Gouty arthritis radiological signs. X-ray method in the diagnosis of joint diseases

Gout is a disease in which uric acid salts are deposited in the joints. The most common method for diagnosing deviations is x-rays. With its help, it is possible to identify a destructive process in the cartilage, for example, a “punch” symptom, characterized by the formation of a number of nodular formations (tophi), and other bone defects. Most of the signs of gout show up on x-rays.

Gouty arthritis of the upper extremities has similar symptoms to rheumatoid arthritis, so the two conditions are difficult to distinguish.

Gout: what are the causes and what are the symptoms?

Gouty arthritis occurs when:

• violations of the metabolism of purine bases, which is associated with excessive consumption of products containing purine;
• genetic predisposition to the disease;
• the patient has heart failure, hemoblastosis, hormonal pathologies;
• malfunction of the excretory system.

It manifests itself in the form of sudden acute attacks that occur for 3-10 days, and then suddenly disappear. Their occurrence is provoked:

• joint injuries;
• infections;
• drinking alcohol, fatty and fried;
• hypothermia.

More often the disease makes itself felt at night. With a deviation, the following symptoms occur:

• pain in the injured joint;
• high temperature: 38-39 degrees Celsius;
• swelling at the site of the joint acquires a blue tint.

X-ray as one of the diagnostic methods

X-rays help to accurately determine the type of disease. This type of diagnosis is one of the most accurate, since no other method is able to give a specific classification of the disease. For example, during an exacerbation, the level of urates sharply decreases - they all go to the diseased joint, so a blood test can no longer determine gout.

X-ray signs of gout

The main sign that helps to confirm gouty arthritis is the “punch symptom”. On x-ray, such a pathology looks like a cystic formation located on the edge of the bone with clear boundaries. The more calcium inclusions in neoplasms, the better they are visible on the pictures. This diagnostic technique highlights other radiological signs:

• expansion of the joint due to the deposition of uric acid;
• changes in the end sections of the bones.

Gout- a disease associated with a violation of purine metabolism, characterized by an increase in the content of uric acid in the blood (hyperuricemia) and the deposition of urates in the articular and / or periarticular tissues. Detection of hyperuricemia is not enough to establish a diagnosis, tk. only 10% of persons with hyperuricemia suffer from gout. The most common causes are decreased excretion or increased production of uric acid. Chronic gout is characterized by the formation of tophi.

Code according to the international classification of diseases ICD-10:

• M11.1

Causes

Genetic Aspects. The activity of phosphoribosyl pyrophosphate synthetase 1 (311850, PRPS1 gene, Xq22 q24) is controlled by the X chromosome, so only males get sick.
Pathogenesis gouty attack. As a result of prolonged hyperuricemia, microtophi (accumulations of crystals) form in the synovial membrane and cartilage. Due to trauma, fever in the joint, or changes in the concentration of uric acid in the blood or synovial fluid, the microtophi are destroyed, and the crystals enter the joint cavity. Synovial cells produce IL - 1, IL - 6, IL - 8, which act as chemoattractants for neutrophils. Immunoglobulins and complement components opsonize (envelop) urates, stimulating the phagocytic activity of neutrophils. The phagosomes of neutrophils that have absorbed the crystals fuse with lysosomes, and lysosomal enzymes destroy the protein shell of the crystals. Crystals damage neutrophils, and lysosomal enzymes released into the synovial cavity trigger inflammation.

Symptoms (signs)

Clinical picture(according to the stages of the flow)
. Asymptomatic hyperuricemia is elevated blood uric acid in the absence of clinical evidence of crystal deposition (i.e. no arthritis, tophi, nephropathy, or urate stones).
. Acute gouty arthritis - the second stage and the first manifest form of gout - a sudden onset of arthritis with severe pain. A typical attack - more often one joint on the legs is affected, and in 50% of patients the I metatarsophalangeal joint suffers. Most gouty attacks occur at night and are accompanied by a rapid increase in erythema and temperature around the joint, swelling and tenderness. Inflammation can also go to soft tissues, forming a clinical picture of cellulite or phlebitis. Severe cases are accompanied by an increase in body temperature. The usual duration of an attack is a few days, rarely a few weeks. After an attack, the joint returns to its normal shape. In some cases, a polyarticular variant is also possible.
. The interictal period - the third stage of gout - occurs after the end of the first attack and may be interrupted by the next acute attack .. Repeated monoarticular attacks. In 7% of patients, after the first episode of gout, repeated attacks are not noted. However, 62% have recurrent attacks within the first year of illness. In typical cases, in the interictal period, patients do not complain, but if the patient does not receive treatment, then each subsequent attack is more severe and the interictal period is shortened. Progression of the disease. Over time, the attacks become more severe and acquire the character of polyarthritis. In some patients, chronic gouty arthritis develops quickly, almost without remissions - in such cases, differential diagnosis with rheumatoid arthritis is carried out.
. Chronic gouty arthritis (chronic tophi gout) occurs when left untreated; it is considered the final stage of gout. Tofus form clusters of urate crystals surrounded by inflammatory cells and fibrous masses. Tophi are firm, mobile, cream or yellowish in color, with a chalk-like discharge when ulcerated. Typical localization of tophi: auricle; over the affected joints; subchondral articular surfaces; on the extensor surface of the forearm; in the elbow area; over the Achilles and hamstrings.
. Kidney damage: nephrolithiasis, tubulo-interstitial nephritis.
Laboratory data. Leukocytosis in the blood with a shift to the left and acceleration of ESR during acute attacks. Elevated levels of uric acid in the blood. In 10% of cases, the concentration of uric acid in the blood is within the normal range. In the synovial fluid of leukocytes 10-60109/l, mainly neutrophils. Of diagnostic importance are the determination of needle-shaped urate crystals located intracellularly and birefringent light when examined under a polarizing microscope. In the aspirate of the contents of tophi - crystals of uric acid. The study of daily excretion of uric acid is carried out after a 3-day diet that excludes purines.
instrumental data. On the roentgenogram, there are pronounced erosions (symptom of a "punch") in the subchondral zone of the bone, most often in the I metatarsophalangeal joint and in the phalanges of the fingers, but it is also possible in other joints. Periarticular osteoporosis is not typical.
Diagnostic criteria. The presence of characteristic crystalline urates in the joint fluid and / or. Tofus (proven) containing crystalline urates, confirmed by chemical or polarization microscopy. The presence of 6 of the 12 signs listed below: .. More than one attack of acute arthritis in history.. Inflammation of the joint reaches a maximum on the first day of illness.. Monoarthritis.. Hyperemia of the skin over the affected joint.. Swelling and pain in the first metatarsal - phalangeal joint.. Unilateral lesion of the first metatarsal - phalangeal joint.. Unilateral damage to the joints of the foot.. Suspicion of tophi.. Hyperuricemia.. Asymmetric joint edema (X-ray) .. Subcortical cysts without erosion (X-ray) .. Negative results in bacteriological examination of the synovial fluid.
Differential Diagnosis. infectious arthritis. pyrophosphate arthropathy. Hydroxyapatite arthropathy. Osteoarthritis. Amyloidosis. Hyperparathyroidism. Rheumatoid arthritis.

