X-ray signs of gout. Gouty arthritis and the clinic of radiological manifestations of the punch symptom. The punch symptom on the radiograph.

A disease of modern society is gout, which belongs to the group of metabolic diseases. The disease is characterized by a long and persistent course and can provoke severe destructive processes in the joints.

Here it is worth mentioning for the first time the true enemy of humanity - gouty arthritis.

Essence of the disease

The inflammatory manifestation of gout or gouty arthritis develops in the process of accumulation of uric acid crystals in the joints, which subsequently has a destructive effect on the periarticular tissues and hyaline cartilage.

In more detail, the list of pathological changes accompanying the development of the disease consistently includes:

an increase in the amount of uric acid in the blood;
accumulation of its crystals in joints;
irritation, subsequent damage to the structure of the joints and the start of the inflammatory process;
gradual development of consequences;
the appearance of periarticular tumor-like growths.

The toes are most often affected, but the hands and fingers may also be affected. Gouty arthritis of the knee, elbow and ankle joints is extremely rare, and the disease does not affect the pelvic area and shoulders at all.

Causes and forms of the disease

The reasons for the development of the disease have not yet been fully identified. However, it has been proven that the occurrence and course of the disease is significantly influenced by the hereditary factor, as well as metabolic processes in the body.

Among the clearly negative factors, peculiar triggering mechanisms:

In addition to the traditional acute and chronic forms of gouty arthritis, there are also:

Rheumatoid-like, the course of which is characterized by its own duration. The inflammatory process develops in the area of the wrist, metacarpophalangeal and interphalangeal joints.
Pseudophlegmonous, in which only one joint (large or medium) is affected. Local or general reactions of the body are observed: swelling, redness of the skin in the area and outside the joint, hyperleukocytosis, fever.
Subacute, characterized by subtle clinical symptoms. The lesion is concentrated in the area of the big toe.
Aesthetic, which is characterized by slight redness of the skin, no swelling, and an average degree of pain in the affected area.
Periarthritic. In this case, the inflammatory process spreads to the bursae and tendons localized in the area of undamaged joints.

Symptoms of the disease

The developing disease includes the following three stages:

Latent (the content of lactic acid increases, salts accumulate in the area of bone and cartilage tissues and joint capsules). There are most often no symptoms.
Acute, in which severe pain is observed, joints and adjacent tissues become inflamed.
Chronic, characterized by long periods of remission.

The first symptoms of gouty arthritis are acute.

Among them:

pain in the joint area;
skin redness;
increased pain in the affected area when moving;
increase in body temperature.

After a few days, acute symptoms reduce their severity until discomfort disappears almost completely.

The following symptoms may appear at this stage:

formation of tophi (subcutaneous formations) in the area of the damaged joint, their breakthrough;
increasing the duration of the period of exacerbation of the disease;
reduction of intervals between attacks;
destruction of the structure of hyaline cartilage and the development of a chronic form of the disease.

At the last stage of arthritis development, the skin in the area of the affected joints becomes rough, dry, and itching may occur.

The mobility of the limbs is largely limited due to deformation of bone and cartilage tissue and the progression of arthrosis of the joints.

Diagnosis of the disease

The key point in diagnosing the disease is the detection of urate salts in the synovial fluid of the joints.

In addition, a biochemical blood test and urine test are performed to assess the amount of uric acid. The contents of the tophi can also be examined.

In case of prolonged course of the disease, an x-ray examination is prescribed. If the result is positive, the image shows bone defects, cartilage destruction, and punctures.

Treatment method

Treatment of gouty arthritis has a number of goals:

normalization of metabolism in the patient’s body;
relief of the acute form of the disease;
restoration of functionality of damaged internal organs;
treatment of chronic disease.

A set of measures to combat the disease primarily includes drug therapy:

anti-gout drugs to eliminate pain and activate the process of urate elimination;
NSAIDs (Diklak, Voltaren, Movalis, etc.) to relieve swelling, inflammation and pain;
glucocorticosteroids (hydrocortisone) in case of severe pain, are injected once into the affected area.

As the symptoms of the acute form subside, basic therapy is prescribed:

In the treatment of gouty arthritis, one cannot do without physiotherapeutic and hardware procedures. During exacerbation of the disease, electrophoresis and ultraviolet irradiation are prescribed.

At the remission stage - mud applications, drinking mineral waters, radon and bromine baths.

Taking into account the fact that one of the reasons for the development of the disease is poor nutrition, it is impossible to completely recover from the disease without following some dietary rules.

Patient's lifestyle

For effective treatment, the patient should pay close attention to his weight. If it increases, you need to take care of yourself.

Follow a diet, spend more time in the fresh air, visit the bathhouse (sauna) more often, do regular exercise and don’t forget about therapeutic exercises.

Do:

swings and circular rotations with arms;
flexion and extension of the joints of the arms and legs;
finger rotation;
raising legs (lying);
"Bicycle" exercise.

