home Audience 2 X-ray sign of joint damage due to gout. Gout. Causes, symptoms and signs, diagnosis and treatment of pathology Results of a general urine test

X-ray sign of joint damage due to gout. Gout. Causes, symptoms and signs, diagnosis and treatment of pathology Results of a general urine test

Gout is a disease characterized by impaired purine metabolism and the deposition of urate crystals in the form of uric acid in various tissues. This disease has been known to medicine since ancient times; it is often called the “disease of kings,” since most aristocrats suffered from gout due to eating large amounts of meat and wine.

Approximately 2% of the world's population suffers from gout. Recently, the incidence of this arthropathy has increased, which is due to physical inactivity, overeating, and drinking large amounts of alcohol. Mostly men (80-90%) of working age are affected.

Since gout is a disease of the whole body, and not just the joints, many organs and systems are involved in the pathological process, but most often the disease manifests itself as gouty arthritis. According to ICD 10, gout falls under category M 10.

Causes of the disease

Depending on the causes of the disease, gout can be primary or secondary. Primary gout always develops in individuals who have a genetic predisposition to impaired purine metabolism. In most cases, people are not aware of this “feature” of their metabolism.

If an organism that is prone to the deposition of uric acid crystals is exposed to provoking environmental factors, it will most likely develop gouty polyarthritis.

Risk factors:

eating foods that are rich in purines (meat, legumes, etc.);
alcohol abuse;
stress;
injuries, physical fatigue;
infectious diseases;
chronic diseases of internal organs;
use of certain medications (cytostatics, thiazide and loop diuretics, aspirin, ethambutol, pyrazinamide, B vitamins, muscle relaxants).

Very often, gout is secondary in nature and develops against the background of other pathological conditions:

chronic renal failure;
kidney diseases (glomerulonephritis, polycystic amyloidosis, diabetic nephropathy);
side effects of chemotherapy, radiotherapy and pharmacotherapy;
thyroid diseases;
pathology of the cardiovascular system;
obesity;
liver diseases.

The essence of the disease

Several pathological processes play a role in the development of gouty polyarthritis. In people with a genetic predisposition, one of the links in protein metabolism is disrupted, resulting in the formation of much more purine substances than necessary, and then uric acid. Its concentration in the blood increases - hyperuricemia.

This situation leads to increased excretion of urate by the kidneys and deposition of uric acid crystals in peripheral tissues (inner lining of joints, skin, renal tubules). This causes the main symptoms of the disease: urate stones form in the kidneys (urolithiasis), peculiar nodules grow in the skin - tophi, which consist of uric acid crystals, and aseptic (non-infectious) inflammation develops in the joints with the development of acute gouty arthritis.

Symptoms of joint damage

Acute gouty arthritis develops so typically and characteristically that the diagnosis can be established based on the symptoms of arthritis alone.

Clinical symptoms:

the onset is sudden and acute;
often pain in the joint wakes the patient at night;
As a rule, the big toe (1 metatarsophalangeal joint) is affected;
body temperature rises;
pain in the joint is severe, bursting;
mobility in the joint is limited due to pain, the area is painful even to touch;
the joint swells, the skin becomes hot and red;
An acute attack lasts 4-5 days, then passes without a trace.

Over time, attacks of acute gouty arthritis become longer, and the time intervals between them become shorter. There comes a time when the pain syndrome becomes constant, there are no periods of remission. This condition is called chronic gout arthritis.

At this stage of the disease, articular cartilage is destroyed, defects are formed in the bones, which are filled with urate crystals. Clinically, this manifests itself in joint deformities and loss of functional activity, which often leads to disability and decreased performance.

The above describes classic acute gouty arthritis. But there are several more atypical clinical forms of arthritis with gout:

Subacute form. Characterized by mild clinical symptoms. More often observed in women.
Rheumatoid form. The interphalangeal, metacarpophalangeal, and wrist joints are affected, which is more typical for rheumatoid arthritis.
Pseudophlegmonous form. Monoarthritis (1 joint is affected) with severe symptoms of synovitis and periarthritis, fever, severe signs of inflammation of the joint, which resembles a purulent lesion.

How to make a diagnosis?

Symptoms of gouty arthritis allow one to suspect the disease, but additional examination methods are required for an accurate diagnosis.

Diagnosis of gout includes:

complete blood count (increased ESR and leukocytosis);
concentration of uric acid in the blood (increased);
rheumatic tests (increased levels of CRP and other indicators of the inflammatory process);
general urinalysis (urate crystals);
X-ray examination of the affected joints (characteristic changes - “piercer symptom”);
biopsy of subcutaneous tophi;
joint fluid analysis;
renal function test.

Principles of treatment

Treatment of gout can be divided into 2 stages:

elimination of an acute attack of arthritis;
basic therapy between exacerbations for their prevention.

During an acute attack of gouty arthritis, it is necessary to provide functional rest to the affected joint. Fasting is contraindicated; you must adhere to diet No. 6, drink 2.5 liters of alkaline liquid per day.

To eliminate the symptoms of inflammation and pain, the doctor will prescribe one or more medications from the following:

colchicine;
non-steroidal anti-inflammatory drugs (meloxicam, celecoxib);
glucocorticoid hormonal drugs (hydrocortisone, methylprednisolone).

Under no circumstances should you take these medications without a doctor's prescription. These are serious medications that have many contraindications and side effects. Therefore, self-medication can only make things worse for yourself.

Physiotherapeutic treatment is also widely used: ultraviolet irradiation of the joint, electrophoresis, applications with dimexide.

Basic anti-relapse therapy includes:

taking uricodepressants (drugs that prevent the formation of uric acid) - alopurinol, orotic acid, thiopurinol;
uricosurics (medicines that promote the excretion of uric acid by the kidneys) - anturan, benemid, ketazone;
uricolytics (drugs that dissolve urinary stones and prevent their re-formation) - citrate mixtures (blemarene, soluran, urodan) and enzymes (urate oxidase, hepatocatalase).

Diet food

An integral part of treatment is diet for gouty arthritis.

It is necessary to exclude from your diet fatty, high-calorie foods with a large amount of meat and fish dishes, foods rich in purines - kidneys, liver, brain, tongue, veal, chicken, meat and fish broths, herring, smoked and salted foods, sausages, canned food , chocolate, strong coffee and tea, legume dishes, asparagus, sorrel, spinach, alcohol.

Gouty arthritis is a serious disease that must be treated not only during exacerbations, but also between relapses, and the basis of therapy should be dietary nutrition. This is the only way to protect yourself from the progression of the disease and its complications.

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Gout: diagnosis and treatment of “Disease of Kings”

Gouty arthritis is a chronic disease caused by problems with uric acid metabolism. As a result of this process, the amount of urates (crystals of sodium salt of uric acids) increases and their accumulation in tissues.

Clinically, this disease manifests itself as periodic exacerbation with the formation of gouty nodes (tophi) due to oversaturation with extracellular fluid.

Gout is a well-known and very common disease. Until recently, it was believed that it affects only the male half of the population. However, more and more often, lumps on the joints are diagnosed in women of different ages.

How often is the disease detected?

The incidence of diagnosing this type of acute arthritis and hyperuricemia (high uric acid levels) varies. The prevalence of excessive salt levels has reached 4-14 percent and is trending upward.

The vast majority of researchers note that residents of those countries where the standard of living is high get sick. Gouty arthritis practically does not affect children and women who are in the premenopausal period.

According to statistics, approximately 85% of patients are middle-aged and older people who have had asymptomatic hyperuricemia over the previous 20-30 years. Of these, at least 95% are men who have crossed the age limit of 40 years.

This pattern is explained by the different states of purine metabolism and the characteristics of hormonal levels. As for women, an inverse relationship was found between:

the amount of estrogen in the patient’s body;
the concentration of uric acid salts.

With a decrease in hormonal levels during menopause, not only hyperuricemia is observed, but also a very noticeable deposition of urate crystals in tissues and joints.

A detailed analysis of cases where patients sought emergency medical help showed that 15% of people suffering from joint problems were actually diagnosed with an acute attack of gouty arthritis.

In recent years, the proportion of sick people with a history of rheumatic pathologies has increased by 8%.

Features of the disease are that it has become:

debut at a younger age;
early complications with frequent and prolonged exacerbations;
manifested by pronounced hyperuricemia and numerous tophi.

What does the patient feel during an attack?

The clinical picture of gouty arthritis usually consists of damage to the joints and a number of problems of internal organs. The beginning of the disease is considered to be its very first attack.

However, often gout may not make itself felt or may manifest itself only as one of the symptoms, for example, renal colic, which is caused by urate nephrolithiasis.

The main clinical manifestation of gout will be joint damage:

acute gouty arthritis;
chronic arthritis with accumulation of paraarticular tophi;
intermittent arthritis.

It follows that there are several periods (stages) of the disease: asymptomatic hyperuricemia (premorbid period), which is characterized by an increased level of uric acid salts without symptoms of gout, acute gouty arthritis, recurrent arthritis (intermittent), chronic gout, chronic tophi gouty arthritis.