Treatment

TREATMENT
General tactics. Assign diet number 6. Treatment with antigout drugs is carried out with primary gout for life, with secondary gout, depending on the elimination of the situation that provokes the development of gout. Mode. In the acute period - rest.
Diet. Products whose consumption should be excluded.. alcoholic beverages (especially beer) .. animal parenchymal organs (liver, kidneys) .Food products whose consumption should be limited.. fish (caviar, Baltic herring, sardines, etc.; more than large fish), crustaceans.. meat (veal, pork, poultry, broths) .. some vegetables (peas, beans, mushrooms, cauliflower, asparagus, spinach) .Foods that can be consumed without restrictions.. cereals (bread, cereals, bran) .. dairy products (milk, sour cream, cheese) .. all fruits and fruit juices .. fats (butter, margarine, cooking oil) .. coffee, tea, chocolate. most vegetables (potatoes, lettuce, cabbage, tomatoes, cucumbers, pumpkins, onions, carrots, beets, radishes, celery) .. sugar (but: causes weight gain!) .. spices.

Drug treatment
. Management of asymptomatic hyperuricemia is mainly observational. Examine the level of excretion of uric acid. If it is within the normal range, it is rational to limit yourself to dietary recommendations. According to some researchers, when the normal excretion of uric acid is exceeded, the appointment of allopurinol is necessary, but the advantage of using this drug over non-drug management of the patient has not been shown (due to the possibility of developing side effects from treatment, as well as its high cost).
. In the treatment of acute gouty arthritis, rest and cool wraps are very important. An important place is occupied by colchicine, prescribed at 0.5 mg every hour until the arthritis subsides, or until side effects (vomiting, diarrhea), but not less than 6-8 mg / day . For the treatment of an acute attack of gout, colchicine is used for no more than a day.
. NSAIDs (indomethacin, ibuprofen, naproxen, piroxicam, but not salicylates) are usually used in large doses and for a short course (2-3 days). Special care should be taken in concomitant diseases of the liver and kidneys, especially in elderly patients.
. The introduction of HA into the joint cavity in acute gouty arthritis is dangerous due to the possible presence of unrecognized septic arthritis that debuted under the mask of gout or against its background. In addition, the extreme soreness of the joint with gout makes any manipulation difficult.
. Uricostatic and uricosuric drugs are not used during an acute attack, since any fluctuations in the concentration of urate in the blood can prolong an attack of gout.
. With reduced urate excretion, preserved kidney function and the absence of urinary stones, both uricosuric and uricostatic agents can be used. Allopurinol + benzbromarone, used 1 tablet 1 r / day, combines these properties. Probenecid, proposed in foreign guidelines for uricostatic purposes, is not registered in the Russian Federation. Allopurinol is considered a generally recognized uricostatic (i.e., blocking the production of urates) drug. Allopurinol is prescribed at a starting dose of 100 mg / day, followed by a gradual increase in dose to 300 mg / day over 3-4 weeks. If the GFR is reduced to 30–60 ml/min, the dose of allopurinol should not exceed 100 mg/day, and if the GFR is 60–90 ml/min, it should not exceed 200 mg/day.
. With increased excretion of uric acid in the urine and / or gouty kidney damage, allopurinol is preferred. In the first weeks of allopurinol therapy in such patients, the use of drugs that increase the solubility of uric acid in the urine is indicated.
. In secondary gout against the background of hematological, oncological diseases during the period of cytotoxic or radiation therapy, allopurinol remains the treatment of choice.
The prognosis is favorable with early recognition and adequate treatment. Prognostically unfavorable factors: the development of the disease at the age of 30 years, persistent hyperuricemia over 0.6 mmol / l, persistent hyperuricosuria over 1100 mg / day, the presence of urolithiasis in combination with urinary tract infection, progressive nephropathy, especially in combination with diabetes and arterial hypertension. Hyperuricemia is a predictor of MI and death in patients with hypertension and congestive heart failure.
Age features. Children and adolescents: the onset of the disease in this age group indicates the presence of congenital metabolic disorders. Elderly people: gout is usually associated with taking drugs. Women in the premenopausal period get sick very rarely.

