X-ray sign of joint damage due to gout. Gout on the big toe begins its run. The main morphological manifestations of changes in gout

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 the joint has already experienced structural changes. Confirm results are correct X-ray examination Laboratory tests help.

If joint pain occurs, you should immediately seek help from a specialist. Similar diseases There are doctors of different specializations. 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:

If you suspect gouty arthritis, you need to take a urine test. If a joint lesion is present, the sample will reveal increased content urates. In addition, during periods of exacerbation of pathology, urine becomes brown in color. The presence of a large volume of uric acid confirms the course of gout in the patient. One more a clear sign The disease is increased acidity.
A general blood test is also mandatory diagnostic measures. During periods of exacerbation, accelerated erythrocyte sedimentation is detected in the sample. An increase in the number of leukocytes is also observed. All these results indicate the development of an acute inflammatory process in the human body that needs to be combated. The results of the blood test do not change in the periods between excesses.
Biochemical analysis of urine can reveal the presence of increased amounts of uric acid. If its content is normal, then the kidneys are working correctly. An increased or decreased volume of this substance indicates a malfunction of this organ.
A test for uric acid in the blood must be done before starting therapy and after it is completed. The resulting indicators should not exceed acceptable standards. In women it is 360 µmol/l, and in men – 420 µmol/l.
With an exacerbation of gout in a person, the amount of C-reactive protein increases several times. To check its content, rheumatoid tests are required. With their help, it is possible to determine the rheumatic factor, which allows one to exclude the development of other diseases with similar symptoms in the patient.
Desirable diagnostic measures include analyzes of tophi and synovial fluid. They are prescribed only in extreme cases.
One of the most important procedures for gouty symptoms is X-ray examination. Thanks to him, the whole picture of joint disease becomes clear. An x-ray of a joint affected by gouty arthritis helps determine the presence of pathological changes, which are caused by formations of salt crystals. In the case of chronic gout, light spots will be clearly visible on the image, indicating the location of the lesion.

What does an x-ray show for gout?

On x-rays The manifestations of such arthritis are clearly visible. 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 drawn, he can judge current state patient 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 pathological process in the joint helps in short time defeat the disease and prevent it from becoming chronic.

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 who 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.

The disease inevitably progresses, causes pathological changes in internal organs and threatens disability. Correct examination allows you to avoid a false diagnosis and slow down the progression of the disease.

Criteria for diagnosing gout

Joint diseases have similar symptoms, have a hidden course and inevitably become chronic. This significantly complicates the differentiation of ailments and prevents timely treatment. In 1961, the global medical community defined general diagnostic criteria for gout:

increased concentration of uric acid in the blood, urine, joint fluid;
a history of sudden attacks of acute arthritis lasting up to 1-2 days;
detection of uric acid crystals, urates in soft tissues, articular cavity;
visual detection salt deposits – .

The detection of two or more criteria from the above list serves as a valid basis for diagnosing gout. American scientists expanded this list to 12 points:

excess content of uric acid and salts;
pathological absence of microflora in the synovial fluid;
the presence of non-erosive subcortical cysts on x-rays;
a medical history of 2 or more attacks of gouty arthritis;
the acute phase during attacks is observed on the first day;
prolonged inflammation in the metatarsophalangeal joint on the legs;
unilateral form of damage to the joints on the foot;
asymmetric type of joint damage;
signs of arthritis in one joint of the foot;
hyperemia (redness) of the skin in the joint area;
confirmed presence of tophi;
damage to one metatarsophalangeal joint.

On a note!
The diagnosis of gout is made when six of these criteria are met or uric acid and urate crystals are detected in the tophi (or synovial fluid).

Clinical picture and external examination

When diagnosing important role plays the collection of data for anamnesis. By studying the medical history, the doctor receives valuable information for identifying the disease. To diagnose gout, it is necessary to distinguish it from similar diseases (rheumatism,). During an external examination, the following facts are established:

time of appearance and duration of the first symptoms;
change in the appearance of the joint - swelling, redness, deformation;
Availability surgical operations, injuries, pathologies;
complicated heredity and predisposition;
the patient's lifestyle, habits.

