X-ray sign of joint damage in gout. X-ray method in the diagnosis of diseases of the joints Gouty arthritis x-ray

Definition. Gout- a disease of heterogeneous origin, characterized by the deposition in various tissues of urate crystals in the form of sodium monourate or uric acid (Bunchuk N.V., 1997).

Historical information

The term gout comes from the Latin "gutta” (drop) and reflects the idea that the disease is the result of fasting malicious infusion (drop by drop). Another name for gout is also known - “the disease of kings”.

In the history of the study of gout, the following milestones can be distinguished ( M. coher, B . Emmerson, 1994):

5th century BC - description of gout by Hippocrates ("Gout is not bald and not a eunuch");

3rd century AD - Galen : describes tophi;

1679 - Van Leeuwenhoek identifies crystals in tophi;

1798 - Wallaston: revealed the presence of uric acid in tophi;

1814 - shows the effectiveness of colchicine in gout;

1913 - Folin, Denis offer a biochemical determination of the concentration of urate in the blood serum

1936 - Prophylactic efficacy of colchicine noted;

1963 Rundles proved the effectiveness of allopurinol for the prevention of gout attacks;

1967 - Kelly revealed etiopathogenetic deficit value hypoxanthylguanine phosphoribosyl transferase (GKGFT) for the development of gout.

Prevalence

Gout mostly affects men over 40 years of age. Women get gout about 20 times less often, but after 50 years this ratio decreases slightly. The rarer development of gout in women is due to the greater excretion of urate in the urine due to the effect of estrogens.

According to an epidemiological study conducted in the 1980s in the USSR, the frequency of gout among residents over the age of 15 was 0.1%, which is higher than in Japan (0.05%), but lower than in most European countries and USA (0.5-3.5%). In certain ethnic groups of residents of Polynesia, the Philippines and New Zealand, the incidence of gout reaches 10%. A study of the dynamics of incidence in the United States showed an increase in the frequency of gout - from 1967 to 1992. 7 times. An upward trend in incidence has also been noted in other developed countries.

Etiology

The determining factor in the development of gout are different in origin disorders of uric acid metabolism(synthesis and / or excretion), leading to a persistent increase in its level in the blood - hyperuricemia . Allocate primary and secondary gout (and hyperuricemia). Secondary gout is recognized when it is one of the syndromes of another disease, in which, for one reason or another (congenital or acquired), disturbances in the metabolism of uric acid occur. For example, secondary gout due to increased formation of uric acid develops in acute and chronic leukemia, multiple myeloma, lymphoma, kidney carcinoma and other malignant tumors, hyperparathyroidism, psoriasis, hemoglobinopathies, von Willebrand disease and some other diseases. Chronic renal failure is the most common cause of secondary gout due to slower excretion of uric acid by the kidneys. The development of secondary gout is also possible with sarcoidosis, hypothyroidism, salicylates, cyclosporine, and some other drugs.

In the case of primary gout, no diseases that could cause it are found. Among patients with primary gout, those who have increased urate synthesis make up only 10%. Specific enzymatic defects are detected in these patients only in isolated cases. In the vast majority of patients with primary gout, the cause of the disease is a violation of the excretion of uric acid by the kidneys. In these patients, both isolated defects in the various phases of uric acid excretion (decreased secretion, increased reabsorption) and combined disorders can be observed.

Persistent long-term hyperuricemia is a mandatory and main condition for the development of gout. In those who develop primary gout, hyperuricemia reaches its maximum severity by the age of 25, while the average age of patients with gout is approximately 47 years. The incidence of gout in individuals with hyperuricemia averages 2.7-12% and depends on the level of hyperuricemia. The development of primary gout requires a combination of hyperuricemia with such acquired factors in adult life as the consumption of large amounts of foods rich in purines, alcohol, overweight, which increase the already existing disorders of uric acid. There is a well-known aphorism: "Partners of hyperuricemia are friends of abundance."

Alcohol is one of the important factors contributing to the development of hyperuricemia. Mechanism hyperuricemic the effects of alcohol are presumably associated with an increase in the content of lactic acid, which makes it difficult for the kidneys to excrete urates ( J. Cameron et al ., 1981). In addition, alcohol contributes to the formation of urates, increasing the rate of ATP breakdown. Beer contains a significant amount guanosine-purine base, which becomes an additional load ( R. Janson, 1999).

It is widely believed that there is a direct relationship between a high level of uric acid in the blood and a person’s intelligence, about a special predisposition to the development of gout in men who have achieved success in life and have leadership qualities ( J. Wyngaarden, W Kelly , 1976). For example, Isaac Newton, Michelangelo, Benjamin Franklin, Charles Darwin suffered from gout.

The source of uric acid is purine bases (adenine and guanine) - components of nucleic acids (both endogenous and, to a much lesser extent, supplied with food), as well as purine nucleosides from which ATP is formed, and similar compounds. The metabolism of purine bases is regulated by several enzymes. Currently, the presence of two enzymatic defects has been proven, which are accompanied by a sharp increase in the synthesis of uric acid and the development of gout already in childhood: deficit hypoxanthine-guanine phosphoribosyl transferase (HCGFT) and increased activity of 5-phosphoribosyl-1-synthetase. These enzymes are controlled by genes associated with the X chromosome, so males are more likely to get sick.

It is well known that gout is often inherited: cases of this disease in relatives occur, according to various sources, in 6-81% of patients, and hyperuricemia is found in 25-27% of relatives of patients with primary gout. A six-generation family with gouty arthritis and progressive nephropathy has been described in Japan ( M. Yokota et al., 1991).

Information about the change in the main complex histocompatibility very little in patients with gout. A weak association of gout with HLA B 14 (B. Cassium et al., 1994).

Pathogenesis

If the content of uric acid in the blood or tissue fluid is more than 0.42 mmol / l (at a temperature of 37 0 C), there is a danger of urate crystallization. It remains unclear why some people with higher uremia do not develop either gouty arthritis or tophi. With a decrease in temperature, the crystallization of uric acid is facilitated, which explains the predominant deposition of urate crystals in avascular tissues (articular cartilage and cartilage of the auricles), in a relatively poor blood-supplied structures (tendons, ligaments) or relatively poorly blood-supplied anatomical areas (in particular, in the feet). The favorite onset of gout is from the metatarsophalangeal joints of the big toes, possibly due to the fact that it is in them that degenerative-dystrophic changes in the cartilage occur earlier and most often, which predisposes to the deposition of urates.

A gout attack is associated with the formation of sodium urate crystals ( M. Cohen et al ., 1994). The crystals are “coated” with a protein shell, as a result of which they have the ability to initiate inflammatory reactions.Ig G , adsorbed on crystals, reacts withFc-receptors of inflammatory cells, activating them, and apolipoprotein B, also included in the protein shell of urates, inhibits phagocytosis and cellular immune response. Thus, urates stimulate the production of chemotaxis factors, cytokines (interleukins 1,6,8 and tumor necrosis factor), prostaglandins, leukotrienes and oxygen radicals by neutrophils, monocytes and synovial cells. Cytokines cause an influx of neutrophils into the joint cavity, in addition, the complement system and the release of lysosomal enzymes by neutrophils are activated.

The very fact of the appearance of urate crystals in the joint cavity, apparently, is not enough for the onset of arthritis, since urate crystals are often found in the synovial fluid during the interictal period of gout (in about 52-58% - in the knee and first metatarsophalangeal joints).

self-passingthe nature of inflammation in the joint with gout is determined by the ability of phagocytes to digest crystals and the release of a number of anti-inflammatory factors, in particular platelet growth factor - beta. The predominant development of arthritis in gout at night is explained by the fact that tissue hydration decreases at rest and there is an increase in the concentration of uric acid in the joint fluid.