Traditional medicine to help

In parallel with the main therapy, you can help yourself with folk remedies:

Decoction of onion peels. Pour a glass of husk into a liter of boiling water and put on fire for ¼ hour, then filter and take ½ glass several times a day.
Chamomile with salt. 2 tbsp. l. pour a glass of boiling water over chamomile flowers and leave for 1.5 hours, then mix ½ glass with salt (1 glass) and water (10 l.). We take baths in the morning and evening.
Rub the sore spots with salted lard.

Complications

All complications that can overtake the patient can be divided into three groups:

articular (development of the process of joint deformation);
renal (the occurrence of urolithiasis and gouty kidney, which entail the development of arterial hypertension);
other complications (formation of tophi in other tissues and organs).

Prognosis for the patient

The prognosis in this case is generally favorable. Among the disappointing factors in the development of the disease:

age up to 30 years;
the presence of persistent hyperuricemia and hyperuricosuria;
urolithiasis and urinary tract infection;
nephropathy in a progressive stage.

Urolithiasis develops in 20-25% of clinical cases.

Preventive measures

Fundamental preventive measures in the case of gouty arthritis are:

maintaining a healthy lifestyle;
diet;
body weight control (excluding sudden changes in weight);
increased physical activity;
organization of work and rest schedules;
dealing with stress.

Gouty arthritis is a very serious disease, the development of which can be caused by seemingly trivial factors.

If a disease is suspected, it must be followed by timely diagnosis and treatment, otherwise the further course of the disease can lead to permanent immobilization of the limbs.

General information
Causes
Development and classification
Types of disease
Symptoms
Treatment

If crystals of a substance known as calcium pyrophosphate dihydrate are deposited in a person's connective tissue, then we are dealing with pyrophosphate arthropathy.

General information

Imagine that you are under 55 years old. Most likely, the disease will bypass you. With age, the frequency of crystallization increases - this is evidenced by X-ray data. The disease belongs to the group of so-called microcrystalline arthritis. Doctors distinguish 3 clinical variants of this disease:

pseudogout;
pseudoosteoarthrosis;
pseudorheumatoid arthritis.

Over time, chronic arthropathy may develop. Acute attacks of pseudogout are also observed. Young people (20-30 years old), adolescents and children are not susceptible to chondrocalcinosis.

Causes

There is no clear information about the reasons for crystallization of the bone structure. However, there is reason to believe that a number of factors contribute to this. Let's list some:

age (over 55 years);
hereditary predisposition (autosomal dominant trait);
joint injury;
hemochromatosis (clearly associated with chondrocalcinosis);
endocrine and metabolic disorders;
Gitelman syndrome (hereditary renal tubular pathology);
hypocalciuric hyperkalemia (familial);
hypothyroidism.

Development and classification

The accumulation of crystals occurs in cartilage, which is located near the surface of chondrocytes. One of the likely mechanisms of crystallization is increased activity of the enzymes nucleoside triphosphate-pyrophosphate hydrolase. Vesicles formed as a result of the breakdown of collagenase (concentrated in articular cartilage) are saturated with enzymes of the mentioned group.

If you carefully examine the crystals through a microscope, you will notice that they have a rhombic (or rectangular) shape and are significantly different from monosodium urate, which has a needle-like structure.

PFA (pyrophosphate arthropathy) is divided into primary and secondary. Primary PFA is familial, and secondary is associated with metabolic diseases:

hemochromatosis;
primary hyperparathyroidism;
Konovalov-Wilson disease;
hypomagnesemia;
hypophosphatasia.

Symptoms

One of the main symptoms is an acute gout attack. It always develops suddenly, for no apparent reason. The disease is accompanied by:

The knee joint is often affected, but in some cases the big toe, small and large joints are affected. In case of calcification of intervertebral discs, there is a possibility of developing radicular syndrome.

Arthritis can sometimes be quite intense, which entails its misdiagnosis as “septic.” The disease develops spontaneously, sometimes after a cerebral crisis, heart attack or phlebitis. In 25% of cases, a pseudogout form is observed, in 5% - a pseudorheumatoid form.

Diagnostics

The affected area is the wrist, shoulder, knee or metacarpophalangeal joints. The following types of examinations help identify the disease:

Physical. The affected joint is characterized by swelling, pain, and the joint is asymmetrical or deformed. With pseudarthrosis, swelling of Bouchard's and Heberden's nodes can be observed.
Laboratory. The main symptom is the presence of crystals in the synovial fluid. When detecting them, the most popular method is polarization microscopy.
Instrumental. X-rays of the pelvis, joints and hands are taken. The goal is to identify specific and nonspecific signs.
Differential. There is a comparison of PFA with septic and rheumatoid arthritis, gout, and osteoarthritis.

Treatment

If therapy is ineffective and the disease worsens, hospitalization is required. In addition, they practice:

Drug treatment.
Non-drug treatment.
Surgical intervention.

The chances of recovery are quite good. Practice shows that 41% of patients recover. Surgery is required in 11% of cases.

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X-ray manifestations of gout first described by G. Huber in 1896. Later, many studies were carried out that showed that at the early stage of the disease there are no characteristic changes. Radiographs then show signs of bone and cartilage destruction due to deposition of sodium urate crystals in the subchondral bone.

