Medication relief of an acute attack of gout

Gout is a disease associated with impaired metabolism of special nitrogen-containing substances - purine bases. Purine bases are part of nucleic acids - DNA and RNA, which are responsible for the storage, transmission and implementation of hereditary information in each cell. With gout, the end product of purine base metabolism, uric acid, accumulates in the body.

Uric acid in excess amounts is deposited in the form of crystals, most often with the formation of gouty nodes (tophi) in small joints, causing their inflammation (gouty arthritis), as well as in the kidneys, which leads to the development of urolithiasis. In later stages, uric acid crystals are deposited in other organs and tissues (especially in cartilage, near joints).

Gout is accompanied by severe pain in the affected joints (usually the small joints of the toes or hands), which occurs in the evening, intensifies at night and subsides in the morning. In this case, there may be an increase in temperature - fever.

To treat gout, a special group of drugs is used, called anti-gout drugs.

Classification of drugs for the treatment of gout

Antigout drugs are classified into:

• drugs that inhibit the formation of uric acid (uricodepressants): allopurinol, febuxostat;
• drugs that increase the excretion of uric acid (uricosuric drugs): citric acid + trisodium citrate + potassium bicarbonate, sulfinpyrazone, benzobromarone, probenecid;
• anti-inflammatory drugs: colchicine, glucocorticosteroids (prednisolone, triamcinolone, methylprednisolone), non-steroidal anti-inflammatory drugs (diclofenac, indomethacin, naproxen, ibuprofen, ketoprofen, nimesulide).

Pharmacotherapy of gout

Treatment of gout seems to be an exhausted topic. Over the past 25 years, not a single fundamentally new anti-gout drug has been created. However, practice shows that not all issues in the treatment of gout have been resolved. One of the important problems is timely and accurate diagnosis of the disease.

The most common are the so-called Rome diagnostic criteria for gout (1961) (see box). It is necessary to make a number of comments regarding these diagnostic criteria.

They do not take into account the kidney damage that naturally occurs with gout and, in particular, the significant fact that in 40% of patients the detection of kidney stones precedes the first articular attack. The upper limits of normal uricemia given in the Rome criteria were determined using manual methods (colorimetric and enzymatic uricase). The use of the now most common automated methods for determining uric acid has led to a recalculation of normal values ​​- they increase by 0.4–1.0 mg% or by 24–60 µmol/l (see table).

Errors in the diagnosis of gout result from ignorance of the fact that during an acute attack, the level of uric acid in many patients (according to various sources, in 39–42%) decreases to normal levels.

The most reliable diagnostic method is the detection of urate crystals using polarization microscopy

. But one must take into account the relatively low sensitivity of this research method (69%), the dependence of the results on the experience and thoroughness of the microscopist, as well as on the number of crystals and their sizes. Crystals of monosodium urate in the synovial fluid can be found (usually outside the cells) in patients with joint damage of other etiologies with concurrent asymptomatic hyperuricemia, for example, in psoriatic arthritis, hyperparathyroidism, sarcoidosis, malignant tumors, renal failure.

The striking effect of colchicine, previously considered a diagnostic sign of gout, is now not considered as such, as it can be observed in pseudogout and a number of other acute arthritis.

Methods for relieving acute gouty arthritis

There are two classic approaches to relieving a gout attack: colchicine or nonsteroidal anti-inflammatory drugs (NSAIDs)

.
It is now recognized that the overall effectiveness of these two methods is the same.
The differences are only in the speed of onset of the effect and tolerability. Colchicine begins to act faster: between 12 and 48 hours (NSAIDs - between 24 and 48 hours), but undoubtedly causes side effects more often. In the only double-blind, placebo-controlled study, colchicine

proved effective in 2/3 of patients with acute gout (placebo – in 1/3 of patients); treatment was more successful if it was started within the first 24 hours after the onset of the attack. More than 80% of patients experienced nausea, vomiting, diarrhea, or abdominal pain before complete resolution of arthritis (MJ Ahbern et al.). The standard method of using colchicine for an acute attack of gout is to administer 0.5 mg of the drug every hour. Treatment is carried out until the onset of effect, the development of side effects, or the maximum dose is reached (usually no more than 6 mg over 12 hours; in patients with renal failure and the elderly, the dose should be lower).