Measures for diagnosing gout

If the pathology stage is early, then even an X-ray photo does not show any changes in the joint. Only in more advanced cases will an x-ray show signs of destructive processes in cartilage and bone tissue, which are caused by the accumulation of urate crystals in the subchondral bone.

Medicine knows several classifications of characteristic changes in gouty arthritis:

large cysts in the deep layers of bone tissue and subchondral bone (sometimes soft tissue compaction is possible);
large-sized neoplasms, small erosions on the surface of the joints. There is a constant compaction of the soft tissue around the joint (sometimes calcification is possible);
erosions become large, but no more than a third of the size of the joint surface. There is osteolysis of the epiphysis, significant compaction of soft tissue and accumulation of lime in the joint.

There is another classification. According to it, important radiological signs will be compactions in soft tissues, eccentric darkness caused by tophi, clearly visible articular surfaces (bones, joints), absence of juxtaarticular osteoporosis, marginal sclerosis, perforation (erosive processes).

Thus, these classifications differ significantly from each other. This requires unification of a number of radiological symptoms for this form of arthritis.

Instrumental and laboratory diagnostics of gout

If during an acute attack of gout the patient donates blood from a finger for a general analysis, leukocytosis will be detected with an increase in erythrocyte sedimentation rate (ESR) and a neurophilic shift to the left.

Tests for gout in the blood serum in such cases determine an excessive concentration of uric acid salts. In men we are talking about indicators of more than 7 mg (0.42 mmol per liter), in women 6 mg (0.36 mmol per liter).

A study to determine uric acid salts should be carried out 3 days after the start of a special diet that excludes purine foods (red meat, fish, broths, beans, cocoa, teas, coffee, chocolate, alcoholic beverages).

The volume of urine excreted by the body per day, the concentration of uric acids and creatinine in it are determined. If we talk about norms, then about 300-600 mg should be secreted in 24 hours (1.8-3.6 mmol per liter).

Uric acid crystals are often found in the contents of tophi. Typical of the disease will be cyst-like neoplasms inside the bones. They can be of different sizes, and are caused by the same tophi.

This disease of kings, if chronic, is accompanied by the destruction of cartilage (narrowing of the joint space) and the active development of bone erosions along the edge. A characteristic symptom will be a “punch” - this is a marginal bone or cyst-like growth of the correct shape. It is distinguished by clear contours (sometimes sclerotic).

As the pathological condition develops, obvious destruction occurs not only in the subchondral part of the bone, but also in the epiphysis and diaphysis, forming osteopis inside the joint.

Gout is most pronounced in the joints of the diseased first toe. Moreover, there are cases when x-rays showed the presence of pathological changes in the joints:

shoulder;
hip;
sacroiliac;
spine.

Bone deformities in the disease rarely decrease, even if adequate treatment is carried out.

It is equally important to conduct a study of the joint fluid. This procedure makes it possible to detect the presence of salt crystals and leukocytes specific for gout. Of diagnostic importance is the identification of needle-shaped salt crystals in the lubricant, which are located inside cells that birefringent light during examination using polarizing microscopes.

Another important indicator for an acute attack of this disease is the cellular composition of the synovial fluid, namely the number of leukocytes in it.

Visceropathy

A disease associated with gout is visceropathy, which often affects the patient’s kidneys. Speaking in numbers, from 50 to 75% of patients are susceptible to this problem. In some cases, the formation of gouty nodes in the liver provokes hepatopathy (poisoning with liver poisons).

The likelihood of kidney damage in people suffering from gout is almost proportional to the duration of the disease and the severity of hyperurinemia. In some cases, urate nephropathy precedes the development of articular syndromes.

The incidence of kidney damage ranges from 30 to 70% of cases.

As is known, the clinical symptoms of disruptions in purine metabolism will be isolated urinary nephropathy. Quite often it occurs latently, and for a long time. This condition is called a precursor to gouty arthritis. Often, urate nephropathy becomes the only sign of metabolic disorders.

Back in the late 80s of the last century, the Sechenov Institute conducted a study that confirmed that the presence of problems with purine metabolism, namely long-term hyperurinemia, becomes the cause of clinically latent glomerulonephritis. This disease of kings occurs with a predominance of hematuria and active progression towards chronic kidney failure (CKF).

From all of the above, a logical conclusion should be drawn that gouty kidney is a collective concept. It includes:

renal pathology, which is observed with gout;
tophi in the kidney parenchyma;
uric acid stones;
glomerulosclerosis;
interstitial nephritis;
atherosclerosis with transition to nephrosclerosis.

Other methods for diagnosing gout

Kings disease, as gout is often called, can be detected using other methods. Thus, in 1963, at an international symposium, several criteria for diagnosing pathology were developed.

Its development is indicated by symptoms: tophi, increased levels of uric acid in the blood, acute pain attacks that usually occur unexpectedly and pass quickly, the presence of crystals of uric acid salts in the joint fluid and tissues (diagnosed by chemical examination or microscopic).

The doctor will be able to make a final diagnosis of gouty arthritis if the patient has two points at once. The listed criteria include a third symptom characteristic of the disease. The presence of tophi on the joints, as is known, cannot be an early sign. For this reason, this symptom is not sufficiently informative at the beginning of the pathological process.

Similar criteria were proposed a little later in 1977:

the presence of monosodium urate crystals in the joint fluid;
tophi was confirmed by polarization microscopy and chemical analysis;
the presence of at least 6 of the 12 radiological and laboratory symptoms listed below (maximum inflammatory process in the joint in 1 day, monoarthritis, the presence of more than 1 attack of arthritis, redness of the joints, asymmetric manifestations of inflammation, suspicion of the presence of tophi, pain and inflammation of the metatarsophalangeal joint of the big toe , unilateral lesion of the tarsal joint, absence of pathological microorganisms in the culture of joint fluid, hyperuricemia, subcortical cystic ulcers identified by x-ray).

Disease of kings and treatment

If the preliminary diagnosis is confirmed during research, then the disease should be treated as early as possible.

Depending on the characteristics of the disease, the optimal treatment will be selected. It is also necessary to take into account the stage of the disease:

acute attack;
interictal period;
chronicle.

Treatment of gouty arthritis requires relief of a painful attack and procedures in the inter-attack period. Preventive measures are provided to prevent re-exacerbation of articular syndrome, treatment of extra-articular symptoms of the disease (tendonitis, myositis, gouty nephropathy).

Doctors identify three main tasks when carrying out treatment:

relief of symptoms;
relapse prevention;
preventing the disease from becoming chronic.

Treatment of gout will be of high quality only if the doctor’s instructions are strictly followed. Diet plays an important role in this matter. Without a properly prescribed diet, treatment will not be successful.

Treatment is supplemented with traditional medicine recipes. However, such methods should not exclude treatment with medications and physical procedures.

Spondylosis is a degenerative-dystrophic disease of the spine caused by pathological deposition of calcium salts in the ligamentous apparatus of the spinal column. On radiographs, the disease can be seen in the form of bone “spikes” located along the lateral parts of the vertebral bodies.

The terms “dystrophic” and “degenerative” were introduced in medicine to describe the pathogenetic links of the process caused by a violation of the supply of nutrients, as well as changes in the blood supply to anatomical structures.

Spondylosis belongs to the group of dystrophic diseases, as it occurs against the background of a lack of chemical compounds necessary for the normal development of the musculo-ligamentous apparatus of the spine, as well as for the healing of tissues after damage.

Degenerative-dystrophic spondylosis of the spine is observed mainly in old age, although recently there have been trends towards its rejuvenation. After 50 years, the spinal column undergoes reverse involutional changes. The process is significantly accelerated against the background of other pathologies:

Diseases of the cardiovascular system;
Violations of vascular permeability;
Deposits of cholesterol plaques in the artery wall;
Multiple ruptures of muscles and ligaments;
Metabolic diseases.

With heart disease, microcirculation is disrupted, so the spine lacks oxygen. Against this background, even with minimal damage to the ligaments, multiple ruptures form. Initially, repair occurs due to the overgrowth of damaged areas with non-functional fibrous (connective) tissue.

If the process continues for a long time, salts of the mineral calcium (Ca) are deposited at the rupture sites. They are clearly visible on the x-ray. Osteophytes irritate the nerve receptors of the muscular-ligamentous apparatus, and a “aching” pain appears.

Violation of vascular permeability is accompanied by multiple small hemorrhages. If they appear in the small capillaries of the muscular-ligamentous system of the spine, inflammation occurs in the tissues. Bone “spikes” occur when the process persists for a long time.

Similar changes occur with traumatic injuries to the muscles and ligaments of the spine and atherosclerosis (formation of cholesterol plaques in the walls of blood vessels).

In metabolic diseases (for example, gout), ossification of soft tissues may appear primarily as a result of an excess of chemical compounds. With gout, uric acid accumulates in the ligaments, which causes damage. The deposition of calcium salts in such structures is intended to reduce the mobility of the damaged area, but excessive accumulation leads to serious pathological changes.