X-ray picture of gouty arthritis of the feet

X-ray picture of gouty arthritis of the right leg

There are several classifications of radiological changes in gout. Thus, E. Kavenoki-Mintz distinguishes three stages of chronic gouty arthritis (1987):

I - large cysts in the subchondral bone and in deeper layers. Sometimes hardening of soft tissues;
II - large cysts near the joint and small erosions on the articular surfaces, constant compaction of the periarticular soft tissues, sometimes with calcifications;
III - large erosions, but less than 1/3 of the articular surface, osteolysis of the epiphysis, significant compaction of soft tissues with lime deposits.

A more recent classification is proposed by M. Cohen, B. Emmerson (1994), according to which the main radiological signs of gout include the following:

in soft tissues - compactions;
eccentric darkening caused by tophi;
bones (joints) - the articular surface is clearly represented;
no juxtaarticular osteoporosis;
erosions (perforation, marginal sclerosis).

Thus, the presented classifications differ significantly and require unification of a number of radiological signs for gout.

Instrumental and laboratory studies.

Clinical blood tests during acute attacks of gout in patients reveal leukocytosis with a neutrophilic shift to the left and an increase in ESR.

An increased content of uric acid is determined in the blood serum: in men more than 7 mg% (0.42 mmol/l), in women - 6 mg% (0.36 mmol/l). A study of uric acid excretion should be carried out after a 3-day diet excluding purines (meat, broths, fish, poultry, legumes, 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 (1.8-3.6 mmol/l) of uric acid is excreted per day.

Uric acid crystals are found in the contents of tophi. It should be borne in mind that during histological examination of tophi tissue, they should not be fixed with formaldehyde in order to avoid dissolution of urate crystals.

Typical are intraosseous racemose formations of various sizes caused by tophi. Chronic gouty arthritis may be accompanied by cartilage destruction (narrowing of the joint space) and the development of marginal bone erosions. A characteristic sign is the “piercer symptom” - marginal bone or racemose formations of regular shape with clear, sometimes sclerotic contours; over time, pronounced destruction forms not only in the subchondral part of the bone, but also in the epiphysis and even in the diaphysis, forming intra-articular osteolysis. Radiologically, the most pronounced pathology is observed in the joints of the feet (primarily in the joints of the big toe). Rarely, radiological changes in the shoulder, hip, sacroiliac joints and spine can occur. Bone changes in gout rarely decrease with specific therapy.

Examination of synovial fluid.

The current literature on the composition of synovial fluid in patients with gout indicates the importance of its study for the diagnosis of joint diseases. According to many researchers, the detection of urate crystals in synovial fluid and especially in leukocytes is specific for gout. Of diagnostic significance is the detection of needle-shaped urate crystals located intracellularly and birefringent light when examined using a polarizing microscope. The threshold concentration of urate crystals in synovial fluid that is still available for identification is about 10 μg/ml.

The sensitivity of this test ranges from 85-97%.

Another important indicator of synovial fluid for an acute attack of gout is its cellular composition, mainly the number of leukocytes, which reaches the following values: from 10. 10 9 to 60 10 9 /l, with a predominance of neutrophils.

Joint diseases
V.I. Mazurov

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

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

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

Gouty arthritis occurs when:

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

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

joint injuries;
infections;
consumption of alcohol, fatty and fried foods;
hypothermia.

With gout, the temperature mainly rises at night.

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

pain in the damaged joint;
high temperature: 38-39 degrees Celsius;
swelling at the joint site takes on a blue tint.

X-ray as one of the diagnostic methods

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

X-ray signs of gout

The main sign that helps confirm gouty arthritis is the “punch sign”. On X-ray, this pathology looks like a cystic formation located on the edge of the bone with clear boundaries. The more calcium inclusions there are in the tumors, the better they are visible in the photographs. This diagnostic technique also identifies other radiological signs:

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

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.

In case of 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 (blemaren, 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 from this that there are several periods (stages) of the disease: asymptomatic hyperuricemia (premorbid period), which is characterized by an increased level of urate 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, 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 standards, 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 deformations 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 using chemical examination or microscopic examination).

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 (tendinitis, 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 lifting your leg 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 – lumboischialgic pain is observed when bending the head;
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 (ischialgic 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.

Joint diseases are among the most common in the world. And gout is also the most painful of them all. The disease affects both young and elderly patients. And this is due to poor nutrition and abuse of fast food.

The main reason for the development of the disease is a violation of metabolic processes in the body. An increased content of uric acid and its salts leads to the formation of crystals that destroy the cartilage tissue of the joint and lead to the formation of tophi.

Gouty arthritis can be triggered by pathologies of the central nervous system (CNS), thyroid gland and brain.

Incorrect or untimely diagnosis of gout and lack of adequate treatment increases the risk of complications.

Special Correspondent: Treatment of joints with expensive pacifiers - rheumatologists have been deceiving patients across the country for 12 years.
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Diagnosis of gout

It is quite difficult to identify gout on your own. Only an experienced specialist can rule out other diseases with similar symptoms and make a diagnosis of gout. Diagnosis begins with a visual examination of the patient and collection of anamnesis.