Among NSAIDs, preference is given to the most effective in anti-inflammatory terms: previously, as a rule, phenylbutazone was prescribed (now it is almost never used due to the risk of hematological complications), currently diclofenac sodium

or
indomethacin
(in doses up to 200 mg per day). There is a known method of simultaneous use of colchicine (in low doses of 1–1.5 mg per day) and NSAIDs.

Judging by survey data from American and Canadian doctors, the vast majority of them prescribe NSAIDs for acute gouty arthritis (E. McDonald and S. Marino; M. Harris et al.). In France, on the contrary, among 750 rheumatologists surveyed, 63% prefer colchicine, 32% prefer the combined use of this drug and NSAIDs, and only 5% prefer the isolated use of NSAIDs (S. Rozenberg et al.).

There are two alternative methods for relieving a gout attack: intravenous colchicine and the use of glucocorticosteroids.

(intra-articular, orally or parenterally) or
ACTH
.

The first report of the successful intravenous use of colchicine was published in 1954. After several years of enthusiasm for this method, it was almost abandoned due to the possibility of developing severe complications (primarily inhibition of hematopoiesis), in some cases leading to death. However, even now this method is still used, for example, in the development of severe arthritis after surgery, when other anti-inflammatory drugs are contraindicated.

It is recommended to strictly adhere to the following rules

(S. Wallace and J. Singer):

• a single dose should not exceed 2 mg, and the total dose should not exceed 4 mg (usually, 1 mg of colchicine dissolved in 20 ml of isotonic sodium chloride solution is first administered for at least 10 minutes);

• if the patient received colchicine orally the day before, this drug should not be used intravenously; after intravenous administration of a full dose, colchicine should not be used in any form for at least 7 days;

• in the presence of kidney or liver disease, the dose of colchicine should be reduced (by half if creatinine clearance is below 50 ml/min; if this figure is below 10 ml/min, colchicine is not used); in elderly patients, before intravenous use of colchicine, it is advisable to study creatinine clearance (if this is not possible, the dose is halved);

• Precautions should be taken to eliminate the risk of colchicine entering outside the vein. The onset of action of intravenously administered colchicine occurs within 6–12 hours.

It is much safer to use glucocorticosteroids. In addition to the long, although infrequently practiced, intra-articular administration of these drugs, they can be taken orally: prednisolone

in the initial daily dose of 30–50 mg. After 1–2 days, the dose is quickly reduced, and after an average of 10 days the drug is discontinued. The indication for this method of relieving a gout attack is the inability to use NSAIDs or colchicine due to intolerance to these drugs, renal failure or ulcerative lesions of the gastrointestinal tract (in the latter case, corticosteroids are administered parenterally). According to one study, oral prednisolone therapy led to improvement in all patients within 48 hours; complete disappearance of arthritis symptoms in most cases was noted on average after 3.8 days and no later than 7 days. Relapse of arthritis immediately after discontinuation of prednisolone was observed in only one case. Tolerability was good, side effects (transient hyperglycemia) were detected in only 1 of 12 patients (G. Groff et al.).

Anti-gout therapy itself

Despite many years of experience in gout therapy, two fundamental points remain not completely clear:

when to start treatment for bestophous gout, and which drug is best to choose in the absence of urate hyperexcretion.