Uric acid lithiasis approximately 40% of patients with gout precede articular manifestations. Hyperuricemia plays an important pathogenetic role in the development of urolithiasis, but plays an even greater role hyperuricosuria . With the release of less than 700 mg of uric acid per day, urolithiasis is observed in 21% of patients, and with the release of 1100 mg / day or more - in 50% of patients ( T.-F. Ju, A . b. Gutman, 1987). Other predisposing factors include impaired solubility of uric acid due to acidic urine. Stone formation is also facilitated by urinary stasis (congenital anomalies of the urinary tract, prostatic hypertrophy, etc.) and its infection.

Kidney damage in gout can be presented urate nephropathy, for which the deposition of monosodium urate crystals in the interstitial tissue is typical. Of primary importance in its origin is chronic hyperuricemia. The deposition of microtophi in the interstitium predisposes to arterial hypertension. Another type of kidney damage is characterized by the formation and deposition of uric acid crystals in the collecting ducts, calyces, pelvis, or ureter. Since both types of kidney damage in gout are often detected in one patient, this division is conditional.

Pathological picture

During acute gouty arthritis, urate crystals are found in the superficial layer of the synovial membrane. Synovitis is nonspecific. Histopathological changes include fibrin deposits, synovial cell proliferation, and marked neutrophilic leukocyte infiltration. Even in the early stages, infiltration by lymphocytes and plasma cells can be seen. Tophi in the synovial membrane are usually observed in patients with repeated attacks of gout. In tophi, there is a large accumulation of urate crystals, surrounded by granulomatous tissue containing giant multinucleated cells. In some cases, over time, tophi can calcify and even ossify. Joint damage in chronic gout is characterized by significant destruction of cartilage, and often subchondral bone, changes in tendons, ligaments and synovial bags.

Clinical picture

It is customary to count the onset of gout from the first attack of arthritis, although before that, on average 10 years earlier, 10-40% of patients develop one or more renal colic caused by urate lithiasis.

There is a classic description of a typical gout attack: “The victim goes to bed and falls asleep in good health. Around two in the morning she wakes up with pain in her big toe, less often in her heel or ankle. This pain is similar to that which occurs when the joint is dislocated, another part of the patients compares the pain with the feeling of cold water pouring on the joint. This is followed by chilliness and a feeling of trembling with low temperature. The pain, which is mild at first, gradually becomes intense. After a while, the attack peaks, bones, ligaments of the metatarsus and tarsus are involved. Now - this is an incredible tension of the ligaments and the feeling that the latter are torn apart - this is already a gnawing pain. So a refined and cheerful person, stricken with a disease, sleeps off his feet. He can't put on heavy night clothes, he can't walk around the room, everything gets on his nerves.

The night passes in torment, without sleep, the patient constantly changes position, which leads to constant pain in the joints and worsening of the attack. From this time on, all efforts aimed at relieving pain by changing the position of the trunk or limbs remain in vain ”( J. Wyngaarten et al.,1976).

With gout, acute and chronic arthritis is distinguished.

Acute arthritis. For the first "attack" of gout in men, monoarthritis and predominant damage to the joints of the foot are typical. Acute arthritis of the joints of the big toe during the entire period of the disease is observed in almost all patients, but during the first attack of gout it is observed only in 50%. Less typical for gout is inflammation of the elbow and wrist joints. Oligo- or polyarthritis at the onset of gout in men is not typical, but is typical for women. Another feature of gout in women is the more frequent involvement of the joints of the hands. In both men and women, the first to be affected with gout are those joints that were previously changed for some reason. It is known, for example, the involvement of the distal interphalangeal joints of bones altered due to osteoarthritis.

In classic cases, suddenly, often at night or early in the morning, a sharp pain develops in one joint, usually in the lower limb. The pain quickly, within a few hours, increases to intolerance, there is a pronounced swelling of the affected joint, usually accompanied by reddening of the skin over it. Movement in the inflamed joint becomes almost impossible, as well as support on the affected limb. The pain is significant even without movement, often its intensification is caused even by a light touch of the joint with a blanket. Pain, swelling of the joint and hyperemia of the skin over it can be so pronounced that they resemble phlegmon. During an attack of gout, moderate fever, leukocytosis, and an increase in ESR are often noted.

A characteristic feature of gouty arthritis is the spontaneous (without treatment) complete regression of symptoms in a few hours or more often in a few days.

The course of untreated gout is very variable. The most characteristic is the constant increase in the "attacks" of arthritis, a tendency to their more protracted nature. In rare cases, there is a clinical course of gout with an almost complete absence of light intervals between attacks of arthritis and the rapid development of tophi.

The development of acute gouty arthritis is facilitated by any abrupt changes in the content of uric acid in the blood, both upward and downward, and the latter, perhaps even to a greater extent. Acute gouty arthritis can be triggered by trauma, exercise, emotional stress, sudden changes in diet (both overeating and fasting), drinking alcohol, bleeding, infections, myocardial infarction, surgery (usually after 3-4 days), certain drugs (diuretic, mainly thiazide, vitamin B 12, allopurinol, chemotherapeutic anticancer drugs, intravenous heparin, cyclosporine, administration of protein drugs), as well as radiation therapy.

Allocate atypical forms of gout(V.A. Nasonova, M.G. Astapenko, 1989): rheumatoid-like, pseudophlegmonous, polyarthritic(migratory), subacute form, asthenic, periarthritic a form with localization of the process in the tendons and bursae (most often in the calcaneal tendon) with intact joints.

Chronic gout. It is characterized by the development of certain permanent manifestations of the disease: tophi(significant accumulations of urate crystals) of various localization, chronic arthritis, kidney damage or urolithiasis. From the first "attack" of the disease to the development of chronic gout, an average of 11.6 years passes (from 3 to 42 years). The rate of progression of the disease depends on the severity of hyperuricemia and kidney damage.

The most frequent localization of subcutaneous or intradermal located visible during direct examination tophi- in the area of ​​the fingers and toes, knee joints, protrusions on the ulnar surface of the forearms, as well as synovial bags (especially the elbows), tendons and auricles. Tophi are often concentrated around persistently altered joints. Sometimes the skin over the tophus can ulcerate, while their contents are spontaneously released, which have a pasty consistency and white color. It should be noted that intraosseous tophi, found only on radiographs, can often develop earlier than subcutaneous ones. There are known clinical descriptions of tofus lesions of the spine, compression of the spinal cord, changes in the myocardium, heart valves, conduction system, various structures of the eye and larynx. In very rare cases, tophi are determined before the development of gouty arthritis.

Joint damage . Chronic arthritis and gout can involve a variable number of joints. The small joints of the hands and feet are often affected. Articular syndrome may include destructive signs, deformity and stiffness joints. Infiltration of articular tissues with urates is accompanied by an inflammatory reaction of the tissues surrounding the joint.

An X-ray examination helps to assess changes in the joints in detail. Gout is characterized by intraosseous cystic formations of various sizes, caused by tophi. Chronic gouty arthritis may be accompanied by cartilage destruction (narrowing of the joint gap) and the development of marginal bone erosions. Over time, pronounced destruction is noted not only subchondral part of the bone, but also the entire epiphysis and even part of the diaphysis ( intra-articular osteolysis). At the same time, there is a significant expansion of the “corroded” articular sections of the bones and sharpening of their edges. The so-called “punch” symptom is marginal bone erosion or cystic formations of the correct form with clear, sometimes sclerosed contours - observed in gout infrequently and nonspecific. Bone ankylosis in gout is extremely rare. X-ray changes are most pronounced in the joints of the feet (primarily in the joints of the thumbs) and hands. More rare localization of radiographic changes in gout are the shoulder, hip, sacroiliac joints and spine. Bone changes in gout rarely improve with specific therapy. Tophi located in soft tissues can also be detected by X-ray, especially if they are calcified.

Main x-ray signs of gout summarized in Table 1.

Table 1.