Typically, spondylosis occurs simultaneously with osteochondrosis - a decrease in the height of the intervertebral discs. These diseases are dependent on each other, since the pathogenetic links of one of them lead to the other, and vice versa.

There are other reasons for the formation of the disease, but they are observed more rarely.

Stage 1 spondylosis does not have pronounced clinical symptoms. Minor damage to the muscular-ligamentous apparatus in rare cases causes aching pain. True, there is specificity of the disease depending on the location.

Degenerative-dystrophic spondylosis in the cervical spine is dangerous not so much because of the pain syndrome as because of the likelihood of impaired blood supply to the brain. The vertebral artery passes through the transverse processes of the cervical vertebrae, supplying blood to approximately 25% of the structures of the brain. With ossification of the neck ligaments, compression of this vessel may occur.

The first symptoms appear with stage 2 cervical spondylosis at the level of the lower segments (C5, C6, C7). As a result of such changes, the following changes are formed:

Vegetative;
Static;
Neurological.

We'll talk about them below.

Spondylosis of the thoracic spine of the 1st degree is asymptomatic, since the mobility of the area is “fixed” by the ribs. A slight displacement of the vertebrae in this form does not lead to pinching of nerve fibers or serious compression of blood vessels.

At stage 2 of the pathology, pain along the ribs (intercostal neuralgia) and painful sensations in the heart area due to damage to the cardiac nerve are possible.

More pronounced symptoms of spondylosis are observed when bone osteophytes are localized in the lumbar and sacral regions. In these areas there are large nerve plexuses responsible for the functionality of the abdominal cavity, small pelvis and lower extremities. As a result, grade 2 spondylosis in the lumbar region forms:

Pain syndrome in the lower back;
Radiation of pain to the legs and buttocks;
Loss of sensitivity of the skin of the lower extremities;
Loss of nerve reflexes (knee, Achilles).

Advanced spondylosis of all localizations is accompanied by serious clinical manifestations caused by secondary damage to internal organs against the background of pathological impulses from the nervous system.

Neurological symptoms

To properly treat spondylosis, you should study the characteristics of the neurological symptoms that are observed with it. They can be caused by both ossification of ligaments and intervertebral hernias. These pathogenetic links of the pathological process require a different approach to treatment.

Neurological symptoms of spondylosis:

Ankylosing spondylitis is a pain syndrome on the affected side when lifting the healthy leg up. It appears due to the mobility of the damaged nerve fiber;
Lasègue's symptom is pain when raising your legs up. The syndrome disappears when the leg is straightened at the knee joint. When you lift your leg up to an angle of 30 degrees, the pressure on the nerves increases, so the pain intensifies;
Neri – when bending the head, lumboischialgic pain is observed;
Bragarda - with a positive Lasègue symptom, the pain syndrome intensifies with dorsiflexion of the foot;
Wasserman - when extending the leg, pain occurs in the knee joint;
Matskevich - lying on the stomach increases pain when bending the leg at the knee joint.

Dystrophic spondylosis of 1st and 2nd degrees is accompanied by vegetative syndromes. If the osteophyte is localized in the thoracic region:

Heart rate increases;
Blood pressure increases;
Colicky pain occurs in the chest when turning the body;
Breathing becomes difficult.

Autonomic disorders in the presence of ossification of ligaments in the neck:

Headache and dizziness;
Spasmodic contractions of the shoulder muscles;
Inability to raise your arm up;
Difficulty bending the head forward and backward.

What is observed with spondylosis of 1st and 2nd degree in the lumbar spine:

Aching pain in the back, buttocks and lower extremities;
Increased urination and defecation disturbance;
Loss of sensation in the skin of the legs;
Impaired blood supply to the veins.

Static syndromes of the disease are manifested by impaired mobility of the upper and lower extremities with paraplegia and paralysis.

They arise due to straightening or strengthening of lordosis and kyphosis of the spine against the background of pathology. The changes described below are compensatory in order to reduce the shock-absorbing pressure on the spinal column when walking and lifting loads:

Limitation of mobility of the spinal column;
Decreased flexion amplitude of the back;
Difficulty with maximum lateral bending;
Forced posture to compensate for pain (schialgic scoliosis).

Neurological manifestations include loss and weakening of the body's reflexes. So. Grade 3 spondylosis can lead to decreased impulses in the ligaments of the lower extremities. In this case, when you tap the kneecap with a neurological hammer, the knee does not rise up, as is normal.

A neurologist can detect serious spinal injuries just by looking at the patient. It is detected by trophic disorders:

Blueness of the skin of the back;
Peeling of the skin;
Decreased skin temperature;
The eye twitches when the nerves are pinched.

It is possible to cure neurological disorders only after eliminating the pathogenetic link that led to their appearance.

Features of compression syndrome

Radicular compression appears in the disease not only due to the formation of bone osteophytes, but also due to the secondary formation of intervertebral hernias. If it is present, any attempt to turn the body or move causes acute pain, similar to the sensations when an electric current passes through the body.

With cervical spondylosis, pain is observed in the upper limb and can reach the tips of the 4th and 5th fingers. It gets worse when sneezing or lifting heavy objects.

With lumbar localization, similar symptoms are observed in the lower limb. Upon examination, the neurologist will detect a weakening of muscle strength on one or both sides.

Cervical spondylosis manifests itself more as sympathalgia rather than radiculalgia (as with lumbar localization of the disease). Their peculiarity lies in the presence of a primary focus, and the irradiation exactly corresponds to the course of the nerve. With radicular symptoms, the pain syndrome is diffuse, and the primary focus of its origin is difficult to identify even for a qualified neurologist.

Lumbar or cervical dyscalgia are secondary syndromes that form against the background of intervertebral hernias. They differ from primary sympathalgia in their high intensity. Against the background of dyscalgia, there is a decrease in muscle strength and low mobility of the cervical muscles.

How to treat the disease

Spinal spondylosis can be treated only after a thorough diagnosis of the symptoms.

Unfortunately, it is impossible to completely get rid of the pathology, but symptomatic therapy can restore a person’s ability to work and reduce the risk of disability.

The diagnosis of spondylosis can be made only after using x-ray methods:
Computed and magnetic resonance imaging;
X-ray of the spine in two projections.

The main stages of treatment for spondylosis:

Anesthesia;
Normalization of skeletal muscle tone;
Elimination of neurological disorders;
Manual therapy;
Rehabilitation complex;
Normalization of diet;
Maintaining hygiene of the musculoskeletal system and changing work and sleep patterns.

Spondylosis of the 1st and 2nd degrees is manifested by aching pain, which can be effectively treated with non-steroidal anti-inflammatory drugs: movalis, ketorolac, ibuprofen, nise, diclofenac.

Reflexology and acupuncture are used as additional procedures for pain relief.

The basis of treatment of the disease is therapeutic exercises. It is designed to normalize the condition of the muscular frame of the back, which will maintain the correct position of the spine. A set of exercises is developed by doctors based on the individual characteristics of the pathology.

Spondylosis with neurological disorders requires treatment with drugs to improve blood supply: Cavinton, Trental, pentoxifylline. To normalize muscle tone, muscle relaxants are used: mydocalm.

Unfortunately, if a doctor diagnoses spondylosis, it is radically impossible to treat it. Complex therapy allows you to eliminate the main manifestations of the disease and create comfortable conditions for a person’s life. At the same time, he must carefully follow all the doctor’s recommendations. Otherwise, it is difficult to prevent disability.

Gout is one of the common systemic diseases that are related to impaired purine metabolism. X-ray is one of the ways to detect this pathology. The diagnostic procedure is informative only if structural changes have already occurred in the joint. Laboratory tests help confirm the accuracy of the X-ray results.

If joint pain occurs, you should immediately seek help from a specialist. Doctors of different specializations deal with such diseases. If you complain about discomfort in the joints, it is customary to go to an appointment with a therapist, nephrologist, hepatologist or rheumatologist. The last option is considered more optimal.

To understand what exactly is troubling the patient, he first needs to undergo a full examination in the clinic. A referral for diagnostic procedures is issued by the doctor with whom he is being seen. Several types of tests will be required:

What does an x-ray show for gout?

The manifestations of such arthritis are clearly visible on x-rays. On x-rays, the specialist recognizes places where there is an accumulation of salt crystals. Therefore, when symptoms of this disease appear, the doctor first of all sends the patient to undergo such an examination. It makes it clear whether signs of gout are really present, and not of another joint pathology.

The main essence of the diagnostic procedure is the absorption of rays by the tissues of the affected area. This area is subsequently projected on film or a computer monitor. The information received is processed by the doctor. Based on the conclusions made, he can judge the patient’s current condition and select the optimal treatment for him.

X-rays help determine the extent of destruction of bone structures due to gout.

X-ray signs of gout

X-rays help to accurately determine the type of disease; this type of diagnosis is one of the most accurate

The swelling of soft tissues characteristic of the disease helps identify arthritis in the early stages of development. The development of bone inflammation cannot be ruled out. Due to the active course of the disease, bone destruction occurs. Destructive processes can occur both inside and outside the joint.

