Diet for gout: how to eat properly if you have gout?

Gout is a disease consisting of a disorder of uric acid metabolism.
Gout is usually classified as a joint disease because excess uric acid forms salts (urates), which are deposited primarily in the joints. The first joint affected is the joint of the big toe. An inflamed bump on the thumb is a characteristic symptom of gout. Genetically, men are more predisposed to this disease. Among the sick, almost 95% of them are. The peak incidence in men occurs at the age of 40-50 years, in women – from 60 years and older. However, gout can also affect people at a younger age.

General information about the disease

Gouty arthritis is a systemic metabolic disease associated with the deposition of uric acid salts in articular and periarticular tissues. Men get sick more often after 40 years of age. In women, gout is less common and begins later - in the postmenopausal period after 50-60 years. In total, gout affects about 2.5% of these populations. With age, this percentage increases significantly and by the age of 80 it is 9% in men and 6% in women. The ICD-10 code is M10.

Gouty arthritis is comorbid (often combined) with kidney diseases and chronic renal failure, cardiovascular diseases (angina pectoris, high blood pressure), type 2 diabetes mellitus, and obesity.

Despite the fact that treatment for this disease has been developed, it is not always possible to keep gout attacks under control. This mainly occurs due to patients’ misunderstanding of the mechanism of development (pathogenesis) of gout and refusal or irregular maintenance therapy.

Read more about arthritis, its symptoms and treatment in this article.

Causes of gout

• Taking medications:
  thiazide diuretics, aspirin (2 g per day), cyclosporines.
• Diseases leading to the appearance of gout symptoms:
  coronary heart disease (CHD), arterial hypertension, metabolic syndrome, chronic renal failure, psoriasis, some blood diseases. The development of gout can also be promoted by organ transplantation and the introduction of a contrast agent during X-ray examinations.
• Abuse of foods rich in purine bases can provoke and aggravate the development of this disease:
  fatty meats and fish, alcohol, carbonated drinks, legumes, eggs, chocolate, mushrooms.

Cause and mechanism of development (etiology and pathogenesis) of the disease

The cause of gouty arthritis is a disorder of purine metabolism. Purines are chemical compounds that form the basis of nucleic acids necessary for the formation of DNA and RNA molecules. As cells break down, purines are broken down into uric acid (UA). The latter enters the intercellular space and into the blood plasma, where it combines with sodium, forming a salt - monosodium urate (MUN).

An increased level of urate in the blood (hyperuricemia - GU) may be a consequence of a genetic predisposition (the kidneys do not eliminate MUN completely), high blood pressure (BP), consumption of large amounts of animal food, and alcohol.

With an excess of urates, when they can no longer dissolve in the surrounding fluid (EOR concentration more than 0.4 mmol/l), the salts crystallize, deposit in the articular and periarticular tissues and are surrounded by protein rings. This formation is called tophi. The release of MUN from the tophi causes an immunological reaction: a large number of neutrophils (one of the types of leukocytes responsible for cellular immunity) appear in the synovial membrane and joint fluid.

Neutrophils ingest MUN crystals, which causes the release of proinflammatory (inflammation-causing and maintaining inflammation) cytokines and the development of an acute inflammatory response in the synovium. Acute attacks in the form of synovitis are very painful, but do not leave any consequences. The long-term chronic course of the disease with frequent repeated attacks leads to the destruction of articular cartilage, proliferation of bone tissue, deformation and dysfunction of the joint. Deposition of MUN in the kidneys causes a decrease in their function.

Factors contributing to increased urate levels in the blood:

• the presence in the diet of a large number of meat dishes, offal, eggs, alcoholic beverages,
• overweight;
• taking certain medications - diuretics, aspirin, nicotinic acid, medications to lower blood pressure (Concor), etc.;
• lead poisoning;
• increased breakdown of purines in blood diseases, psoriasis, etc.;
• increased formation of purines;
• impaired renal function and uric acid excretion.

Why is gout dangerous?

If gout is not treated, the joints will gradually deteriorate. Every year it will become more difficult to walk, and attacks will occur more often. Elderly people whose disease is in an advanced stage become bedridden patients, as the progressive disease is accompanied by fragility of joints and bones.

In addition, untreated gout leads to the formation of kidney stones. Therefore, during the course of treatment, various diagnostics are always prescribed, which will tell about the condition of the internal organs.