X-ray signs of gout
( M. Cohen and B. Emmerson , 1994)

Kidney damage. Factors favoring the development of nephropathy in gout are uricosuria over 700 mg/day. diuresis and decrease Ph urine (X. Kappen, 1990). Massive "excretion" of uric "acid" can lead to damage to the tubular apparatus of the kidneys and, secondarily, to the interstitium of the kidneys. Later, damage to the glomeruli may occur with the development immunocomplex jade. Gout is characterized by a predominance of disorders of tubular functions (especially a violation of the concentration function) over a decrease in glomerular. The most common sign of renal dysfunction in gout is mild proteinuria, which occurs in 20-40% of patients with gout and may be intermittent. The more pronounced the clinic of articular gout, the more significant the damage to the kidneys. With tofus gout, proteinuria, slight disturbances in the concentration function and a decrease in glomerular filtration are observed. Over time, changes in the kidneys gradually increase. Among the clinical manifestations of gout, it is nephropathy that most often determines the prognosis of the disease. Approximately 10% of patients with gout die of kidney failure. With the development of severe renal failure, there is a tendency to infrequent development of acute arthritis. Hemodialysis also leads to a decrease in articular "attacks".

According to Shukurova S.M. (1997), echolocation of the kidneys revealed changes in 75.4% of cases. Stones were determined with the greatest frequency (in 1/3 nephrolithiasis was bilateral). In 23% of cases, changes in the pelvicalyceal segments and calculi were simultaneously detected, which, in combination with leukocyturia, made it possible to discuss the diagnosis of concomitant pyelonephritis. Kidney cysts were determined in only 13% of patients.

Accompanying illnesses. Common diseases associated with gout include obesity, arterial hypertension, hyperlipidemia, impaired glucose tolerance (metabolic syndrome), and coronary heart disease.

According to epidemiological studies, approximately 78% of gout patients are over 10% overweight, and 57% are over 30% (Brochner-K. Morteus, 1984). Reduced glucose tolerance is found in 7-74% of patients with gout, although diabetes mellitus develops infrequently.

Hypertriglyceridemiaobserved in 50-75% of patients with gout, and hyperuricemia in 82% of patients with hypertriglyceridemia. Especially often this type of hyperlipidemia in gout is observed in patients who abuse alcohol. Although a number of patients with gout also have hypercholesterolemia, several studies have shown no correlation between uricemia and cholesterol levels.

Arterial hypertension is noted in ¼-½ of patients with gout. This may be due to decreased renal blood flow. Obesity may be an important link between arterial hypertension and hyperuricemia. In turn, hyperuricemia is detected in 22-38% of patients with arterial hypertension. It is assumed that an increase in the level of uric acid in the blood may be an indicator of damage to the vessels of the kidneys (or renal tubules) in arterial hypertension.

It is noted that young patients with coronary heart disease often have hyperuricemia. More than half of the causes of death in patients with gout are cardiovascular diseases.

Diagnostics. The most common criteria for the diagnosis of gout, adopted at the international symposium in Rome (1961):

Hyperuricemia- uric acid in the blood more than 0.42 mlmol/l in men and more than 0.36 mlmol/l in women

Presence of gouty nodules (tophi)

Detection of urate crystals in synovial fluid or tissues

A history of acute arthritis accompanied by severe pain that began suddenly and subsided in 1-2 days

/ The diagnosis of gout is considered reliable if any two signs

Later, S. Wallace et al. (1974), also proposed to take into account the peculiarities of the course of gouty arthritis - unilateral lesion I metatarsophalangeal joint, accompanied by redness and pain, the maximum development of symptoms on the first day, asymmetric changes in the joints on the x-ray, the absence of flora when sowing the joint fluid.

In an acute attack of gout, an increase in the level of uric acid in the blood is usually noted, but the normal value of this indicator is no exception. Of greatest value in the diagnosis of gout is polarizing microscopy of synovial fluid and other tissues (for example, tophi), in which it is possible to detect characteristic urate crystals that have a needle-like shape, and most importantly, peculiar distinctive light-optical properties - negative birefringence and a number of others. The main diagnostic value is the detection of intracellular crystals, and their extracellular location may be accompanied by asymptomatic hyperuricemia (5%) or chronic renal failure (approximately 20%). The sensitivity of this study is 69%, the specificity is about 97% ( C. Gordon et al ., 1989). The threshold concentration of urate crystals in the synovial fluid, still available for identification, is about 10 µg/ml. There are cases of acute arthritis in gout, when using polarizing microscopy, urate crystals were not detected due to their small size, but were detected by electron microscopy. Errors are possible in the presence of other crystals in the synovial fluid, in particular lipid ones. It is especially easy to identify urate crystals in superficially located tophi using polarizing microscopy.

It is important to determine the daily excretion of uric acid in the urine. Normally, after a 3-day restriction of purines in the diet, 300-600 mg (1.8-3.6 ml mol) of urates are excreted, and with normal nutrition - 600-900 mg. It is advisable to conduct this study before dieting and 7 days after it (meat, meat soups and sauces, poultry, fish, legumes, oatmeal, tea, coffee, cocoa, alcohol are excluded). Initially and in dynamics simultaneously determine the volume of urine, Ph urine, uric acid and creatinine levels in the blood. It has been established that with an increase in the daily excretion of urate in the urine of more than 1100 mg, the risk of kidney damage is 50%.

The therapeutic effect of colchicine is of particular importance in the diagnosis of acute gouty arthritis. However, it should be borne in mind that a striking effect with gout is not always observed and, conversely, with pyrophosphate arthropathy and calcifying tendonitis colchicine can be very effective.

Treatment

Treatment of gout involves a differentiated strategy depending on the stage of the disease - an acute attack or an interictal period, a tofus form.

Allocate main tasks in the treatment of goutPanrotsky J., 1996):

End an acute attack as soon as possible;

- Prevent relapse.

Prevent or reduce the manifestations of chronic gout, primarily the formation of kidney stones and tophi.

In a number of gout patients with relatively low hyperuricemia and infrequently recurrent arthritis, measures such as dietary restrictions, weight loss, refusal to drink beer and strong alcoholic beverages can bring a significant therapeutic effect and should be tried before prescribing drugs, but even very strict a low-purine diet can reduce uricemia by no more than 0.06 mlmol / l, and daily uricosuria - by no more than 200-400 mg, which is clearly not enough in most patients. Dietary recommendations include the exclusion of broths and sauces, the restriction of meat and fish products, legumes, strong coffee and tea, and alcohol. The amount of proteins is reduced to 1 g / kg, fat - less than 1 g / kg, the need for calories is satisfied mainly due to carbohydrates. A slight increase in the amount of fluid you drink (up to 2-3 liters per day), regular visits to the bath or sauna are useful, which contributes to the extrarenal excretion of uric acid. It is also important to control the maintenance of normal body weight and blood pressure, glucose and blood lipids. An important place in the treatment of gout is occupied by the education of the patient, the purpose of which is to understand the role of various factors that positively and negatively affect his disease.

Before choosing a therapy, each patient with gout should be properly examined. The magnitude and persistence of hyperuricemia and daily uricosuria, kidney function and the state of the urinary tract should be analyzed, the stage of the disease and concomitant diseases should be determined.

Treatment of asymptomatic hyperuricemia . To address the issue of treatment tactics, the results of determining the daily excretion of uric acid in the urine are of primary importance. When a persistent hyperuricosuria more than 900 mg per day, which is not eliminated by a low-purine diet, the question of the constant use of allopurinol should be considered. If the daily excretion of uric acid in the urine is not increased, then anti-gouty drugs are not indicated and a low-purine diet, weight loss and other preventive measures are of primary importance in the treatment.

