arthritis is observed with the gradual formation of deformation, and sometimes contracture of the joint. In acute gouty arthritis with sharp pain, fever, significant swelling and hyperemia of the skin around the joint, erysipelas may be suspected. But at the same time, there is no roller-like infiltration along the periphery, characteristic of erysipelas, sharply limiting the affected area, 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 with chondrocalcinosis (pseudogout), which gives an identical clinical picture. However, in this disease there is no 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 area of the elbow joints are mistaken for rheumatoid nodules. The difference is that with gout, exacerbations of arthritis are more severe and shorter. Joint deformation is not explained by proliferative phenomena in the periarticular tissues, but by the infiltration of articular and periarticular tissues with urates with the destruction of these tissues and bone growths around the articular surfaces (secondary osteoarthritis).
On x-rays of joints with gout, characteristic bone defects are observed - “punches”. Gouty nodules (tophi) are denser and more irregular in shape than rheumatoid nodules, and can sometimes be very large (the size of a chicken egg or larger). The skin over large tophi is thinned, and the whitish contents are visible through it, and sometimes there is a fistula with the release of a pasty mass of urates. Histological examination allows one to clearly differentiate tophi from rheumatoid nodule.
In some cases, when a patient with chronic gout clinically and radiologically has signs of secondary deforming arthrosis, a diagnosis of primary osteoarthritis is mistakenly made, and gouty attacks (especially if they occur subacutely) are mistaken for recurrent reactive synovitis. However, with 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 are much milder than with gout, without significant swelling and without hyperemia of the skin, quickly subside with rest, and there are no tophi, and on radiographs there are no “punches” characteristic of gout.
When diagnosing gout, the question of whether gout is secondary is very important. It is resolved through careful questioning and examination of the patient for the presence of factors that may 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 frequency of women affected, the absence of family cases of the disease, higher rates of hyperuricemia and uricosuria with very frequent formation of stones in the urinary tract.
Treatment of gout should be aimed at preventing and stopping an acute attack and deposition of urate in tissues, as well as their resorption.
With the help of modern therapeutic drugs, it is possible to quickly stop an acute attack of gout and normalize the level 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 level 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, no treatment is required.
Treatment of an acute attack of gout. The most powerful drug that suppresses acute gouty arthritis is the crocus drug - colchicine. According to modern views, the mechanism of action of colchicine lies mainly in its suppressive effect on the functions of polymorphonuclear leukocytes - migration and phagocytosis of urate crystals. In addition, colchicine affects the excretion of urate and its solubility in tissue.
Colchicine is used from the very beginning of an 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 reduction in the dose. On the 2nd and 3rd days, 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 attack stops, colchicine therapy is continued for 3-4 days. Colchicine causes toxic effects from the gastrointestinal tract (diarrhea, nausea, vomiting), as a result of which it is sometimes necessary to quickly reduce the dose or even discontinue the drug before the end of the attack. A few days after colchicine is discontinued, its toxic effect disappears.
Under the influence of colchicine, after 24-48 hours, pain and swelling of the joint sharply decrease in 60-75% of patients. In the remaining 40-25% of patients, colchicine may be ineffective due to significant side effects, which does not allow the required dosage to be achieved, or incorrect treatment methods, when colchicine is prescribed late - a few days after the onset of the attack or in 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 drugs are also effective treatments for acute gout. Pyrazolone drugs - butadione, reopirin, ketazone, phenylbutazone - are quite effective and less toxic than colchicine. They have a pronounced anti-inflammatory effect and, in addition, increase the release of urates from the body. They are prescribed at a dose of at least 200 mg in the first few days with its subsequent reduction.
Indole drugs - indocid, indomethacin, methindole - give a good therapeutic effect, although less pronounced than pyrazolone derivatives. On the 1st day the drugs 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 their distinct anti-inflammatory effect, can be prescribed for an acute attack of gout, especially for patients in whom all of the above drugs had no effect or caused a drug reaction. However, corticosteroids do not provide a lasting effect, and after they are stopped, signs of arthritis may return. 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 for gout. We believe that in case of resistance to other drugs, prednisolone can be used for several days (20-30 mg/day with subsequent dose reduction), but always against the background of small doses of butadione or indocide tolerated by patients. After the end of the attack and discontinuation of prednisolone, these drugs are continued for another week or 10 days.
In case of severe pain in the joint in the first 1-2 days of the attack, when the effect of the drugs used has not yet manifested itself, a rapid analgesic and anti-inflammatory effect can be obtained by intra-articular injection of 50-100 mg of prednisolone into a large or medium joint and 25 mg into a small joint. After this, pain and exudation in the joint decrease sharply within a few hours.
