Gouty arthritis and the clinic of radiographic manifestations of the punch symptom. Gout - description, causes, symptoms (signs), treatment Gouty arthritis x-ray

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

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

Pathologies of the central nervous system (central nervous system), thyroid gland and brain can provoke gouty arthritis.

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

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 exclude other diseases with similar symptoms and diagnose gout. Diagnosis begins with a visual examination of the patient and the collection of anamnesis.

Interrogation of the patient

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

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

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

Surgical operations;
Kidney dysfunction;
Long-term use of antibiotics or steroids.

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

Clinical researches

An experienced doctor can identify gout without testing. However, it is possible to make a final diagnosis, determine the acute or chronic form of the course of the disease only on the basis of the results of the tests. For differential diagnosis, the following examinations are prescribed:

Biochemical blood test for gout for uric acid, sialic acids, fibrin and the presence of protein (with C-reactivity). Such self-diagnosis is used to determine the quantitative indicators of urates and their presence in the bloodstream. For men, the norm of uric acid is 460 μM / l, for women the normal values are lower - 330 μM / l. Guided by one biochemical analysis, it is impossible to diagnose gout of the joints. But an elevated level of urate indicates dysfunction of the urinary tract and disruption of the kidneys. The pathology of the kidneys is also indicated by a decrease in the level of creatinine (normally it is 115 mmol / l). Additionally, a biochemistry analysis shows the amount of nitrogen, ammonia, glucose, lipids and bilirubin. A sharp increase in their indicators indicates a violation of the functioning of various body systems;

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

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

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

Urinalysis for gout allows you to clarify the cause of the pathology. The results of the analysis show the amount of uric acid and the overall level of acidity. Urine is given during the day. This helps to explore the change in acidity results throughout the day.

An increase in indicators indicates the development of urolithiasis.

Puncture of synovial fluid. This method allows you to diagnose gout joints. In a healthy person, synovial fluid has no color, but resembles water in consistency. A change in color and a decrease in fluidity indicate an increase in acidity, a metabolic disorder. The analysis also shows the level of neutrophilic lymphocytes;
X-ray is used to diagnose gout of the joints of the lower extremities, as well as fingers. The picture shows the development of the pathological process in the joint, the deposition of salts. Radiographic signs of gout include white spots, with a diameter of 0.5 millimeters to 3 centimeters. They are due to the presence of tophi, resulting from the deposition of uric acid salts in the periarticular tissues. The formation of tophi takes about five years. Exacerbation of gout can accelerate their formation. Sometimes an x-ray image captures the complete or partial destruction of the endocrine gland, and its cells are replaced by uric acid crystals. X-ray examination will be effective for all joints. It helps to determine the type of gout, fix the transition of the disease to the periarticular bag or tendons and the occurrence of inflammation in them. In this case, an additional biopsy test is prescribed;

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

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

What tests need to be done for gout, the attending physician will tell you. He will draw up a scheme for conducting studies to clarify the diagnosis, especially with secondary gout.

Rules for preparing for analyzes

Analyzes for gouty arthritis are given comprehensively. Otherwise, their results may be unreliable. This will lead to misdiagnosis and ineffective treatment. In order for the analyzes to be the most informative, the following rules should be observed:

Eliminate the use of alcohol for at least a day before taking tests;
Reduce the intake of foods containing high doses of vitamin C, otherwise deviations from the norm may be overestimated;
Caffeine can also interfere with test results. Therefore, it is recommended to give up coffee and tea 8-10 hours before their delivery;
Aspirin increases the level of acidity, so you should refuse it;
Diuretics lower test levels;
All tests for gout should be taken on an empty stomach. The last meal should be no earlier than 8-10 hours before delivery;
Following a diet for 2-3 days before testing minimizes the distortion of test results. The use of vegetable and lactic acid products is recommended;
You should also refrain from excessive exercise before conducting research.

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

False results

Failure to comply with the rules for preparing for the delivery of tests can lead to a change in their results:

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

The patient should be aware that chronic gout of the joints cannot be completely cured. But with the help of therapeutic methods, you can reduce the number of acute attacks, reduce pain.

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

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

Diagnosis of gouty arthritis

Radiological manifestations of gout first described by G. Huber in 1896. Later, many studies were carried out that showed that at an early stage of the disease there are no characteristic changes. Then, radiographs show signs of bone and cartilage destruction due to the 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. So, E. Kavenoki-Mints distinguishes three stages of chronic gouty arthritis (1987):

I - large cysts in the subchondral bone and in deeper layers. Sometimes soft tissue hardening;
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 erosion, but less than 1/3 of the articular surface, osteolysis of the epiphysis, significant compaction of soft tissues with lime deposition.

More recent is the classification proposed by M. Cohen, V. Emmerson (1994), according to which the following are the main radiological signs in gout:

in soft tissues - seals;
eccentric darkening due to tophi;
bones (joints) - the articular surface is clearly presented;
juxta-articular osteoporosis is absent;
erosion (punch, marginal sclerosis).

Thus, the presented classifications are significantly different and require the unification of a number of radiological signs in gout.

Instrumental and laboratory research.

In a clinical blood test during acute attacks of gout, patients reveal leukocytosis with a neutrophilic shift to the left and an increase in ESR.

In the blood serum, an increased content of uric acid is determined: in men, more than 7 mg% (0.42 mmol / l), in women - 6 mg% (0.36 mmol / l). A uric acid excretion study should be performed after a 3-day purine-free diet (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.

In the contents of tophi, crystals of uric acid are found. It should be borne in mind that during histological examination of tophi tissues, they should not be fixed with formalin 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 - “a symptom of a punch” - marginal bone or racemose formations of the correct form with clear, sometimes sclerotic contours, over time, pronounced destruction is formed not only in the subchondral 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 thumb). Rarely, radiological changes in the shoulder, hip, sacroiliac joints and spine can occur. Bone changes in gout rarely decrease with specific therapy.

The study 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 the synovial fluid and especially in leukocytes is specific for gout. Diagnostic value 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 the synovial fluid, 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.

Gout and x-ray

Gout is a systemic disease associated with impaired 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. In the diagnosis of the disease, laboratory tests and X-ray procedures of the affected areas play a very important role.

Signs of the disease

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

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

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X-ray examination of gout

The diagnostic method consists in the absorption of rays by the affected area and further projection on films or a PC monitor. Further, the doctor processes the information and makes recommendations. To clarify the degree of destruction of the skeleton in gouty arthritis, x-rays of the affected joints are prescribed. Such an x-ray phenomenon as a “punch” symptom, which is characteristic of the late stages of the disease, is very well known. This is a bone defect with a size of 5 mm, which is most often localized at the first metatarsophalangeal joint.

Early x-rays of gout can show transient osteoporosis.

A manifestation of the initial stages of gout can be diffuse compaction of soft tissues (swelling). Sometimes they find an inflammatory process of the bone substance - transient arthritis. During the disease, destruction of the patient's bone often occurs. Erosion and destruction can occur inside and outside the joint. X-ray 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:

X-ray for gout

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

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

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

Gouty arthritis occurs when:

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

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

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

With gout, the temperature mainly rises at night.

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

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

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X-ray as one of the diagnostic methods

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

X-ray signs of gout

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

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

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Other ways to confirm the diagnosis

A blood test is also performed to detect gout, which determines the amount of uric acid, the presence of alpha-2 globulin, fibrinogen, and C-reactive protein. The laboratory method of research is effective only in the absence of deterioration. Otherwise, the analysis will not be able to detect the presence of urate crystals in the blood, because they will all go to 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. It's very annoying, but easy to manage. treatment disease.