Classification

Based on the causes of occurrence, gouty arthritis is divided into forms:

• primary
  – associated with hereditary characteristics of purine metabolism and excretion of MUN by the kidneys;
• secondary
  – the cause of development is some other diseases, nutritional disorders, bad habits, etc.

According to the mechanism of accumulation of MUN, gout is divided into types:

• metabolic
  – increased internal production of purines during their normal excretion by the kidneys;
• renal
  – impaired excretion of uric acid by the kidneys;
• mixed
  .

By severity:

• mild course
  - attacks of gouty arthritis no more than 2 times a year with damage to no more than two joints; single tophi no more than 1 cm in diameter; there are no complications from the kidneys or impaired joint function;
• moderate severity
  - no more than 5 attacks per year affecting no more than 4 joints with minor changes in cartilage and bone tissue; a large number of small tophi; stones in the kidneys;
• severe
  – attacks of gouty arthritis more than 5 times a year, multiple large tophi and arthritis; decreased kidney function.

What to do during exacerbations

Exacerbations, which are accompanied by acute pain, can last from several hours to a week. The frequency of repetition varies in each specific case. It happens that a patient experiences acute pain only once, but such cases are rare.

The main task during exacerbations is to relieve inflammation and pain. Most often, the doctor prescribes non-steroidal anti-inflammatory drugs. They are used in a course until the pain in the joint completely subsides. If exacerbations occur frequently, in parallel the patient takes medications to remove uric acid from the body. By itself, this medicine does not reduce the symptoms of inflammation, but works well in conjunction with other drugs.

Symptoms of gouty arthritis

The appearance of the first symptoms of gouty arthritis is sometimes preceded by a long-term increase in the concentration of urate in the blood. Therefore, men after 40 years of age, and women after menopause, need to periodically check the content of uric acid salts (UA) in the blood. This is especially important for those who have close relatives suffering from gout. Gouty arthritis develops when the concentration of urate in the blood exceeds 0.4 mmol/l. But with such an indicator, arthritis manifests itself only in a fifth of patients; the rest may not be aware of their risk of developing gout.

Primary signs

The first attack of acute gouty arthritis begins suddenly. Sharp pain appears in the affected joint, the tissue over it swells, and the skin turns red. The pain is very strong. The body temperature may rise and the general condition of the patient may be disrupted.

Severe pain in the affected joint, high body temperature and poor condition of the patient are the first signs of gouty arthritis.

In half of the cases, gouty arthritis begins with damage to one joint. This is usually the first metatarsophalangeal joint of the foot. The knee, elbow, small joints of the hand, etc. may also be affected.

Symptoms of gouty arthritis are especially pronounced at night.

Obvious symptoms

The attack of gouty arthritis lasts from 2 days to 2 – 3 weeks. Then complete remission occurs without any consequences. The next attack usually develops within a year, but sometimes remission lasts several years.

Acute gouty arthritis can recur over a number of years, but gradually its course becomes chronic. Several joints are asymmetrically affected, including the first metatarsophalangeal joint on the lower extremities.

Under the skin on the extensor surface of the joints, as well as in the area of ​​the ears, tophi appear - small superficial nodules or larger subcutaneous nodes with a cartilaginous consistency. They are painless, but can become inflamed during an exacerbation of gouty arthritis. In this case, they become painful and sometimes break through to the surface of the skin in the form of a whitish mass.

Attacks of urolithiasis may occur - urates are deposited on the walls of the urinary tract, as well as in the kidneys, which leads to disruption of their function.

When you need to see a doctor urgently

You should seek medical help if:

• joint pain appeared, accompanied by severe redness and swelling of the tissues; body temperature increased, chills and malaise appeared;
• severe paroxysmal pain appeared in the lower back - an attack of urolithiasis;
• joint pain also bothers you during the interictal period - a sign of the chronic course of gouty arthritis.

Recommendations for antihyperuricemic therapy

The goal of antihyperuricemic therapy is to prevent the formation and dissolution of existing monosodium urate crystals by maintaining uric acid (UA) levels below 360 µmol/L.

• Allopurinol

  – promotes adequate long-term antihyperuricemic therapy. The drug is recommended at a dose of 100 mg daily, if necessary, the dose is increased by 100 mg every two to four weeks. Patients with renal failure require dose adjustment of this drug.