Questioning the patient

During the interview with the patient, the doctor finds out what symptoms are bothering him and how they manifest themselves. At the initial stage of the disease, small joints on the legs and arms are affected, then the disease spreads to large joints.

The diagnostic criterion for gout is the presence of genetic determination. If close relatives of the patient have been diagnosed with gout, then the risk of developing this particular disease increases.

The doctor also finds out previous diseases that can provoke gouty arthritis. These include:

Surgical operations;
Impaired kidney function;
Long-term use of antibiotics or steroids.

It also turns out that the patient has bad habits and food addictions.

Clinical studies

An experienced doctor can determine gout without tests. However, a final diagnosis and determination of the acute or chronic form of the disease can only be made on the basis of test results. To carry out differential diagnosis, the following examinations are prescribed:

Biochemical blood test for gout for uric acid, sialic acids, fibrin and the presence of protein (with C-reactivity). Such auto-diagnosis is used to determine the quantitative indicators of urates and their presence in the bloodstream. For men, the normal level of uric acid is 460 µM/l; for women, the normal level is lower - 330 µM/l. It is impossible to diagnose joint gout based on biochemical analysis alone. But an increased level of urate indicates dysfunction of the urinary tract and impaired renal function. A decrease in creatinine levels (normally it is 115 mmol/l) also indicates kidney pathology. Additionally, biochemistry analysis shows the amount of nitrogen, ammonia, glucose, lipids and bilirubin. A sharp increase in their indicators indicates a disruption in the functioning of various body systems;

With the development of gout, the results of a biochemistry analysis look like this: the amount of protein during an attack significantly exceeds the norm, in some there is a noticeable increase in glucose and creatinine. Indicators of calcium, lipids, and lipoproteins will also be elevated.

General blood test. Quantitative indicators of neutrophils in a blood test for gout help identify inflammation in the joint. This research method is effective for kidney dysfunction. An indicator of gout based on a general blood test is the presence of crystalline urates in the resulting sediment;

A high concentration of urates in the blood indicates the development of gout of the joints.

A urine test for gout allows you to clarify the cause of the pathology. The test results show the amount of uric acid and the overall acidity level. Urine is collected within 24 hours. This helps to examine the change in acidity results throughout the day.

An increase in indicators indicates the development of urolithiasis.

Puncture of synovial fluid. This method allows you to diagnose gout of the joints. In a healthy person, synovial fluid is colorless and has a consistency similar to water. A change in color and a decrease in fluidity indicates an increase in acidity and metabolic disorders. The analysis also shows the level of neutrophil lymphocytes;
X-rays are used to diagnose gout in the joints of the lower extremities and fingers. The picture shows the development of the pathological process in the joint, the deposition of salts. X-ray signs of gout include white spots with a diameter of 0.5 millimeters to 3 centimeters. They are caused by the presence of tophi, resulting from the deposition of uric acid salts in the periarticular tissues. Tophi take about five years to form. An exacerbation of gout can accelerate their formation. Sometimes an X-ray image shows complete or partial destruction of the endocrine gland, and its cells are replaced by uric acid crystals. X-ray examination will be effective for all joints. It helps to determine the type of gout, to record the transition of the disease to the periarticular bursa or tendons and the occurrence of inflammation in them. In this case, an additional biopsy test is prescribed;

The puncture symptom in gout is known as a phenomenon of the late stage of the disease. This is the “bone” on which the joint at the base or head of the phalanx rests. Such a defect can be up to 5 millimeters in diameter. In most cases, it is located in the first metatarsophalangeal joint of the foot.

Ultrasound and tomography - this technique is used only during an exacerbation of gout. During an attack, the interarticular space increases noticeably, swelling, hardening and inflammation of the soft tissues near the affected joint are observed. This clinical picture can be observed a week after an acute attack of gout. But during remission, ultrasound will not detect changes. In case of chronic gout, ultrasound can detect joint deformation, as well as the presence of an inflammatory process. The analysis also allows you to determine the deposition of salts in the kidneys and ureter;
A biopsy is a highly accurate analysis that allows you to identify quantitative indicators of uric acid deposits in the joints. For analysis, intra-articular fluid is collected. This technique allows you to clarify the cause of the development of gout.

Your doctor will tell you what tests you need to take for gout. He will draw up a research plan to clarify the diagnosis, especially with secondary gout.

Rules for preparing for analysis

Tests for gouty arthritis are carried out comprehensively. Otherwise, their results may be unreliable. Which will lead to an erroneous diagnosis and ineffective treatment. In order for the analyzes to be the most informative, the following rules should be followed:

Avoid drinking alcohol for at least a day before taking tests;
Reduce consumption of foods containing high doses of vitamin C, otherwise deviations from the norm may be overestimated;
Caffeine can also affect test results. Therefore, it is recommended to give up coffee and tea 8-10 hours before taking them;
Aspirin increases acidity levels, so you should avoid it;
Diuretics reduce test levels;
All tests for gout should be taken on an empty stomach. The last meal should be no earlier than 8-10 hours before delivery;
Following a diet for 2-3 days before taking tests will minimize distortion of test results. The consumption of plant and lactic acid products is recommended;
You should also avoid excessive exercise before conducting research.