Meets gout relatively infrequently. Although the very word "gout" I have to hear almost every day. For example, most grandmothers call arthrosis of the big toe “gout”. Usually they say this: “I have gout on my leg.”

In fact, gout, although it affects all the same big toes, is most often the lot of 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 has become much more common in them than, for example, a century ago.

In addition, gout in women has become more common due to the use of certain drugs, primarily medicines for high blood pressure. Some drugs to reduce high blood pressure with long-term use lead to an increase in the concentration of uric acid in the body.

But all the same, in men, gout manifests itself much more acutely and “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 about what kind of diet you need to follow with this disease.

Signs of gout

"Classic" gout belongs to the group of arthritis. It develops in people who have a hereditary predisposition to this disease. Moreover, a 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 right, then the disease may not manifest itself in them and will exist all their lives only in a latent, latent form.
And our potential patient, who has a predisposition to this disease, will provoke a disease in himself only if he leads a lifestyle that is not entirely healthy (in terms of a tendency to gout).

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

With the abuse of these products, an increased formation of uric acid in the blood occurs, which, in turn, forms a poorly soluble salt of sodium urate. When the concentration of uric acid in the blood reaches the limit 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 him. But nevertheless, the crystals can be asymptomatic in the joint for a long time - until any provocation (physical overload, stress, prolonged fasting, or, conversely, the enumeration of "purine foods" and alcohol) provokes an acute gouty attack, that is gout attack. 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, thumbs, knee, ankle, elbow joints, calcaneal tendons become inflamed, and very rarely, wrist joints.

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

However, after some time, the pain just as suddenly repeats itself. 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, then everything changes with time. Attacks become longer and longer, and the intervals between them become shorter.

In the end, there comes a point when the pain in the joints becomes constant, and the intervals between attacks are practically absent. This condition is called "gouty status" or chronic gouty arthritis. In chronic gouty arthritis, the destruction of the articular cartilage occurs, and in the bones adjacent to the joint, special defects are formed - "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 mushy mass. Such nodules are called tophi, and most often they are located on the auricles 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 breakthrough of tofus, the wound heals without consequences.

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

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

Diagnosis of gout

Assuming that the patient has gouty arthritis (and in classic cases this is quite easy), a competent rheumatologist or arthrologist will refer the patient to x-rays of the hands and feet, as well as to 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 just need to choose the right treatment.

The problem, however, is that if you do a uric acid test at the very moment of an attack (and usually at this time the patient goes to the doctor), then such an analysis may not fix any deviations. 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 interictal periods. But for this, patients with gout often do not have the patience. As soon as the next attack “fades to naught”, they often completely stop thinking about their health again.

Meanwhile, without proper 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 want to note that, despite the frequent mention of the term "gout" in the literature and in conversations, in fact it turns out that the correct diagnosis of patients with gout is not always made and often with great delay. 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 they amputated the toe that was inflamed with gout. Literally after 3 weeks, his big toe on the other leg became inflamed, and they were going to amputate the patient too! Fortunately, the man guessed that this time he should have consulted with another doctor, and turned to me for help. On 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 in just one day! From the imaginary gangrene the next day there was no trace left.

Another patient was treated for arthrosis for seven years, while 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 the patient, in numerous blood tests taken from a vein, uric acid just went off scale. She was more than twice the norm! But the doctors over and over again managed to ignore it. And they continued to bend their line. In one of the attacks, the man even managed to operate on his knee and removed a completely healthy meniscus. But the operation, of course, 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 in front of me a pile of tests, which clearly read a constant increase in the level of uric acid, the patient was finally selected an adequate anti-gout treatment. And already 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

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

Although here, as is often the case, it cannot do without a "fly in the ointment in a barrel of honey." Yes, gout is very well treated, but many gout patients are unwilling to accept the conditions that are needed for recovery - because the "conditions" are the rejection of those foods (and alcohol) that caused the metabolic disorder. And when I tell patients that in order to get rid of the disease it is necessary to give up their favorite foods and alcohol, they often simply do not want to hear me.

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

The classic but outdated version of the gout diet is here.

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

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

To stop an acute gouty attack, non-steroidal anti-inflammatory drugs (Voltaren, ibuprofen, movalis, nimulide, etc.), or a special short-acting anti-gout drug - colchicine, are successfully used. Locally on a sore joint, you can put a vodka compress.

Preparations for the relief of an acute attack are used for a short time, a short three-seven-day course. And directly for the treatment of gout, in the absence of contraindications, for several months or years they use a drug that reduces the formation of uric acid in the body - purinol, aka allopurinol.

Compliance with the diet and the use of purinol (allopurinol) leads to the normalization of the condition of patients during the first month of therapy. Although the first week, against the background of therapy with purinol or allopurinol, an exacerbation of the disease may even occur. But then the attacks become weaker and happen less and less, and eventually stop altogether.

And about a year later, with the good health of my ward, I allow some relief in his regimen. I ask the patient what he would like to stop - diet or medication, because then we can 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 can hardly tolerate dietary restrictions, then you can abandon the diet, but continue taking medication. However, the drugs will have to be used for several years - which, in general, is not terrible, since purinol (allopurinol) rarely causes any side effects and is generally well tolerated by patients.

Article by Dr. Evdokimenko © for the book "Arthritis", published in 2004.
Edited in 2011
All rights reserved.

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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, Faculty of Postgraduate Medical Education, Volgograd State Medical University, Director of the Federal Budgetary State Institution "Research Institute of Clinical and Experimental Rheumatology" of the Russian Academy of Medical Sciences, 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 the description by Hippocrates of 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 been undulating, usually associated with the discovery some new perspective.

But the data on the study of crystals that cause gouty arthritis are especially interesting. It is shown that these are monosodium urate crystals, the detection of which is of absolute diagnostic value. In fact, by the end of the 20th century, gout began to be considered as a disease of the accumulation of urate crystals in the structure of the joint, subcutaneous tissue and bones, 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 in them, and then destructively. - sclerotic changes.

Refers to multifactorial diseases.

Epidemiology

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

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

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

Gout affects mainly men (in 95-98%), usually older than 30 years.

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 the tissues.

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

IV. The features of the disease in recent decades are its occurrence at a younger age, earlier formation of complications. Frequent involvement in the process of the kidneys and the cardiovascular system. In young people, a severe course of the disease is more often observed with multiple lesions of the joints, frequent and prolonged exacerbations, multiple tophi and more pronounced 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 a prerequisite for the crystallization of urates. However, the blood contains substances that increase solubility, so usually crystallization does not occur even at a serum uric acid concentration of 4800 µmol/l (80 mg%).

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

Synthesis and breakdown of purines occur in all tissues, but uric acid is formed only where there is xanthine oxidase, 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 excretion. 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 rest is mainly excreted in the 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 in these tubules, and then about 40% is reabsorbed again. As a result, only 8-12% of filtered uric acid enters the urine.

Serum uric acid concentration depends on sex and age, and in adults - on height, weight, blood pressure, kidney function and alcohol consumption. In most children, it is 180 - 240 µmol / l (3 - 4 mg%). With puberty in men, the concentration increases, and in women it remains low until menopause. The reason for this difference has not been definitively 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 postmenopausal women, the concentration of uric acid in serum increases in women and approaches the concentration characteristic of men.

II. The occurrence of gout is associated with both genetic conditioning and alimentary 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 it usually occurs between the ages of 40 and 60, and in women after menopause.

III. However, it must be emphasized that the detection of 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 attacks of acute arthritis. And 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 hence hyperuricemia is a clinical syndrome distinct from gout.