On a note!
The clinical picture of a chronic, long-term disease often has a pronounced, clearly identifiable character. An experienced specialist is able to determine gout without tests, guided by own experience, skills and knowledge. However, most often a preliminary diagnosis is made, which requires confirmation and justification by an appropriate examination.

Features of differential diagnosis

At the first signs of damage to the joints on the legs, a rheumatologist, surgeon, or traumatologist is required. After studying the clinical picture, the doctor decides what tests need to be taken for gout. Differential diagnosis allows you to accurately determine the causes of the disease based on the results of laboratory tests of blood, urine, and instrumental examination.

Lab tests

The first stage in diagnosing any disease is laboratory testing of blood and urine. The results of the analysis indicate changes in the composition, rheological properties liquids. These data suggest the cause and patterns of development of the disease. To identify gout you will need:

results general analysis blood, urine;
data from their biochemical study;
results of studying the composition of joint fluid;
study of the contents of tophi.

General blood test results

A constant excess of uric acid and crystallization of urates is accompanied by metabolic disorders and inflammatory processes in the joints. These factors inevitably lead to changes chemical composition fluids in the body. Blood test indicators for gout according to general parameters:

increased proportion of neutrophils;
change in leukocyte formula;
decrease in the number of lymphocytes;
increase in erythrocyte sedimentation rate (ESR).

On a note!
At the initial stage of gout, there may be no deviations from the norm in a general blood test.

Features of biochemical blood analysis

With a complete biochemical blood test, the value of various indicators is established. Their specific change and ratio suggests the presence of gout and determines the degree of neglect.

Established and generally accepted standards for blood parameters:

Tests for gout (indicator)	Children (1-14 years old)	Men	Among women
Total protein value	48-82 g/l	64-83 g/l
Albumin content	33-55 mg/l	33-50 mg/l
C-reactive protein content	None	up to 0.5 g/l
Creatinine value	35-110 µm/l	63-115 µm/l	54-97 µm/l
Meaning of uric acid	0.15-0.28 µmol/l	0.13-0.21 µmol/l	0.16-0.41 µmol/l
Calcium value	0.94-1.16 mmol/l	1.04-1.27 mmol/l	2.14-2.5 mmol/l
Total bilirubin value	17- 67 µmol/l	3.5-20.7 µmol/l	3.41-17.0 µmol/l
Meaning of high-density lipoprotein cholesterol	0.9-1.9 mmol/l	0.7-1.83 mmol/l	0.9-2.2 mmol/l
Low density lipoprotein cholesterol value	1.6-3.5 mmol/l	2.1-4.7 mmol/l	1.91-4.5 mmol/l

The results of a biochemical blood test for uric acid in gout are overestimated. For self-diagnosis and establishment of hyperuricemia, increased levels of C-reactive protein, sialic acids, and fibrin are taken into account. If dysfunction of the kidneys or urinary system is suspected, the value of bilirubin, prothrombin, and liver enzymes is studied.

Results of a general urine test

With hyperuricemia, there is an increase in the level of uric acid, urate in the urine, crystallization of salts in the urinary tract, kidneys, bladder. General analysis is effective with concomitant. Based on the results of a urine test for gout, the following is determined:

increased concentration of uric acid;
alkaline pH>7 at the late stage of gout;
deviation in color due to changes in composition;
the presence of urate crystals in the dry residue of urine;
detection of protein molecules (albumin);
small amounts of blood, epithelium.

Study of synovial fluid

An important step in the differential diagnosis of gout in the legs is the study of joint (synovial) fluid. Its composition is close to blood plasma, differs in content hyaluronic acid. The norm is the presence of cholesterol, cells (synovocytes, lymphocytes, monocytes, neutrophils). By puncture, synovial fluid is extracted from the joint cavity for bacteriological and bacterioscopic examination. Changes in its indicators indicate gout:

violation of color, density, viscosity;
the appearance of turbidity, mucin clots;
deviation from the norm pH=7.3 to 7.6;
detection of erythrocytes, leukocytes;
the appearance of phagocytes, destroyed cells;
study of synoviocytogram;
crystals of urates, phosphates.