Compliance with the rules for preparing for tests is a guarantee of the reliability of the results, correct diagnosis and prescription of adequate treatment.

False results

Failure to follow the rules for preparing for tests can lead to changes in their results:

Uric acid levels are elevated;
An X-ray or ultrasound before taking tests may affect the results;
Abuse of fatty foods and alcohol consumption provoke distortion of research results;
During gout therapy, tests will not be productive.

The patient should know that chronic gout of the joints cannot be completely cured. But with the help of therapeutic methods it is possible to reduce the number of acute attacks and reduce pain.

Self-medication for gouty arthritis of the joints is unacceptable. This can cause the progression of the disease and the development of complications. Uncontrolled use of drugs can distort test results, artificially lowering their indicators.

Prescribing adequate therapy for gout is possible only by a specialist, based on the results of tests and instrumental studies. Gouty arthritis does not always have visual manifestations, so it is very difficult to diagnose it only during a medical examination. A comprehensive examination allows you to diagnose the disease, identify its stage, and the presence of concomitant diseases.

Diagnosis of gouty arthritis

X-ray picture of gouty arthritis of the feet

X-ray picture of gouty arthritis of the right leg

There are several classifications of radiological changes in gout. Thus, E. Kavenoki-Mintz distinguishes three stages of chronic gouty arthritis (1987):

I - large cysts in the subchondral bone and in deeper layers. Sometimes hardening of soft tissues;
II - large cysts near the joint and small erosions on the articular surfaces, constant compaction of the periarticular soft tissues, sometimes with calcifications;
III - large erosions, but less than 1/3 of the articular surface, osteolysis of the epiphysis, significant compaction of soft tissues with lime deposits.

A more recent classification is proposed by M. Cohen, B. Emmerson (1994), according to which the main radiological signs of gout include the following:

in soft tissues - compactions;
eccentric darkening caused by tophi;
bones (joints) - the articular surface is clearly represented;
no juxtaarticular osteoporosis;
erosions (perforation, marginal sclerosis).

Thus, the presented classifications differ significantly and require unification of a number of radiological signs for gout.

Instrumental and laboratory studies.

Clinical blood tests during acute attacks of gout in patients reveal leukocytosis with a neutrophilic shift to the left and an increase in ESR.

Examination of synovial fluid.

The sensitivity of this test ranges from 85-97%.

Another important indicator of synovial fluid for an acute attack of gout is its cellular composition, mainly the number of leukocytes, which reaches the following values: from 10 10 9 to 60 10 9 / l, with a predominance of neutrophils.

Gout and X-ray

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 the characteristic signs of other diseases. The initial stage is asymptomatic, X-ray studies will be uninformative. If pain occurs in the joints, a number of tests are prescribed. To determine gout, the following examinations are used:

general urinalysis;
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.

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X-ray examination of gout

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 the late stages of the disease. 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.

A manifestation of the initial stages of gout can be diffuse hardening of soft tissues (edema). 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 edges of the bones in the form of a shell or shell. There are several X-ray signs that are presented in the table:

X-ray for gout

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

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

Gouty arthritis occurs when:

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

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

joint injuries;
infections;
consumption of alcohol, fatty and fried foods;
hypothermia.

With gout, the temperature mainly rises at night.

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

pain in the damaged joint;
high temperature: 38-39 degrees Celsius;
swelling at the joint site takes on a blue tint.

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X-ray as one of the diagnostic methods

X-ray signs of gout

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

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Other ways to confirm the diagnosis

To detect gout, a blood test is also performed, which determines the amount of uric acid, the presence of alpha-2-globulin, fibrinogen and C-reactive protein. The laboratory research method is effective only if there is no deterioration. Otherwise, the analysis will not be able to detect the presence of urate crystals in the blood, because they will all go into the affected joint.

Gout, gouty arthritis: symptoms, signs and treatment

Gout, or gouty arthritis is a disease in which a metabolic disorder occurs in the body, and uric acid salts are deposited in the joints. This is very unpleasant, but easy to manage treatment disease.

Occurs gout relatively infrequently. Although I hear the word “gout” almost every day. For example, most grandmothers call arthrosis of the big toe “gout.” This is what they usually say: “Gout has grown on my leg.”

In fact, gout, although it affects the same big toes, most often affects men. In women, gout (real, true gout) is several times less common.

Previously, some 100 years ago, gout was generally considered an exclusively male disease. But in our time, due to the fact that women began to eat better, eat more meat and sausages, gout began to occur much more often among them than, for example, a century ago.

In addition, gout in women has become more common due to the use of certain medications, primarily medications for high blood pressure. Some drugs to reduce high blood pressure, when used for a long time, lead to an increase in the concentration of uric acid in the body.

But still, in men, gout manifests itself much more acutely and “more aggressively,” since male sex hormones have a noticeable effect on the concentration of uric acid.

Below I will tell you about symptoms, signs And gout treatment, as well as what diet to follow for this disease.

Signs of gout

“Classical” gout belongs to the group of arthritis. It develops in people who have a hereditary predisposition to this disease. Moreover, the potential patient may not even be aware of his heredity.