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

The causes 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. Factors predisposing to urate deposition and joint inflammation in individuals with hyperuricemia are unknown to date (with the exception of familial cases).

CLASSIFICATION OF THE CAUSES OF HYPERURICEMIA

metabolic hyperuricemia

Primary idiopathic hyperuricemia

Excess activity of phosphoribosyl pyrophosphate synthetase

Most of the signs of gout show up on x-rays.

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

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

Gouty arthritis occurs when:

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

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

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

With gout, the temperature mainly rises at night.

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

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

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X-ray as one of the diagnostic methods

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

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Other ways to confirm the diagnosis

X-ray with gouty polyarthritis stage 3

The picture clearly shows the "punch symptom" - rounded voids in the distal third of the 1st metatarsal bone on the left (shown with a red arrow). The articular surfaces of the metatarsophalangeal joints (PFJ) are compacted and sclerotic, narrowing of the joint spaces, especially pronounced in the I metatarsophalangeal joints on both sides.

Destruction of bone tissue in the area of the 1st metatarsophalangeal joints on both sides, marginal erosions in the same place (yellow arrow), deformation and subluxation of the 1st MTPJ on the right, as well as pronounced edema and compaction of soft tissues in the area of the ankle joints (green arrows) are determined.

Conclusion: X-ray signs of podargic polyarthritis stage 3, to confirm the diagnosis, determine the level of uric acid in the blood, the presence of urates (MUN crystals) in the joint fluid, perform a biopsy of tophi.

Gout is a chronic articular pathology that occurs with periods of exacerbation and remission, the main causes of which are hyperuricemia and the body's reaction to it. The frequency of this pathology averages 25 cases per 1000 of the population, men suffer more often by 5-6 times.

The management of a patient with gouty arthritis includes the following activities:

Lifestyle correction, strict diet with the exclusion of foods high in purines, weight loss.
Achieving compensation for chronic diseases that affect the frequency of exacerbations (IHD, hypertension, dyslipidemia, diabetes mellitus).
Appointment of NSAIDs, glucocorticosteroids (intra-articular injections), colchicine in the acute period;

Uric acid lowering drugs - allopurinol, febuxostat, probenecid, sulfinpyrazone, benzbromarone, benziodarone.

Punch symptom

Punch symptom. The symptom of the punch is that during palpation of the stomach filled with a contrast agent, single or multiple rounded forms of enlightenment with even, clear contours, of various sizes are determined. The punch symptom becomes reliable only with the stability of localization, shape, size of enlightenment and is also combined with a change in the direction of the mucosal folds and a hoop symptom. It is observed in benign epithelial and non-epithelial tumors of the stomach (polyps, adenoma, neurinoma, leiomyoma, etc.), aberrant pancreas.

Recognized by fluoroscopy and radiography using a contrast agent in various projections in a vertical and horizontal position.

Gout and x-ray

Gout is a systemic disease associated with impaired 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. In the diagnosis of the disease, laboratory tests and X-ray procedures of the affected areas play a very important role.

Signs of the disease

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

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X-ray examination of gout

Early x-rays of gout can show transient osteoporosis.

X-ray signs of gout

Gouty arthritis and the clinic of radiographic manifestations of the punch symptom

Gout is a chronic progressive disease caused by a violation of purine metabolism, characterized by an increased (normal for adult women μmol / l; for adult men μmol / l) content of uric acid in the blood (hyperuricemia), followed by the deposition of urates in the articular and / or periarticular tissues. Detection of hyperuricemia is not enough to establish a diagnosis, since only 10% of individuals who suffer from this disease have gout. Nearly 95% of people diagnosed with gout are men in their 40s and 50s, although the disease is said to be "getting younger".

The rest are menopausal women. Gout has become more and more often accompanied by such individual diseases as obesity, hypertriglyceridemia (increased levels of neutral fats in the blood) and insulin resistance (violation of the amount of insulin in the blood). It can be concluded that gout is not a cause, but a consequence of a metabolic disorder 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 excretion of urate by the kidneys. And the causes of secondary gout are kidney failure, blood diseases accompanied by increased catabolism (processes aimed at the destruction of substances in the body), and the use of a number of drugs (diuretics, salicylates, etc.).

Lesions

The main function of the kidneys is filtration and absorption actions, 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 mg, while 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 is due to an increase in the activity of the kidneys and the deposition of urates in the soft tissues of the 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 (permeability of 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. Increasing the diffusion of water from the joint increases the concentration of crystallized urates.

It has been proven that the 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 the peripheral joints (ankles, phalanges of the fingers) contributes to the accelerated crystallization of urates and the formation of microtophi. With a high concentration of microcrystals in tissues (cartilage of the joints, epiphyses of bones, etc.), the formation of micro- and macrotophi begins. Sizes range from millet grain to chicken eggs. The accumulation of urate leads to the destruction of cartilage. Further, uric acid salts begin to be deposited in the subchondral bone (the foundation for cartilage, which ensures its trophism) with its destruction (the x-ray name is a symptom of a punch).

Uric acid also accumulates in the kidneys (gouty kidney or gouty nephropathy). In all patients with gout, the kidneys are affected, so that renal failure is not considered as a complication, but as one of the visceral (internal) manifestations of the disease. Gouty kidney (nephropathy) may present with 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 diseased joints and limbs;
sometimes a symptom of a slight fever;
a symptom of returning pain, which occurs with a prolonged course of gouty arthritis;
a symptom of the formation of hard white lumps under the skin (tophi);
symptom of kidney 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 an increased amount of uric acid in the body and / or the passage of urate stones with or without colic attacks. This period can be quite long. The onset of attacks of the first gouty crisis indicates that the disease began to develop actively.

Gouty arthritis

In the intermittent period, acute attacks of gouty arthritis alternate with asymptomatic intervals between them. Long-term hyperuricemia and exposure to provoking factors (alcohol consumption, prolonged fasting, eating foods rich in purines, trauma, drug use, etc.) in 50-60% lead to nocturnal acute attacks of gouty arthritis. The beginning of the attack is a sharp pain in the first metatarsophalangeal joint of the leg (thumb). The site of the lesion quickly swells, the skin becomes hot from a sharp rush of blood, the edema stretches the skin, which acts on pain receptors. Shiny, tense, red skin soon turns bluish-purple, which is accompanied by peeling, fever, leukocytosis. There is a violation of the function of the joint, the attack is accompanied by fever. Other spherical joints, joints of the foot are also affected, somewhat less often - the ankle and knee joints.

Less common are the affected elbow, wrist and hand joints; extremely rare - shoulder, sternoclavicular, hip, temporomandibular, sacroiliac and spinal joints. Acute gouty bursitis is known (inflammation of the mucous bags, mainly of the joints), usually the prepatellar (located under the skin in front of the kneecap) or elbow bag is affected. Under the influence of synovitis (inflammation of the synovial membranes of the joint), the joints are deformed, the skin in the focus of inflammation becomes tense, shiny, stretched, and when pressed, the fossa disappears. The boundaries of hyperemia (impaired circulation) are indistinct, 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 begins to go away after a few days with proper treatment. At first, the redness of the skin disappears, its temperature normalizes, and later the pain and swelling of the tissues disappear. The skin is wrinkled, its abundant pityriasis peeling, local itching are noted. Sometimes gout-specific tophi appear. The early stages of intermittent gout are characterized by rare attacks (1-2 times a year). But the longer the disease progresses, the more often the symptoms of gouty arthritis return, becoming longer and less acute.