In addition to the use of medications, during an acute attack of gout, complete rest, a low-calorie diet and abundant alkaline drinking 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, low 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 in boiled form 23 times a week. Among meat products, chicken and ham are recommended, as they are relatively low in purines. The amount of protein should not exceed 1 g/kg. Since excess dietary lipids prevents the elimination of uric acid at night and provokes an acute attack of gout, foods rich in fat should be excluded: eggs, sausages, fatty milks 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. If you are overweight, a hypocaloric diet and fasting (vegetable or fruit) days are recommended once a week or 10 days. Alcoholic drinks, strong tea and strong coffee are prohibited. It has long been noted that the use of these substances can provoke gout attacks.
A study of the mechanism of the hyperuricemic effect of alcohol showed that lactic acid, formed during the metabolism of ethyl alcohol, can temporarily inhibit the renal excretion of uric acid. When loaded with alcohol and food rich in purines, the content of uric acid can increase by 26.1% compared to the original, which leads to a change in the concentration of uric acid in the synovial fluid, the release of sodium urate microcrystals from the intra-articular cartilage of the tophi and the development of acute arthritis. Since a gout attack can be triggered not only by a rapid increase in the level of uric acid in the blood, but also by a rapid decrease, fasting is not recommended for gout patients. For sufficient removal of uric acid, patients must have good diuresis (at least 1.5 l/day), so it is recommended to drink plenty of fluids up to 2-2.5 l per day (if there are no contraindications from the cardiovascular system and kidneys). Alkaline drinking (soda water, mineral waters such as Borjomi) is recommended, since alkalinization of urine reduces the conversion of sodium urate into 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 complete normalization of uric acid levels when they increase significantly. The decrease in uric acid content only when following a diet is small.
Basic therapy for gout consists of long-term use of medications that normalize the level of uric acid in the blood. The issue of indications for the use of anti-gout drugs remains controversial. In patients with rare attacks (without tophi and chronic arthritis) when the level of uric acid in the blood is below 0.4-7 mmol/l, one can limit oneself to diet only. However, according to WN Kelley, anti-gout drugs are indicated in the tissues and development of gouty nephropathy.
The basic principle of basic therapy for gout is long-term and almost continuous use of anti-gout drugs throughout the patient’s life, since after their withdrawal the uric acid content again reaches its previous levels and gout attacks resume.
All anti-gout drugs used for long-term treatment of gout:
Curicodepressive drugs include allopurinol and its analogues milurite, thiopurinol, as well as hepatocatalase and orotic acid. The most effective of these drugs is allopurinol (hydroxypyrazolopyrimidine). The mechanism of allopurinol suppression of uricosynthesis is not only the inhibition of the enzyme xanthine oxidase, but also 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 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 level of uric acid in the blood to normal over several days and 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 reduction 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 for secondary gout caused by diuretins or blood diseases when treated with cytostatics, when, under the influence of the use of these drugs, 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 normal levels of uric acid in the blood). The drug is well tolerated. Allergic reactions (itching, skin rash, allergic Quincke's edema) are observed only occasionally.
All of the above also applies to the Hungarian drug milurite, an analogue of allopurinol. Thiopurinol (mercaptopyrazolopyramidine) reduces uricemia as effectively as allopurinol, but is much better tolerated by patients. The mechanism of its action consists mainly in inhibition of the synthesis of new purines due to inhibition of the aminotransferase enzyme. 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 phosphoribosol pyrophosphate (usually no 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 beef liver preparation 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, 10,000-25,000 units.
The group of uricosuric drugs includes drugs such as anturan, ketazone, probenecid (benemide), etamide, and acetylsalicylic acid. The general mechanism of their action is a decrease in tubular reabsorption of urate. resulting in increased excretion of uric acid by the kidneys. However, it has been established that their mechanism of action is more complex. Thus, ketazone, probenecid and anturan appear to reduce the binding of urates to plasma proteins and, therefore, increase their filtration by the glomeruli.
The disadvantage of all uricosuric drugs is that by increasing the secretion 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 drugs in case of high levels of uric acid in the urine (over 3.5-6 mmol/day), and it is better to prescribe uricodepressive drugs to these patients.
The use of uricosuric drugs should 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 renal failure if the patient has a “gouty kidney”.
Probenecid (benemid) is a benzoic acid derivative that is 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). A daily dose of this drug has a rapid uricosuric effect within 24 hours. Benemide is quite well tolerated, but in some cases it can cause disturbances (skin rashes, itching, fever, etc.).
While taking probenecid, patients should not be prescribed acetylsalicylic acid, which interferes with the uricosuric effect.
Anturan (sulfinpyrazone) is an analogue of phenylbutazone. It has been used as a uricosuric agent since 1958. It is used in tablets of 100 mg (no more than 600 mg/day). Its uricosuric effect is longer lasting than probenecid, 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, and leukopenia. Acetylsalicylic acid is also an antagonist of the uricosuric action of anturan.
Probenecid and anturan are contraindicated in cases of renal failure, urolithiasis, gastritis, gastric and duodenal ulcers, hepatitis, and leukopenia.