An absolute indication for starting anti-gout therapy is the detection of tophi

(see picture).
From a practical point of view, it is advisable to classify as tophi not only subcutaneous nodules, but also destructive changes typical of gout, found on radiographs of the joints, as well as characteristic changes in the kidneys (urate nephropathy and urolithiasis). The latter is especially important, since it is kidney damage that determines the prognosis of gout
in many patients.
It is recommended to carry out appropriate examinations:
x-rays of those joints that were most often attacked, kidney studies and urine tests. It is well known that gouty nephropathy is characterized by an asymptomatic course. Therefore, it is important to pay attention to even small changes in urine tests (microproteinuria, microleukocyturia, microhematuria, and, especially, persistent sharply acidic reaction of urine - pH 4.5–5.5, with a norm of 7.4–7.5), carefully study the medical history (renal colic, pain in the kidney area, gross hematuria), do not forget to monitor blood pressure and conduct an ultrasound examination of the kidneys in search of stones.

In approximately 20% of cases, stones in patients with gout are composed of calcium oxalate and calcium phosphate. However, in most cases, a central urate “core” is detected in stones of this composition (S. Noda et al.), this explains the decrease in the incidence of calcium stones during treatment with allopurinol.

There are three different opinions regarding the time to start therapy for bestophous gout. According to the first, specific therapy should be delayed until symptomatic prophylactic treatment has been exhausted or tophi formation has been noted. This opinion is justified by the fact that tophi and chronic arthritis develop only in a minority of patients with gout.

Most experts make the prescription of anti-gout therapy dependent on the frequency of gout attacks during the year, considering the number 3-4 “critical”.

The third, less common opinion is that specific therapy should be started after the first joint attack, since even after the attack subsides, microtophus and urate crystals can be detected in the synovial membrane - a sign of chronic inflammation. However, there is no convincing evidence of the development of joint destruction in asymptomatic gout. Due to the fact that in some patients a second attack of gout may occur only many years after the first, and given the seriousness of the decision to use anti-gout therapy (lifelong nature, risk of adverse reactions), this approach to the treatment of gout is not used in practice.

Preventive anti-inflammatory therapy

Most often, it involves the daily use
of colchicine
in a small daily dose (0.5–1.5 mg). Tolerability of long-term use of colchicine in these doses is usually satisfactory; side effects (mainly diarrhea) are observed in only 4% of patients. The incidence of complications increases in case of impaired renal function. It is in these patients that depression of hematopoiesis, proximal myopathy (weakness in proximal muscle groups and increased creatine phosphokinase) and peripheral neuropathy more often develop. By 1990, 16 cases of death were known from complications of low-dose colchicine therapy. It is recommended to exercise caution in patients with impaired liver function, as well as with the simultaneous use of cimetidine, tolbutamide and erythromycin (they slow down the metabolism of colchicine).

Choosing between allopurinol and uricosuric drugs

To resolve this issue, they resort to measuring the daily excretion of uric acid.

This allows us to identify that relatively small subpopulation of gout patients in whom urate excretion is increased (more than 800 mg per day in the case of a study without dietary restrictions or 600 mg after preliminary use of a low-purine diet), which is considered a sign of overproduction of uric acid. Before this study, you should ensure normal renal function (in the case of decreased creatinine clearance, a decrease in uric acid excretion does not exclude its overproduction), and also exclude possible drug effects on the excretion of urate. It is believed that in such patients only allopurinol should be used, and uricosuric drugs are dangerous due to the increased risk of developing nephropathy and urolithiasis.

Allopurinol

.
The dose of allopurinol is selected individually and can range from 100 to 800 mg per day.
It is recommended to start therapy with a relatively small dose (100–300 mg per day), avoiding a very sharp decrease in uricemia: optimally no more than 0.6–0.8 mg% for 1 month of therapy. This helps reduce the risk of developing gout attacks after prescribing anti-gout drugs (N. Yamanaka et al.). When choosing the dose of allopurinol, you need to keep in mind that the maximum effect is achieved no later than 14 days. Side effects occur in approximately 5–20% of patients, with allopurinol discontinuation required in almost half of them. The most common are allergic skin rashes (usually maculopapular in nature), dyspepsia, diarrhea and headache. Serious complications are rare and are more common in renal failure and in patients taking thiazide diuretics. The greatest danger is represented by a symptom complex considered to reflect hypersensitivity to allopurinol: a combination of dermatitis, signs of liver damage, renal dysfunction, leukocytosis, eosinophilia or hematopoietic suppression.