ICD-10. M10 Gout

Appendix. Calcium familial gout exists in two forms (*118600, 5p, CCAL1 gene, ; chondrocalcinosis with early manifestation of osteoarthritis, *600668, 8q, CCAL2 gene, ). Clinically: arthropathy, acute intermittent arthritis, ankylosing of the joints, chondrocalcinosis. Laboratory: crystals of calcium pyrophosphate in the synovial fluid with a normal level of serum calcium, a decrease in the activity of pyrophosphohydrolase in the synovial fluid. Synonyms: limited calcification, calcium pyrophosphate accumulation disease, familial chondrocalcinosis articular.

ICD-10. M11.1 Hereditary chondrocalcinosis

Gout is a systemic tophi disease that develops due to inflammation at the site of sodium monourate (MUN) crystal deposition in individuals with hyperuricemia (HU) caused by environmental and/or genetic factors.

Differential Diagnosis

It is necessary to emphasize the importance for the differential diagnosis of a thorough analysis of the history, previous events and the nature of arthritis, summarized in Table. one.

Nevertheless, it must be remembered that arthritis of the first metatarsophalangeal joint (PFJ) that has arisen for the first time can be observed with soft tissue infections, bursitis of the big toe, osteoarthritis with acute inflammation, sarcoidosis, psoriatic arthritis, pseudogout and other conditions.

Causes of acute monoarthritis of the metacarpophalangeal joint of the first finger:

Frequent causes:

- microcrystalline arthritis (MUN, calcium pyrophosphate, hydroxyapatites, calcium oxalates);

- trauma;

- hemarthrosis;

- septic arthritis;

- osteoarthritis;

- osteomyelitis;

- aseptic necrosis of the bone.

Possible reasons:

- reactive arthritis;

- sarcoidosis;

- juvenile arthritis;

- psoriatic arthritis;

- hemoglobinopathies;

- osteosarcoma.

Rare causes:

- Behçet's syndrome;

- mediterranean fever;

- intermittent hydrarthrosis;

- vilolesionodular synovitis;

- relapsing polychondritis;

- synovioma;

- Still's syndrome;

- metastases of tumors in the synovial membrane.

Traumatic arthritis

Septic and especially traumatic arthritis have the greatest similarity with gout in terms of severity of inflammatory manifestations, although their frequency of occurrence is much lower compared to gout. In the case of traumatic arthritis, finding out the provoking factor can only partially help in making the correct diagnosis, since gout often has a chronological relationship with trauma, which explains why patients first of all turn to a traumatologist or surgeon. X-ray examination of the distal feet can be uninformative, since at the first attack of gouty arthritis there is not yet a characteristic radiological symptom of a "punch" (to be discussed later). The level of uric acid at the time of an attack may also not exceed the laboratory norm, which is explained by the redistribution of urates in the blood with their precipitation into crystals. In this case, almost the only method for verifying the diagnosis is the puncture of the affected joint. In classical cases, the identification of hemarthrosis will testify in favor of traumatic arthritis. In the absence of blood impurities, it is necessary to assess the level of the inflammatory response, which can be difficult due to the small amount of synovial fluid obtained from this joint. However, to detect EOR crystals, it is sufficient to obtain a minimum amount of liquid (no more than a drop). An additional fact that testifies in favor of gouty arthritis may be the rather rapid relief of the last NSAID, especially at the onset of the disease.

Septic arthritis

Septic arthritis is clinically similar to gouty arthritis and is also characterized by the development of hyperemia, hyperthermia, pain, swelling, and dysfunction of the joint. Septic arthritis is accompanied by fever, increased ESR, leukocytosis, which is not typical for gout or is observed in its late chronic polyarticular course. The causes of septic arthritis can be intra-articular injections of drugs for rheumatoid arthritis (RA) and osteoarthritis (OA), as well as immunosuppression.

Gout and septic arthritis can develop in the same patient, so if bacteria are found in the synovial fluid, it should also be examined for the presence of MUN crystals.

Pyrophosphate arthropathy

Pyrophosphate arthropathy (PAP) is a type of microcrystalline arthropathy. It develops mainly in the elderly (usually not younger than 55 years), approximately equally often in men and women. Clinical and radiographic differences between gout and PAP are summarized in Table 1. 2. Cases of detection of both types of crystals in one patient are described. In 90% of cases, PAP affects the knee, shoulder and small joints of the hands. It is noteworthy that the onset of gout with arthritis of the knee joints is not casuistry, especially in the presence of a history of trauma, and vice versa, pseudogout with involvement of the PFS occurs. Involvement of the small joints of the hand in gout occurs more often in the late stage of the disease, and the shoulder joints can be considered "exception" joints even at an advanced stage.

To verify the diagnosis at an early stage, the key point is polarizing microscopy of the synovial fluid, which makes it possible to identify calcium pyrophosphate crystals. In the later stages of PAP, a characteristic radiological picture appears: chondrocalcinosis, more often of the menisci, but also of the articular cartilage.

Acute calcifying periarthritis

Episodes of pain and inflammation in the joints, including in the area of ​​the PFS of the first finger, can be observed in acute calcific periarthritis. Large joints are most often affected: hip, knee, shoulder. Deposits of amorphous hydroxyapatites that form in the acute stage in the ligaments or joint capsule may subsequently disappear and then reappear, causing repeated attacks of arthritis. More often, calcifying periarthritis occurs in women or in patients with uremia who are on hemodialysis.

Classification criteria for gout

A. Detection of urate crystals in synovial fluid.

B. Verification of crystals for suspected tophi.

C. Analysis of 12 clinical and laboratory signs (at least 6 are required for the diagnosis):

1. Maximum inflammation of the joint on the first day.

2. Having more than one attack of arthritis.

3. Monoarthritis.

4. Redness of the joints.

5. Pain and inflammation of the PFS of the first finger.

6. Asymmetric PFS inflammation.

7. Unilateral lesion of the tarsal joints.

8. Suspicion of tophi.

9. Hyperuricemia.

10. Asymmetric inflammation of the joints.

11. Subcortical cysts without erosions on x-ray.

12. Absence of microorganisms in the culture of synovial fluid.

Clinical picture of gouty arthritis

Classic gouty arthritis: acute, sudden onset, usually at night or in the morning, pain in the area of ​​the metatarsophalangeal joint of the first finger.