X-ray manifestations of joint disease are primarily observed at the edges of bone structures. They take on the appearance of a kind of shell or shell. There is a whole classification of stages according to the signs of gout, which can be seen on x-rays:

First stage. Cysts and accumulations of urates form in the affected area. Soft tissue compaction is observed.
Second stage. Large cysts characteristic of the pathology form in the joint area. Erosive processes also begin on the surface of the joint.
Third stage. Tissues are subject to severe erosion. It can occupy about a third of the entire joint. As a result, partial destruction of the bone occurs and salt crystals are deposited in the empty cavities.

X-ray changes are usually observed during the 1st and 2nd stages of gouty arthritis. They are formed over 9 years. After about 10-15 years, irreversible destruction occurs in the joint area. If the patient begins to properly treat his disease in a timely manner, he will be able to avoid negative consequences and serious complications that can even lead to disability.

Timely recognition of the pathological process in the joint helps to quickly defeat the disease and prevent its transition to a chronic form.

Where to get an x-ray

When prescribing a referral for an X-ray examination to a patient with suspected gouty arthritis of the joint, the doctor will immediately inform him where exactly this diagnosis can be carried out. As a rule, x-rays are taken in the same clinic where the appointment took place. Such diagnostics are carried out by public and private medical institutions that have the necessary equipment.

The cost of an x-ray of a joint for gout depends on where exactly the diagnosis is carried out. Usually the price of the procedure is in the range of 800-2500 rubles.

Gout is a disease associated with a disorder of purine metabolism, characterized by an increase in uric acid in the blood (hyperuricemia) and the deposition of urate in articular and/or periarticular tissues, kidneys and other organs. Detection of hyperuricemia is not sufficient to establish a diagnosis, since only 10% of individuals with hyperuricemia have 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 with a history of asymptomatic hyperuricemia for 20-30 years. Men suffer from gout 20 times more often. Before menopause, women rarely become ill, possibly due to the effect of estrogen on uric acid excretion. An acute attack of gout in adolescents is rarely observed.

ETIOLOGY

The accumulation of excess amounts of uric acid in the blood can 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 that develops when prescribed various drugs.

HYPERPRODUCTION OF URIC ACID

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

Primary overproduction 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 hyperproduction occurs only in males. When an excess 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, and dry wine.

Secondary overproduction is caused by increased cell breakdown during hemoblastosis, paraproteinemia, chronic hemolysis, antitumor chemotherapy, and is also typical for people who abuse alcohol. Hyperuricemia often accompanies psoriasis, although clinical manifestations of gout rarely develop.

REDUCED URIC ACID EXCRETION

Normally, about 60-70% of uric acid is excreted by the kidneys, the rest by the intestines and skin. Excretion of urate by the kidneys involves four stages: glomerular filtration, reabsorption of 95% of filtered uric acid, secretion in the proximal tubules, and reabsorption of 40-44% of 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 the crystallization of urates in the kidneys against the background of an increase in their excretion (more than 800 mg/day) with 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. There are known epidemic outbreaks of “lead gout” caused by metal intoxication through the use of lead paints, consumption of alcohol substitutes containing this element, etc.

PATHOGENESIS

DEPOSITS OF URATE CRYSTALS

Plasma supersaturation with urates occurs when uric acid concentrations exceed 0.42 mmol/l, but crystallization of uric acid does not occur for a long time, probably due to counteraction by an unidentified solubilizing ability of the plasma. As the temperature decreases, crystallization is facilitated, so urate deposits form primarily in areas with poor blood supply (ligaments, cartilage).

ACUTE GOUT ARTHRITIS

The pathogenesis of acute gouty arthritis is presented in Fig. 52-1. As a result of crystallization of uric acid, microtophi (clusters of crystals) are formed in the synovial layer and cartilage. Due to injury, increased temperature in the joint, or changes in the concentration of uric acid in the blood or synovial fluid, the microtophi are destroyed and the crystals are released into 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.

Rice. 52-1. Pathogenesis of acute gouty arthritis.

KIDNEY DAMAGE

At a urine pH of more than 7, uric acid dissociates completely, 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 attack of gout, urate crystals are detected in the form of microtophus, resembling boils during arthroscopy. Tophi in tissues are urate deposits surrounded by granulomatous tissue, which contains multinucleated giant cells. In some cases, tophi may become calcified.

Stones in the urinary tract are often urate in composition, but in 10-12% they contain admixtures of calcium oxalate or calcium 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. Atrophic changes in the renal tubules and deposition of lipofuscin in the tubular epithelium are possible.

CLINICAL PICTURE

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

ASYMPTOMATIC HYPERURICEMIA

Asymptomatic hyperuricemia is a condition characterized by elevated levels of uric acid in the blood in the absence of clinical signs of crystal deposition (i.e., no arthritis, tophi, or kidney damage).

ACUTE GOUT ARTHRITIS

The typical clinical picture is represented by sudden onset arthritis with severe joint pain. The disease is triggered by injury, physical activity, sauna use, emotional stress, diet changes (both overeating and fasting), drinking alcohol, bleeding, infection, surgery, and the use of medications (most often thiazide diuretics, chemotherapeutic anticancer drugs). More often, one joint of the lower extremities is affected, and in 50% of patients the first metatarsophalangeal joint is involved. Inflammation of the elbow and wrist joints is less common; distal interphalangeal joints are affected more often against the background of existing osteoarthritis; the hip joints are usually not affected. More often, gout attacks occur at night and occur with a rapid increase in erythema and temperature around the joint, its swelling and pain. Inflammation can spread 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 several days, less often several weeks. After an attack, joint deformities do not occur. The above-described features of a gout attack are specific and important for making a correct diagnosis.

INTER-ATTICAL PERIOD

The interictal period begins after the end of the attack and lasts until the next acute attack. In 60% of patients, repeated attacks occur during the first year of the disease. In typical cases, during 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. Some patients quickly develop chronic gouty arthritis, with virtually no remissions.

CHRONIC GOUT ARTHRITIS

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

Localization of tophi: subcutaneously or intradermally in the area of the fingers and toes, knee joints, elbows, ears, although tophi can form in almost any part of the body and in internal organs. In postmenopausal women, tophi are often located in the area of Heberden's nodes. 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 detected. The functions of the tubules are mainly impaired. In 10% of cases, end-stage chronic renal failure develops. In acute obstructive uric acid nephropathy (blockade of tubules by urate crystals), a renal variant of acute renal failure can develop.

LABORATORY AND INSTRUMENTAL STUDIES

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

A biochemical blood test reveals an increased level of uric acid in the serum.

A study of uric acid excretion is carried out after a 3-day diet excluding 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/day of uric acid is released.

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

Uric acid crystals are found in the contents of tophi. During histological examination of tophi tissue, samples should not be fixed with formaldehyde to avoid dissolution of urate crystals.

X-rays of the bones reveal intraosseous cyst-like formations of various sizes, 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 cyst-like formations with clear contours (the “puncture” symptom) are rarely observed in gout. More typical is the destruction of the subchondral part of the bone that occurs over time (intra-articular osteolysis), the epiphysis, and part of the diaphysis. Periarticular osteoporosis and bone ankylosis are rarely found. X-ray changes are most often found in the joints of the feet (primarily in the joints of the thumbs), as well as the hands.

DIAGNOSTICS

CLASSIFICATION CRITERIA

To make a diagnosis, the classification criteria developed by Wallace et al. are used.

A. 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 chemically or by polarization microscopy.

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

1. History of more than one attack of acute arthritis

2. Joint inflammation reaches its maximum on the 1st day 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 damage to the joints of the foot

8. Suspicion of tophi

9. Hyperuricemia

10. Asymmetric joint swelling

11. Subcortical cysts without erosions (radiography)

12. Negative results on synovial fluid culture

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

DIFFERENTIAL DIAGNOSTICS

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

Basic calcium phosphate crystal deposition disease manifests itself primarily not as arthritis, but as calcific tendonitis and bursitis. The diagnosis must be based on the identification of the detected 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 imitates the clinical picture of osteoarthritis or rheumatoid arthritis, therefore, determination of uric acid in the blood serum and examination of synovial fluid using polarization microscopy are considered necessary elements in the differential diagnosis of arthritis.

Patient education:

nelimination of risk factors for exacerbation of arthritis: weight loss, avoidance of alcohol intake;

ndetailed information about the nature of clinical manifestations in acute gouty arthritis and the consequences of uncontrolled hyperuricemia;

nneed to quickly relieve acute gouty arthritis (keep an effective NSAID with you at all times);

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 GOUT ARTHRITIS

To relieve 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.

Non-steroidal anti-inflammatory drugs

In the absence of contraindications, the drug of choice is NSAIDs in full therapeutic doses: 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).

No differences in effectiveness have been established between NSAIDs.

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

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

Colchicine

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

Colchicine should not be prescribed to patients with severe damage to the kidneys, gastrointestinal tract, or cardiovascular system, as the risk of severe side effects increases.

Potential indications: NSAIDs are ineffective or have contraindications (eg, warfarin treatment) for their use.