Management of acute gouty arthritis usually administered with colchicine or non-steroidal anti-inflammatory drugs (NSAIDs). It is believed that colchicine is able to eliminate the symptoms of acute gouty arthritis in about 80% of patients within 48 hours after the start of therapy. In the case of using the drug in the first few hours after the onset of an attack, the effectiveness increases to 90%. The physician prescribing colchicine must be aware of the patient's comorbidities. Colchicine (Colchicum - Dispert,Solvay Pharma) is administered orally, at an initial dose of 0.5 mg (in accordance with the recommendations of other authors - 1 mg). Then, every hour, an additional 0.5 mg of the drug is prescribed (or 1 mg of the drug every 2 hours) until the arthritis is completely relieved or until diarrhea (vomiting) appears, but not less than 6-8 mg per day. The dose of the drug should be reduced with a decrease in creatinine clearance below 50-60 ml / min. In most patients, the effect is already noted from 0.5 mg of colchicine and becomes distinct by 12 hours of treatment. For more than one day, colchicine is usually not used to treat a gout attack. Perhaps parallel use in acute gouty arthritis of colchicine in small doses (0.5 mg 2 times a day) and NSAIDs. Sometimes, when oral colchicine cannot be administered, for example, after surgery, the drug is used intravenously.

Among NSAIDs, preference is given to drugs with a rapid onset of action and the most active in anti-inflammatory respect: diclofenac sodium and phenylbutazone, but not acetylsalicylic acid. Diclofenac sodium at the first appointment, it is prescribed orally at a dose of 50-100 mg or intramuscularly at a dose of 75 mg. Phenylbutazone (butadione) - at a dose of 0.3 g. Then, if necessary, every 2-3 hours, NSAIDs are repeated: diclofenac sodium at a dose of 25-50 mg up to 200 and even 400 mg per day, and phenylbutazone - up to 0.6 g in 3-4 doses. Due to frequent adverse reactions (edema, arterial hypertension, gastrointestinal disorders, hematological disorders), phenylbutazone is almost never used. For the relief of acute gouty arthritis, ibuprofen at a dose of 2,000-3,200 mg / day can also be used, taking into account the good tolerability of the drug. For all NSAIDs, the same principle remains as for colchicine - the earliest possible appointment at a sufficiently high initial dosage.

An acute attack of gout can be stopped by injecting into the inflamed joint glucocorticosteroids, having previously evacuated the synovial fluid, as well as prescribing these drugs orally (prednisolone 20-40 mg for 3-4 days) or intramuscularly. This method of treatment should be resorted to if colchicine or NSAIDs are ineffective or poorly tolerated.

Treatment anti-gouty means ( allopurinol, benzbromarone) is carried out only after the relief of gouty arthritis, usually not earlier than after 3 weeks.

Treatment of frequently recurrent gouty arthritis. With absence hyperuricosuria, signs of kidney damage and urolithiasis There are two possible approaches to treatment.

The issue of starting specific therapy is resolved positively with a significant severity of uricemia (more than 0.6 mlmol / l) and the presence of tophi. In this situation, it is possible to use both allopurinol and uricosuric funds.

The dose of allopurinol is selected individually. Most often, it is recommended to start treatment with the appointment of 0.3-0.4 g of the drug per day, once. Sometimes a smaller dose is enough. The effectiveness of treatment is monitored by repeated determination of the level of uric acid in the blood. The desired level of this indicator is less than 0.36 mlmol / l (in men), and the ideal level is within the range of 0.24-0.3 mlmol / l. It must be borne in mind that the dissolution of urates in the extracellular fluid and tissues occurs only if the uricemia is less than 0.42 mlmol / l. Usually, under the influence of allopurinol, the level of uric acid decreases after 24-48 hours and normalizes when an adequate dose is selected after 4-14 days. The selection of a maintenance dose of allopurinol is carried out so as to ensure not only a stable normal level of uricemia, but also to prevent recurrence of arthritis and kidney damage. Resorption of subcutaneous tophi is observed no earlier than after 6-12 months of continuous allopurinol therapy. In this situation, the choice between allopurinol and uricosuric drugs are administered empirically.

probenecidappoint an initial dose of 0.25 g 2 times a day. Uricosuric The effect of the drug develops after 30 minutes. After 3-4 days, with insufficient reduction in uricemia, every 1-2 weeks increase the dose of the drug by 0.5 g. The disadvantage of the drug is often developing resistance to treatment.

Treatment sulfinpyrazone start with a dose of 0.05 g, appointing it 2 times a day. The first dose of the drug is recommended to be taken as early as possible in the morning, and the last - as late as possible in the evening. After 3-4 days, in the absence of a sufficient decrease in the level of uric acid in the blood, the daily dose sulfinpyrazone gradually, every week, increase by 0.1 g. But not more than 0.8 g / day, increasing the number of doses during the day to 3-4. Usually the maintenance dose of the drug is 0.3-0.4 g / day.

Benzbromarone (hipurik, dezurik, normurat) compares favorably with others uricosuric means of prolonged action, can be administered 1 time per day. The usual dose is 0.08-0.1 g per day, the maximum is 0.6 g.

In the treatment of gout, it is possible to use a combination of allopurinol with uricosuric means (usually sulfinpyrazone or with benzobromarone, but not with probenecid), as well as a combination of individual uricosuric funds among themselves. However, a significant “benefit” from combination therapy for gout is usually not achieved.

In primary gout, drugs are usually prescribed for lifelong daily intake, their cancellation or interruptions in treatment lead to a rapid (within 1-3 weeks) increase in the level of uric acid in the blood and the resumption of the clinical manifestations of the disease. In the first days and weeks of treatment, any antigout drugs can provoke the development of gouty arthritis. Therefore, at first, either colchicine (1.5 mg per day) or NSAIDs in average daily doses are additionally prescribed. While taking anti-inflammatory drugs, the amount of fluid you drink should be increased to 3 liters / day, so that the daily amount of urine would be at least 2 liters. It is important that diuresis is sufficient at night.

If uricemia does not reach 0.6 mlmol / l, no hyperuricosuria and tophi , for constant use, colchicine is prescribed at a dose of 0.5-1.5 mg / day or NSAIDs in medium doses, and a low-purine diet is also recommended. The advantage of this non-specific therapy lies in the good tolerability of the drugs. placebo controlled The study showed that prophylactic administration of colchicine at a dose of 0.5 mg 2 times a day prevented arthritis relapses in 74% of patients and reduced their severity in 20%. Colchicine is generally well tolerated when taken long-term at the indicated dose.

With increased excretion of uric acid in the urine and / or in the presence of kidney damage due to urolithiasis preference is certainly given to allopurinol. Uricosuric funds are contraindicated. When choosing the dose of allopurinol in patients with reduced kidney function, it is conditionally considered that every 30 ml / min of filtered urine corresponds to a daily dose of the drug, which is 0.1 g. Allopurinol can lead to the gradual dissolution of existing urate stones, reduce the severity of gouty kidney damage, and also prevent the formation of both uric acid and oxalate stones. In the first weeks of allopurinol therapy in such patients, especially with a significant severity of kidney damage or urolithiasis, the appointment of agents that increase the solubility of uric acid in the urine is indicated. More often they use a mixture of citrate salts (magurlite, uralit- U etc.), which increases Ph -urine to alkaline values, optimum Ph is 6-7. These drugs are taken before meals, 3-4 times a day, 2-3 hours before the maximum value. Ph urine. The daily dose of citrates is usually from 6 to 18 g. Contraindications are acute and chronic renal failure and urinary tract infection. These drugs also reduce the saturation of urine with calcium oxalate, nucleation and crystal growth of this composition. The dose is selected individually, under control Ph urine. It is possible to use sodium bicarbonate for the same purpose at a dose of about 2 g per day, until alkaline values ​​\u200b\u200bare reached. Ph urine. Rapid and effective alkalinization of urine can also be achieved with the help of the diuretic drug acetazolamide (diacarb, etc.). It is administered orally at a dose of 125-250 mg every 6-8 hours. Due to the rather sharp and rapidly advancing increase Ph urine carbonic anhydrase inhibitors (acetazolamide) are usually prescribed to patients with severe urolithiasis, when it is especially important to achieve alkalization of urine at night, as well as in acute renal failure in patients with "gouty kidney". Acetazolamide is used short-term, usually within 3-5 days. If necessary, the drug is repeated after a break of 2-3 days.