Since in some patients allopurinol is the only effective drug in the treatment of gout, in the event of hypersensitivity to it, “desensitization” may be necessary, sometimes allowing therapy to be resumed. This procedure is advisable for the development of mild reactions, mainly recurrent dermatitis. Aqueous suspensions of the drug are prepared in very small concentrations (0.05 mg in 1 ml). Slowly (once every 3 days) and gradually (each time no more than 2 times) the concentrations of allopurinol are increased. The entire “oral desensitization” procedure takes about 30 days (T. Gillott et al.).

If there is no hyperuricosuria, allopurinol and uricosuric drugs are equally indicated, the choice between them being determined mainly by personal preference and the experience of the physician. Almost no objective comparisons have been made to fully weigh all the advantages and disadvantages of these two groups of funds. There is an opinion that it is preferable to prescribe uricosuric drugs to patients under the age of 60 years, with satisfactory renal function (creatinine clearance of at least 50 ml/min) and in the absence of urolithiasis.

Benzbromarone

. Benzbromarone receives the most attention for the following reasons:

• it not only enhances the excretion of urates by the kidneys (inhibits tubular reabsorption), but also inhibits the synthesis of purine bases and the absorption of uric acid from the intestine;

• its dose may not be reduced in case of moderate renal failure (unlike allopurinol);

• it is not characterized by serious adverse reactions (3-4% of patients develop diarrhea and itchy skin rashes);

• the drug is easy to use (the daily dose, usually 100–200 mg, is taken once).

The benefits of benzbromarone over allopurinol have been established in two recent studies. The first, an open-label, parallel-arm study, compared the effectiveness of benzbromarone (100 mg daily) with allopurinol (300 mg daily) in 86 men with chronic gout in the absence of uric acid hyperexcretion. With the help of benzbromarone, it was possible to achieve a more significant reduction in uric acid levels than with allopurinol treatment: uricemia decreased by 5.04 and 2.75 mg%, respectively. Improvement in renal function and the absence of new stone formation was noted only in patients receiving benzbromarone (F. Perez-Ruiz et al., 1998). It should be noted that the lack of effectiveness of allopurinol found in this study could have resulted from the use of an incomplete dose of the drug (no more than 300 mg). In terms of the degree of reduction in uricemia, benzbromarone (in a daily dose of 100–200 mg) was more effective than allopurinol (100–300 mg/day) also in patients with chronic gout in the presence of renal failure (F. Perez-Ruiz et al., 1999). Moreover, benzbromarone was effective in patients receiving diuretics (in these cases, the effect of allopurinol was clearly worse), and had a sufficient effect when allopurinol was ineffective.

Other uricosurics

Probenecid, the “oldest” uricosuric drug, is still used in the treatment of gout, with the use of which in 1949 the “era” of specific therapy for this disease began.

Probenecid

prescribed at an initial dose of 0.25 g 2 times a day. If the level of uric acid in the blood is not sufficiently reduced, the dose of the drug is increased by 0.5 g every 1–2 weeks (the maximum daily dose is 3 g). The disadvantages of probenecid are the often developing resistance, as well as the relatively frequent occurrence of adverse events (about 8% of patients have gastric dyspepsia, and 5% have allergic skin rashes). Rare serious adverse reactions include liver necrosis, nephrotic syndrome and aplastic anemia. Probenecid can prolong the effect of penicillin, cephalosporins, rifampicin and a number of other drugs, and also increases the blood concentration of naproxen and indomethacin. Acetylsalicylic acid completely blocks the uricosuric effect of probenecid.