Application tactics.

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

nIn some cases (especially with exacerbation of gout in the postoperative period), colchicine is used intravenously (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 hypercoagulation, hepatonecrosis, hypocalcemia, convulsions, heart failure).

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

Combination therapy with colchicine and NSAIDs has no advantages over NSAID monotherapy.

Glucocorticoids

Used when there are contraindications for the use of NSAIDs and colchicine.

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

In case of multiple joint damage, 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 the administration after 24 hours.

ANTIHYPERURICEMIC THERAPY

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

During treatment, uric acid concentrations should be maintained at ‹400 µmol/l.

Antihyperuricemic therapy should be continued throughout life.

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

Consider the use of colchicine to prevent exacerbation of arthritis when initiating antihyperuricemic therapy.

Indications:

nincreasing frequency of attacks up to 2 or more per year;

nchronic tophi gout.

Contraindications.

nAntihyperuricemia therapy is not used in patients with asymptomatic hyperuricemia (with the exception of patients with hyperuricemia during chemotherapy for malignant neoplasms).

nIf there are contraindications, it is possible to use small doses of NSAIDs or GCs (i.m.) in the form of short courses.

nDo not use uricosuric agents in patients with nephrolithiasis.

The effectiveness of antihyperuricemic therapy is determined by 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 prescribing allopurinol:

frequent attacks of acute gouty arthritis,

nclinical and radiological signs of chronic gouty arthritis;

nformation of tophi in soft tissues and subchondral bone;

ncombination of gout with renal failure;

nephrolithiasis;

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

ndaily excretion of uric acid more than 1100 mg;

ncarrying out cytotoxic therapy or radiotherapy 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 monitoring uric acid levels every 2 weeks). With the correct dose of allopurinol, the decrease in uric acid levels should be no more than 10% of the initial level within 1 month.

nThe 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.

nWhen selecting the dose of allopurinol, the creatinine clearance should be taken into account (if the clearance decreases to less than 30 ml/min, the dose of allopurinol must 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 supervision.

FORECAST

The prognosis is favorable with early diagnosis and adequate treatment. Unfavorable prognostic factors include the development of the disease before 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 a urinary tract infection, nephropathy, especially in the presence of diabetes mellitus and hypertension.

Gout- a systemic tophi disease that develops due to inflammation at the site of deposition of monosodium urate (MSU) crystals 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 anamnesis, previous events and the nature of the arthritis, summarized in table. 1.

However, it must be remembered that new-onset arthritis of the first metatarsophalangeal joint (MTPJ) can be observed with soft tissue infections, bunions, osteoarthritis with acute inflammation, sarcoidosis, psoriatic arthritis, pseudogout and other conditions.

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

Common reasons:

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

- injury;

- hemarthrosis;

- septic arthritis;

- osteoarthritis;

- osteomyelitis;

- aseptic bone necrosis.

Possible reasons:

- reactive arthritis;

- sarcoidosis;

- juvenile arthritis;

- psoriatic arthritis;

- hemoglobinopathies;

- osteosarcoma.

Rare reasons:

- Behcet's syndrome;

- Mediterranean fever;

- intermittent hydrarthrosis;

- vilolesionodular synovitis;

- relapsing polychondritis;

- synovioma;

- Still's syndrome;

- metastases of tumors into the synovium.

Traumatic arthritis

Septic and especially traumatic arthritis are most similar to gout in terms of the severity of inflammatory manifestations, although their incidence is significantly lower compared to gout. In the case of traumatic arthritis, identifying the provoking factor can only partially help in making the correct diagnosis, since with gout there is often a chronological connection with injury, which explains why patients primarily turn to a traumatologist or surgeon. X-ray examination of the distal parts of the feet may not be informative, since at the first attack of gouty arthritis there is still no characteristic X-ray symptom of a “punch” (to be discussed further). 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, practically the only method for verifying the diagnosis is puncture of the affected joint. In classical cases, the presence of hemarthrosis will indicate traumatic arthritis. In the absence of blood, the level of inflammatory response must be assessed, which may be difficult due to the small amount of synovial fluid obtained from the joint. However, to detect EOR crystals, it is enough to obtain a minimal amount of liquid (no more than a drop). An additional fact in favor of gouty arthritis may be the fairly 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 joint dysfunction. Septic arthritis is accompanied by fever, increased ESR, and leukocytosis, which is not typical for gout or is observed in late chronic polyarticular course. Septic arthritis can be caused by 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 detected 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 predominantly in older people (usually no younger than 55 years), approximately equally often in men and women. Clinical and radiological differences between gout and PAP are summarized in Table. 2. Cases of detection of both types of crystals in one patient are described. In 90% of cases, PAP affects the knee, shoulder joints 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 PFJ occurs. Involvement of the small joints of the hands in gout is observed more often at a late stage of the disease, and the shoulder joints can be considered “exception” joints even at a late stage.

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

Acute calcific periarthritis

Episodes of pain and inflammation in the joints, including in the area of the PFJ of the first finger, can occur with acute calcific periarthritis. Large joints are most often affected: hip, knee, shoulder. Deposits of amorphous hydroxyapatites, which form in the acute stage in the ligaments or joint capsule, may subsequently disappear and then reappear, causing repeated attacks of arthritis. Calcific periarthritis is more common in women or in patients with uremia 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 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 PFJ of the first finger.

6. Asymmetric inflammation of the PFJ.

7. Unilateral damage to the tarsal joints.

8. Suspicion of tophi.

9. Hyperuricemia.

10. Asymmetric inflammation of the joints.

11. Subcortical cysts without erosions on X-ray examination.

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 development of severe pain and swelling of the joint, which reaches a maximum 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 severe hyperemia and swelling in combination with severe pain in the PFJ of the first finger makes clinicians think specifically about gouty arthritis.

Typical provoking factors are: alcohol intake, heavy consumption of meat and fatty foods, visiting a bathhouse (hypovolemia), surgery, microtrauma associated with prolonged stress on the foot or a forced position (while driving, on an airplane, etc.).

Common mistakes

The combination of arthritis with high levels of uric acid in the blood makes diagnosis easier. But, as our observations show, the diagnosis of gout is established only in 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 pain relief with the use of non-steroidal anti-inflammatory drugs (NSAIDs) or analgesics. The characterological characteristics of patients are important: 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 inflammation that occurs in response constitute the pathogenetic essence of the disease. The study of the phenomenon of formation of EOR crystals showed their uniqueness and obligatory nature for gout. Their detection is the absolute certainty of the diagnosis (Fig. 2a).

Tophi. EOR crystals, resulting from GI, 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, macrotophus are also formed.

Tophi 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, and polysaccharides are also components of tophi. Subcutaneous tophi are the most famous because they are easily detected. More often they are localized in the area of the toes and hands, knee joints, elbows and ears. The same deposits are formed in the kidneys, heart, joints, and structures of the spine. Finally, we recently discovered the phenomenon of deposition of EOR crystals in the gastric mucosa.

Synovial fluid is the most accessible for research, 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 variations, the sensitivity and specificity of this method are considered to be high.

Radiological features of gouty arthritis

The diagnosis of gout is based on clinical data; in the early stages of the disease, X-ray examination of the affected joints is not very informative. The radiological phenomenon typical of late gout is quite well known - the “punch” symptom. This phenomenon was first described in 1896 by Huber as a defect of the subchondral bone, with a diameter of 5 mm or more, located in the medial part of the base of the diaphysis or in the head of the phalanx, most often the first metatarsophalangeal joint. As experience accumulated, it became clear that the opposite situation is more often observed, when radiographic 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. However, despite the low sensitivity and specificity, this radiological sign was included in the clinical and laboratory list of criteria for gout.

When discussing the “punch” symptom, it is necessary to note a number of points that determine the significance of its identification. Firstly, the pathomorphological substrate of this X-ray phenomenon is intraosseous tophi (the impression of a cystic formation is created due to the fact that MUN crystals do not block X-rays). By identifying the “puncture”, we determine the stage of the disease as chronic tophi. It is generally accepted to consider tophi of any location a direct indication for starting anti-gout therapy.

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

An early radiographic sign of 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 emphasized contours. The latter is very typical for erosions in gout, in contrast to those in rheumatoid arthritis, tuberculosis, sarcoidosis, syphilis, and leprosy. Erosion can be found both in the joint itself and outside the joints. When tophi are located intra-articularly, the edges of the joints are more often damaged. Subsequently, destructive changes spread to the central parts of the joint. Extra-articular erosions are usually localized in the cortical layer of the metamyphyses and diaphysis of the bones. Extra-articular erosions are often associated with adjacent soft tissue tophi and are defined as round 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, involving deeper layers of bone tissue and resembling “rat bites”. Asymmetrical erosions with destruction of cartilage are typical; Bone ankylosis rarely develops.