• Uricosuric agents

  (probenecid, sulfinpyrazone) are used as an alternative to allopurinol in patients with normal renal function. These drugs are relatively contraindicated in patients with urolithiasis.

• Benzbromarone

  - powerful uricozourik; the drug is more effective than allopurinol. It is used for moderately reduced renal function, but requires monitoring due to hepatotoxicity.

• Colchicine

  can be used as a prophylaxis for joint attacks during the first month of antihyperuricemic therapy (0.5-1.0 grams per day) and/or NSAIDs.

It is worth noting that in patients with gout, diuretics should be discontinued if possible (except for cases where diuretics are prescribed for health reasons).

• Losartan and fenofibrate
  have a moderate uricosuric effect. These drugs are recommended for use in patients who are resistant to or intolerant of allopurinol or other uricosurics, in the presence of hypertension or metabolic syndrome. However, the clinical significance of such therapy and its cost-effectiveness are still unknown.

At the Clinic of High Medical Technologies named after. N.I. Pirogov patients will be able to determine the serum level of uric acid and other important biochemical blood parameters, as well as undergo clinical blood and urine tests, and receive qualified advice from a rheumatologist on treatment both during the interictal period of the disease and during the attack of an acute gouty arthritis.

Stages of gouty arthritis

Gouty arthritis occurs in 4 stages:

1. Asymptomatic
   - Increased levels of MUN in the blood without the presence of crystals and gout attacks.
2. Asymptomatic
   - increased levels of MUN in the blood with the presence of crystals in the synovium and joint fluid, but without signs of gouty arthritis and the presence of tophi.
3. Intermittent
   - deposition of MUN crystals in tissues in combination with attacks of acute gouty arthritis.
4. Chronic tophi
   - the presence of tophi in articular and periarticular tissues in combination with chronic arthritis, destruction of cartilage tissue, impaired joint function and kidney damage.

Any form of arthritis has serious complications, so you should not delay treatment.
See how easily the disease can be cured in 10-12 sessions.

If gouty arthritis is not treated

If you suspect gouty arthritis, you should immediately contact a rheumatologist. The disease requires treatment, both during an attack and in the interictal period. The main reason why the development of gout attacks cannot be brought under control is the refusal of patients to undergo treatment in the inter-attack period, which inevitably leads to:

• hyperuricemia – increased urate levels in the blood;
• resumption of attacks of gouty arthritis;
• transition of acute gouty arthritis to chronic;
• joint destruction and disability;
• severe complications from the kidneys and cardiovascular system.

What to do during exacerbations

If severe joint pain occurs in combination with severe swelling and redness of tissues, increased body temperature, and malaise, you should:

• take any sedative + medicine from the group of non-steroidal anti-inflammatory drugs (NSAIDs) - Diclofenac (oral tablet or rectal suppository), Ibuklin, Nise, etc. Apply ointment or gel from the same group (Voltaren, Pentalgin, etc.) to the skin over the sore joint. ;
• call a doctor at home;
• lie down and take a position that minimizes joint pain.

Drugs for the treatment of exacerbation of gouty arthritis

Treatment methods for gout

Treatment of gout consists of both pharmacological and non-pharmacological methods, and should take into account the following factors:

• uric acid concentration, number of previous arthritis attacks,
• stage of the disease (asymptomatic increase in uric acid, interictal period, acute or intermittent arthritis, chronic tophi gout,
• age, gender, obesity, hyperuricemic drugs, polypharmacy.

It should be remembered that asymptomatic hyperuricemia does not equate to gout. Currently, there is no data proving the need for drug therapy to maintain normouricemia in such patients; the main method of therapy in this case is the treatment of comorbid diseases, dietary correction and lifestyle modification.

In the treatment of gout, a combination of non-pharmacological and pharmacological treatments is more effective than monotherapy. When treating, it is necessary to take into account the phase of the disease: acute attack of arthritis, inter-attack period, chronic form, tophi form, serum uric acid concentration, number of arthritis attacks, the presence of comorbid conditions such as diabetes mellitus (DM), arterial hypertension, coronary artery disease, and risk factors for hyperuricemia.

The main aspect of therapy is teaching the patient a healthy lifestyle, weight loss, diet, and reducing alcohol intake, especially beer. Dietary restriction of purine-rich animal products and weight loss help reduce serum uric acid levels.