Sulfinpyrazone

is an analogue of the metabolite of phenylbutazone, which explains the possibility of developing side effects such as inhibition of hematopoiesis and liver dysfunction, and has led to a gradual reduction in the use of this drug. The initial daily dose of sulfinpyrazone is 100 mg, divided into 2 doses throughout the day. After 3–4 days, in the absence of a sufficient decrease in the level of uric acid in the blood, the daily dose is gradually (every week) increased by 100 mg (but not more than 800 mg). The drug is able to inhibit platelet aggregation, which is valuable given the frequent presence of cardiovascular diseases in patients with gout. The most common side effect is gastric dyspepsia.

In the treatment of gout, it is possible to use a combination of allopurinol with uricosuric drugs

(usually with sulfinpyrazone or benzbromarone, but not with probenecid). This method is justified in particularly severe patients, after establishing torpidity to monotherapy. In these cases, careful selection of doses of individual drugs is required, since uricosuric drugs increase the excretion of allopurinol. A combination of individual uricosuric agents is also possible. There have been no special studies evaluating the advantages and disadvantages of such combinations of anti-gout drugs.

When prescribing both allopurinol and uricosuric drugs, two important circumstances should be remembered.

First. Due to the increased excretion of uric acid, already in the first days of using these drugs, the risk of stone formation and the development of urate nephropathy increases. In this regard, a preliminary examination of the condition of the kidneys and urinary tract is necessary (determining the level of creatinine, its clearance, ultrasound examination of the kidneys), as well as a study of urine pH. Paper analyzers, usually included with commercial citrate preparations, can be used to test urine pH. In patients with persistently low urine pH

(less than 6) before prescribing anti-gout drugs,
it is advisable to achieve its alkalization by using citrates
, sodium bicarbonate or acetozolamide (carbonic anhydrase inhibitor). These drugs are used by regularly checking the pH of the urine, the optimal level of which is 6.2–6.6. In order to prevent stone formation, it is also necessary to drink plenty of fluids (diuresis should be at least 2 liters per day). Preventive measures are taken during the entire period of selecting the optimal dose of the anti-gout drug (usually at least 1–2 months).

Second. After prescribing anti-gout medications for 6–12 months, the risk of developing gout attacks increases. Therefore, as a rule, it is recommended not to start therapy if arthritis is not yet complete.

colchicine
in small doses (0.5–1.5 mg per day) or NSAIDs for several months for prophylactic purposes The use of colchicine has been shown to prevent the occurrence of acute arthritis in approximately 85% of patients who are started on anti-gout therapy. At the same time, a number of experts express doubts about the advisability of mandatory use of preventive therapy, pointing to the relatively small risk of exacerbation of gout and the potential toxicity of colchicine.

Criteria for the effectiveness of anti-gout therapy

In the first months of therapy, the main criterion for effectiveness is the achievement of an optimal level of uric acid in the blood.

. It is no more than 6 mg% (in men), and ideally 4–5 mg%. If the concentration of uric acid does not fall below 6.8 mg%, the dissolution of urate in the extracellular fluid and tissues does not occur, and the risk of gout progression remains. After 6 months of therapy, its effectiveness is also determined by the reduction of gout attacks, the resorption of subcutaneous tophi, the preservation of renal function and the absence of progression of urolithiasis.

The list of references can be found on the website https://www.rmj.ru
References
1. Ahbern MJ, Reid C., Gordon TP Does colchicine work? Results of the first controlled study in gout. Austr. NZJ Med. 1987; 17: 301–4.

2. Gillott TJ, Whallett A., Zaphiropoulos G. Oral desensitization in patients with chronic tophaceous gout and allopurinol hypersensitivity. Rheumatology 1999; 38:85–6.

3. Groff GD, Frank WA, Raddatz DA Systemic steroid therapy for acute gout: a clinical trial and review of the literature. Seminars in Arthr. Rheum. 1990; 19: 329–36.