The gouty “puncture” on the radiograph (Fig. 3) looks like a cyst, close to the edge of the bone, framed by a clear sclerotic rim. In fact, this formation is not a true cyst, since it contains MUN crystals. In the case of calcium deposits in the tophi structures, X-ray positive inclusions can be detected, which sometimes stimulate chondromas. The joint space width of the affected joints usually remains normal until the late stages of the disease. According to some authors, these changes can mimic osteoarthritis. In our opinion, more often in such cases both diseases occur.

In chronic gout, pronounced proliferative periosteal changes can be detected, which reflects the reaction of the periosteum to adjacent soft tissue tophi. Typical sites for such changes are the first MCP joints, 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 joint may mimic gouty arthritis. However, this clinical situation usually does not cause great difficulties. If a sufficient amount of synovial fluid is obtained from a large joint, it is possible to perform not only polarization microscopy to search for crystals, but also a full analysis, including the determination of rheumatoid factor (RF). If synovial fluid analysis is not available, an additional criterion may be the results of the use of NSAIDs or glucocorticoids (intra-articular). This treatment usually completely relieves gouty arthritis, unlike rheumatoid arthritis.

There is often a situation where the late polyarticular form of gout involving small joints is confused with RA. However, RA is characterized by symmetrical damage to the joints with inflammation of the proximal interphalangeal, wrist, temporomandibular joints, and cervical spine, while gout is characterized by asymmetry of inflammation of the joints of the hands, even at a late stage of the disease, and 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 “puncture” symptom. Laboratory tests, morphological studies of nodules, determination of RF and the level of sUA in the blood help to finally resolve diagnostic difficulties. The combination of RA and gout is a casuistry, since the synovial fluid of RA patients inhibits crystal formation.

Osteoarthritis

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

Psoriatic arthropathy

The differential diagnosis of gout with psoriatic arthropathy causes serious difficulties. The latter is characterized by damage to the distal interphalangeal joints, although any joints can become inflamed. X-ray changes in the joints may be similar (with the exception of the classic “pencil in a glass” and “punch” picture). The main symptom that prompts a diagnostic search is GU, 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 cutaneous psoriasis, the final diagnosis of joint damage is established after examining the synovial fluid for crystals. In our practice, we encountered a combination of skin psoriasis and gout, confirmed by the detection of crystals.

Reiter's syndrome

Reiter's syndrome, like gout, affects mainly males, and the joints of the lower extremities become inflamed, most often the large ones, but also the small joints of the feet. Distinctive features of Reiter's syndrome are conjunctivitis and urethritis, which precede arthritis. In this situation, a thorough history taking and examination of synovial fluid help 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 gender, frequent involvement of the joints of the lower extremities, monoarthritis, sudden onset of arthritis. However, the clinical picture of AS has its own characteristics. These are pain in the spine with stiffness and limited excursion of the chest, night pain in the lower back with radiation to the buttocks, long duration of arthritis (from several weeks to months). X-ray examination shows the presence of sacroiliitis. The determination of HLA-B27, detected in almost 90% of patients, helps in diagnosing AS.

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

Second stagegout called intermittent or “interval” gout. There is already a gradual deposition of urates in the joints and in the kidney tubules. The disease occurs in the form of exacerbations ( acute gout attacks) and periods of remission. During an exacerbation, joint symptoms are usually observed, which will be presented in detail below. The formation of kidney stones in intermittent gout is rare.

Exacerbations and acute joint symptoms are usually caused by the following reasons:

injury;
excessive alcohol consumption ( even disposable in large quantities);
surgical intervention;
acute infectious disease ( usually ARI - acute respiratory disease, or ARVI - acute respiratory viral infection).

The attack lasts 3 to 7 days, after which complete remission occurs, and patients do not experience any pain or any discomfort even with stress on the affected joint.

Third stage of gout called chronic. It occurs when the patient develops actual tophi with uric acid crystals. Outwardly, they look like bumps that are hard to the touch, which can reach large sizes and severely deform the joint. It should be noted that tophi are externally determined only in 50 - 60% of patients, and they are not the main criterion for the onset of the third stage. To guide the diagnosis, take the frequency of acute gout attacks and their duration in comparison with periods of remission. Also at the third stage, urolithiasis develops with a corresponding clinical picture.

The main symptoms of gout from the joints are:

Pain

The pain of gout can be very severe. The attack usually begins at night, often under the influence of external factors. The pain radiates ( distributed by) throughout the entire limb. Even light pressure on the affected joint can cause increased pain. Conventional painkillers are ineffective during an attack.

As noted above, the small joints of the feet and hands are usually affected. In more than 55% of patients, the first attack of gout is localized in the area of the first metatarsophalangeal joint ( base of the big toe). As a rule, the joint on only one limb is affected; symmetrical development of the inflammatory process on both limbs is not typical for gout.

Frequency of damage to various joints in gout in the early stages

Joint or anatomical area	Frequency of lesion
I metatarsophalangeal joint	56%
Phalanges of fingers	18%
Wrist joints	11%
Elbow joint	4%
Spine, hip and knee joints	less than 3%
Ankle and Achilles tendon	5%
Damage to 2 - 5 joints simultaneously (oligoarthritis)	17 - 34% (more common in women)

The pain of gout is caused by urate deposits in soft tissues and the presence of crystals in the joint fluid. Solid particles directly injure the tissue and cartilage surfaces inside the joint, leading to severe pain. To a lesser extent, pain is caused by inflammatory edema.

Redness of the joint

Redness of the joint develops quickly, in parallel with the increase in pain. It is more typical during an exacerbation, while during remission it may disappear. The redness is due to a rush of blood to the affected area. Due to microtrauma of soft tissues, cellular elements of the blood migrate to the lesion ( mostly neutrophils). These cells are capable of secreting biologically active substances that increase the permeability of vascular walls and the expansion of capillaries. Under the influence of these substances, blood supply to the affected area increases, causing redness and swelling.

Formation of tophi

Tophi is a symptom specific to gout. As mentioned above, they are a collection of uric acid salts located subcutaneously or intradermally. Usually from the first symptoms of the disease ( first attack) it takes at least 3-5 years for tophi to form ( in rare cases 1 - 1.5 years). These formations grow slowly, but in advanced cases of gout they can reach several centimeters in diameter. Due to impaired blood supply to the skin, trophic ulcers may appear over the tophi. A white paste-like mass, or even just urates in the form of a white powder, is released from them.

The preferred places for the formation of tophi are:

phalangeal joints on the fingers and toes;
metacarpophalangeal and metatarsophalangeal joints ( base of finger);
knee joint area;
elbow joint area;
ankle joint;
ears;
brow ridges.

In atypical forms of gout, early formation of tophi may also be observed ( one year after the first attack of the disease).

Early appearance of tophi is typical for the following categories of patients:

patients with juvenile gout ( cases of gout in children and adolescents);
Elderly women who developed gout while taking diuretics ( diuretics);
patients with severe diseases of the hematopoietic system;
for chronic kidney diseases accompanied by hyperuricemia.

Inflammation of periarticular tissues

The inflammatory process can affect not only the joint area, but also other anatomical structures located nearby. Against the background of gout, diseases such as tendonitis are often observed ( tendon inflammation), tenosynovitis ( inflammation of the tendon sheath), bursitis ( inflammation of the joint capsule, characteristic mainly of large joints).

Limitation of joint mobility

The main reason for limited mobility of a joint affected by gout is severe pain. It appears mainly in the acute period of the disease and does not allow any movement, or even a slight load on the entire limb.

During the period of remission, when the pain subsides, joint stiffness can still be observed. It is partly explained by inflammatory edema, partly by concomitant inflammatory processes in the tendons and other periarticular anatomical structures.

Local temperature rise

The local increase in temperature is explained by increased blood supply to the affected joint and acute inflammatory processes. By touch, the patient can easily determine that the reddened area of skin is much hotter than the surrounding surface tissue. Above tophi, the skin temperature is also almost always 1 - 2 degrees higher, regardless of their location.

Depending on the causes of gout, concomitant diseases and the individual characteristics of the patient’s body, the course of gout can take several clinical forms. Each of them is characterized by certain features and a set of typical symptoms. Often it is the clinical form of gout that becomes the main criterion for choosing treatment.

Currently, the following clinical forms of gout are distinguished:

Typical acute attack

This clinical form occurs in 60 - 80% of patients with gout. Essentially, it includes symptoms that are not observed constantly, but during the exacerbation phase. With the intermittent course of gout, exacerbations are observed quite rarely. In the chronic stage, most symptoms are observed constantly. The duration of attacks, depending on the severity of the disease and the nature of treatment, varies from several days to several weeks.

The main symptoms during an acute attack are:

acute pain in the joints;
general weakness;
headache;
a sharp rise in temperature from a subfebrile level ( 37 - 38 degrees) up to 38.5 - 39 degrees;
the skin over the affected joint quickly turns red and then becomes bluish.

During an acute attack, characteristic changes are observed in these laboratory tests, which will be discussed in detail below ( increased ESR - erythrocyte sedimentation rate, increased levels of sialic acids in the blood, fibrin, seromucoid, and the appearance of C-reactive protein).