An acute attack with rapid onset of severe pain and joint swelling that peaks within 6-12 hours is a highly diagnostic sign for gout, especially when it is accompanied by skin erythema (Fig. 1).

Arthritis of this localization can also occur in other diseases, however, the presence of such typical signs as pronounced hyperemia and swelling, combined with severe pain in the PFS of the first finger, makes clinicians think of gouty arthritis.

Provocative factors are characteristic: alcohol intake, abundant consumption of meat and fatty foods, bathing (hypovolemia), operations, microtraumas associated with a prolonged load on the foot or a forced position (driving, on an airplane, etc.).

Common Mistakes

The combination of arthritis with high levels of uric acid in the blood makes it easier to diagnose. But, as our observations show, the diagnosis of gout is established only at the 7-8th year of the disease. This is primarily due to the peculiarity of the course of gouty arthritis, especially at the onset of the disease: fairly rapid relief of arthritis even without treatment, rapid relief of pain when using non-steroidal anti-inflammatory drugs (NSAIDs) or analgesics. The characterological features of patients matter: an extremely low level of compliance, which is partly due to the sexual dimorphism of the disease: gout affects mainly men of socially active age (45-50 years).

MUN crystals. An independent and sufficient sign for the diagnosis of gout is the detection of MUN crystals in the most accessible media for research - synovial fluid. The formation of MUN crystals and the resulting inflammation constitute the pathogenetic essence of the disease. The study of the phenomenon of the formation of EOR crystals showed their uniqueness and obligatory nature for gout. Their detection is the absolute reliability of the diagnosis (Fig. 2a).

Tophi. EOR crystals, being a consequence of HU, are deposited in the form of deposits called tophi. As a rule, microdeposits are found in many organs and tissues, and in the case of chronic gout, macrotophi are also formed.

Tofus is described by morphologists as a kind of granuloma consisting of crystalline masses surrounded by an infiltrate of inflammatory cells (Fig. 2b). Proteins, lipids, calcium, polysaccharides are also components of tofus. The best known are subcutaneous tophi, as they are easily detected. More often they are localized in the area of ​​​​the toes and hands, knee joints, on the elbows and auricles. The same deposits are formed in the kidneys, heart, joints, and in the structures of the spine. Finally, we have recently discovered the phenomenon of the deposition of MUN crystals in the gastric mucosa.

Synovial fluid is the most accessible for examination, and crystals can be found even in non-inflamed joints. Polarizing microscopy is used to identify crystals. EOR crystals are birefringent, needle-shaped, blue or yellow in color depending on their location relative to the beam; their size can vary from 3 to 20 mm. Overall, despite interlaboratory differences, the sensitivity and specificity of this method are rated as high.

Radiological features of gouty arthritis

The diagnosis of gout is based on clinical data; in the early stages of the disease, an X-ray examination of the affected joints is not very informative. The radiological phenomenon typical of late gout is well known - the “punch” symptom. This phenomenon was first described in 1896 by Huber as a defect in the subchondral bone, 5 mm in diameter or more, located in the medial part of the base of the diaphysis or in the head of the phalanx, more often than the first metatarsophalangeal joint. With the accumulation of experience, it became clear that the opposite situation is more often observed, when radiological changes are not detected in patients with gouty arthritis.

When developing classification criteria for gout, it was shown that subcortical cysts without erosions were found in 11.9% of patients with gout and in 1-3.4% of patients with pseudogout, RA and septic arthritis. Nevertheless, despite the low sensitivity and specificity, this radiographic sign was included in the clinical and laboratory list of criteria for gout.

Discussing the symptom of a "punch", it is necessary to note a number of points that determine the significance of its detection. Firstly, the pathomorphological substrate of this radiological phenomenon is intraosseous tophus (the impression of cystic formation is created due to the fact that EOR crystals do not delay X-rays). Revealing the "punch", we define the stage of the disease as chronic tofus. It is generally accepted that tophi of any localization is a direct indication for starting anti-gout therapy.

Based on our own research, we concluded that the “punch” symptom in patients with primary gout is a late symptom associated with a long course of the disease and chronic arthritis.

An early radiological sign in gout is reversible diffuse soft tissue thickening during an acute attack. In this case, transient local osteoporosis can be detected. As the disease progresses, bone destruction may occur. Initially, a small marginal erosion may form in the form of a shell or shell with overhanging bone edges, with underlined contours. The latter is very typical for erosions in gout, in contrast to those in rheumatoid arthritis, tuberculosis, sarcoidosis, syphilis, and leprosy. Erosions can be found both in the joint itself and outside the joints. With intra-articular localization of tophi, the edges of the joints are more often damaged. In the future, destructive changes spread to the central parts of the joint. Extra-articular erosions are usually localized in the cortical layer of metamyphyses and diaphyses of bones. Often, extra-articular erosions are associated with the adjacent soft tissue tophi and are defined as rounded or oval marginal bone defects with pronounced sclerotic changes at the base of the erosion. If treatment is not carried out, the described changes increase in size, capturing deeper layers of bone tissue and resembling "rat bites". Asymmetric erosions with cartilage destruction are typical; rarely formed bone ankylosis.