One of the mandatory conditions for the treatment of gout is the control of comorbid diseases - dyslipidemia, alternative hypertension, diabetes mellitus, as well as weight loss and smoking cessation.

Treatment of an acute attack of gouty arthritis

Nonsteroidal anti-inflammatory drugs (NSAIDs) and colchicine (when taken orally) are used to treat an acute attack of gout. One effective treatment is removal of synovial fluid and intra-articular injection of long-acting steroids. This treatment method is effective and safe.

Localizations

With gout, gouty arthritis of the joints of the lower extremities most often develops. There may be other localizations, including damage to the joints of the upper extremities. Gout is also characterized by asymmetrical joint lesions.

Gouty arthritis of the lower extremities

During a primary gouty attack, the pathological process in half of the cases involves the 1st metatarsophalangeal joint of the foot. And even if this joint is not the first to be affected, gouty arthritis will still develop in it later. The periarticular tissues swell, the skin turns red. Subsequently, small and large tophi appear on the dorsum of the foot.

Gouty arthritis of the ankle is less common and most cases occur with repeated attacks. The ankle becomes inflamed, swollen and red, and the inflammation spreads to the heel. There is severe pain and the inability to step on the foot.

The knee is often affected, the lesions are asymmetrical, often combined with lesions of the 1st metatarsophalangeal and elbow joints. Severe pain, swelling and redness are initially combined with impaired limb function due to pain, but with prolonged gout, joint deformation and ankylosis (immobility) occur.

Hip gouty arthritis is rare and the redness and swelling are not so noticeable under the thick layer of muscles and ligaments. But the pain can be severe.

Chondroprotectors: what are they, how to choose, how effective are they?

Joint pain at rest

Gouty arthritis of the upper extremities

The small joints of the hand and fingers often become inflamed, and the fingers become like sausages. The pain, inflammation and swelling are very severe. Large tofuses appear on the back of the hand.

The elbow is no less often affected. The lesions are asymmetrical and are often combined with the involvement of small joints of the hand and foot. Small and large tophi appear on the extensor surface of the shoulder and forearm.

Brachial gouty arthritis develops much less frequently, but is painful. Swelling and redness are not expressed, tophi appear on the flexor surface of the shoulder.

Lesions in gouty arthritis of the upper extremities are usually asymmetrical

Tofus lesion of the spine

In the mid-50s of the last century, spinal damage due to gout was first identified. In this case, tophi grow in the soft tissues and joints of the spine with the destruction of their structures.

The lumbar region is most often affected, followed by the cervical region. Pain appears in the back, which is often mistaken for symptoms of osteochondrosis. When the vertebrae are destroyed and the spinal nerves and spinal cord are compressed, neurological symptoms appear. When the cervical spine is affected, this results in paresis and paralysis of the upper limbs, and radicular pain.

When the lumbosacral region is affected, it can be complicated by compression of the final part of the spinal cord - the cauda equina. In this case, the function of the pelvic organs is disrupted - involuntary urination, defecation, and potency disorders occur.

Diagnostics

Despite the fact that gouty arthritis has pronounced symptoms, only 10% of patients can be correctly diagnosed during the first attack. In other cases, a diagnosis of other types of arthritis is made. Diagnostic criteria for gout are:

• acute arthritis of the 1st toe;
• the presence of large and small tophi;
• increased levels of uric acid in the blood;
• detection of EOR crystals in joint fluid and tissues.

If at least two criteria are identified, the diagnosis of gouty arthritis is considered reliable.

Laboratory research:

• general blood test
  - signs of inflammation;
• biochemical blood test
  - uric acid content more than 0.32 mmol/l; increased levels of C-reactive protein (a sign of an inflammatory reaction);
• general urine analysis
  ;
• examination of synovial fluid using polarization microscopy
  - identification of MUN crystals and a large number of leukocytes.

Instrumental studies:

• Ultrasound of joints
  - detection of EOR crystals on the surface of cartilage and tophi;
• radiography of the joints
  - in the early stages there are no changes; later, bone changes are revealed;
• computed tomography (CT)
  - reveals the presence of changes in the spine.

Treatment of gouty arthritis

The goal of treatment for gouty arthritis is to improve disease outcomes. For this purpose, mainly medicinal treatment methods are used. Non-drug methods are of auxiliary value.