Subacute form

The subacute form differs from an attack by less intense symptoms. In particular, the inflammatory process is usually limited to one joint ( monoarthritis), the pain is moderate, and the swelling is not so severe. Subacute damage to several joints can occur in the early stages in young people. Gradually, the subacute form progresses to more severe variants of the course with frequent acute attacks.

Rheumatoid-like form

The rheumatoid-like form is called so because gout with this course is difficult to distinguish from some rheumatic diseases. Features of this form are damage to small joints ( finger and toe joints, wrist joint) at the onset of the disease, as well as prolonged attacks of moderate intensity. The duration of attacks in the rheumatoid-like form can be up to several months. This creates serious problems for doctors in making the correct diagnosis.

Pseudophlegmonous form

The pseudophlegmonous form is characterized by an acute inflammatory process around the joint, while the symptoms typical for gout fade into the background. The leading symptom in this course of the disease will be a temperature of 39 - 39.5 degrees, chills, an increase in the level of leukocytes in the blood to 12 - 15 million/ml, and an increase in ESR. All these symptoms are more reminiscent of phlegmon - acute diffuse purulent inflammation of soft tissues. However, tissue necrosis and pus formation usually do not occur with this form of gout.

Infectious-allergic polyarthritis

Infectious-allergic polyarthritis is an independent disease in which one or more joints alternately become inflamed. In rare cases ( up to 5%) gout can mimic this clinical picture. In this case, damage to new joints appears quickly ( within 24 hours), however, the inflammatory process is not as intense as during a typical exacerbation of gout.

Low-symptomatic form

The asymptomatic form of gout also poses serious difficulties for diagnosis. With it, patients complain of moderate pain, usually in one joint. Upon examination, there may be no signs of inflammation such as swelling or redness of the skin.

It should be remembered that these six clinical forms of gout are characteristic mainly of the initial stages of the disease. Gradually, the disease progresses with the formation of tophi and an increase in typical attacks. However, the above forms can be observed for several years until the disease takes a more characteristic course.

In addition to damage to the joints, gout often affects the urinary system. This occurs in the later stages of the disease and is characterized by the deposition of urate in the kidney tissues ( tubules, renal pelvis). Gouty nephropathy ( kidney damage due to gout) occurs, according to various sources, in 30 - 50% of patients with this pathology.

The main symptoms of gouty nephropathy are:

Acute pain in the lower back. The pain is a consequence of the movement of stones in the renal pelvis. The crystals damage the epithelium of the renal pelvis, leading to the development of inflammation.
Hematuria ( detection of blood in urine). Hematuria is manifested by redness of the urine or the detection of blood elements in it during a laboratory test. Hematuria is caused by minor bleeding that occurs as a result of the movement of stones.
Renal colic. This syndrome involves the sudden onset of severe lower back pain for no apparent reason. Renal colic in gout is caused by blockage of the ureter with a large stone, or by its getting stuck directly at the mouth of the pelvis. Colic may be accompanied by vomiting, urination problems, and a moderate increase in temperature.
The appearance of tophi-like formations in the kidneys. Sometimes, against the background of gout, urates are formed not in the pelvis, but directly in the brain tissue of the kidneys. In this case, this gradually leads to overgrowing of the renal tubules with connective tissue and chronic renal failure.

Diagnosis of gout

As mentioned above, diagnosing gout often presents serious difficulties even for experienced doctors. The fact is that when visiting a doctor, patients most often complain of joint pain, which can be caused by a variety of diseases. To significantly increase the chance of making the correct diagnosis, it is best to contact the rheumatology department. Rheumatologists have more experience in treating arthritis than other specialists and will be able to recognize gout more quickly.

The diagnosis is made directly on the basis of clinical and paraclinical ( laboratory and instrumental) examinations. For some patients, the diagnosis does not take much time, while others have to undergo a series of tests and examinations. First of all, it depends on the cause of the disease and the severity of the symptoms.

The following stages can be distinguished in the diagnosis of gout:

anamnesis ( patient interview);
assessment of the clinical picture of the disease;
instrumental studies;
laboratory research.

Anamnesis

Taking an anamnesis plays an important role in making a diagnosis, as it allows you to immediately exclude several joint diseases with similar symptoms. When interviewing the patient, the doctor must clarify what the first symptoms of the disease were and in what order they appeared. Most patients are able to recall joint pain in the past. Usually these are acute painful sensations in the small joints of the feet and hands. Large joints ( knee, elbow, hip) and the spine are rarely affected first.

Another important point when collecting anamnesis is the history of gout in the family. As mentioned above, hereditary factors play an important role in the pathogenesis of this disease, so such cases facilitate diagnosis.

An indispensable question that the doctor will try to clarify during the examination is the patient’s diet and some bad habits. In particular, an abundance of meat food, alcohol abuse, smoking and significant physical activity give reason to suspect gout. Another dietary feature that plays a role in the onset of gout is not drinking enough fluids during the day.

Often the doctor also asks about illnesses that occurred in the past. For gout, serious surgical interventions, kidney disease with decreased filtration, and long-term use of certain medications are of greatest importance ( cytostatics, thiazide diuretics).

Assessment of the clinical picture of the disease

The clinical picture of the course of the disease is a combination of symptoms of a disease and changes in the patient’s condition over time. An experienced doctor, carefully observing the patient, can with a high degree of probability make the correct diagnosis even without paraclinical studies.

The main criterion when assessing changes in the condition over time is the staging of gout. In almost any patient who undergo regular medical examinations and tests, the following three stages of disease development can be identified:

Hyperuricemia and accumulation of urates in the body. This stage can last for years without causing serious inconvenience to the patient. However, it is this that sooner or later leads to the second stage. Occasionally in medical practice, there are cases when gout appears without a prior increase in uric acid levels.
Deposition of urates in tissues. Urates, as mentioned above, are small crystals that begin to make themselves felt as soon as the first of them are deposited in the soft tissues. It is at this stage that the first obvious symptoms of gout appear, which usually lead the patient to the doctor.
Acute gouty inflammation. This stage occurs only when a significant amount of urate accumulates. In addition to multiple microtraumas caused by crystals in soft tissues, there is also a response of the body to foreign substances. The main role is played by neutrophils and tissue phagocytes, which capture ( phagocytose) crystals.

Kidney damage, as noted above, occurs after several years of the disease.

Instrumental studies

Instrumental studies are prescribed for almost all patients who come in for joint pain. In case of gout, most instrumental methods are uninformative in the early stages, since morphological ( structural) practically no changes in tissues are observed. However, this type of diagnosis allows us to exclude a number of other rheumatological pathologies. The appointment of one or another instrumental diagnostic method is made by the attending physician as necessary. With a pronounced clinical picture with typical manifestations of gout, instrumental diagnosis may not be necessary.

The following instrumental research methods are used in the diagnosis of gout:

Ultrasound ( ultrasound examination of joints);
scintigraphy with technetium pyrophosphate;
X-ray of the affected joints.

Ultrasound
With an intermittent course of gout, changes on ultrasound will be noticeable only during an exacerbation of the disease. In the first 3 to 4 days of an acute attack, widening of the joint space, swelling and hardening of the soft tissues around the affected joint are observed. Already 5 - 7 days after an acute attack, the above changes are barely noticeable, and after 10 - 12 days, an ultrasound of the joint may not reveal any abnormalities.

In the chronic form of gout in the later stages, ultrasound of the joint can reveal moderate deformation of the articular surfaces and deep-seated tophi. In addition, ultrasound can detect stones ( clusters) urate in the kidneys and bladder in urolithiasis.

Technetium pyrophosphate scintigraphy
This study is prescribed mainly for patients with a vague clinical picture of the disease, when the doctor has problems making an accurate diagnosis. Scintigraphy involves the introduction of a specific substance into the blood ( technetium pyrophosphate), which selectively accumulates in places where urate is deposited. Subsequent scanning of the body makes it possible to accurately determine the localization of the pathological process. Scintigraphy can indicate gout even in the early stages, when tophi have not yet begun to form. In addition, it can be used to quickly identify accumulations of urate in atypical places ( spine, sternoclavicular region). The disadvantages of this study include its high cost.

CT scan
Computed tomography provides a series of high-precision x-ray images. With its help, you can determine the degree of joint deformation in the later stages of the disease and the exact localization of tophi. In the early stages, the images will only show the hardening of the soft tissue around the joint during an exacerbation.

X-ray of affected joints
Single X-ray images at an early stage of the disease are prescribed for the purpose of differential diagnosis with other arthropathy ( joint diseases). In gout, they do not reveal significant changes. Only in the chronic course of the disease can a diagnosis be assumed from an x-ray image.

Radiological signs of gout

Tested tissue	Characteristic changes
Soft periarticular tissues	Diffuse ( spilled) compaction due to the inflammatory process, darkened areas with blurred contours ( tophi).
Bones and joints	The articular surface of the bone is clearly visible, no signs of osteoporosis are observed; in chronic gout, signs of erosion are observed. Darkened areas against the background of a light image of the bone may indicate intraosseous accumulation of urates ( intraosseous tophi). In radiology, this sign is also called a “punch”. Symptom of the “overhanging edge” of the joint.