The Soviet drug etamide has a weaker uricosuric effect than previous drugs. 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, minor 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 long-term treatment of gout.
All uricosuric drugs reduce hyperuricemia less actively than uricodepressive drugs. When using them, the level of uric acid in the blood rarely decreases below 0.36 mmol/l.
With long-term use of anti-gout medications against the background of an anti-gout diet, a decrease in the level of uric acid in the blood, a reduction in attacks or even their complete disappearance, and a decrease in the manifestations of chronic arthritis are achieved. Due to a decrease in tissue infiltration with urates, the “punches” on the radiograph may decrease or even disappear. There is a softening and reduction in the size of the 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, attacks of gout, 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, patients must simultaneously be prescribed continuous colchicine therapy in small doses (1 mg/day) in the first months of treatment.
Choice of medications 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 the internal organs, the presence of allergies, and the individual reactivity of the patient.
With a mild course of the disease (rare relapses, 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 medications such as orotic acid, etamide, which are well tolerated by patients . With moderate and severe cases and higher levels of hyperuricemia, it is necessary to continuously take active medications. The correct choice of a specific therapeutic drug can be made only after a thorough clinical and laboratory examination of the patient, determining not only the level of uric acid in the blood, but also its daily excretion in the urine and its clearance.
With the metabolic type of hyperuricemia with a high level of uric acid in the blood with good secretion and good clearance (uricuria over 3.5-6 mmol/day, clearance 6-7 ml/min), the patient should be prescribed drugs that reduce the synthesis of uric acid during long-term treatment , i.e. allopurinol, milurite or thiopurinol. Anturan, probenecid and other uricosuric drugs are not indicated in these cases. They should be prescribed when there is insufficient excretion of uric acid in the urine - less than 3.5-6 mmol / day (renal type of hyperuricemia), but only to patients who do not have renal failure and kidney stones, diseases of the liver and gastrointestinal tract. In the presence of this pathology, only uricodepressive drugs (allopurinol, etc.) are used. If a patient with high hyperuricemia has a reduced secretion 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 adjusted depending on the content of uric acid in the blood and in daily urine. The use of anti-gout drugs is continued for a year, after which you can take a break for 2 months (if the uric acid level is normal) or prescribe another drug.
Physical and resort factors. A patient with gout is a patient in whom, along with uric acid metabolism, other types of metabolism are often disrupted, which aggravates the course of gout. This necessitates the use of general impact factors that improve metabolism and blood circulation. In the presence of chronic gouty arthritis and secondary osteoarthritis, patients, in addition. need physiotherapy and balneotherapy that have a resolving and analgesic effect. Such means can be prescribed diathermy, iontophoresis with lithium, phonophoresis with hydrocortisone, mud and paraffin baths, diadynamic currents, massage, exercise therapy.
By improving local metabolism, tissue trophism and blood circulation, these procedures help reduce pain and inflammation. Processes in the periarticular tissues are improved (Puncture of the joints. General radon or hydrogen sulfide baths are especially indicated for patients with gout, which have a general effect on metabolism and blood circulation, which helps to improve metabolic processes, reduce signs of arthritis, resolve tophi, improve the general condition of patients. It is better to take balneotherapeutic procedures in resort conditions (Pyatigorsk, Sochi, Essentuki, Tskhaltubo, etc.) annually.Physiobalneotherapy should be used against the background of ongoing treatment with anti-gout drugs.
Surgery. For large tophi and massive infiltration of periarticular tissues, especially with skin ulceration and the presence of fistulas, surgical removal of urate deposits is recommended, since these formations usually do not resolve with the use of anti-gout drugs; they can become infected and significantly limit joint function. Sometimes, in the presence of significant destruction of the cartilage and epiphyses, which disables the patient, it is necessary to resort to reconstructive surgical operations such as arthroplasty, etc.
In some patients, especially with good excretion of urate by the kidneys, gout for many years proceeds easily - without the formation of tophi, arthropathy, without kidney pathology; patients remain able to work for a long time. In more severe cases (with massive tophi with destruction of the joint and especially with the development of a gouty kidney, severe atherosclerosis of the coronary or cerebral vessels), the patient may become disabled within several years.
The life expectancy of patients with gout depends on the development of renal and cardiovascular pathology. Literature data indicate that the most common cause of death in patients with gout is uremia, which develops as a result of gouty nephropathy (up to 41% of patients). However, it is believed that patients die no less often from coronary disease or from cerebrovascular complications.
If there is a person with gout in the family, then it is advisable to examine all family members and immediate relatives (brothers, sisters) to identify asymptomatic hyperuricemia. If the level of uric acid in the blood is high, it is recommended to limit the consumption of alcohol and foods rich in purines and fats. With hyperuricemia (more than 0.5-3 mmol/l) and especially with the development of kidney stones (even before a gout attack), long-term use of allopurinol is necessary to prevent gout; Sports activities, systematic gymnastics, and walking are recommended, which increases the release of uric acid from the body.
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