Drug treatment

The main objectives of drug treatment of gouty arthritis are:

• relieving inflammation and pain in acute arthritis;
• preventing attacks of arthritis by reducing uric acid in the blood.

Treatment of an acute attack of arthritis

The following drugs are used to relieve an attack of gouty arthritis:

1. Colchicine
   is a dry extract of autumn crocus seeds. Available in tablets. Effective in the first 12 hours from the onset of a gout attack. The result of its use is the elimination of swelling and pain. The drug is prescribed in small dosages. The daily dose is divided into several doses. First, most of the daily dose is prescribed, then an hour later - a smaller one. If necessary, the dose can be repeated several times a day. A day after the onset of an attack, minimum dosages cannot be used; they are increased, which contributes to the manifestation of side effects, mainly from the gastrointestinal tract. All dosages are selected by the doctor.
2. Nonsteroidal anti-inflammatory drugs (NSAIDs)
   – relieve inflammation, pain and swelling. These drugs are divided into 2 groups: non-selective and selective. Non-selective or 1st generation NSAIDs suppress the action of biologically active substances - prostaglandins, which support inflammatory processes. But they do not act selectively, also suppressing the action of prostaglandins that protect the gastric mucosa. Therefore, drugs such as Diclofenac, Indomethacin, Ibuprofen have side effects from the gastrointestinal tract (GIT). However, they are suitable for some patients and are often prescribed, both orally and intramuscularly. Selective NSAIDs (Nimesulide, Etoricoxib, Celecoxib) belong to the second generation. They act selectively on pro-inflammatory prostaglandins and have almost no effect on the gastrointestinal tract. The selection of the drug is carried out individually, in accordance with the characteristics of the patient’s body.
3. Glucocorticoid hormones (GCs)
   - quickly relieve inflammation, pain and swelling, but are not suitable for everyone, as they can increase blood pressure, blood sugar and cause exacerbation of peptic ulcer disease. Prescribed in short courses orally (Prednisolone), intramuscularly (Betamethasone), in the form of intra-articular injections. Currently, they are trying to use mainly drugs from the NSAID group and only if there are contraindications for their use, GCs are used.
4. Canakinumab (trade name Ilaris)
   is a monoclonal antibody to interleukin-1beta (IL-1b). IL-1b is a messenger protein molecule (cytokines) responsible for the inflammatory response. Antibodies bind to IL-1b and neutralize its action, which leads to the elimination of inflammation and pain. Canakinumab is used in an individually selected dosage for patients who have contraindications to the use of Colchicine, NSAIDs and GCs.

Drugs for the treatment of gouty arthritis

Decrease in uric acid levels in the blood during the interictal period

Outside of attacks, patients suffering from gouty arthritis are prescribed long-term courses of urate-lowering therapy (UST), which lower the content of uric acid (UA) in the blood serum, preventing the formation of UA crystals in tissues. With a low content of uric acid in the blood, the crystals already present in the tissues gradually dissolve. In the presence of chronic gouty arthritis and tophi, the UA content is reduced to a minimum (below 0.3 mmol/l), which contributes to the accelerated elimination of tophi. In the absence of tophi, an acceptable UA content of 0.36 mmol/l is acceptable.

For urate-lowering therapy for gouty arthritis, the following groups of drugs are used:

• A group of drugs that interfere with the formation of uric acid. They suppress the action of the enzyme involved in the formation of uric acid. When prescribing them, constant monitoring of UA content in blood serum is necessary. These medications include:
  Allopurinol is a drug that has been used to treat gout for more than 50 years. It is prescribed in long courses 2 weeks after the end of a gout attack with small doses, which are gradually increased to the required levels. Sometimes it gives side effects from the kidneys, liver, severe allergic skin reactions. At the initial stage of treatment, it often causes an exacerbation of gouty arthritis, so it is combined with the prescription of NSAIDs.
• Febuxostat (trade names: Adenuric, Azurix) is a more modern drug of this group; it acts selectively on only one enzyme involved in the synthesis of uric acid. It does not inhibit other enzymes, so it has fewer side effects. It works softly and effectively. Doses are selected individually and initially combined with the use of NSAIDs.
• Drugs that enhance the excretion of sUA through the kidneys. Prescribed for intolerance to drugs of the first group or ineffectiveness of their use:
  Probenecid - prescribed in long courses, contraindicated in the presence of kidney stones.
• Enzymes that are absent in humans can reduce the level of sUA in the blood. The enzyme uricase is present in the blood of some mammals and reduces the level of UA in the blood, but it is not present in human blood. The drug rasburicase (recombinant bacterial uricase) was produced using genetic engineering from bacteria, which is used for gouty arthritis if other methods fail to reduce UA in the blood. The disadvantage of the drug is increased allergenicity, so it is used strictly according to indications.