Allopurinolis the drug of choice in patients with secondary gout that develops in hematological diseases or malignant tumors of any localization during the period of active cytotoxic or radiation therapy, when the risk of developing acute gouty nephropathy sharply increases.

Treatment of "acute gouty kidney". Treatment of acute renal failure due to blockade intrarenal urine outflow with urate crystals is classified as critical and requires immediate intensive care. The patient must be urgently hospitalized. Measures are being taken to stimulate forced diuresis - intravenous administration of a large amount of fluid and the simultaneous use of saluretics in large doses (furosemide up to 2 g per day). Allopurinol is prescribed orally at a daily dose of 8 mg / kg and urine alkalizing agents (sodium bicarbonate intravenously, acetazolamide orally). The ongoing therapy is considered effective if diuresis of at least 100 ml per hour is achieved within 1-2 days. In the absence of the desired effect, hemodialysis is used.

The prognosis of gout in most cases is favorable, especially with timely recognition and rational therapy. Most predictively unfavorable factors are considered: early development of the disease (up to 30 years), persistent hyperuricemia exceeding 0.6 mlmol / l, persistent hyperuricosuria exceeding 1.100 mg / day, the presence of urolithiasis in combination with urinary tract infection, progressive nephropathy, especially in combination with diabetes mellitus and arterial hypertension.

LITERATURE:

1. WyngaardenJ.D., Kelly W.N. Gout and Hyperurecemia. New York, Grune and Stratton, 1976.

2. Kelly W.N., Schumacher H.R. Gout - In: Textbook of Rheumatology Fourth Edition. Ed. Kelly W. Et al., WB Saunders Co. - 1993.-p. 1291-1336

3. Gordon C. et al. Detection of crystals in synovial fluids by light microscopy: sensitivity and reliability// Ann. Rheum. Dis. - 1989. - Vol. 48.-p.737-742

4. Bunchuk N.V. "Microcrystalline arthritis"// In the book "Rheumatic diseases" Nasonova V.A., Bunchuk N.V. / Moscow. "Medicine" - 1997. - p. 363-374

5. ShukurovaCM. ed. prof. Alekberova Z.S. "Gout" - Moscow, Institute of Rheumatology RAMS, 1997. - 71 p.

6. PawlotskyJ. Treatment of gout.// Rheumatology in Europe. - 1996. - Vol.25. - p.142-144

7. BalkrovTHEM. Allomaron in the treatment of hyperuricemia // Clinical pharmacology and therapy. - 1993. Volume 3, No. 1. - p.35

8. Benevolenskaya L.I., Brzhizovsky M.M. "Epidemiology of rheumatic diseases".// Moscow. "Medicine" - 1998. - p.240

9. Mukhin N.A. "Gout yesterday and today".// "Clinical Medicine" - 1991. - No. 5. - p.103-107

10. Mukhin N.A., Balkarov I.M., Maksimov M.L. Clinical manifestations of disorders of purine metabolism in the practice of an internist.// Ter. Archive. - 1994. - No. 1. - p.35-39

11. Mukhin N.A. Gout - is it only a disease of the joints?// Clinical pharmacology and therapy. - 1994. - No. 1. - p.31-33

12. Nasonova V.A. Diagnosis and treatment of gout.// Ter. Archive. - 1987. - No. 4. - p.3-7

13. Allen M., Reid C., Gordon T. et al. Does colchicine work? Results of he first controlled study in gout.// Aust N.Z. J.Med. - 1987. - vol.17. - p.301-304

14. Curatino C., Rucci C., Giacomello A. Relationship between fractional urate excretion and serum tryglyceride concentration.// Ann. Rheum Dis. - 1996. - vol. 55 - p.934

15. Batuman V. Lead nePhropathe gout and hypertension.// Am. J. Med. Sci. - 1993. - vol.305. - p.241-247

16. Nishioka K. Hyperuricemia and atherosclerosis.// Nippom Rinsho. - 1993. - vol.51. - p.2177-2181

17. Peters T., Ball G. Gout and hyperuricemia .// Current Opinion in Rheumat . - 1992. - vol.4. - p.566-573

18. Cameron J. What is the pathogenesis of familial gouty nePhropathy .// Adv. Exp. Med. Biol. - 1991. - vol. 309A. - p.185-189

Joint diseases are one of the most common in the world. And gout is also the most painful of them. The disease affects both young and elderly patients. And this is due to malnutrition and the abuse of fast food.

The main reason for the development of the disease is a violation of metabolic processes in the body. An increased content of uric acid and its salts leads to the formation of crystals that destroy the cartilage tissue of the joint and lead to the formation.

Interesting!

Pathologies of the central nervous system (central nervous system), thyroid gland and brain can provoke gouty arthritis.

Incorrect or late diagnosis of gout and the lack of adequate treatment increases the risk of complications.

Diagnosis of gout

It is quite difficult to identify gout on your own. Only an experienced specialist can exclude other diseases with similar symptoms and diagnose gout. Diagnosis begins with a visual examination of the patient and the collection of anamnesis.

Interrogation of the patient

During the interview of the patient, the doctor finds out what symptoms bother him, how they manifest themselves. At the initial stage of the disease, small joints on the legs and arms are affected, then the disease spreads to large joints.

The diagnostic criterion for gout is the presence of genetic determinism. If close relatives of the patient have been diagnosed with gout, then the risk of developing this particular ailment increases.

The doctor also finds out previously transferred diseases that can provoke gouty arthritis. These include:

• Surgical operations;
• Kidney dysfunction;
• Long-term use of antibiotics or steroids.

It also turns out that the patient has bad habits, food addictions.

Clinical researches

An experienced doctor can identify gout without testing. However, it is possible to make a final diagnosis, determine the acute or chronic form of the course of the disease only on the basis of the results of the tests. For differential diagnosis, the following examinations are prescribed:

• Biochemical blood test for gout for uric acid, sialic acids, fibrin and the presence of protein (with C-reactivity). Such self-diagnosis is used to determine the quantitative indicators of urates and their presence in the bloodstream. For men, the norm of uric acid is 460 μM / l, for women the normal values ​​​​are lower - 330 μM / l. Guided by one biochemical analysis, it is impossible to diagnose gout of the joints. But an elevated level of urate indicates dysfunction of the urinary tract and disruption of the kidneys. The pathology of the kidneys is also indicated by a decrease in the level of creatinine (normally it is 115 mmol / l). Additionally, a biochemistry analysis shows the amount of nitrogen, ammonia, glucose, lipids and bilirubin. A sharp increase in their indicators indicates a violation of the functioning of various body systems;

Interesting!

With the development of gout, the results of the analysis for biochemistry look like this: the amount of protein during an attack significantly exceeds the norm, in some, an increase in glucose and creatinine is noticeable. Calcium, lipids, lipoproteins will also be overestimated.

• General blood test. Quantitative indicators of neutrophils in the blood test for gout help to identify inflammation in the joint. This research method is effective for kidney dysfunction. An indicator of gout in the general blood test is the presence of crystalline urates in the resulting sediment;

On a note!

A high concentration of urates in the blood indicates the development of gout of the joints.

• Urinalysis for gout allows you to clarify the cause of the pathology. The results of the analysis show the amount of uric acid and the overall level of acidity. Urine is given during the day. This helps to explore the change in acidity results throughout the day.

Attention!

An increase in indicators indicates the development of urolithiasis.