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

The location of tophi is different: it can be auricles, 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 a long time, the formation of tophi occurs everywhere: in cartilage, in internal organs and bone tissues. Subcutaneous or intradermal formations, consisting of monocrystals of sodium urates in the area of the fingers and toes, knee joints, on the elbows and auricles, are a sign that gouty arthritis has passed into the chronic stage. Sometimes it is possible to note ulcers on the surface of tophi, from which spontaneous discharge of a white pasty mass is possible. The formation of tophi on the bone space is called a symptom of a punch or a break, which can be diagnosed using an x-ray.

Nephrolithiasis (kidney stone disease) with 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 more likely it is that tofus formations will appear in the early stages of the disease. Often this is observed against the background of chronic renal failure in elderly women taking diuretics; in some forms of juvenile gout, myeloproliferative diseases (associated with disruption of the brain stem cells) and post-transplant (cyclosporine) gout. Usually, 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, it resembles reactive arthritis in its course. Therefore, an important part of the diagnosis of gout is the analysis of the content of uric acid in the blood, in daily urine and clearance (clearance rate) of uric acid.

During the attack, laboratory acute-phase reactions are detected, a small proteinuria, leukocyturia, and microhematuria are possible in the analysis of urine. The deterioration of the concentration 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 (proliferation of connective tissue in the kidneys). In the synovial fluid, there is a decrease in viscosity, high cytosis, and an acicular structure of sodium urate crystals is visible under a microscope. A morphological study of subcutaneous tofus reveals a whitish mass of sodium urate crystals against the background of dystrophic (degrading) and necrotic tissue changes, around which an inflammatory reaction zone is visible. 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, single tophi are observed.

The moderate course of gout is characterized by a more frequent (3-5 times a year) exacerbation of the disease, which progresses immediately in 2-4 joints, moderate skin-articular destruction, multiple tophi, and kidney stone disease is diagnosed. In severe cases of the disease, attacks are observed with a frequency of more than 5 times a year, multiple joint lesions, pronounced osteoarticular 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 uninformative. The radiological phenomenon typical of late gout is well known - the “punch” symptom. This is a defect in the bone on which the joint rests, it can be 5 mm or more in diameter, located in the middle part of the base of the diaphysis (the middle part of the long bones) or in the head of the phalanx, more often than the first metatarsophalangeal joint. But with the accumulation of information, it became clear that more often there is a situation where X-ray changes are not detected in patients with gouty arthritis.

Manifestation of a symptom of a puncher

It is necessary to note a number of points that make the radiographic symptoms of a punch significant. The pathomorphological (i.e., internal structure that differs from the norm) substrate of this radiological phenomenon is intraosseous tophus, which is similar to a cystic (having a separate wall and cavity) formation, due to the fact that uric acid salt crystals do not delay X-rays. The identified "punch" determines the stage of the disease as chronic tofus. It is worth noting that the detection of tofus of any location is a direct indication for the start of anti-gout therapy. In general, the “punch” symptom in patients with primary gout is a late sign, associated with a long course of the disease and chronic arthritis.

On the other hand, an early radiological sign in gout is a reversible diffuse thickening of the soft tissues during an acute attack due to the fact that during inflammatory processes there is a rush of blood and the deposition of solid crystalline forms in the areas of edema. In this case, local rarefaction of the bone substance (transient arthritis) can be detected, and with the course of the disease, destructive processes in this area can also occur. Radiological manifestations: at first, 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 in gouty arthritis, in contrast to rheumatoid arthritis, tuberculosis, sarcoidosis, syphilis, leprosy. Erosive 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 a close adjacent soft tissue tophi and is defined as rounded or oval marginal bone defects with pronounced sclerotic changes at the base of the erosion. Without treatment, such “holes” increase in size, covering deeper layers of bone tissue. X-rays resemble "rat bites". Asymmetric erosions with cartilage destruction are typical, bone ankylosis (fusion of articular surfaces) is rarely formed. If calcium is present in the tophi structures, then X-ray positive inclusions may appear, which sometimes stimulate chondromas (a tumor consisting of cartilage tissue). The width of the joint space of the affected joints usually remains normal until the advanced stages of gouty arthritis. These changes can mimic osteoarthritis (degradation of the joint), 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 seals - gouty arthritis is just developing;
large tophi formations near the joint and small erosions of the articular surfaces, increasing density of the periarticular soft tissues, sometimes with a certain amount of calcium - gouty arthritis is manifested by acute attacks;
severe erosion on at least 1/3 of the joint surface, complete aseptic resorption of all articular tissues of the epiphysis, significant compaction of soft tissues with calcium deposits - chronic gouty arthritis.

Prediction of the consequences of gout

With timely recognition and treatment of gout, unpleasant consequences or overflow into the chronic form of the disease can be avoided. Adverse factors that affect 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 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 pathology. In conclusion, it should be noted that gout is a systemic disease that is difficult to diagnose, the symptoms of which are different and often overlap with various other diseases.

Only in 10% of cases, the doctor can 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 state of the blood. Blood is an indicator of a person's condition. Timely diagnosed gout will allow you to choose the most effective method of 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 surgery and a long rehabilitation period will help without a guarantee that the disease will not return again. Be healthy!

Diagnosis of gouty arthritis

X-ray manifestations in gout were first described by G. Huber in 1896. Later, many studies were carried out that showed that there are no characteristic changes at an early stage of the disease. Then, radiographs show signs of bone and cartilage destruction due to the 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. So, E. Kavenoki-Mints distinguishes three stages of chronic gouty arthritis (1987):

I - large cysts in the subchondral bone and in deeper layers. Sometimes soft tissue hardening;
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 erosion, but less than 1/3 of the articular surface, osteolysis of the epiphysis, significant compaction of soft tissues with lime deposition.

More recent is the classification proposed by M. Cohen, V. Emmerson (1994), according to which the following are the main radiological signs in gout:

in soft tissues - seals;
eccentric darkening due to tophi;
bones (joints) - the articular surface is clearly presented;
juxta-articular osteoporosis is absent;
erosion (punch, marginal sclerosis).

Thus, the presented classifications are significantly different and require the unification of a number of radiological signs in gout.

Instrumental and laboratory research.

Gout: what is it, treatment, symptoms, signs, causes

What is gout

Gout is a metabolic disease with a pronounced tissue localization (in the synovial membranes and cartilage of the joints), studied mainly from the point of view of a violation of the purine fraction of protein metabolism.

The disease was already well known in ancient medicine. A clear description of gout, in particular, acute joint attacks, was given by Sydenham at the end of the 17th century. At present, gout occurs almost exclusively in the atypical form, without the classic acute gouty articular attacks.

Gout is a disease characterized by a sharp increase in the level of uric acid in the blood (up to 0.25-0.50 mmol / l), which is due to a violation of the metabolism of nitrogenous bases. As a result, acute and then chronic arthritis and kidney damage develop first. The development of arthritis occurs as follows: due to impaired metabolism, uric acid salts are deposited in the form of crystals in the joints and periarticular tissue. The defeat of the urinary system occurs due to the formation of stones, consisting of uric acid and its salts, in the kidneys and urinary tract, as a result of which nephritis develops in the future.

The term "gout" in Greek means "foot trap", that is, it indicates damage to the joints and impaired mobility.

The accumulation of uric acid in the body occurs as a result of the following processes: a decrease in the excretion of uric acid by the kidneys, although its content in the blood does not exceed the norm and / or an increase in the formation of uric acid in the body.

Predispose to the development of gout obesity, high blood levels of certain fats, insulin, uncontrolled use of certain drugs, such as vitamin B 12. Gout provoking factors are the use of alcoholic beverages and fatty meat foods the day before, hypothermia, long walking, and the presence of concomitant infectious diseases.