The gouty "punch" on the radiograph (Fig. 3) looks like a cyst, close to the edge of the bone, framed by a clear sclerotic corolla. In fact, this formation is not a true cyst, as it contains EOR crystals. In the case of deposition in tofus structures of calcium, X-ray positive inclusions can be detected, which sometimes stimulate chondromas. The width of the joint space of the affected joints usually remains normal until the later stages of the disease. According to some authors, these changes can mimic osteoarthritis. In our opinion, both diseases are more common in such cases.

In chronic gout, pronounced proliferative periosteal changes can be detected, which reflects the reaction of the periosteum to the adjacent soft tissue tophi. Typical sites for such changes are the first PFS, tarsal joints, and knee joints.

Rheumatoid arthritis

In some cases, differential diagnosis of gout is carried out with RA. Monoarticular onset of RA with isolated involvement of the knee and elbow can mimic gouty arthritis. However, this clinical situation usually does not cause great difficulties. When a sufficient amount of synovial fluid is obtained from a large joint, it is possible to conduct not only polarizing microscopy to search for crystals, but also a complete analysis, including the determination of rheumatoid factor (RF). If the analysis of synovial fluid is not available, the results of the use of NSAIDs or glucocorticoids (intra-articular) may serve as an additional criterion. This treatment usually completely stops gouty arthritis, unlike rheumatoid arthritis.

Often there is a situation when the late polyarticular form of gout involving small joints is confused with RA. However, RA is characterized by symmetrical joint damage with inflammation of the proximal interphalangeal, radiocarpal, temporomandibular joints, and cervical spine, while gout is characterized by asymmetric inflammation of the hand joints even at a late stage of the disease, with a tendency to predominantly affect the joints of the lower extremities. Ulnar deviation and amyotrophy of the hands are observed only in isolated cases with gout, in contrast to PA. In both diseases, subcutaneous nodules are formed, which can be quite difficult to distinguish. Radiologically, RA is characterized by marginal bone erosions, and gout is characterized by a “punch” symptom. Laboratory tests, morphological studies of nodules, determination of the RF and the level of UA in the blood help to finally resolve the diagnostic difficulties. The combination of RA and gout is casuistry, since the synovial fluid of RA patients inhibits crystal formation.

Osteoarthritis

OA and gout may coexist in the same patient, especially in the elderly. Heberden's and Bouchard's nodes may be involved in the process of microcrystalline inflammation. Changes in the synovial fluid in OA are characterized by mild inflammation, crystals that differ from MUN can be detected, they consist of liquid lipids and calcium pyrophosphatases.

Psoriatic arthropathy

Serious difficulties are caused by the differential diagnosis of gout with psoriatic arthropathy. The latter is characterized by damage to the distal interphalangeal joints, although any joint can become inflamed. X-ray changes in the joints may be similar (with the exception of the classic picture of "pencil in a glass" and "punch"). The main sign forcing a diagnostic search is HU, which often accompanies psoriatic arthritis and is an indirect sign of the activity of skin manifestations. It should be remembered that even in the presence of skin psoriasis, the final diagnosis of joint damage is established after examining the synovial fluid for crystals. In our practice, there was a combination of skin psoriasis and gout, confirmed by the detection of crystals.

Reiter's syndrome

Reiter's syndrome, like gout, affects mainly males, while the joints of the lower extremities become inflamed, often large, but also small joints of the feet. The hallmarks of Reiter's syndrome are conjunctivitis and urethritis preceding arthritis. In this situation, a careful history taking and examination of the synovial fluid help to verify the diagnosis.

Ankylosing spondylitis

Quite often it is necessary to distinguish between gout and ankylosing spondylitis (AS). This is due to the fact that these diseases are characterized by the similarity of a number of signs, namely: male sex, frequent involvement of the joints of the lower extremities, monoarthritis, sudden onset of arthritis. Nevertheless, the clinical picture of AS has its own characteristics. These are pains in the spine with stiffness and limitation of chest excursion, night pains in the lower back radiating to the buttocks, a long duration of arthritis (from several weeks to months). X-ray examination shows the presence of sacroiliitis. Helps in the diagnosis of AS is the determination of HLA-B27, which is detected in almost 90% of patients.

* Criteria A and B (detection of crystals) are independent.

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.

Gout is a disease associated with a violation of purine metabolism, characterized by an increase in the content of uric acid in the blood (hyperuricemia) and the deposition of urates in the articular and / or periarticular tissues, kidneys and other organs. Detection of hyperuricemia is not enough to establish a diagnosis, since only 10% of individuals with hyperuricemia suffer from gout.

According to epidemiological studies, the normal concentration of uric acid in the blood in men does not exceed 0.42 mmol / l, in women - 0.36 mmol / l. The prevalence of hyperuricemia in the population ranges from 4 to 12%, with a significant tendency to increase with age, especially in women. Gout affects about 0.1% of the population. The majority of patients (80-90%) are middle-aged or older people with previous asymptomatic hyperuricemia for 20-30 years. Men are 20 times more likely to get gout. Before menopause, women rarely become ill, possibly due to the effect of estrogen on uric acid excretion. Rarely, an acute attack of gout occurs in adolescents.

ETIOLOGY

The accumulation of an excess amount of uric acid in the blood may be due to either its high production (increased synthesis of endogenous purines), or low excretion, or a combination of these mechanisms. There are primary and secondary gout. The secondary form includes gout, which developed during the appointment of various drugs.

OVERPRODUCTION OF URIC ACID

The sources of uric acid are the purine bases adenine and guanine. There are two types of overproduction of uric acid.

Primary hyperproduction is associated with defects in the enzymatic system for the synthesis of uric acid. To date, the presence of two such defects has been proven: deficiency of hypoxanthine-guanine phosphoribosyl transferase and increased activity of ribose phosphate pyrophosphokinase. These enzymes are controlled by genes linked to the X chromosome, so primary overproduction occurs only in males. When an excessive amount of substrates for the formation of purines enters the body with food, hyperproduction of uric acid begins. A large amount of purines is found in anchovies, sardines, fatty meats, kidneys, liver and meat extracts, dry wine.