4. Harris MD, Siegel LB, Alloway JA Gout and hyperuricemia. Am. Fam. Physician. 1999; 15:925–34.

5. McDonald E., Marino C. Stopping progression to tophaceous gout. When and how to use urate-lowering therapy. Postgrad. Med. 1998; 104:117–27.

6. Noda S., Hayashi K., Eto K. Oxalate crystallization in the kidney in the presence of hyperuricemia. Scanning Microsc. 1989; 3:829–36.

7. Perez-Ruiz F., Alonso-Ruiz A., Calaabozo M. et al. Efficacy of allopurinol and benzbromarone for control of hyperuricemia: a pathogenic approach to the treatment of primary chronic gout. Ann. Rheum. Dis. 1998; 57:545–9.

8. Perez-Ruiz F., Calaabozo M., Fernandez-Lopez J. et al. Treatment of chronic gout in patients with renal function impairment: an open, randomized, actively controlled study. J. Clin. Rheumatol. 1999; 5:49–55.

9. Rozenberg S., Lang T., Laatar A., ​​Koeger AT et al. Diversity of opinions on the management of gout in France: a survey of 750 rheumatologists. Rev. Rhum. 1996; 63:255–61.

10. Singer JZ, Wallace SL The allopurinol hypersensitivity syndrome. Unnecessary morbility and mortality. Arthr. Rheum. 1996; 29:82–7.

11. Talbott JH, Terplan KL The kidney in gout. Medicine 1960; 39: 405–68.

12. Wallace SL, Singer JZ Review: systemic toxicity associated with the intravenous administration of colchicine – guidelines for use. J. Rheumatol. 1988; 15: 495–9.

13. Yamanaka H., Togashi R., Hakoda M. et al. Optimal range of serum urate concentrations ti minimize risk of gouty attacks during anti-hyperuremic treatment. Adv. Exp. Med. Biol. 1998; 431:13–8.

14. Yu: TF., Gutman AB Uric acid nephrolitiasis in gout: pridisposing factors. Ann. Intern. Med. 1967; 67:1133–48.

15. Yu: TF. Urolitiasis in hyperuricemia and gout. J. Urol. 1981; 126:424–30.

Gout Treatment Basics

Diet plays a major role in the treatment of gout. If you have gout, you should limit your consumption of foods rich in purines - red meat, legumes, cheese, cottage cheese, chocolate. In addition, you must avoid drinking alcohol (especially beer and wine).

If you have gout, it is important to maintain adequate water balance - drink at least two liters of water per day. Alkaline drinking is especially recommended (a teaspoon of soda per liter of water, alkaline mineral waters), since uric acid is more easily excreted in the alkaline environment of urine. In an acidic environment, uric acid precipitates in the form of crystals and is deposited in the kidneys.

Colchicine, glucocorticosteroids and non-steroidal anti-inflammatory drugs are used for an acute attack of gout.

During the interictal period, to reduce the level of uric acid in the blood and prevent gout attacks, drugs that inhibit the formation of uric acid - allopurinol and febuxostat - are used.

A combined drug containing citric acid, trisodium citrate and potassium bicarbonate is prescribed for urolithiasis to alkalize urine to facilitate the dissolution and removal of urinary stones.

Causes and symptoms of gout

Gout belongs to the group of arthritis. Arthritis is any disease of the joints. The term “gout” is used when talking about the deposition of uric acid salts in various tissues of the body, most often in joints and cartilage. Why does this process occur?

Uric acid is a product of the breakdown of purines - special substances that are produced in our body and also come to us with food. We get a large amount of purines when we eat fatty meat and fish (herring, sardines, cod), meat by-products (sausages, sausages), and fast food. And also when we drink alcohol (especially beer and grape wine), unnatural juices, sweet carbonated drinks, coffee. In this case, a huge amount of uric acid is synthesized in the body, and the kidneys cannot cope with its elimination. Another cause of gout is when the body produces a normal amount of this acid, but the kidneys are unable to remove it due to some pathology.