Peguricase is a uricase with polyethylene glycol, which suppresses increased allergenicity. A more modern drug, but it is also used strictly according to indications.

Crunching in joints - when to worry

Intra-articular injections of hyaluronic acid

Non-drug treatment

This type of treatment includes:

• diet;
• control over the course of comorbid (often combined with gout and aggravating its course) diseases;
• physiotherapeutic procedures;
• folk remedies.

Diet for gouty arthritis

Patients suffering from gouty arthritis should not consume foods rich in purine bases. But recent studies have found that only animal products have a negative effect. This is fatty red meat, offal (liver, kidneys, heart, brains), strong meat broths, canned fish in oil, canned meat and pates.

On the contrary, plant foods containing purine bases should not be completely excluded from the diet. These are nuts, peas, beans, lentils, legumes, cocoa and coffee. Dairy-vegetable diets with low-fat dairy products, a variety of vegetables and fruits are very useful. Especially useful are foods rich in vitamin C, which helps eliminate uric acid.

Alcohol should be excluded from the diet: strong spirits and beer, including non-alcoholic beer. Only a small amount of dry wine is allowed. You should not consume sweets, baked goods, and especially sweet carbonated drinks. It is also necessary to stop smoking.

Monitoring the course of comorbid diseases

Gouty arthritis is often combined and aggravated by obesity, diabetes mellitus, cardiovascular and kidney diseases.

Obesity requires constant monitoring of body weight. This includes following a diet with a reduced daily caloric intake, an active lifestyle, and courses of therapeutic exercises.

Diabetes mellitus also requires constant monitoring, laboratory monitoring and supportive treatment.

Frequent concomitant diseases with gouty arthritis are also arterial hypertension (consistently high blood pressure) and coronary heart disease with angina attacks. Currently, there are medications that can stabilize the condition of such patients, but this requires constant monitoring by a cardiologist.

Any renal pathology also complicates the course of gouty arthritis. She also needs to be observed and treated.

Physiotherapeutic procedures

Physiotherapy is an additional treatment for gouty arthritis. During a gouty attack, electrophoresis with glucocorticoid hormones and ultraviolet irradiation of the affected area are prescribed.

Electrophoresis with glucocorticoid hormones and ultraviolet irradiation are used to treat gouty arthritis.

During the period of remission, courses of magnetic and laser therapy are prescribed to improve blood microcirculation and restore damaged joint tissue.

In the absence of gout attacks, sanatorium treatment can be carried out for six months. The Caucasian Mineralnye Vody and Crimea sanatoriums are suitable.

Read about other methods of treating arthritis in this article.

Folk remedies

To relieve inflammation, swelling and pain during a gout attack, traditional medicine recommends compresses with activated carbon. Previously, charcoal was used for this purpose, today it is enough to take 50 tablets of activated carbon, crush, dilute with water to the consistency of homemade sour cream, add a tablespoon of vegetable oil, mix and apply to the inflamed area, apply a napkin, compress paper, cotton wool on top, bandage and leave all night long. Perfectly relieves inflammation, swelling, reduces pain.

Surgery

For large tophi, which often suppurate and compress surrounding tissues, disrupting their function, they are removed.

Surgical operations aimed at restoring joint function are carried out strictly according to indications, in case of destruction of cartilage tissue, proliferation of bone tissue with articular deformation and loss of limb function. If the joint is completely destroyed, it is replaced with an artificial one (endoprosthetics).

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.

Approach to the treatment of gouty arthritis at the Paramita clinic

Our clinic has developed a unique method for treating gouty arthritis. There are two opposing approaches to identifying and treating this disease. First of all, a thorough clinical, laboratory and instrumental examination of the patient is carried out. After establishing the final diagnosis and concomitant diseases, individually selected comprehensive treatment is prescribed, including:

• modern Western techniques, including the use of the latest medications; this allows you to eliminate inflammation and pain during a gout attack and maintain the desired level of uric acid in the blood serum during the inter-attack period;
• traditional oriental techniques that have a regulating effect on the body as a whole and on the site of inflammation; techniques allow you to eliminate pain after the first session; After the course of treatment, the patient feels a surge of strength and complete renewal.