Secondary overproduction is due to increased cell breakdown in hemoblastosis, paraproteinemia, chronic hemolysis, antitumor chemotherapy, and is also characteristic of people who abuse alcohol. Hyperuricemia often accompanies psoriasis, although clinical manifestations of gout rarely develop.

REDUCED EXECRETION OF URIC ACID

Normally, about 60-70% of uric acid is excreted by the kidneys, the rest - by the intestines and skin. Urate excretion by the kidneys involves four steps: glomerular filtration, reabsorption of 95% filtered uric acid, proximal tubular secretion, and reabsorption of 40-44% uric acid. As a result, only 8-12% of the initially filtered uric acid is excreted in the urine, which is 400-600 mg / day. Excretion disorders can be induced by urate crystallization in the kidneys against the background of an increase in their excretion (more than 800 mg / day) during primary hyperproduction of uric acid. In these cases, urate tubulointerstitial nephritis develops. A decrease in renal excretion of urates is also observed under the influence of diuretics, alcohol, small doses of acetylsalicylic acid, aminophylline, diazepam, diphenhydramine, dopamine, drugs containing caffeine, vitamins B 12 and C, lead. Epidemic outbreaks of "lead gout" are known, caused by metal intoxication when using lead paints, using alcohol surrogates containing this element, etc.

PATHOGENESIS

URATE CRYSTAL DEPOSITS

Supersaturation of blood plasma with urates occurs at a concentration of uric acid above 0.42 mmol / l, however, crystallization of uric acid does not occur for a long time, probably due to the counteraction of an unidentified solubility of the plasma. With a decrease in temperature, crystallization is facilitated, therefore, urate deposits are formed, first of all, in areas with poor blood supply (ligaments, cartilage).

ACUTE GOUTY ARTHRITIS

The pathogenesis of acute gouty arthritis is shown in Fig. 52-1. As a result of crystallization of uric acid, microtophi (accumulations of crystals) are formed in the synovial layer and cartilage. Due to trauma, fever in the joint, or changes in the concentration of uric acid in the blood or synovial fluid, the microtophi are destroyed, and the crystals enter the joint cavity. Synovial cells produce cytokines: IL-1, IL-6, IL-8, TNF-γ, which act as chemoattractants for neutrophils. Immunoglobulins and complement components opsonize urates, stimulating the phagocytic activity of neutrophils.

KIDNEY DAMAGE

At a urine pH of more than 7, uric acid completely dissociates, at neutral values ​​it dissociates by half, and at a pH of less than 5 it practically does not dissociate. With the release of more than 1100 mg/day of uric acid, urolithiasis develops in 50% of patients. In addition, uric acid crystals can be deposited in the interstitial tissue of the kidneys and cause interstitial gouty nephritis, leading to the development of secondary hypertension.

PATHOMORPHOLOGY

In the joints during an acute gouty attack, urate crystals are detected in the form of microtophi, resembling boils during arthroscopy. Tophi in tissues are urate deposits surrounded by granulomatous tissue, which includes multinucleated giant cells. In some cases, tophi can be calcified.

Stones in the urinary tract are more often urates in composition, but in 10-12% they have impurities of calcium oxalate or phosphate. In the interstitial tissue of the kidneys, deposits of sodium urate monohydrate predominate, and in the lumen of the collecting ducts - uric acid crystals. Possible atrophic changes in the tubules of the kidneys, the deposition of lipofuscin in the epithelium of the tubules.

CLINICAL PICTURE

The clinical picture of gout consists of damage to the joints, tophi and kidney damage (interstitial nephritis and nephrolithiasis). Obesity, hyperlipidemia, disorders of carbohydrate metabolism, hypertension and coronary artery disease are often detected.

ASYMPTOMATIC HYPERURICEMIA

Asymptomatic hyperuricemia - a condition characterized by an increased content of uric acid in the blood in the absence of clinical signs of crystal deposition (i.e. without arthritis, tophi, kidney damage).

ACUTE GOUTY ARTHRITIS

A typical clinical picture is represented by a sudden onset of arthritis with severe pain in the joints. The disease is provoked by trauma, physical activity, sauna visits, emotional stress, dietary changes (both overeating and fasting), alcohol consumption, bleeding, infection, surgery, medication (most often thiazide diuretics, chemotherapeutic anticancer drugs). More often, one joint of the lower extremities is affected, and in 50% of patients, the I metatarsophalangeal joint is involved. Less often, inflammation of the elbow and wrist joints is noted; distal interphalangeal joints are affected more often against the background of existing osteoarthritis; the hip joints are usually not affected. More often, gouty attacks occur at night and proceed with a rapid increase in erythema and temperature around the joint, its swelling and soreness. Inflammation can also go to the surrounding soft tissues, forming a clinical picture of inflammation of the subcutaneous tissue or phlebitis. Severe cases are accompanied by an increase in body temperature. The usual duration of an attack is a few days, rarely a few weeks. After an attack of deformities of the joint does not occur. The above features of a gouty attack are specific and important for making the correct diagnosis.

INTERACTION PERIOD

The interictal period begins after the end of the attack and lasts until the next acute attack. In 60% of patients, recurrent attacks occur within the first year of illness. In typical cases, in the interictal period, patients do not complain, but if the patient does not receive treatment, then each subsequent attack is more severe, the interictal period is shortened. In some patients, chronic gouty arthritis develops rapidly, with little or no remission.