Gout is characterized by impaired purine metabolism, hyperuricemia, as well as in periarticular and intraarticular structures, and recurrent episodes of arthritis.

In women, gout occurs in the postmenopausal period.

Frequency. Up to 5% of men over the age of 40 suffer. Women get sick during menopause. The ratio of men and women is 20:1. The prevalence of the disease reaches 1-3% among the adult population.

gout classification

Distinguish between primary and secondary gout.

Primary gout is a hereditary disease caused by the presence of several pathological genes. But it should be noted that not only hereditary factors are of great importance in its development, but also nutritional characteristics: the consumption of foods containing a lot of proteins, fats, and alcohol.

Secondary gout is the result of an increase in the level of uric acid in the blood in some pathologies: endocrine, cardiovascular, metabolic diseases, tumors, kidney pathologies. In addition, minor injuries to the joints, as well as taking certain medications that increase the level of uric acid in the blood, can be its causes. Injury to the joint causes its swelling, due to which there is a rapid local increase in the content of uric acid.

In gout, the following stages of the disease are distinguished.

The first is acute gouty arthritis, which lasts for several years.
The second is interictal gout.
The third is chronic gouty arthritis. The fourth is chronic nodular gout.

Causes of gout

The cause of gout is hyperuricemia over 360 µmol/l, especially long-term. Contribute to this obesity, hypertension, taking thiazide diuretics, alcohol, foods rich in purines (liver, kidneys), kidney disease. There are cases of congenital increase in the production of urates.

Gout affects, according to classical descriptions, mainly men over the age of 35-40 years. On the contrary, predominantly menopausal women get sick with atypical gout. Old doctors pointed to the probable connection of the disease with overeating, especially meat, and the abuse of wine. In some cases, gout has been associated with chronic lead poisoning. The connection between the course of gout and the influence of nervous shocks was also tarnished. It becomes clear that under the influence of the named hazards acting in a number of generations, the disease can occur in several family members, and with a deeper change in the chemistry of tissues and its nervous regulation, it can take on the character of hereditary suffering.

An increase in uric acid in the blood is most likely due to both hereditary defects in its synthesis linked to the X chromosome (deficiency of the enzyme hypoxanthine-guanine phosphoribosyl transferase) (only men are ill), and a decrease in the excretion of uric acid by the kidneys (both men and women are ill). Hyperuricemia is caused by foods containing a large amount of purines: fatty meat, meat broths, liver, kidneys, anchovies, sardines, dry wine.

Secondary gout occurs with increased cell breakdown (hemolysis, the use of cytostatics), psoriasis, sarcaidosis, lead intoxication, renal failure, and alcoholics.

Pathologically, the most characteristic are inflammatory foci in the synovial membranes, tendon sheaths, cartilage with the deposition of sodium urate crystals and a connective tissue reaction. Being located in the periarticular tissue, on the earlobe, etc., these foci give characteristic nodules (tophi), which facilitate the intravital recognition of the disease, especially if the presence of uric acid salts can be proved by self-opening of the nodules to the outside or by biopsy. The deposition of urate salts in the kidneys in advanced cases of gout, with the development of nephroangiosclerosis, as well as atherosclerotic changes in the coronary vessels or often stated general obesity, etc., are not so much related to gouty metabolic disorders, but to hypertension, atherosclerosis with their consequences and to other metabolic diseases, with which gout is often combined along the lines of a general metabolic disorder.

Pathogenesis. Violation of purine metabolism, of course, represents only the most obvious side of complex pathological metabolic changes in patients with gout, however, it is the deposition of uric acid salts in the joints and the often observed blood overload by them that continue to be at the center of the study of the pathogenesis of this disease. In gouty arthritis, the formation of uric acid crystals in the joint cavity, chemotaxis, phagocytosis of crystals and exocytosis of lysosomal enzymes by neutrophils are important.

According to modern views, the most important for the development of gout symptoms is a violation of tissue metabolism in areas poorly supplied with blood, with a perversion of the general nervous regulation of metabolism. A well-known, although not completely elucidated role, obviously, is played by liver failure, as, probably, in other metabolic diseases, although it is not possible to connect this violation, for example, with the absence of any specific enzyme in the body. Thus, gout can be put on a par with obesity, in which, apparently, tissue disorders also play a leading role, along with a violation of regulatory processes. Classical acute articular gouty attacks are largely in the nature of hyperergic inflammation with clear signs of damage to the entire nervous system in the form of a kind of crisis.

The retention of uric acid in the body, in particular, its increased content in the blood, apparently reflects only one of the phases of the disease, especially at the height of the paroxysm and in the late period. The content of uric acid in the blood can be significantly and sometimes long-term increased in chronic uremia, leukemia, liver disease, but there are no gouty paroxysms. The theory of primary functional insufficiency of the kidneys in relation to the release of uric acid has also not been confirmed; the kidneys are affected in gout only secondarily due to the development of hypertension and atherosclerosis.

Synthesis of uric acid. Normally, 90% of the degradation products of nucleotides (adenine, guanine, and hypoxanthine) are reused for the synthesis of AMP, IMP (inosine monophosphate) and GMP with the participation of adenine phosphoribosyl transferase (APRT) and hypoxanthinguanine phosphoribosyl transferase (HGPRT), respectively. The reason for the development of gout in hyperuricemia is the low solubility of urates (especially uric acid), which decreases even more in the cold and at low pH (pKa of urates / uric acid = 5.4).

Hyperuricemia occurs in approximately 10% of the population in industrialized Western countries: 1 in 20 develop gout; in men more often than in women. 90% of patients with this disease have a genetic predisposition to primary gout. In rare cases, hyperuricemia is caused by a partial deficiency of HGPRT, in which the amount of recycled metabolites of nucleotides decreases.

Since the temperature of the fingers is lower than that of the torso, accumulations of urate crystals (microtophi) are more likely to form in the distal joints of the legs.

A gout attack occurs when urate crystals (perhaps as a result of injury) are suddenly released from microtophi and are recognized by the immune system as foreign bodies. Aseptic inflammation (arthritis) develops, neutrophils are attracted to the area of inflammation, which phagocytize urate crystals. The neutrophils then disintegrate, and the phagocytosed uric acid crystals are released again, maintaining inflammation. Severe pain develops, swelling of the joints, which become dark red. In % of cases, the first attacks occur in one of the proximal joints of the toes.

Acute urate nephropathy. With a sudden significant increase in plasma uric acid concentration and primary urine (usually with secondary gout, see below), and/or concentrated urine (with a decrease in fluid intake), and/or low urine pH (for example, with a diet rich in proteins) in the collecting ducts, a large amount of uric acid / urates precipitates, clogging their lumen. This can cause acute kidney failure.

Repeated attacks in chronic gout lead to damage to the joints of the hands, knees, etc. Against the background of constant pain, a pronounced deformity of the joints develops, accompanied by the destruction of cartilage and atrophy of bone tissue. Foci of deposition of urate crystals (tophi) are formed around the joints or along the edge of the auricles, as well as in the kidneys with the development of chronic gouty nephropathy.

The so-called secondary hyperuricemia, or gout, develops, for example, in leukemia, the treatment of tumors (high nucleotide metabolism) or kidney failure of another etiology.

There is a deposition of monosodium urate crystals in the cartilage and less intensively in the tendons and ligaments. Subsequently, the crystals are deposited in the kidneys, joints, for example, in case of cartilage injury. Macrophages phagocytize crystals, triggering an inflammatory reaction, which is also initiated by interleukins, TNF-α, etc. During inflammation in an acidic environment, crystals precipitate and form conglomerates in the form of tophi and the development of urolithiasis.