We combine proven techniques of the East and innovative methods of Western medicine.
Read more about our unique method of treating arthritis

A completed course of treatment and properly selected urate-lowering therapy allows the patient to forget about gout attacks for a long time (in most cases until the end of life). You can get more detailed information about treatment at the clinic on our website.

Criteria for the diagnosis of gout

Example of using diagnostic criteria:

• Attack of arthritis of the first metatarsophalangeal joint - +2 points
• Characteristics of the episode: erythema over the joint, inability to tolerate touch/pressure, great difficulty walking/inability to use the affected joint +3 points
• More than 1 “typical episode of arthritis” – +2 points
• Hyperuricemia (548 µmol/l) – +3 points

General clinical recommendations for patients with gouty arthritis

All patients suffering from gout are advised to:

• follow a diet, lead an active lifestyle;
• follow all doctor's orders, including taking prescribed urate-lowering medications;
• monitor your weight;
• treat concomitant diseases: diabetes, obesity, angina pectoris, high blood pressure, chronic kidney disease.

Prevention of gout

Gout is most often associated with hereditary metabolic characteristics. There are also no factors predisposing to the development of this disease. If you eliminate their influence, then even if you have a family history, you can significantly reduce the risk of developing the disease. To do this, you need to follow the following recommendations:

• do not overeat, reduce the calorie content of your daily diet, do not consume offal, red meat, alcohol, quit smoking;
• get rid of excess weight;
• Take any medications in consultation with your doctor - some of them increase the concentration of uric acid (diuretics, nicotine, acetylsalicylic acid, etc.);
• regularly treat chronic diseases: diabetes, obesity, kidney and cardiovascular diseases;
• men over 40 years old, and women over 50, periodically check the level of uric acid in the blood.

Prevention of gout

You need to adhere to the basics of proper nutrition: remove smoked meats and sausages from your diet, eat less fatty foods. Regular physical activity will have a positive effect on the body's condition - walking or light exercise in the morning is enough.

If you get rid of bad habits in the form of frequent alcohol consumption, the risk of encountering gout will significantly decrease. You should also undergo regular examinations to understand the condition of your internal organs.

As soon as you notice the first signs of arthritis, you should immediately consult a doctor so as not to start the disease.

https://text.ru/spelling/616bf65070647 — 100%

Frequently asked questions about the disease

Is it possible to get disability?

For chronic tophi gouty arthritis with impaired joint function.

Which doctor treats you?

Rheumatologist.

What prognosis do doctors usually give?

With proper systematic treatment under the supervision of a physician, the prognosis is favorable.

Gouty arthritis requires constant monitoring by a rheumatologist, urate-lowering therapy, diet and all doctor’s recommendations. If treated correctly, you can forget about gout attacks forever. Doctors at the Paramita clinic have extensive experience in treating gout. Contact us!

Literature:

1. Fedorova A. A., Barskova V. G., Yakunina I. A., Nasonova V. A. Short-term use of glucocorticoids in patients with prolonged and chronic gouty arthritis. Part III. Frequency of development of adverse reactions // Scientific and practical rheumatology. 2009; No. 2. pp. 38–42.
2. Eliseev M. S. Gout. In the book: Russian clinical guidelines. Rheumatology / Ed. E. L. Nasonova. M.: GEOTAR-Media, 2022. pp. 372–385.
3. Rainer TH, Cheng CH, Janssens HJ, Man CY, Tam LS, Choi YF Oral prednisolone in the treatment of acute gout: a pragmatic, multicenter, double-blind, randomized trial // Ann Intern Med. 2016; 164(7):464–471.
4. Reinders M., van Roon E., Jansen T., Delsing J., Griep E., Hoekstra M. et al. Efficacy and tolerability of urate-lowering drugs in gout: a randomized controlled trial of benzbromarone versus probenecid after failure of allopurinol // Ann Rheum Dis. 2009; 68:51–56.

Themes

Arthritis, Joints, Pain, Treatment without surgery Date of publication: 01/25/2021 Date of update: 02/02/2021

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