CHRONIC GOUTY ARTHRITIS

Chronic gouty arthritis (chronic tophi gout) occurs when left untreated and is considered the final stage of gout. It is characterized by the formation of tophi - accumulations of urate crystals surrounded by inflammatory cells and fibrous masses. Tophi are dense, mobile formations of a whitish-yellowish color, from which, when ulcerated, chalk-like contents are released.

Localization of tophi: subcutaneously or intradermally in the area of ​​the fingers and toes, knee joints, on the elbows, auricles, although tophi can form in almost any part of the body and in internal organs. In postmenopausal women, tophi are often located in the region of Heberden's nodules. Sometimes there is ulceration of the skin over the tophi with spontaneous release of the contents in the form of a pasty white mass.

Early appearance of tophi is observed: in some forms of juvenile gout, in elderly women taking diuretics, in myeloproliferative diseases and some kidney diseases, leading to severe hyperuricemia.

KIDNEY DAMAGE

Kidney damage can occur at any stage of the disease and is manifested by nephrolithiasis and tubulointerstitial nephritis. With nephritis, moderate proteinuria, a decrease in the relative density of urine, the development of hypertension and nephrolithiasis are found. Basically, the functions of the tubules are disturbed. In 10% of cases, the end stage of chronic renal failure develops. In acute obstructive uric acid nephropathy (blockade of the tubules by urate crystals), a renal variant of acute renal failure may develop.

LABORATORY AND INSTRUMENTAL STUDIES

A general blood test during acute attacks reveals leukocytosis with a shift to the left, an increase in ESR.

In a biochemical blood test, an increased content of uric acid in the serum is found.

The study of uric acid excretion is carried out after a 3-day diet that excludes foods rich in purines (meat, broths, poultry, fish, legumes, oatmeal, 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 of uric acid is secreted per day.

When analyzing the synovial fluid obtained from the affected joint, an increase in the content of leukocytes up to 10-60×10 9 /l with a predominance of neutrophils is found. Diagnostic value is the detection of needle-shaped urate crystals located intracellularly and birefringent light when examined using a polarizing microscope.

In the contents of tophi, crystals of uric acid are found. During histological examination of tophi tissue, specimens should not be fixed with formalin to avoid dissolution of urate crystals.

On radiographs of the bones, intraosseous cystic formations of various sizes are detected, caused by tophi, which can be located within the joint, next to it, and even at a distance. Severe erosions in the subchondral zone of the bone or cystic formations with clear contours (the “punch” symptom) are observed in gout infrequently. More characteristic is the destruction of the subchondral portion of the bone (intra-articular osteolysis), the epiphysis, and part of the diaphysis that occurs over time. Periarticular osteoporosis, bone ankylosis are rare. X-ray changes are found most often in the joints of the feet (primarily in the joints of the thumbs), as well as the hands.

DIAGNOSTICS

CLASSIFICATION CRITERIA

The classification criteria developed by Wallace et al. are used to make the diagnosis.

BUT. The presence of characteristic uric acid crystals in the joint fluid.

B. The presence of tophi, the content of uric acid crystals in which is confirmed by chemical or polarizing microscopy.

IN. Presence of 6 of the 12 features listed below:

1. More than one attack of acute arthritis in history

2. Joint inflammation peaks on day 1 of illness

3. Monoarthritis

4. Hyperemia of the skin over the affected joint

5. Swelling and pain in the first metatarsophalangeal joint

6. Unilateral lesion of the first metatarsophalangeal joint

7. Unilateral foot injury

8. Suspicion of tophi

9. Hyperuricemia

10. Asymmetric swelling of the joints

11. Subcortical cysts without erosion (X-ray)

12. Negative synovial fluid culture results

Six or more clinical criteria were identified in 88% of patients with gout, less than 3% of patients with septic arthritis, and 11% of patients with pyrophosphate arthropathy.

DIFFERENTIAL DIAGNOSIS

Pseudogout [a disease of calcium pyrophosphate crystal deposition (pyrophosphate arthropathy)] got its name because of its resemblance to gout. Differential diagnosis is based on a comparison of the physicochemical data of crystals: urates are X-ray negative, under a microscope they have a needle-like appearance and have the property of birefringence in a polarizing microscope. Calcium pyrophosphate crystals are X-ray positive (they are visible on radiographs of the joints, more often knee and wrist, in the form of dotted lines parallel to the joint space), have a wedge-shaped shape under the microscope and do not have the property of birefringence. Secondary pyrophosphate arthropathy occurs with hyperparathyroidism, hemochromatosis, hemosiderosis, Wilson-Konovalov's disease.

The disease of deposition of crystals of basic calcium phosphates is manifested mainly not by arthritis, but by calcific tendonitis and bursitis. The diagnosis must be based on the identification of detectable chemical compounds: crystals of basic calcium phosphates, unlike pyrophosphates and urates, do not have characteristic optical properties. For screening diagnostics of basic calcium phosphate crystals, staining with alizarin red dye is recommended, but the sensitivity and specificity of the method are low.

In some cases, gout mimics the clinical picture of osteoarthritis or rheumatoid arthritis, so the determination of uric acid in the blood serum and the study of synovial fluid using polarizing microscopy are among the necessary elements of the differential diagnosis of arthritis.

Patient education:

elimination of risk factors for exacerbation of arthritis: weight loss, refusal to take alcohol;

detailed information on the nature of clinical manifestations in acute gouty arthritis and the consequences of uncontrolled hyperuricemia;

the need for rapid relief of acute gouty arthritis (always have an effective NSAID with you);

ninformation about the side effects of drug therapy.

Diet. A low-calorie and low-carbohydrate diet with the inclusion of polyunsaturated fatty acids leads to a decrease in uric acid levels.

Treatment tactics acute gouty arthritis and complications associated with hyperuricemia are different.