For example, if his parents or relatives lead a healthy lifestyle, do not abuse alcohol and eat properly, then the disease may not manifest itself in them and will exist all their lives only in a latent, hidden form.
And our potential patient, who has a predisposition to this disease, will provoke the disease in himself only if he leads a not entirely healthy (from the point of view of a tendency to gout) lifestyle.

Thus, a typical gout is often (but not always) an overweight man who abuses either alcohol or so-called “purine foods”: meat, meat soups, smoked meats, fish and salted foods, offal (liver, kidneys), beans, beans , chocolate, grape wine.

When these products are abused, there is an increased formation of uric acid in the blood, which, in turn, forms a poorly soluble sodium urate salt. When the concentration of uric acid in the blood reaches a maximum level, its salts in the form of microcrystals are deposited in the joint cavity, forming a kind of “depot” there.

The presence of microcrystals of sodium urate in the joint cavity is a serious irritant for it. But nevertheless, crystals can remain in the joint for a long time asymptomatically - until some provocation (physical overload, stress, prolonged fasting or, conversely, too much “purine foods” and alcohol) provokes an acute gouty attack, that is attack of gout. It is regular acute attacks of gout that are the main symptom of this disease.

Gout symptoms

The first attacks of gouty arthritis are almost always short-lived. The attack usually begins suddenly, most often at night. In most cases, the joint of the big toe becomes inflamed (sometimes one, sometimes both). Less commonly, the thumbs, knees, ankles, elbow joints, heel tendons and, very rarely, the wrist joints become inflamed.

The pain is such that, according to my patients, it makes you want to literally “climb the wall.” The affected joint swells, turns red, and the skin over it becomes bright red or purplish and hot to the touch. Even a light touch to the inflamed joint or the slightest movement in it causes unbearable pain. The patient suffers for 3-4 days, when suddenly the attack passes, as if nothing had happened.

However, after some time, the pain just as suddenly recurs. Moreover, if at the beginning of the disease the intervals between attacks are quite long, from one to eight months, and the attacks themselves are short-lived, then over time everything changes. The attacks are becoming longer and longer, and the intervals between them are becoming shorter.

Eventually, there comes a time when the pain in the joints becomes constant, and there are practically no intervals between attacks. This condition is called "status gouty", or chronic gouty arthritis. In chronic gouty arthritis, articular cartilage is destroyed, and special defects are formed in the bones adjacent to the joint - “punches”, which are a cavity filled with microcrystals of sodium urate.

In addition, sodium urate crystals can be deposited even under the skin, forming whitish, hard nodules filled with a pasty mass. Such nodules are called tophi, and most often they are located on the ears or near the joints. Sometimes tophi break through and uric acid crystals are released through the resulting fistula. Fortunately, usually within a few days after the tophi breaks through, the wound heals without consequences.

In addition to the above troubles, gout, especially if advanced, is almost always accompanied by the deposition of urate in the kidneys, which leads to urolithiasis and sometimes to inflammation of the kidneys (pyelonephritis).

Female variants of gout are usually much milder. Women very rarely have acute gouty attacks, and tophi and punctures in the bones are much less likely to form. Most often, female gout manifests itself as mild chronic pain in the knee or ankle joint. And an experienced doctor can guess that this is not arthrosis only by the severe swelling of the inflamed joint, which is uncharacteristic of arthrosis.

Diagnosis of gout

Having assumed that the patient has gouty arthritis (and in classical cases this is quite easy), a competent rheumatologist or arthrologist will refer the patient for an X-ray of the hands and feet, as well as a biochemical blood test.

With advanced gout, the doctor can easily detect characteristic gouty “punches” in the periarticular bones on x-rays of the hands and feet. A blood test will show an increase in uric acid levels. If such an increase is clearly expressed and is combined with the presence of “punches” in the bones and characteristic gouty symptoms, then the diagnosis is considered reliable, and then we only need to select the correct treatment.

The problem, however, is that if you do a uric acid test at the very moment of the attack (and usually it is at this time that the patient goes to the doctor), then such an analysis may not record any abnormalities. That is, at the time of an attack, the level of uric acid in the blood may turn out to be normal (after all, at the time of an attack, the maximum amount of uric acid goes into the inflamed joint).

Therefore, it is necessary to measure the level of uric acid in the blood several times, including between attacks. But gout patients often don’t have the patience for this. As soon as the next attack “subsides,” they often completely stop thinking about their health again.

Meanwhile, without correct diagnosis and without proper treatment, gout can lead to very undesirable consequences not only for the joints, but also for the kidneys.

Continuing the topic, I would like to note that, despite the frequent mention of the term “gout” in the literature and in conversations, in reality it turns out that the correct diagnosis of gout patients is not always made and is often very late. Sometimes you have to deal with monstrous diagnostic errors.

For example, at the time of an attack, surgeons managed to diagnose one of my patients with “gangrene of the big toe” and amputated the toe inflamed by gout. Literally 3 weeks later, his big toe on his other foot became inflamed, and the patient was about to amputate that too! Fortunately, the man realized that this time he should consult another doctor, and turned to me for help. Upon examination, it immediately became clear that the patient did not have gangrene, but classic gout. I prescribed the anti-gout drug colchicine to the patient, and the attack was eliminated literally in one day! The next day there was no trace left of the imaginary gangrene.