Symptoms and signs of gout

The clinical picture of the disease is mainly due to joint damage in the form of acute gouty arthritis, which then turns into chronic polyarthritis. Kidney damage is most often manifested by urolithiasis, less often by nephritis or glomerulonephritis, which develops when uric acid crystals are deposited in their parenchyma. In addition, there is damage to peripheral tissues due to the deposition of uric acid salts in them, which are detected in the form of specific gouty nodules, which are uric acid crystals surrounded by connective tissue.

The onset of acute gouty arthritis is sudden, due to the accumulation of uric acid salts in the joints and periarticular tissues, which, being a foreign body, cause a response of the immune system. Formed elements of blood accumulate around them, acute inflammation develops. The attack of acute gouty arthritis usually begins at night or in the early morning hours in the form of a lesion of the big toe (98%); less often other joints are affected: knee (less than 35%), ankle (about 50%), elbow, wrist. There is an increase in body temperature up to 39 ° C. When you try to lean on the affected limb, the pain increases sharply. The affected joint increases sharply in volume, the skin over it becomes cyanotic or purple in color, glossy, and there is a sharp pain on palpation. After the end of the attack, which on average lasts from 3 days to 1 week, the function of the joint returns to normal, it acquires a normal shape. As the disease progresses, the duration of attacks increases, and the periods between them shorten. With a long course of the disease, persistent deformity of the joint appears, restriction of movements in it. With a repeated attack of the disease, an increasing number of joints may be involved in the process, and partial destruction of the joint and bone tissue occurs. With the development of chronic polyarthritis, subluxations of the joints of the fingers, contractures of the joints (immobility) appear, a crunch is found in the joints during movement, audible at a distance, the shape of the joint changes even more due to the growth of the articular surfaces of the bones. With a far advanced disease, patients lose their ability to work, can move with great difficulty.

When the kidneys are affected by urolithiasis, attacks of renal colic, symptoms of urolithiasis appear in the clinical picture of the disease. Perhaps independent discharge of stones. Kidney damage also entails an increase in blood pressure, protein, blood, and a large amount of uric acid salts are detected in the urine. It should be noted that when the kidneys are damaged, the reabsorption of substances in the renal tubules is impaired to a greater extent compared to filtration in them. In rare cases, renal failure may develop.

In the peripheral parts of the body, gouty nodes most often appear on the auricles, elbow and knee joints, less often on the toes and hands. In some cases, gouty nodes can open on their own. As a result, fistulas are formed, from which uric acid salts are released in the form of a yellowish mass.

A specific radiological sign of the disease is the “punch” symptom, due to the development of bone erosion around the affected joint.

An attack of acute gouty arthritis must be distinguished from acute rheumatic fever. For rheumatic polyarthritis, the onset of the disease at an early age and damage to the heart are characteristic. Rheumatoid nodules first appear on the joints of the thumbs, and then the joints of the toes are affected; with gout, the opposite is true. In addition, rheumatoid nodules never open.

Gouty nodes must be distinguished from those that form in osteoarthritis. The former have a dense texture and are localized on the joints of the 1st and 5th fingers. In addition, osteoarthritis most often affects the joints of the spine, hip and knee joints, which rarely suffer from gout.

Gout is most often detected in men 30-50 years of age and in women in the postmenopausal period.

With deforming osteoarthritis of the joint of the big toe, there may be similarities with a gouty node, but the inflammatory process will develop gradually, the pain will be less pronounced, the general condition is not disturbed.

An acute gouty attack most often affects the metatarsophalangeal joint of the big toe, less often other joints. An attack is preceded by a kind of prodrome, by which the patient recognizes his approach, - dyspepsia, mental depression, etc. Alcohol abuse, overexertion can lead to an attack. The attack is characterized by a sudden onset, severe pain, swelling and redness of the affected joint, which gives the impression of a severe inflammatory process; in addition, the temperature may be greatly increased, the tongue is coated, the abdomen is swollen, the action of the intestines is delayed, the liver is enlarged and painful. The attack lasts 3-4 days and is more often localized in one joint.

Diagnosis of gout

An ultrasound of the kidneys is performed to detect stones.

differential diagnosis. With gout, non-simultaneous damage to the joints is noted, in contrast to rheumatoid arthritis, morning stiffness is uncharacteristic.

Infectious arthritis can also give an acute onset, hyperemia of the joint. They start after an infection. When sowing the synovial fluid, microorganisms are detected.

Pseudogout is caused by the deposition of calcium pyrophosphate. With it, the course of arthritis is essentially similar to gout, but usually milder, often with damage to the knee joint. X-ray reveals signs of chondrocalcinosis. Calcium pyrophosphate crystals are characterized by the absence or weak birefringence under polarizing microscopy.

chronic gout

After the first attacks, local changes pass almost without a trace; however, in the future, gradually increasing persistent changes are observed - thickening and limitation of mobility in the diseased joint. The soft tissues around the joint remain constantly edematous, gouty nodes increase, the skin over them, thinning, can break through, and white masses of urate salt crystals begin to stand out through the fistula. Gouty arthritis can lead to deformation as a result of contractures, subluxations of the fingers.

atypical gout

Diagnosis of typical cases is based on acute gouty attacks, the presence of gouty nodules, and lesions of other organs characteristic of gout. Radiographically, in advanced cases, gouty arthritis is characterized by round bone defects in the epiphyses, near the articular surface, as a result of the replacement of bone tissue by urates. Elevated levels of uric acid in the blood, hyperuricemia (over 4 mg%), contrary to the idea, is by no means a permanent symptom of gout. Uric acid crystals in the urine sediment speak rather against gout, in which the excretion of uric acid is disturbed for periods; at the same time, the release of a crystalline precipitate is closely related to the deterioration of the conditions for the dissolution of uric acid (a decrease in the protective colloids of urine), which is characteristic not of gout, but of uric acid diathesis. However, the widespread opinion that gout, which is incorrect in essence, can be recognized by urine sediment is not without some basis, if we consider uric acid diathesis and gout from the point of view of ‘close metabolic disorders. The gouty nature of the disease may be indicated by the provocation of an articular attack rich in purines (liver, kidneys, brains). Atypical gout occurs in overweight women, often in the presence of small liver signs (liver spots - chloasma - on the face, deposition of cholesterol nodes in the skin of the eyelids, etc.), varicose veins in the legs, hemorrhoids, migraines, angina pectoris, hypertension, albuminuria with excretion of sand with urine, etc. The joints of the hands and especially the feet are deformed; there are periarticular deposits, a rough crunch in the knee and ankle joints, calluses caused by wearing even ordinary shoes. Pain in the lower back, in the muscles, albuminuria are unstable and improve with active movements.

The prognosis for life with gout is largely determined by progressive cardiovascular lesions: coronary sclerosis, hypertension, nephroangiosclerosis. By themselves, gouty disorders, as a rule, do not shorten life. However, changes in the joints can significantly interfere with movement and reduce the ability of patients to work.

Treatment of gout

Treatment of the disease is complex. Its main tasks are: the removal of an acute attack of gouty arthritis, the mandatory normalization of protein metabolism. With the progression of the pathology, specific treatment of chronic gouty polyarthritis is carried out.

For the relief of acute gouty arthritis, the following drugs are used: meloxicam, nimesulide. Colchicine at a dose of 0.5 mg every hour, but not more than 6 mg of the drug in 12 hours, has a very good effect. When prescribing it, it is necessary to monitor kidney function. Hormonal treatment (triamcinalone at a dose of 30-50 mg per day) is prescribed only in exceptional cases for severe intra-articular pain.