Uric acid salts (urates) are deposited in joints, especially small ones, gradually destroying them. Injured joints are most susceptible to salt deposition. The joint of the big toe (popularly called the “big bone on the foot”) is often the target of damage due to the fact that we wear uncomfortable, narrow shoes. Gout can also lead to the formation of kidney stones, which in turn lead to kidney failure, which in some cases causes death.

Symptoms of gout may include:

• acute joint pain (especially after eating heavy food or large amounts of alcohol). Sometimes the sensations are so unbearable that even having a sheet on your arm or leg hurts. The pain begins at night, goes away during the day, and then returns again. This can happen for several days or even months;
• redness and swelling of the joint;
• increased temperature in the joint area to 39–40° C;
• fever;
• general weakness.

If attacks are repeated again and again, then, for example, gout of the toe can spread to other joints, making them painful and inactive.

Gout is considered a disease of the elderly, but due to the fact that modern people consume a lot of fat and alcohol, in particular beer, this leads to a “rejuvenation” of the pathology. The disease is chronic, that is, it cannot be completely cured. But in order to avoid serious consequences, you should resort to therapy that will stop or slow down the process of joint destruction.

Gout as a joint disease

Gout is a joint disease associated with increased uric acid in the body. Its historical name is “disease of kings.” It was believed that rich people, leading an idle life, overeated and abused alcohol. The consequences were dire: pain in the joints due to salt deposits.

At one time, gout was considered a type of osteoarthritis. In the 17th century, doctors proved that this is a separate disease. The disease is typical for middle-aged males (40-45 years old). Women suffer during climate change.

Formation of tophi in gout

Nutrition and diet for gout

People suffering from gout should eat properly. Meals are four to five times in small portions. Gluttony, as well as fasting, are strictly prohibited, as they can provoke an attack. Without a diet, gout cannot be cured. You need to try to lose those extra pounds, but gradually.

Drink enough fluids - 2 liters per day, and during periods of increased illness - 3 liters.

Below is a table of product consumption for people with gouty arthritis

In conclusion, it must be said that traditional methods of combating gout are used mainly as prevention of the disease, as well as in conjunction with treatment with medications, a healthy diet and exercise.

Causes of gout development

Causes of gout:

• genetics;
• hormonal imbalances;
• poor nutrition;
• passion for strong drinks (especially beer libations);
• taking medications such as Aspirin, Pyrazinamide, Nicotinic acid, Diuretics;
• excess weight and metabolic disorders.

Gout is different in that it primarily affects the legs.

Attacks on them may appear after:

• sports loads;
• surgical intervention;
• driving a car for a long time.

Physiotherapy for gout

In the acute period, applications of dimexide solution are used on the affected joint.
It has analgesic and anti-inflammatory effects. Before starting the procedure, tests are carried out for sensitivity to dimexide (the presence of an allergic reaction), and procedures begin 24 hours after the test. For applications, use a 30-50% solution of dimexide (pure dimexide is diluted with boiled water). A napkin soaked in the solution is placed on the sore joint. Initially, the duration of the procedure is 10 minutes, later it is increased to 2 hours. During the period of remission, applications with mud, paraffin, and ozokerite are used, which helps improve joint function and reduces the urate content in them. During the period of remission, patients are recommended to undergo sanatorium-resort treatment. Health measures have a beneficial effect on the health status of patients and the course of the disease:

• dietary food,
• taking alkaline mineral waters,
• balneotherapy,
• mud therapy

Diagnosis of gout

1. Blood chemistry. Detection of hyperurecemia: increased uric acid levels in men over 0.42 mmol/l, in women over 0.36 mmol/l. Determination of blood creatinine level - to identify renal failure.
2. Examination of the synovial fluid of the affected joint. Chemical or microscopic examination reveals uric acid crystals; there is no bacterial flora in the culture.
3. X-rays of joints determine changes in chronic gouty arthritis.
4. Ultrasound of the kidneys. Identification of X-ray negative calculi (stones).