X-ray examination

For chronic and advanced forms of gout, radiography is prescribed. The method is effective for diagnosing diseases on the legs, establishing the stage of the disease and detecting complications. X-ray reveals irreversible changes bone structure, cartilage of affected joints. Typical radiological signs of gout:

Research elements	Picture in the picture	Pathological processes
Soft tissues (muscles, membranes)	Local dimming with blurred outline.	Tissue compaction due to inflammation, crystallization of urates.
Joint bones	Visual deformation of the bone surface, detection of an overhanging edge or swelling of the edge, areas with darkening.	Erosion, destruction of the bone surface, cartilage, crystallization of urates around and inside the bones.
Joints	A symptom of a puncture in gout is light-colored areas with a diameter of 0.3-3 cm on an x-ray of the diseased joint.	Formation of intraosseous tophi, destruction of bone tissue at the late stage of gout.

Other diagnostic methods

To establish the diagnosis of gout, modern diagnostic methods are used in medicine. They identify additional signs of the disease that are used to confirm the diagnosis:

Ultrasound, tomography (computer, magnetic resonance) - during the period of exacerbation, they are used to detect narrowing of the interarticular space, inflammation, hardening of soft periarticular tissues, joint deformation, pathology in the kidneys and ureter;
Biopsy – detailed study intra-articular fluid to determine excess uric acid in the synovial fluid in the problem joint.

How to prepare for tests

There are known cases of false blood test results for gout, biased results of urine and joint fluid tests. The reliability and information content of laboratory research increases with proper preparation for delivery of biological material:

3 days before the tests, follow a strict diet - exclude foods prohibited for gout;
10 hours before, stop taking vitamin C;
do not take diuretic medications for 24 hours;
do not engage in sports activities for 3 days;
All tests are taken on an empty stomach, early in the morning.

Following these rules eliminates the possibility of distorting test results and making an erroneous diagnosis.

Gout is a systemic disease associated with a disorder of purine metabolism, which is manifested by the deposition of salts in the body. It affects men more often than women and occurs in 1% of the world's population. Laboratory tests and X-ray procedures of the affected areas play a very important role in diagnosing the disease.

Signs of the disease

Gouty arthritis is difficult to diagnose in the early stages of the disease; its symptoms are often similar to characteristic features other diseases. The initial stage is asymptomatic, X-ray studies will be uninformative. When pain a number of tests are prescribed in the joints. To determine gout, the following examinations are used:

general urine analysis;
study of uric acid concentration;
general and biochemical study of blood;
puncture of the inflamed joint;
studying the contents of tophi;
Ultrasound of joints;
CT, MRI and scintigraphy for a blurred clinical picture.

X-ray examination of gout

The “punch” symptom can be seen in the image at an advanced stage of the disease.

The diagnostic method involves absorption of rays by the affected area and further projection on films or a PC monitor. The doctor then processes the information and makes recommendations. To clarify the degree of skeletal destruction in gouty arthritis, x-rays of the affected joints are prescribed. A very well known X-ray phenomenon is the “punch” symptom, which is characteristic of late dates diseases. This is a bone defect measuring 5 mm or more, which is most often localized at the first metatarsophalangeal joint.

X-rays of gout in the early stages may reveal transient osteoporosis.

X-ray signs of gout

Manifestation initial stages gout may serve diffuse compaction soft tissues (swelling). Sometimes an inflammatory process of bone substance is found - transient arthritis. During illness, destruction of the patient's bone often occurs. Erosion and destruction can occur inside and outside the joint. Radiological manifestations first appear along the edge of the bones in the form of a shell or shell. There are several X-ray signs that are presented in the table:

According to statistics, X-ray changes in the joints, characteristic of stages I-II of gout, occur within 9 years. Irreversible destruction occurs after 10-15 years. With adequate therapy and a decrease in the infiltration of the patient’s joints with urates, “punches” and other signs of bone destruction on the radiograph can significantly decrease or even disappear altogether. If gout is recognized in a timely manner, the disease can be prevented from becoming chronic. To exclude complications, patients are recommended to consult both a rheumatologist and a urologist.