In order to normalize protein metabolism, dietary nutrition is practiced with the exception of foods containing a large amount of protein (meat, fish, legumes), as well as liver, strong coffee, fats, and alcoholic beverages. Nutrition should also be aimed at reducing excess weight. Patients are advised to drink plenty of fluids - at least 2 liters per day.

Almost half of patients with gout develop arterial hypertension. In order to normalize blood pressure, diuretics and antihypertensive drugs are prescribed.

To stabilize protein metabolism, groups of drugs are used that promote the excretion of uric acid and purines from the body. They are prescribed only after the removal of an acute gouty attack.

A good remedy for removing uric acid from the body is sulfinpyrazone. Its initial daily dose is 100 mg divided into 2 doses. Gradually the dose can be increased to 400 mg. During treatment with this drug, plenty of fluid intake is recommended to reduce the risk of developing urolithiasis. The drug has contraindications for use: these include urolithiasis, increased formation of uric acid salts, gouty nephropathy.

One of the best means of normalizing protein metabolism in the body is allopurinol. Its initial daily dose is 100 mg, but then it can be increased to 800 mg. During treatment with this drug, it is recommended to take non-steroidal anti-inflammatory drugs. With long-term treatment with allopurinol, normalization of kidney function and the reverse development of gouty nodes are possible.

Indications for specific treatment are the presence of gouty nodes and the "punch" symptom.

Specific treatment consists of prescribing colchicine 0.5-1.5 mg per day intravenously, benzbromarone 100-200 mg per day (increases excretion and inhibits the formation of uric acid), probenecid 0.25 g 2 times a day, as well as the above drugs.

With the formed chronic gouty polyarthritis, the main goal of treatment is to restore the affected joints. This is achieved with the help of physiotherapy exercises, spa treatment, mud therapy, and the use of therapeutic baths. With an exacerbation of the disease, the above drugs are used.

In an acute attack of gout, rest and cooling compresses are indicated. NSAIDs are used to control inflammation. Salicylates are contraindicated due to their ability to cause hyperuricemia. The use of uricostatic or uricosuric agents may lead to an increase in the duration of a gout attack and is therefore not recommended.

In the interictal period, a diet is indicated with a restriction on the use of alcoholic beverages, liver, smoked meats, canned food, meat and fish dishes, sorrel, lettuce, spinach, legumes, chocolate, coffee and strong tea. In obese patients, it is necessary to reduce the total caloric content of food. The amount of fat should not exceed 1 g/kg. Meat or fish (0.5-1 g / kg) is consumed no more than once a day. In the absence of contraindications from the side of the night, it is advisable to drink plenty of alkaline water. With secondary gout, increased excretion of uric acid or gouty kidney damage, uricostatic drugs are prescribed for a long time. In other cases, it is possible to use uricosuric agents or their combination with uricostatic drugs.

Colchicine is effective when administered in the first hours of illness.

In acute attacks of gout, triamcinolone 60 mg intravenously or oral prednisolone 30 mg / day are also prescribed.

Treatment of chronic tofus gout involves the rejection of alcohol, especially beer, the observance of a low-calorie diet. Alkaline mineral waters are recommended.

Anti-inflammatory drugs are used: NSAIDs, corticosteroids, colchicine, but they do not affect the progression of gout.

Uricosuric drugs (sulfinpyrazone, benzbromarone) are prescribed according to more stringent indications due to contraindications in the form of renal failure, nephrolithiasis, and their hepatotoxicity.

Diuretics are contraindicated in patients with gout. The antihypertensive drug losartan and fenofibrate used to treat dyslipidemia have a slight uricosuric effect.

Prevention of gout

Colchicine is used to prevent relapse. Such therapy is carried out for a short time due to the possibility of developing neuropathy or myopathy.

Preventive measures are reduced to systematic training and sufficient constant physical activity, physical culture and sports, to the appointment of rational food with the exception of overfeeding, to strengthening the nervous system, etc.

For patients with gout, a diet with a sharp restriction of meat food, meat soups, and especially the liver, brains, kidneys, is very important; it is allowed to consume a small amount of only boiled meat and fish (purines mostly pass into a decoction). From vegetables containing purines, peas, beans, lentils, radishes, sorrel, spinach are prohibited. Thus, patients receive simple milk and vegetable food, a lot of fruits, liquids, including alkaline mineral waters.

Of the drugs, atophane (a-denial, tophus-gouty node) is widely used, which selectively increases the excretion of uric acid by the kidneys. Atofan is prescribed in cycles of 3-4 days with breaks for a week; the medicine taken is washed down with alkaline water to avoid the precipitation of uric acid crystals in the urinary tract. By enhancing the activity of the liver, atophane can have a sharply toxic effect and cause even fatal liver necrosis in case of an overdose, which should be remembered, especially when prescribing long courses of treatment with this drug. During acute paroxysms it is better to give T-ga Colchici 15-20 drops 3-4 times a day or (carefully!) pure colchicine. With gout, mechanotherapy and physiotherapy (diathermy, iontophoresis, solux, massage) and balneotherapy are widely used - mineral, hydrogen sulfide, radon baths, mud, alkaline-salt waters, etc. - in the resorts of Essentuki, Pyatigorsk, Sochi - Matsesta, Tskhaltubo, etc. .

Prognosis for gout

Urolithiasis often develops. The prognosis is worse with the development of the disease up to 30 years, the presence of urolithiasis due to the threat of developing chronic renal failure.

Interesting!
Pathologies of the central nervous system (central nervous system), thyroid gland and brain can provoke gouty arthritis.

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

Diagnosis of gout

Interrogation of the patient

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

Surgical operations;
Kidney dysfunction;
Long-term use of antibiotics or steroids.

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

Clinical researches

Biochemical blood test for gout for uric acid, sialic acids, fibrin and the presence of protein (with C-reactivity). Such self-diagnosis is used to determine the quantitative indicators of urates and their presence in the bloodstream. For men, the norm of uric acid is 460 μM / l, for women the normal values are lower - 330 μM / l. Guided by one biochemical analysis, it is impossible to diagnose gout of the joints. But an elevated level of urate indicates dysfunction of the urinary tract and disruption of the kidneys. The pathology of the kidneys is also indicated by a decrease in the level of creatinine (normally it is 115 mmol / l). Additionally, a biochemistry analysis shows the amount of nitrogen, ammonia, glucose, lipids and bilirubin. A sharp increase in their indicators indicates a violation of the functioning of various body systems;

Interesting!
With the development of gout, the results of the analysis for biochemistry look like this: the amount of protein during an attack significantly exceeds the norm, in some, an increase in glucose and creatinine is noticeable. Calcium, lipids, lipoproteins will also be overestimated.

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

On a note!
A high concentration of urates in the blood indicates the development of gout of the joints.

Urinalysis for gout allows you to clarify the cause of the pathology. The results of the analysis show the amount of uric acid and the overall level of acidity. Urine is given during the day. This helps to explore the change in acidity results throughout the day.

Attention!
An increase in indicators indicates the development of urolithiasis.

Puncture of synovial fluid. This method allows you to diagnose gout joints. In a healthy person, synovial fluid has no color, but resembles water in consistency. A change in color and a decrease in fluidity indicate an increase in acidity, a metabolic disorder. The analysis also shows the level of neutrophilic lymphocytes;
X-ray is used to diagnose gout of the joints of the lower extremities, as well as fingers. The picture shows the development of the pathological process in the joint, the deposition of salts. Radiographic signs of gout include white spots, with a diameter of 0.5 millimeters to 3 centimeters. They are due to the presence of tophi, resulting from the deposition of uric acid salts in the periarticular tissues. The formation of tophi takes about five years. Exacerbation of gout can accelerate their formation. Sometimes an x-ray image captures the complete or partial destruction of the endocrine gland, and its cells are replaced by uric acid crystals. X-ray examination will be effective for all joints. It helps to determine the type of gout, fix the transition of the disease to the periarticular bag or tendons and the occurrence of inflammation in them. In this case, an additional biopsy test is prescribed;

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

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

On a note!
What tests need to be done for gout, the attending physician will tell you. He will draw up a scheme for conducting studies to clarify the diagnosis, especially with secondary gout.