Another patient was treated for arthrosis for seven years, despite the fact that his joints became inflamed in attacks, alternately, about once a month, and the inflammation never lasted longer than 5-7 days. The most surprising thing in this story was that in numerous tests of blood taken from a vein, the patient’s uric acid simply went off scale. She was more than 2 times higher than normal! But doctors managed to ignore this over and over again. And they continued to stick to their line. During one of the attacks, the man even had time to have his knee operated on and a completely healthy meniscus was removed. But the operation, naturally, did not bring any relief to the patient. The knee periodically continued to become inflamed along with other joints.

Only after the man came to see me and laid out a pile of tests in front of me, which clearly showed a constant increase in uric acid levels, was the patient finally given adequate anti-gout treatment. And just a month after the start of treatment, gout attacks, for the first time in all the past years, began to disappear. And then they stopped altogether.

Treatment of gout

After diagnosing a patient, I usually say, without any irony, “Congratulations, you have gout.” I really am not being ironic, because of all the possible diagnoses, this is one of the most favorable. Gout is very easy to treat and is not particularly difficult for a competent specialist.

Although here, as often happens, there is a “fly in the ointment.” Yes, gout is very treatable, but many gout patients do not want to accept the conditions that are necessary for recovery - since the “conditions” are the refusal of those foods (and alcohol) that caused metabolic disorders. And when I tell patients that to get rid of the disease they need to give up their favorite foods and alcohol, they often simply don’t want to hear me.

Therefore, every time I have to patiently explain that without a diet there can be no talk of recovery - no matter what “cool” medications are used. Another thing is that in many cases the diet is a temporary measure, and if certain conditions are met, after a year or two the strict restrictions can be lifted.

A classic but outdated version of the gout diet is here

The diet for gout updated and corrected by Dr. Evdokimenko is here

Drug therapy gouty arthritis consists of two components: treatment of an acute attack and therapy of gout itself.

To relieve an acute gout attack, non-steroidal anti-inflammatory drugs (Voltaren, ibuprofen, Movalis, Nimulide, etc.) or a special short-acting anti-gout drug - colchicine - are successfully used. A vodka compress can be applied locally to the sore joint.

Drugs to relieve an acute attack are used for a short period of time, in a short course of three to seven days. And directly for the treatment of gout, in the absence of contraindications, for several months or years a drug is used that reduces the formation of uric acid in the body - purinol, also known as allopurinol.

Compliance with the diet and the use of purinol (allopurinol) leads to normalization of the patients' condition within the first month of therapy. Although during the first week, during therapy with purinol or allopurinol, an exacerbation of the disease may even occur. But then the attacks become weaker and occur less and less often, and over time they stop altogether.

And after about a year, if my ward is feeling well, I allow some relaxations in his regime. I ask the patient what he would like to stop - diet or medication, since we can then limit ourselves to one thing. If the patient is already accustomed to the diet, then there is no point in breaking it. In this case, it is better to reduce the dose of medications taken or stop them altogether.

If the patient finds it difficult to tolerate dietary restrictions, then you can abandon the diet, but continue taking medications. However, the medications will have to be used for several years - which, in general, is not scary, since purinol (allopurinol) rarely causes any side effects and is generally well tolerated by patients.

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GOUT

Irina Aleksandrovna Zborovskaya – Doctor of Medical Sciences, Professor, Professor of the Department of Hospital Therapy with a Course of Clinical Rheumatology of the Faculty of Advanced Training of Physicians of the Volgograd State Medical University, Director of the Federal Budgetary State Institution "Research Institute of Clinical and Experimental Rheumatology" RAMS, Head of the Regional Center for problems of osteoporosis, member of the presidium of the Association of Rheumatologists of Russia, member of the editorial boards of the journals “Scientific and Practical Rheumatology” and “Modern Rheumatology”

Definition

For two and a half millennia - since Hippocrates described the syndrome of acute pain in the area of the big toe, which he called gout (literally from Latin “trap on the foot”), interest in this disease has always had an undulating course, usually associated with the discovery some new look.

But the data on the study of crystals that cause gouty arthritis are especially interesting. It has been shown that these are monosodium urate crystals, the detection of which has absolute diagnostic significance. In essence, by the end of the 20th century, gout began to be viewed as a disease of accumulation of urate crystals in the structure of the joint, subcutaneous tissue and bones, and kidneys in the form of urolithiasis or tubular nephropathy.

So, gout is a disease based on a violation of purine metabolism with an increase in the content of uric acid in the blood, excessive deposition of uric acid salts, primarily in the tissues of the musculoskeletal system and internal organs and with the development of inflammatory and then destructive diseases in them. -sclerotic changes.

Refers to multifactorial diseases.

Epidemiology

I. In Europe and the USA, the incidence of gout is 0.3% of the total incidence, among rheumatic diseases it accounts for 5%, in our country it is 7-8%.