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. IN Lately 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 the body, which is prone to the deposition of uric acid crystals, is affected by provoking factors external environment, then he will probably 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 has secondary character 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 shell 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 pain syndrome becomes permanent, 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 still a few atypical clinical forms arthritis with gout:

Subacute form. Characterized by erased 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 for an accurate diagnosis it is necessary additional methods examinations.

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;
kidney 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 serious illness, which must be treated not only during the period of exacerbation, 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 chronic illness, which is caused by failures of uric acid metabolism. As a result of this process, there is an increase in the amount of urates (crystals sodium salt uric acids) 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 different condition purine metabolism and characteristics of hormonal levels. As for women, it was revealed inverse relationship 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.

Behind last years the proportion of sick people with a history of rheumatic pathologies 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 in only 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 deep layers 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, puncture (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 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 become a “punch” - this is a marginal bone or cyst-like growth correct form. It is distinguished by clear contours (sometimes sclerotic).

As the pathological condition obvious destruction occurs not only in the subchondral part of the bone, but also in the epiphysis, 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 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.

Complement treatment with prescriptions traditional medicine. 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 in the artery wall cholesterol plaques;
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. Passes through the transverse processes of the cervical vertebrae vertebral artery, which supplies blood to approximately 25% of the brain structures. 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 severe symptoms spondylosis are observed when bone osteophytes are localized in the lumbar and sacral regions. In these areas there are large nerve plexuses responsible for functionality abdominal cavity, 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 features neurological symptoms, which are observed with him. 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 - at positive symptom Lasegue's pain increases 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. At the same time, when tapping with a neurological hammer on kneecap, the knee does not rise up as 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 secondary formation intervertebral hernia. 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 individual characteristics 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 human life. At the same time, he must carefully follow all the doctor’s recommendations. Otherwise, it is difficult to prevent disability.

Gout is a chronic progressive disease caused by a disorder of purine metabolism, characterized by an increased (normal for adult women - 150-350 µmol/l; for adult men - 210-420 µmol/l) level of uric acid in the blood (hyperuricemia), with subsequent deposition of urates in articular and/or periarticular tissues. Detection of hyperuricemia is not sufficient to establish a diagnosis, since only 10% of individuals who suffer from this disease have gout. Almost 95% of people diagnosed with gout are men between 40 and 50 years of age, although the disease is noted to be “getting younger.”

The rest are women menopause. Gout more and more often began to be accompanied by such certain diseases such as obesity, hypertriglyceridemia (increased levels of neutral fats in the blood) and insulin resistance (impaired amount of insulin in the blood). We can conclude that gout is not a cause, but a consequence of metabolic disorders in the body. There are two types of gout: primary and secondary. Primary gout is a hereditary disease (11-42% of cases), which is associated primarily with a predisposition to hyperuricemia, which is transmitted in an autosomal dominant manner.

The cause of primary gout is the impaired activity of enzymes that are involved in the formation of uric acid from purine bases or in the mechanisms of urate excretion by the kidneys. And the causes of secondary gout are renal failure, blood diseases accompanied by increased catabolism (processes aimed at destroying substances in the body), and the use of a number of medications (diuretics, salicylates, etc.).

Lesions

The main function of the kidneys is filtration and absorption, which are aimed at removing harmful and dangerous substances from the body, in particular waste products. The reserves of uric acid in the body are 900-1600 mg, and about 60% of this amount is replaced daily by new formation due to the breakdown of nucleotides and erythroblasts and the synthesis of nitrogen-containing compounds.

With prolonged hyperuricemia (with increased formation of uric acid in the body), adaptive reactions develop to reduce the level of uric acid in the blood. This occurs due to an increase in kidney activity and the deposition of urates in the soft tissues of cartilage. The clinical symptom of gout is associated precisely with the deposition of uric acid crystals in soft tissues. Although the mechanism of urate deposition is not fully understood, there are two main factors:

Insufficient vascularization (permeated with blood vessels) of tissues such as tendons and cartilage, in which there is an increased concentration of urates.
Local temperature, serum pH, and the presence of substances that retain urate in the fluid (proteoglycans) all affect the rate of sedimentation of uric acid salts. Increased diffusion of water from the joint increases the concentration of crystallized urate.