TREATMENT OF ACUTE GOUTY ARTHRITIS

For the relief of an acute attack of gout, NSAIDs, colchicine and GC are used (locally and systemically).

Treatment should begin as early as possible, preferably within 24 hours of the onset of arthritis.

Nonsteroidal anti-inflammatory drugs

In the absence of contraindications, NSAIDs in full therapeutic doses are the drug of choice: indomethacin (25-50 mg 4 times a day), naproxen (500 mg 2 times a day), diclofenac (25-50 mg 4 times a day), nimesulide (100 mg 2 times a day).

Differences in efficacy between NSAIDs have not been established.

NSAIDs are more effective than colchicine in patients with long-term acute arthritis.

In patients with cardiovascular risk factors, it is not recommended to use selective NSAIDs due to an increased risk of vascular complications.

Colchicine

Colchicine is rarely used due to the high frequency of side effects (diarrhea, nausea).

Colchicine should not be given to patients with severe kidney, gastrointestinal, or cardiovascular disease, as the risk of severe side effects increases.

Potential indications: failure of NSAIDs or contraindications (for example, treatment with warfarin) for their prescription.

application tactics.

n0.5-0.6 mg orally every hour until relief of arthritis or the appearance of side effects or until the maximum allowable daily dose (6 mg) is reached or on the 1st day - 3 mg (1 mg 3 times after meals), for 2nd day - 2 mg (1 mg in the morning and evening), and then 1 mg / day.

In some cases (especially with exacerbation of gout in the postoperative period), IV colchicine is used (no more than 3 mg in 10-20 ml of saline is administered over 10-20 minutes). Intravenous administration of colchicine can lead to severe toxic reactions (myelosuppression, renal failure, intravascular hypercoagulability, hepatonecrosis, hypocalcemia, convulsions, heart failure).

n To prevent exacerbations of arthritis at the beginning of antihyperuricemic therapy - 0.5-1.5 mg / day (elderly people and those with renal insufficiency should be given the minimum effective dose of colchicine).

Combination therapy with colchicine and NSAIDs has no advantage over NSAIDs alone.

Glucocorticoids

Applied in the presence of contraindications for the appointment of NSAIDs and colchicine.

If 1 or 2 joints are affected (with the exclusion of septic arthritis) - intra-articular injection of triamcinolone (40 mg into large joints, 5-20 mg into small ones, or methylprednisolone aceponate (40-80 mg) into large joints, 20-40 mg into small joints ), or betamethasone (1.5-6 mg).

With multiple lesions of the joints - systemic administration of GCS:

nprednisolone 40-60 mg po on the first day, followed by a dose reduction of 5 mg on each subsequent day;

triamcinolone 60 mg IM or methylprednisolone 50-150 mg iv, if necessary, repeat administration after 24 hours.

ANTIHYPERURICEMIC THERAPY

Antihyperuricemic therapy effectively prevents the recurrence of gouty arthritis and the development of complications associated with uncontrolled hyperuricemia.

During treatment, the concentration of uric acid should be maintained at the level of ‹400 µmol / l.

Antihyperuricemic therapy should be carried out throughout life.

Do not start antihyperuricemic therapy during an acute attack of arthritis until the attack is completely relieved (if an arthritis attack has developed while taking antihyperuricemic drugs, treatment should be continued).

Consider using colchicine to prevent arthritis exacerbations at the start of antihyperuricemic therapy.

Indications:

increased frequency of seizures up to 2 or more per year;

chronic tophi gout.

Contraindications.

n Antihyperuricemic therapy is not used in patients with asymptomatic hyperuricemia (with the exception of patients with hyperuricemia on cancer chemotherapy).

n In the presence of contraindications, it is possible to use small doses of NSAIDs or GCs (IM) in the form of short courses.

nDo not use uricosuric agents in patients with nephrolithiasis.

The effectiveness of antihyperuricemic therapy is determined by the normalization of the level of uric acid in the blood serum, a decrease in the frequency of gout attacks, resorption of tophi, and the absence of progression of urolithiasis.

Allopurinol

Absolute indications for the appointment of allopurinol:

n frequent attacks of acute gouty arthritis,

n clinical and radiological signs of chronic gouty arthritis;

nformation of tophi in soft tissues and subchondral bone;

n combination of gout with renal failure;

nnephrolithiasis;

n an increase in the level of uric acid in the blood > 780 µmol / l in men and > 600 µmol / l in women;

daily excretion of uric acid more than 1100 mg;

n Carrying out cytotoxic therapy or X-ray therapy for lymphoproliferative tumors.

nTo prevent acute attacks of arthritis and severe adverse reactions, allopurinol therapy is started with a small dose (50 mg / day) and gradually increased until normouricemia is achieved (under the control of uric acid levels every 2 weeks). With the correct selection of the dose of allopurinol, the decrease in the level of uric acid should be no more than 10% of the initial level within 1 month.

The effective dose of allopurinol varies widely (from 100 mg/day to 900 mg/day or more).

nAllopurinol at a dose of more than 300 mg / day is prescribed in several doses.

When selecting the dose of allopurinol, creatinine clearance should be taken into account (if the clearance is less than 30 ml / min, the dose of allopurinol should be reduced).

nWhen allopurinol is discontinued, uric acid levels return to baseline within 3-4 days.

nTreatment with allopurinol is associated with the development of side effects (sometimes severe - 5%) and should be carried out under strict control.

FORECAST

The prognosis is favorable with early diagnosis and adequate treatment. Prognostically unfavorable factors include the development of the disease at the age of 30 years, persistent hyperuricemia more than 0.6 mmol/l, persistent hyperuricosuria more than 1100 mg/day, the presence of urolithiasis in combination with urinary tract infection, nephropathy, especially in the presence of diabetes mellitus and hypertension.