• Puncture of synovial fluid. This method allows you to diagnose gout joints. In a healthy person, synovial fluid has no color, but resembles water in consistency. A change in color and a decrease in fluidity indicate an increase in acidity, a metabolic disorder. The analysis also shows the level of neutrophilic lymphocytes;
• X-ray is used to diagnose gout of the joints of the lower extremities, as well as fingers. The picture shows the development of the pathological process in the joint, the deposition of salts. Radiographic signs of gout include white spots, with a diameter of 0.5 millimeters to 3 centimeters. They are due to the presence of tophi, resulting from the deposition of uric acid salts in the periarticular tissues. The formation of tophi takes about five years. Exacerbation of gout can accelerate their formation. Sometimes an x-ray image captures the complete or partial destruction of the endocrine gland, and its cells are replaced by uric acid crystals. X-ray examination will be effective for all joints. It helps to determine the type of gout, fix the transition of the disease to the periarticular bag or tendons and the occurrence of inflammation in them. In this case, an additional biopsy test is prescribed;

Interesting!

The symptom of a gout punch is known as a phenomenon of the late stage of the disease. This is the “bone” on which the joint rests at the base or head of the phalanx. Such a defect can be up to 5 millimeters in diameter. In most cases, it is located in the first metatarsophalangeal joint of the foot.

• Ultrasound and tomography - this technique is used only during an exacerbation of gout. During an attack, the interarticular gap noticeably increases, swelling, thickening and inflammation of the soft tissues near the affected joint are observed. Such a clinical picture can be observed a week after an acute attack of gout. But during remission, ultrasound will not fix changes. In chronic gout, with the help of ultrasound, it is possible to notice the deformity of the joint, as well as the presence of an inflammatory process. Also, the analysis allows you to determine the deposition of salts in the kidneys and ureter;
• A biopsy is a highly accurate analysis that allows you to identify quantitative indicators of uric acid deposits in the joints. For analysis, intra-articular fluid is taken. This technique allows you to clarify the cause of the development of gout.

On a note!

What tests need to be done for gout, the attending physician will tell you. He will draw up a scheme for conducting studies to clarify the diagnosis, especially with secondary gout.

Rules for preparing for analyzes

Analyzes for gouty arthritis are given comprehensively. Otherwise, their results may be unreliable. This will lead to misdiagnosis and ineffective treatment. In order for the analyzes to be the most informative, the following rules should be observed:

• Eliminate the use of alcohol for at least a day before taking tests;
• Reduce the intake of foods containing high doses of vitamin C, otherwise deviations from the norm may be overestimated;
• Caffeine can also interfere with test results. Therefore, it is recommended to give up coffee and tea 8-10 hours before their delivery;
• Aspirin increases the level of acidity, so you should refuse it;
• Diuretics lower test levels;
• All tests for gout should be taken on an empty stomach. The last meal should be no earlier than 8-10 hours before delivery;
• Following a diet for 2-3 days before testing minimizes the distortion of test results. The use of vegetable and lactic acid products is recommended;
• You should also refrain from excessive exercise before conducting research.

Attention!

Compliance with the rules for preparing for analyzes is a guarantee of the reliability of the results, the correct diagnosis and the appointment of adequate treatment.

False results

Failure to comply with the rules for preparing for the delivery of tests can lead to a change in their results:

• Uric acid levels are elevated;
• X-ray or ultrasound before testing may affect their results;
• Abuse of fatty foods, alcohol consumption provoke distortion of research results;
• During gout therapy, tests will not be effective.

The patient should be aware that chronic gout of the joints cannot be completely cured. But with the help of therapeutic methods, you can reduce the number of acute attacks, reduce pain.

Attention!

Self-medication is unacceptable. This can cause the progression of the disease and the development of complications. Uncontrolled intake of drugs can distort the results of tests, artificially lowering their performance.

The appointment of adequate therapy for gout is possible only by a specialist, based on the results of the tests and instrumental studies. Gouty arthritis does not always have visual manifestations, so it is very difficult to diagnose it only during a medical examination. A comprehensive examination allows you to diagnose the disease, identify its stage, the presence of concomitant diseases.

6879 0

Radiological manifestations of gout first described by G. Huber in 1896. Later, many studies were carried out that showed that at an early stage of the disease there are no characteristic changes. Then, radiographs show signs of bone and cartilage destruction due to the deposition of sodium urate crystals in the subchondral bone.

X-ray picture of gouty arthritis of the feet

X-ray picture of gouty arthritis of the right leg

• I - large cysts in the subchondral bone and in deeper layers. Sometimes soft tissue hardening;
• II - large cysts near the joint and small erosions on the articular surfaces, constant compaction of the periarticular soft tissues, sometimes with calcifications;
• III - large erosion, but less than 1/3 of the articular surface, osteolysis of the epiphysis, significant compaction of soft tissues with lime deposition.

More recent is the classification proposed by M. Cohen, V. Emmerson (1994), according to which the following are the main radiological signs in gout:

• in soft tissues - seals;
• eccentric darkening due to tophi;
• bones (joints) - the articular surface is clearly presented;
• juxta-articular osteoporosis is absent;
• erosion (punch, marginal sclerosis).

Thus, the presented classifications are significantly different and require the unification of a number of radiological signs in gout.

Instrumental and laboratory research.

In a clinical blood test during acute attacks of gout, patients reveal leukocytosis with a neutrophilic shift to the left and an increase in ESR.

In the blood serum, an increased content of uric acid is determined: in men, more than 7 mg% (0.42 mmol / l), in women - 6 mg% (0.36 mmol / l). A uric acid excretion study should be performed after a 3-day purine-free diet (meat, broths, fish, poultry, legumes, tea, coffee, cocoa, alcohol, beer). The volume of daily urine, pH, concentration of uric acid and creatinine in urine and blood serum are determined. Normally, 300-600 mg (1.8-3.6 mmol / l) of uric acid is excreted per day.

In the contents of tophi, crystals of uric acid are found. It should be borne in mind that during histological examination of tophi tissues, they should not be fixed with formalin in order to avoid dissolution of urate crystals.

Typical are intraosseous racemose formations of various sizes, caused by tophi. Chronic gouty arthritis may be accompanied by cartilage destruction (narrowing of the joint space) and the development of marginal bone erosions. A characteristic sign - "a symptom of a punch" - marginal bone or racemose formations of the correct form with clear, sometimes sclerotic contours, over time, a pronounced destruction is formed not only in the subchondral area of ​​​​the bone, but also in the epiphysis and even in the diaphysis, forming intra-articular osteolysis. Radiologically, the most pronounced pathology is observed in the joints of the feet (primarily in the joints of the thumb). Rarely, radiological changes in the shoulder, hip, sacroiliac joints and spine can occur. Bone changes in gout rarely decrease with specific therapy.

The study of synovial fluid.

The current literature on the composition of synovial fluid in patients with gout indicates the importance of its study for the diagnosis of joint diseases. According to many researchers, the detection of urate crystals in the synovial fluid and especially in leukocytes is specific for gout. Of diagnostic importance is the detection of needle-shaped urate crystals located intracellularly and birefringent light when examined using a polarizing microscope. The threshold concentration of urate crystals in the synovial fluid, still available for identification, is about 10 µg/ml.

The sensitivity of this test ranges from 85-97%.

Another important indicator of synovial fluid for an acute attack of gout is its cellular composition, mainly the number of leukocytes, which reaches the following values: from 10. 10 9 to 60 10 9 /l, with a predominance of neutrophils.

Joint diseases
IN AND. Mazurov

The disease of modern society is gout, which belongs to the group of metabolic diseases. The disease is characterized by a long and persistent course and is capable of provoking severe destructive processes in the joints.

Here it is worth mentioning for the first time the true enemy of mankind - gouty arthritis.

The essence of the disease

The inflammatory manifestation of gout or gouty arthritis develops in the process of accumulation of uric acid crystals in the joints, which subsequently has a devastating effect on the periarticular tissues and hyaline cartilage.