It has been proven that complete dissolution of uric acid salts occurs at pH = 12.0-13.0 (strongly alkaline solution), which in reality exists inside the human body. Hypothermia of peripheral joints (ankles, phalanges of fingers) promotes accelerated crystallization of urates and the formation of microtophi. With a high concentration of microcrystals in tissues (joint cartilage, bone epiphyses, etc.), the formation of micro- and macrotophus begins. Sizes range from millet grain to chicken egg. The accumulation of urates leads to cartilage destruction. Next, uric acid salts begin to be deposited in the subchondral bone (the foundation for cartilage, providing its trophism) with its destruction (the radiological name is a puncture symptom).

Uric acid also accumulates in the kidneys (gouty kidney or gouty nephropathy). All patients with gout have affected kidneys, so renal failure is considered not as a complication, but as one of the visceral (internal) manifestations of the disease. Gouty kidney (nephropathy) may have manifestations such as urolithiasis, interstitial nephritis, glomerulonephritis or arteriolonephrosclerosis.

Gout symptoms

a symptom of severe pain in one or more joints - the intensity of the pain increases over several hours;
a symptom of swelling or burning, as well as redness of the skin in sore joints and limbs;
sometimes a symptom of slight fever;
a symptom of returning pain, which occurs with prolonged gouty arthritis;
a symptom of the formation of hard white lumps under the skin (tophi);
symptom renal failure, stones.

Gouty arthritis and its classification

In total, there are 4 different clinical stages:

acute gouty arthritis;
interictal (interval) gout;
chronic gouty arthritis (exacerbation, remission);
chronic tophi arthritis.

Gout and its clinic

There are three stages in the development of gout. The premorbid period is characterized by the asymptomatic formation of increased amounts of uric acid in the body and/or the passage of urate stones with or without attacks of colic. This period can be quite long. The onset of attacks of the first gouty crisis indicates that the disease has begun to actively develop.

Gouty arthritis

During the intermittent period, acute attacks of gouty arthritis alternate with asymptomatic intervals between them. Long-term hyperuricemia and exposure to provoking factors (drinking alcohol, prolonged fasting, eating foods rich in purines, trauma, taking medications, etc.) lead to nocturnal acute attacks of gouty arthritis in 50-60% of cases. The beginning of the attack is sharp pain in the first metatarsophalangeal joint of the leg (big toe). The affected area quickly swells, the skin becomes hot from a sudden rush of blood, the swelling tightens the skin, which affects pain receptors. Shiny, tense, red skin soon becomes bluish-purple, which is accompanied by peeling, fever, and leukocytosis. There is a dysfunction of the joint, the attack is accompanied by fever. Other spherical joints, foot joints, and, somewhat less frequently, ankle and knee joints are also affected.

Less commonly affected are the elbow, wrist and hand joints; extremely rare - shoulder, sternoclavicular, hip, temporomandibular, sacroiliac and spinal joints. Acute gouty bursitis (inflammation of the mucous bursae, mainly of the joints) is known; the prepatellar (located under the skin in front of the kneecap) or ulnar bursa is usually affected. Under the influence of synovitis (inflammation synovial membranes joint), the joints are deformed, the skin at the site of inflammation becomes tense, shiny, stretched, and when pressed, the dimple disappears. The boundaries of hyperemia (poor circulation) are unclear, bordered by a narrow strip of pale skin. This picture is observed from 1-2 to 7 days, then local inflammatory processes decrease, but the pain can sometimes continue at night. Gouty arthritis after a few days with proper treatment starts to go away. First, the redness of the skin disappears, its temperature normalizes, and later the pain and swelling of the tissues disappear. The skin wrinkles, there is abundant pityriasis-like peeling and local itching. Sometimes gout-specific tophi appear. The early stages of intermittent gout are characterized by rare recurrences of attacks (1-2 times a year). But the longer the disease progresses, the more often the symptoms of gouty arthritis return, becoming longer lasting and less acute.