Laboratory research

Laboratory studies during gout are very informative, as they allow you to trace the process of formation and excretion of uric acid at various levels. Changes in blood and urine tests are also valuable from the point of view of differential diagnosis, as they make it possible to distinguish gout from other inflammatory diseases of the joints with similar symptoms.

Laboratory tests for gout include the following tests:

blood chemistry;
biochemical urine analysis;
study of synovial fluid of joints;
study of the contents of tophi.

General blood analysis
In the general blood test, no changes may be observed at first. During periods of exacerbation, leukocytosis appears against the background of the inflammatory process ( increase in the number of leukocytes in the blood) with a shift in the leukocyte formula to the left. This means that, in percentage terms, there are more immature rod forms. Adult segmented leukocytes migrate to the site of inflammation and are destroyed there. In addition to leukocytosis, an intense inflammatory process leads to an increase in ESR ( erythrocyte sedimentation rate). Other changes in the general blood test are observed only with concomitant severe kidney damage or when the patient has a secondary form of gout against the background of severe diseases of the hematopoietic system.

Blood chemistry
A biochemical blood test is the most important laboratory test for gout. It is within the framework of this study that the level of uric acid in the blood is determined and hyperuricemia is detected.

Possible changes in the biochemical blood test for gout are:

increased levels of C-reactive protein;
hyperglycemia ( increased sugar levels) occurs in 15-25% of patients with hyperuricemia and is often caused by hereditary enzymopathies;
an increase in creatinine and urea levels is observed mainly with kidney damage;
the amount of lipids and lipoproteins in the blood is usually increased;
elevated calcium levels.

In addition, during a biochemical blood test, it is recommended to check the level of prothrombin, fibrinogen, and liver enzymes ( AlAT and AsAT) and bilirubin. These substances indicate the functioning of other internal organs and can help make the correct diagnosis in cases of secondary gout.

Separately, it should be said about the determination of uric acid in the blood. With gout, in most cases there is an increase in its content ( hyperuricemia). Normally, the content of uric acid in urine varies from 0.18 to 0.38 mmol/L in women and from 0.27 to 0.48 mmol/L in men. Determination of serum uric acid levels is carried out before the start of treatment to clarify the diagnosis and after the start of treatment to monitor its effectiveness. Hyperuricemia has been shown to be a risk factor for gout. But despite this, serum uric acid levels cannot serve as an indicator to exclude or confirm gout. During an acute attack, determining the serum level of uric acid is not informative, since almost half of the patients during this period have increased excretion ( allocation) uric acid by the kidneys, which may cause serum uric acid levels to reach normal levels.

General urine analysis
In a general urine test, pathological changes appear after kidney damage. Determination of urate crystals in urinary sediment is characteristic. Possible albuminuria ( excretion of the albumin fraction of blood proteins in the urine), moderate hematuria ( detection of blood in urine), cylindruria ( detection of columnar epithelial cells in urine). The cause of these changes is direct damage to the epithelium of the renal pelvis by calculi.

Biochemical urine analysis
First of all, this test is necessary to determine the level of uric acid in the urine. Uric acid clearance is usually determined - the amount of substance excreted during the day. Normally it is 250 - 750 mg. Depending on the reasons that led to the appearance of gout, this indicator varies. If the kidneys are not affected by the pathological process, then filtration occurs normally, and the level of uric acid in the urine will increase in parallel with the level of uric acid in the blood. With increased consumption of purines in food, the amount of uric acid increases. If the patient develops gout secondary, against the background of chronic kidney diseases, then less than 250 mg of uric acid will be excreted in the urine during the day due to insufficiently effective filtration.

Study of joint synovial fluid
In the synovial fluid obtained during joint puncture, an increased content of leukocytes, mainly neutrophils, is detected ( 10 - 16*10 9 /l). Polarization microscopy is performed, which reveals a precipitate of needle-shaped crystals of uric acid salts ( size 3 - 30 microns), which have the property of negative birefringence. Individual neutrophils containing sodium urate crystals in the cytoplasm are also visible. This analysis is the most reliable to confirm the diagnosis of gouty arthritis.

Study of the contents of tophi
When puncturing or opening the tophi, a white pasty mass or even white crystalline powder is discovered. This symptom is also characteristic only of gout, but it can only be detected in the later stages of the disease.

In addition to the classical stages of diagnosing gout, there are a number of criteria recommended by WHO ( world health organization). According to WHO, there are 12 key points that a doctor should pay attention to during an examination. If at least 6 of the 12 points are confirmed, the doctor can reasonably make a preliminary diagnosis of gout without additional research. The advantage of diagnostics according to WHO criteria is the speed and high accuracy of diagnosis, the disadvantage is the possibility of confusing the low-symptomatic form of gout with some rheumatic diseases.

As noted above, some rheumatic diseases have similar symptoms and manifestations, so it can be difficult to distinguish them from gout. Such diseases are rheumatoid arthritis, psoriatic arthritis and chondrocalcinosis ( also called pseudogout). To facilitate diagnosis, special criteria for differential diagnosis between these diseases have been developed.

Criteria for differential diagnosis of gout and some rheumatic diseases

Diagnostic criteria	Gout	Rheumatoid arthritis	Psoriatic arthritis	*Chondrocalcinosis ( pseudogout)*
Floor	97% men	75% women	-	M:F - 4:1
Provoking factors	Alcohol, poor diet, stress	-	Stress	-
Predominantly affecting joints	I metatarsophalangeal, arch joints	Small joints of the hand	Distal interphalangeal joints	Knee-joint
hyperuricemia	+	-	-	-
Radiogram ( calcifications, erosions)	As a rule, there are no calcifications, erosions are characteristic	-	-	Chondrocalcinosis and degenerative changes are observed
Crystals: form birefringence	+	-	-	+
	Sodium monourate	-	-	Calcium pyrophosphate
	Needle-shaped	-	-	Rod-shaped
	Negative	-	-	Weakly positive
Damage to internal organs	Kidneys	Heart, lungs	Kidneys, cardiovascular system ( the cardiovascular system)	-

Treatment of gout requires an integrated approach with impact on the pathological chain at various levels. Whenever possible, doctors try to determine the underlying cause of the disease and eliminate it. However, with hereditary enzymopathies, even an accurate determination of the missing enzyme does not eliminate the root cause, so we have to limit ourselves to symptomatic treatment ( aimed at eliminating symptoms and manifestations of the disease and improving the patient’s quality of life).

The main directions in the treatment of gout are:

diet;
anti-inflammatory drugs;
anti-gout drugs;
local treatment;
folk remedies.

Diet

Diet plays a major role in the prevention of gout. The main goal of the diet is to reduce the content of uric acid compounds in the body. When following a diet, practically no purine bases enter the body from the outside. This makes the diagnostic process easier. If on the 5th - 7th day of dietary nutrition the level of uric acid in the blood does not decrease, then we are most likely talking about secondary gout, caused by a strong decrease in filtration in the kidneys or massive breakdown of the body’s own tissues.

The gout diet involves several rules:

Eliminating or limiting the amount of foods rich in purine bases. It is these foods that are in most cases responsible for increasing the level of uric acid in the blood. With their limited consumption, exacerbations of the disease are observed much less frequently and are easier.
Introducing foods that do not contain or are low in purine bases. These products also need to be selected by a nutritionist. They are the main focus of the diet, and they must fully cover the body’s needs for calories and nutrients ( proteins fats carbohydrates).
Administer sufficient fluid. When consuming large amounts of liquid ( at least 2 liters of water per day, not counting liquid dishes) the amount of circulating blood increases and filtration in the kidneys accelerates. Due to the increased blood volume, the concentration of uric acid decreases, and its deposition in the form of salts in soft tissues does not occur. Intensive filtration in the kidneys flushes the urinary system and prevents urine from stagnating. This prevents the deposition of urate in the renal pelvis and bladder. If you have chronic kidney disease, you should check with your doctor about the need to drink plenty of fluids, as in this case it can lead to a sharp rise in blood pressure.
Loss of body weight. In most cases, losing excess weight improves the functioning of internal organs, so that uric acid is better eliminated from the body. In addition, the amount of lipids and lipoproteins circulating in the blood and contributing to the accumulation of uric acid is reduced. The most effective weight loss method for patients with gout is selected individually by the attending physician.

Foods that contain high amounts of purines(more than 150 mg per 100 g of product), are :

beef internal organs ( brains, kidneys, liver, tongue, pancreas);
sardines;
anchovies;
small shrimp;
mackerel;
legumes.

Foods with Moderate Purine Levels (50 - 150 mg per 100 g of product):

most types of meat ( beef, lamb, chicken);
fish;
crustaceans.

Low purine foods(0 - 15 mg per 100 g of product):

The meat of young animals contains more purine bases than the meat of adult animals, so its consumption should be avoided or at least limited. It is also recommended to limit your intake of saturated fats ( sunflower oil, butter), since under conditions of hyperlipidemia, excretion becomes difficult ( allocation) uric acid by the kidneys.