In more detail, the list of pathological changes accompanying the development of the disease consistently includes:

• an increase in the amount of uric acid in the blood;
• the accumulation of its crystals in the joints;
• irritation, subsequent damage to the structure of the joints and the launch of the inflammatory process;
• gradual development of consequences;
• the appearance of periarticular tumor-like growths.

The toes are most commonly affected, but the hands and fingers may be affected. Gouty arthritis of the knee, elbow and ankle joints is extremely rare, and the disease does not affect the pelvic region and shoulders at all.

Causes and forms of the disease

The reasons for the development of the disease have not yet been fully identified. However, it has been proven that the onset and course of the disease is significantly influenced by the hereditary factor, as well as metabolic processes in the body.

Among the clearly negative factors, peculiar triggers:

In addition to the traditional acute and chronic forms of gouty arthritis, there are also:

1. Rheumatoid-like, the course of which is characterized by its own duration. The inflammatory process develops in the area of ​​the wrist, metacarpophalangeal and interphalangeal joints.
2. Pseudophlegmonous, in which only one joint (large or medium) is affected. There are local or general reactions of the body: swelling, redness of the skin in the area and outside the joint, hyperleukocytosis, fever.
3. Subacute, characterized by implicit clinical symptoms. The lesion is concentrated in the area of ​​the big toe.
4. Aesthetic, which is characterized by a slight reddening of the skin, the absence of swelling, the average degree of soreness of the affected area.
5. Periarthritis. In this case, the inflammatory process extends to the bursae and tendons localized in the area of ​​intact joints.

Symptoms of the disease

The developing disease includes the following three stages:

1. Latent (the content of lactic acid increases, salts accumulate in the area of ​​bone and cartilage tissues and joint bags). Symptoms are most often absent.
2. Acute, in which severe pain is observed, joints and adjacent tissues become inflamed.
3. Chronic, characterized by long periods of remission.

The first symptoms of gouty arthritis are acute.

Among them:

• pain in the joint area;
• skin redness;
• increased soreness of the affected area during movement;
• increase in body temperature.

After a few days, acute symptoms reduce their severity to almost complete disappearance of discomfort.

At this stage, the following symptoms may appear:

• the formation of tophi (subcutaneous formations) in the area of ​​the damaged joint, their breakthrough;
• an increase in the duration of the period of exacerbation of the disease;
• reduction of intervals between attacks;
• destruction of the structure of hyaline cartilage and the development of a chronic form of the disease.

At the last stage of the development of arthritis, the skin in the area of ​​\u200b\u200bdiseased joints becomes rough, dry, and itching may appear.

The mobility of the limbs is largely limited due to the deformation of bone and cartilage tissues and the progression of arthrosis of the joints.

Diagnosis of the disease

The key point in diagnosing the disease is the detection of urate salts in the synovial fluid of the joints.

In addition, a biochemical blood test and a urinalysis are performed to assess the amount of uric acid. The contents of tofus may also be examined.

In the case of a long course of the disease, an X-ray examination is prescribed. With a positive result, the image shows bone defects, cartilage destruction, and punches.

Treatment Method

The treatment of gouty arthritis has a number of goals:

• normalization of metabolism in the patient's body;
• relief of the acute form of the disease;
• restoration of the functionality of the affected internal organs;
• treatment of a chronic disease.

A set of measures to combat the disease, first of all, includes drug therapy:

• anti-gout agents to eliminate pain and activate the process of excretion of urates;
• NSAIDs (Diklak, Voltaren, Movalis, etc.) to relieve swelling, inflammation and pain;
• glucocorticosteroids (hydrocortisone) in case of severe pain, are injected once into the affected area.

As the symptoms of the acute form subside, basic therapy is prescribed:

In the treatment of gouty arthritis, physiotherapy and hardware procedures cannot be dispensed with. During the period of exacerbation of the disease, electrophoresis and ultraviolet irradiation are prescribed.

At the stage of remission - mud applications, the use of mineral waters, radon and bromine baths.

Taking into account the fact that one of the causes of the development of the disease is malnutrition, it is impossible to completely recover from the disease without following certain dietary rules.

Patient's lifestyle

For effective treatment, the patient should pay close attention to their weight. In case of its increase, you need to take care of yourself.

Follow a diet, spend more time outdoors, visit a bathhouse (sauna) more often, do warm-ups regularly and do not forget about therapeutic exercises.

Do:

• swings and circular rotations with hands;
• flexion and extension of the joints of the arms and legs;
• finger rotation;
• lifting legs (lying down);
• bicycle exercise.

Traditional medicine to help

In parallel with the main therapy, you can help yourself with folk remedies:

1. A decoction of onion peel. Pour a glass of husk with a liter of boiling water and put on fire for ¼ hours, then filter and take ½ cup several times a day.
2. Chamomile with salt. 2 tbsp. l. chamomile flowers pour a glass of boiling water and leave for 1.5 hours, then mix ½ cup with salt (1 cup) and water (10 l.). We take baths in the morning and evening.
3. We rub sore spots with salted fat.

Complications

All complications that can overtake the patient can be divided into three groups:

• articular (development of the process of joint deformation);
• renal (the occurrence of urolithiasis and gouty kidney, which entail the development of arterial hypertension);
• other complications (formation of tophi in other tissues and organs).

Prognosis for the patient

The prognosis in this case is generally favorable. Among the disappointing factors in the development of the disease:

• age up to 30 years;
• the presence of persistent hyperuricemia and hyperuricosuria;
• urolithiasis and urinary tract infection;
• nephropathy in an advanced stage.

In 20-25% of clinical cases, urolithiasis develops.

Preventive measures

Fundamental preventive measures in the case of gouty arthritis are:

• maintaining a healthy lifestyle;
• dieting;
• control of body weight (elimination of sudden jumps in weight);
• increased motor activity;
• organization of the regime of work and rest;
• fight stress.

Gouty arthritis is a very serious disease, the development of which can be caused, at first glance, by trifling factors.

The emergence of suspicions of an ailment must necessarily be followed by timely diagnosis and treatment, otherwise the further course of the disease can lead to the final immobilization of the limbs.

• General information
• Causes
• Development and classification
• Types of disease
• Symptoms
• Treatment

If crystals of a substance known as calcium pyrophosphate dihydrate are deposited in the human connective tissue, then we are dealing with pyrophosphate arthropathy.

General information

Imagine that you are under 55 years old. Most likely, the disease will bypass you. With age, the frequency of crystallization increases - this is evidenced by X-ray data. The disease belongs to the group of so-called microcrystalline arthritis. Doctors distinguish 3 clinical variants of this disease:

• pseudogout;
• pseudo-osteoarthritis;
• pseudorheumatoid arthritis.

Over time, chronic arthropathy may develop. Acute attacks of pseudogout have also been observed. Young people (20-30 years old), teenagers and children are not susceptible to chondrocalcinosis.

Causes

There is no clear information about the causes of crystallization of the bone structure. However, there are reasons to believe that a number of factors contribute to this. Let's list some:

• age (over 55 years);
• hereditary predisposition (autosomal dominant trait);
• joint injury;
• hemochromatosis (clearly associated with chondrocalcinosis);
• endocrine and metabolic disorders;
• Gitelman's syndrome (canalicular renal pathology of a hereditary nature);
• hypocalciuric hyperkalemia (familial);
• hypothyroidism.

Development and classification

The accumulation of crystals is carried out in cartilage, which is located near the surface of chondrocytes. One of the probable mechanisms of crystallization is an increase in the activity of nucleoside triphosphate pyrophosphate hydrolase enzymes. Enzymes of the mentioned group are saturated with vesicles formed as a result of the breakdown of collagenase (concentrated in the articular cartilage).

If you carefully examine the crystals through a microscope, you will notice that they have a rhombic (or rectangular) shape and differ significantly from monosodium urate, which has an acicular structure.