Each time, the intervals between attacks of the disease shorten and cease to be asymptomatic, and blood tests can reveal an increased content of uric acid. This is an indicator that the disease is becoming chronic. Chronic gout is described by the occurrence of tophi and/or chronic gouty polyarthritis. The disease develops 5-10 years after the first attack and is characterized by chronic inflammation joints and periarticular (periarticular) tissues, the occurrence of tophi (subcutaneous deposits of uric acid crystals), as well as combined damage to the joints (polyarthritis), soft tissues and internal organs (usually the kidneys).

The location of tophi is different: it can be the ears, the area of the elbow joints, hands, feet, Achilles tendons. The presence of tophi indicates a progressive inability of the body to remove uric acid salts at a rate equal to the rate of their formation.

Chronic tophi gout

When gouty arthritis develops for quite some time, the formation of tophi occurs everywhere: in cartilage, in internal organs and bone tissue. Subcutaneous or intradermal formations consisting of monocrystals of sodium urate in the area of the fingers and toes, knee joints, elbows and ears, are a sign that gouty arthritis has entered the chronic stage. Sometimes ulcers can be noted on the surface of the tophi, from which spontaneous discharge of a white pasty mass is possible. The formation of tophi in the bone space is called a puncture or break symptom, which can be diagnosed using x-rays.

Nephrolithiasis (kidney stone disease) in gout occurs due to the deposition of urate in the kidneys, forming stones. The more actively hyperuricemia progresses and the rate of crystal deposition increases, the greater the likelihood that tophi formations will appear in the early stages of the disease. This is often observed against the background of chronic renal failure in elderly women taking diuretics; for some forms of juvenile gout, myeloproliferative diseases (associated with disruption of brain stem cells) and post-transplant (cyclosporine) gout. Typically, the presence of tophi of any localization is combined with chronic gouty arthritis, in which there is no asymptomatic period, and is accompanied by polyarthritis (multiple joint damage).

General diagnostics

Gout is a disease that is difficult to diagnose in the early stages, since most of the time it is asymptomatic, and during periods of acute attacks its course resembles reactive arthritis. Therefore, an important part of the diagnosis of gout is an analysis of the level of uric acid in the blood, in daily urine and the clearance (speed of purification) of uric acid.

During an attack, laboratory acute-phase reactions are detected; a urine test may show slight proteinuria, leukocyturia, and microhematuria. Deterioration in the concentrating ability of the kidneys according to the Zimnitsky test indicates the presence of asymptomatic interstitial nephritis (inflammation of the kidneys) with the gradual development of nephrosclerosis (overgrowth of connective tissue in the kidneys). In the synovial fluid there is a decrease in viscosity, high cytosis, and the needle-like structure of sodium urate crystals is visible under the microscope. Morphological study subcutaneous tophi reveals, against the background of dystrophic (degrading) and necrotic changes in tissue, a whitish mass of sodium urate crystals, around which a zone is visible inflammatory reaction. The mild course of the disease is characterized by rare (1-2 times a year) attacks of gouty arthritis, which occur in no more than 2 joints. There are no signs of articular destruction on radiographs; isolated tophi are observed.

Moderate gout is characterized by more frequent (3-5 times a year) exacerbation of the disease, which progresses in 2-4 joints at once, moderate skin and joint destruction, multiple tophi are observed and kidney stone disease is diagnosed. At severe course diseases, attacks are observed with a frequency of more than 5 times a year, multiple joint lesions, pronounced bone and joint destruction, multiple large tophi, severe nephropathy (kidney destruction).

X-ray diagnostics

In the early stages of gouty arthritis, 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 is a defect in the bone on which the joint rests, can be 5 mm in diameter or more, located in the middle part of the base of the diaphysis (the middle part of the long tubular bones) or in the head of the phalanx, most often the first metatarsophalangeal joint. But as information accumulated, it became clear that a situation is more often observed when radiographic changes are not detected in patients with gouty arthritis.