II. In our country, in the post-war years, apparently due to limited protein nutrition, the frequency of gout decreased, but subsequently increased significantly and acquired greater social significance.

In our country, gout is detected in 0.1% of the population; The true percentage is likely higher because gout is diagnosed late. The incidence of gout is increasing worldwide.

Gout affects mostly men (95-98%), usually over 30 years of age.

However, in recent years, a number of researchers have noted a widespread increase in the number of patients with gouty arthritis among women. An inverse relationship was found between the level of estrogen and the concentration of uric acid. A decrease in the level of these hormones in the blood during menopause contributes to the appearance of hyperuricemia and the formation of deposits in tissues.

III. It is also important that in most patients the diagnosis is not made in a timely manner.

IV. Features of the disease in recent decades are its onset at a younger age and the formation of complications earlier. Frequent involvement of the kidneys and cardiovascular system in the process. Young people are more likely to experience a severe course of the disease with multiple joint damage, frequent and prolonged exacerbations, multiple tophi and more severe hyperuricemia.

Etiopathogenesis

I. Uric acid is the end product of the breakdown of purines in humans. In plasma, extracellular and synovial fluid it is contained mainly in the form of salts (urates). At pH 7.4, uric acid is 98% monosodium salt, which is easily removed from plasma by hemofiltration or dialysis. Uric acid practically does not bind to plasma proteins.

The concentration of a saturated solution of uric acid in serum at a temperature of 37°C is 416 µmol/l (7 mg%). Exceeding this threshold creates the precondition for the crystallization of urates. However, the blood contains substances that increase solubility, so crystallization usually does not occur even at a serum uric acid concentration of 4800 µmol/L (80 mg%).

Uric acid is more soluble in urine than in water, possibly due to the presence of urea, proteins, and glycosaminoglycans. Its solubility depends on pH. At a pH of 5, the solubility of uric acid in urine is 360-900 µmol/l (6-15 mg%), and at a pH of 7, it is 9480-12000 µmol/l (158-200 mg%). Some of the uric acid is found in the urine in the form of salts: monosodium, disodium, potassium, ammonium and calcium.

The synthesis and breakdown of purines occurs in all tissues, but uric acid is formed only where xanthine oxidase is present, primarily in the liver and small intestine. The amount of uric acid in the body is determined by the ratio of the rates of formation of uric acid and its elimination. The rate of formation of uric acid depends on the amount of purines in the diet and the rates of synthesis, regeneration and breakdown of purines. Normally, 66-75% of uric acid is excreted in the urine, and the remainder is excreted mainly in feces.

Approximately 98–100% of uric acid from the glomerular filtrate is reabsorbed in the proximal tubules, but half of this amount is secreted back into these tubules, and then about 40% is reabsorbed again. As a result, only 8–12% of filtered uric acid ends up in the urine.

Serum uric acid concentrations depend on sex and age, and in adults, on height, weight, blood pressure, renal function, and alcohol consumption. In most children it is 180 – 240 µmol/l (3 – 4 mg%). As men reach puberty, the concentration increases, but in women it remains low until menopause. The reason for this difference has not been conclusively established. The upper limit of normal serum uric acid concentration in women of childbearing age and in adult men is 360 and 416 μmol/L (6 and 7 mg%), respectively. In postmenopause, the concentration of uric acid in serum in women increases and approaches the concentration characteristic of men.

II. The occurrence of gout is associated with both genetic and nutritional causes.

In the general population, the prevalence of hyperuricemia is 2–13.2%, and gout is 1.3–3.7%. The higher the serum uric acid concentration, the greater the likelihood of gout. According to one study, the incidence of gout at a serum uric acid concentration of more than 540 µmol/l (9 mg%) was 4.9%, and at a concentration of 415 - 535 µmol/l (7 - 9 mg%) - 0.5% . The course of gout depends on the duration and severity of hyperuricemia. The first attack of gout most often occurs after 20-40 years of persistent hyperuricemia; in men this usually occurs between the ages of 40 and 60, and in women after menopause.

III. However, it must be especially emphasized that identifying hyperuricemia is not enough to establish a diagnosis, since only about 10% of patients with hyperuricemia suffer from gout. In this regard, it is important to emphasize the paradox of the 20th century - all patients with gout have hyperuricemia, but the vast majority of people with hyperuricemia have never suffered an attack of acute arthritis. This means that the development of gout is due to pathophysiological features that determine the deposition of urate crystals in tissues, accompanied by inflammation and subsequent degenerative changes. Thus, hyperuricemia is a necessary but not sufficient antecedent for the development of urate microcrystalline disease, and, therefore, hyperuricemia is a clinical syndrome different from gout.

IV. Therefore, in the development of gout, along with hyperuricemia, other factors are important.

The reasons that self-limit the course of acute gouty arthritis are not completely clear, but are most likely associated with the synthesis of “anti-inflammatory” mediators (IL-1 receptor antagonist, transforming growth factor-B, etc.).

V. To date, factors predisposing to urate deposition and joint inflammation in individuals with hyperuricemia (with the exception of familial cases) are unknown.

CLASSIFICATION OF CAUSES OF HYPERURICEMIA