PFA (pyrophosphate arthropathy) is divided into primary and secondary. Primary PFA is familial, and secondary PFA is associated with metabolic diseases:

• hemochromatosis;
• primary hyperparathyroidism;
• Konovalov-Wilson disease;
• hypomagnesemia;
• hypophosphatasia.

Symptoms

One of the main symptoms is an acute gouty attack. It always develops suddenly, for no apparent reason. The disease is accompanied by:

Often the knee joint is affected, but in some cases the big toe, small and large joints suffer. In the case of calcification of the intervertebral discs, there is a possibility of developing a radicular syndrome.

Arthritis is sometimes quite intense, which entails its erroneous diagnosis as "septic". The disease develops spontaneously, sometimes - after suffering a cerebral crisis, heart attack or phlebitis. In 25% of cases, a pseudogouty form is observed, in 5% - pseudorheumatoid.

Diagnostics

The affected area is the wrist, shoulder, knee or metacarpophalangeal joints. The following types of examinations help to identify the disease:

1. Physical. The affected joint is characterized by swelling, soreness, the joint is asymmetric or deformed. With pseudoarthrosis, swelling of Bouchard's and Heberden's nodules is traced.
2. Laboratory. The main symptom is the presence of crystals in the synovial fluid. When they are detected, the most popular method is polarizing microscopy.
3. Instrumental. X-rays of the pelvis, joints and hands are taken. The goal is to identify specific and non-specific features.
4. Differential. There is a comparison of PFA with septic and rheumatoid arthritis, gout, osteoarthritis.

Treatment

With the ineffectiveness of therapy and exacerbation of the disease, hospitalization is required. In addition, practice:

• Medical treatment.
• Non-drug treatment.
• Surgical intervention.

The chances of recovery are very good. Practice shows that 41% of patients are on the mend. Surgery is required in 11% of cases.

W A disease that occurs due to a violation of the metabolism of purine bases in the body.

• In 40% of cases, it is combined with calcium phosphate deposition disease (as an additional factor in favor of metabolic disease).
• Gouty arthritis - arthropathy with deposition of urate crystals in and outside the joint (eg, in the kidneys)
• Manifests in 10% of patients with hyperuricemia (uric acid levels greater than 6.4 mg / dl, in 20-25% of the male population, especially in prosperous nations)
• Men are affected 20 times more often than women
• Age of onset of gout: after the age of 40 (in women, after menopause)
• In 60%, the disease affects the metatarsophalangeal joints of the big toe (gout on the legs)
• Also commonly affects the ankle (gouty arthritis of the ankle), knee, and metacarpophalangeal joint of the thumb
• This metabolic disease is based on an imbalance between the production and excretion of uric acid.
• When the serum concentration reaches the solubility limit, urate crystals are deposited in the tissues
• Phagocytosis of urate crystals by leukocytes
• Apoptosis with the release of enzymes and mediators that cause damage to the joint.

Primary (familial) hyperuricemia:

• The frequency is 90-95%
• Enzyme defect impairs uric acid excretion or uric acid overproduction
• Violation of the diet in gout.

Secondary hyperuricemia:

• kidney failure
• Diseases with accumulation of high levels of purine derivatives (myeloproliferative and lymphoproliferative disorders)
• Use of cytostatics and diuretics
• Psoriasis
• Endocrine disorders (eg, hyperparathyroidism)
• Alcohol consumption.

Acute gout:

• trigger factors include excessive fluid intake and food cravings ("hunger and overeating"), as well as stress.

CT and MRI diagnosis of gouty arthritis

Selection Methods

• X-ray examination in two projections

What will x-ray show with gouty arthritis

• Early stage or acute gout: asymmetric swelling of the soft tissues in the joint area.
• Late stage gout: latent course for 4-6 years in cases of inadequate gout treatment
• (Para-)articular, well-defined erosive lesion, often with sclerotic borders
• An overhanging margin without overt osteoporosis may be present
• Secondary degenerative changes in the joints during the course of the disease
• Absence of periarticular osteopenia
• Perhaps a combination with chondrocalcinosis.
• Tophi: inflammatory foci in soft tissues surrounded by urate crystals
• Calcifications in damaged kidneys
• Styloid tophi: styloid reaction of the periosteum
• Bone tophi: well-circumscribed, rounded osteolytic lesion with/without sclerotic ring.

Launched gout. X-ray examination of the hand shows pronounced gouty changes in the middle finger. Marginal erosion and swelling of the soft tissues around the metacarpophalangeal joint of the index finger. The "thorn" is defined in the second metacarpal bone. Chondrocalcinosis of the articular disc of the distal radioulnar joint. Destruction is determined in the distal radioulnar joint. Cystic destruction is visualized in the distal ulna

Patient with established gout. X-ray examination of the foot shows erosive changes in the medial part of the first metatarsal head with degenerative changes, which is an indicator of the presence of gout in addition to valgus deformity of the big toe.

a-c Typical signs of a lesion of the big toe in a patient with gout: a - Soft tissue swelling around the metatarsophalangeal joint associated with gout; b ) Radiolucent area in the head of the first metatarsal bone, caused by the formation of a gouty focus in the bone marrow, as well as moderate bony outgrowths in the medial part; c) Manifest erosion; d ) Image in the form of a "halberd" with a common tofus; e ) Pronounced gouty destruction of the metatarsophalangeal joint with saucer-shaped flattening of the articular surfaces and a spiky gouty focus on the proximal phalanx.

What will ultrasound of the joints with gout show

• Hyperechoic gouty nodes (tophi) in soft tissues
• The central acoustic shadow is formed by a centrally located crystal.

What will MRI images of the joints show with gout

• In patients with an unidentified underlying disease, an MRI is necessary to rule out a malignant process.
• Preoperative study to better assess the prevalence of tophi and their relationship with adjacent anatomical structures
• Tophi have heterogeneous signal intensity, possibly hypointense in T2-weighted sequence
• Urate crystals have a low signal intensity.
• Soft tissue: moderate increase in MR signal intensity on T1-weighted image
• More pronounced enhancement of signal intensity in T2-weighted image
• Severe accumulation of contrast agent.

Clinical manifestations

Clinical classification distinguishes four stages:

• Asymptomatic hyperuricemia (significantly more common than overt gout).
• Acute gout.
• Interictal stage (interval between two attacks of gout).
• Chronic gout with the formation of tophus (gouty focus) and irreversible changes in the joint.

Acute gout:

• sudden attack, often at night, extremely painful arthritis in one joint
• Redness
• Local temperature increase
• Swelling
• Generalized signs of the inflammatory process (fever, leukocytosis, increased ESR).

Chronic gout:

• pain syndrome in the joint
• Gouty tophus
• Rarely occurs at present (in patients with inadequate treatment).

Treatment Methods

Diet therapy: weight loss, low purine diet for gouty arthritis, avoidance of alcohol

Drug therapy is aimed at treating the above symptoms of gout: NSAIDs and colchicine in the acute stage;

Long-term therapy with uricostatic drugs, as well as drugs that promote the excretion of uric acid

Course and forecast

• Favorable prognosis with adequate prevention and treatment of signs of gout
• Left untreated or inadequately treated, gouty arthritis can lead to progression of symptoms and chronic damage to the joints and kidneys.

What the attending physician would like to know

• The severity of the joint injury
• In some cases - confirmation of the preliminary diagnosis.

What diseases have symptoms similar to gouty arthritis

pseudogout

Analysis of synovial fluid

No increase in uric acid concentration

Usually no erosive changes

Acute arthritis in one joint/oligoarthritis

Clinical manifestations, no increase in uric acid concentration

Periostitis and bone outgrowths in seronegative spondyloarthropathy

Erosive changes are usually not clearly defined

Active osteoarthritis (first metatarsophalangeal joint)

No erosive changes

Less severe soft tissue swelling (first metatarsophalangeal joint)

Misinterpretation of the lesion as evidence of active osteoarthritis or acute arthritis involving one joint instead of acute gouty arthritis.