Manifestation of the punch symptom

It is necessary to note a number of points that make the radiological symptoms of the punch significant. The pathomorphological (i.e., internal structure different from the norm) substrate of this X-ray phenomenon is intraosseous tophi, which is similar to a cystic (having a separate wall and cavity) formation, due to the fact that the uric acid salt crystals do not retain x-rays. The identified “puncher” determines the stage of the disease as chronic tophi. It is worth noting that identification of tophi of any location is a direct indication for starting anti-gout therapy. In general, 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.

On the other hand, early radiological sign in gout there is a reversible diffuse thickening of soft tissues during an acute attack due to the fact that when inflammatory processes there is a rush of blood and precipitation of solid crystalline forms in places of edema. In this case, local thinning of the bone substance (transient arthritis) can be detected, and as the disease progresses, destructive processes in this area can also occur. X-ray manifestations: initially, erosion can form along the edges of the bone in the form of a shell or shell with overhanging bone edges, with clearly defined contours, which is very typical for gouty arthritis, in contrast to rheumatoid arthritis, tuberculosis, sarcoidosis, syphilis, leprosy. Erosion processes can be detected both in the joint itself and outside it.

With intra-articular localization of tophi, destructive processes begin from the edges and, as they develop, move towards the center. Extra-articular erosions are usually localized in the cortical layer of the metamyphyses (from the medulla of the edges of the long tubular bone) and the diaphysis of the bones. Most often, this erosion is associated with close adjacent soft tissue tophi and is defined as round or oval marginal defects of bone tissue with pronounced sclerotic changes at the base of the erosion. Without treatment, such “holes” increase in size, covering deeper layers of bone tissue. X-ray images resemble “rat bites.” Asymmetrical erosions with destruction of cartilage are typical; bone ankylosis (fusion of articular surfaces) is rarely formed. If calcium is present in the tophi structures, then X-ray positive inclusions can be detected, which sometimes stimulate chondromas (a tumor consisting of cartilage tissue). The joint space width of the affected joints usually remains normal until the late stages of gouty arthritis. These changes can mimic osteoarthritis (joint degradation), but in some cases both conditions occur.

Stages of joint damage

tophi in the bone adjacent to the joint capsule and in deeper layers, rarely - manifestations of soft tissue compaction - gouty arthritis is just developing;
large tophi formations near the joint and small erosions of the articular surfaces, increasing compaction of the periarticular soft tissues, sometimes containing a certain amount of calcium - gouty arthritis manifests itself in acute attacks;
severe erosion on at least 1/3 of the surface of the joint, complete aseptic resorption of all articular tissues of the epiphysis, significant compaction of soft tissues with calcium deposits - chronic gouty arthritis.

Forecast of the consequences of gout

With timely recognition and treatment, gout can be avoided. unpleasant consequences or progression into a chronic form of the disease. Unfavorable factors that influence the degree of development of the disease: age under 30 years, persistent hyperuricemia exceeding 0.6 mmol/l (10 mg%), persistent hyperuricosuria exceeding 1100 mg/day, the presence of urolithiasis in combination with a urinary tract infection; progressive nephropathy, especially in combination with diabetes mellitus And arterial hypertension. Life expectancy is determined by the development of renal and cardiovascular pathologies. In conclusion, it is worth noting that gout is a difficult to diagnose systemic disease, the symptoms of which are varied and often overlap with various other diseases.

Only in 10% of cases can a doctor immediately diagnose gout, since its early form is sluggish, almost asymptomatic. That is why it is important to monitor diseases that have obvious external manifestations (pain or deformation of any part of the body), and the condition of the blood. Blood is an indicator of a person's condition. Timely diagnosed gout will allow you to choose the most effective method treatment. And if the final diagnosis was made only at a late stage, then in order to be able to move normally (gout affects the joints, deforming them), only surgical intervention and a long rehabilitation period with no guarantee that the disease will not return again. Be healthy!

Be sure to consult your doctor before treating any illness. This will help take into account individual tolerance, confirm the diagnosis, ensure the correctness of treatment and eliminate negative drug interactions. If you use prescriptions without consulting your doctor, it is entirely at your own risk. All information on the site is presented for informational purposes and is not a medical aid. All responsibility for use lies with you.