Rules for preparing for analyzes

Eliminate the use of alcohol for at least a day before taking tests;
Reduce the intake of foods containing high doses of vitamin C, otherwise deviations from the norm may be overestimated;
Caffeine can also interfere with test results. Therefore, it is recommended to give up coffee and tea 8-10 hours before their delivery;
Aspirin increases the level of acidity, so you should refuse it;
Diuretics lower test levels;
All tests for gout should be taken on an empty stomach. The last meal should be no earlier than 8-10 hours before delivery;
Following a diet for 2-3 days before testing minimizes the distortion of test results. The use of vegetable and lactic acid products is recommended;
You should also refrain from excessive exercise before conducting research.

Attention!
Compliance with the rules for preparing for analyzes is a guarantee of the reliability of the results, the correct diagnosis and the appointment of adequate treatment.

False results

Failure to comply with the rules for preparing for the delivery of tests can lead to a change in their results:

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

The patient should be aware that chronic gout of the joints cannot be completely cured. But with the help of therapeutic methods, you can reduce the number of acute attacks, reduce pain.

Attention!
Self-medication is unacceptable. This can cause the progression of the disease and the development of complications. Uncontrolled intake of drugs can distort the results of tests, artificially lowering their performance.

Gout is a disease that is characterized by a violation of 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 the consumption of large amounts of meat and wine.

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

Since gout is a disease of the whole organism, and not just of 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 belongs to the heading M 10.

Causes of the disease

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

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

Risk factors:

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

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

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

The essence of the disease

Several pathological processes play a role in the development of gouty arthritis. In people with a genetic predisposition, one of the links in protein metabolism is disrupted, as a result of which much more purine substances are formed than necessary, and then uric acid. In the blood, its concentration increases - hyperuricemia.

This situation leads to an increased excretion of urates by the kidneys and the deposition of uric acid crystals in peripheral tissues (the inner lining of the joints, skin, renal tubules). This causes the main symptoms of the disease: urate stones (urolithiasis) form in the kidneys, 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 already be made from the symptoms of arthritis alone.

Clinical symptoms:

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

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

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

The classic acute gouty arthritis is described above. But there are several more atypical clinical forms of arthritis in gout:

Subacute form. It is characterized by blurred clinical symptoms. More commonly seen in women.
Rheumatoid form. Interphalangeal, metacarpophalangeal, radiocarpal 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, pronounced signs of inflammation of the joint, which resembles a purulent lesion.

How to establish a diagnosis?

Symptoms of gouty arthritis make it possible to suspect the disease, but additional examination methods are needed for an accurate diagnosis.

Diagnosis of gout includes:

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

Principles of treatment

Treatment of gout can be conditionally divided into 2 stages:

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

In an acute attack of gouty arthritis, it is necessary to provide the affected joint with functional rest. Starving is contraindicated, you must adhere to diet No. 6, consume 2.5 liters of alkaline liquid per day.

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

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

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

Physiotherapeutic treatment is also widely used: UVR 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 (drugs that promote the excretion of uric acid by the kidneys) - Anturan, Benemide, Ketazon;
uricolytics (drugs that dissolve urinary stones and prevent their re-formation) - citrate mixtures (blemaren, soluran, urodan) and enzymes (uratoxidase, hepatocatalase).

Diet food

An integral part of the treatment is a diet for gouty arthritis.

It is necessary to exclude from your diet fatty, high-calorie foods with a lot 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 an exacerbation, but also between relapses, and the basis of therapy should be dietary nutrition. Only in this way will you protect yourself from the progression of the disease and its complications.

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Gout: Diagnosis and Treatment of "The Disease of Kings"

Gouty arthritis is a chronic disease that is caused by malfunctions of uric acid metabolism. As a result of this process, there is an increase in the number of urates (crystals of the sodium salt of uric acids) and their accumulation in the tissues.

Clinically, this disease is manifested by periodic exacerbation with the formation of gouty nodes (tophi) due to supersaturation with extracellular fluid.

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

How often is the disease diagnosed?

The frequency of diagnosing this type of acute arthritis and hyperuricemia (high uric acid levels) fluctuates. The prevalence of excessive salt levels has reached 4-14 percent and there is an upward trend in these indicators.

The predominant 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 during 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 state of purine metabolism and the peculiarities of the hormonal level. For women, an inverse relationship was found between:

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

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

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

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

Features of the disease is that it has become:

debut at a younger age;
early to form complications with frequent and prolonged exacerbations;
manifested by bright hyperuricemia, numerous tophi.

What does the patient feel during an attack?

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

However, often gout may not be felt or manifested only by 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.

From this it follows that several periods (stages) of the disease are distinguished: 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 stage of the pathology is early, then even an x-ray photo does not show any changes in the joint. Only in more advanced cases, the radiograph will show signs of destructive processes in the 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 at once:

large cysts in the deep layers of bone tissue and subchondral bone (sometimes soft tissue hardening 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 (calcification is sometimes possible);
erosions become large, but not more than a third of the size of the joint surface. Osteolysis of the epiphysis, significant compaction of the soft tissue and accumulation of lime in the joint are noted.

There is another classification. According to her, the important radiological signs will be seals in soft tissues, eccentric darkening caused by tophi, clearly visible articular surfaces (bones, joints), absence of juxta-articular osteoporosis, marginal sclerosis, punch (erosive processes).

Thus, these classifications are seriously different from each other. This requires the unification of a number of radiological symptoms in this form of arthritis.

Instrumental, laboratory diagnosis of gout

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

Tests for gout in the blood serum in such cases, an excessive concentration of uric acid salts is determined. 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 for the determination of uric acid salts should be carried out after 3 days from 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 is determined. If we talk about the norms, then about 300-600 mg should be secreted in 24 hours (1.8-3.6 mmol per liter).

In the contents of tophi, crystals of uric acids are often detected. Typical for 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 it is chronic, is accompanied by the destruction of cartilage (narrowing of the joint space) and the active development of bone erosion along the edge. A characteristic symptom will be a "punch" - this is a marginal bone or cystic outgrowth of the correct form. It is distinguished by clear contours (sometimes sclerosed).

As the pathological condition develops, a clear destruction occurs not only in the subchondral bone, but also in the epiphysis, diaphysis, forming osteopiz inside the joint.

Gout is most pronounced in the joints of the patient's first toe. Moreover, there are cases when an x-ray showed the presence of pathological changes in the joints:

shoulder;
hip;
sacroiliac;
spine.

Bone deformities with an illness rarely decrease, even if adequate treatment is carried out.

It is equally important to conduct a study of the joint fluid. This procedure allows you to identify the presence in it 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 should be called the cellular composition of the synovial fluid, namely the number of leukocytes in it.

visceropathy

The disease associated with gout is visceropathy, which often affects the patient's kidneys. Speaking in numbers, from 50 to 75% of patients are prone 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 with 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 frequency of kidney damage ranges from 30 to 70% of cases.

As you know, isolated urinary nephropathy will become clinical symptoms of failures in purine metabolism. Quite often it proceeds latently, and for a long time. This condition is called the precursor of 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, causes clinically latent glomerulonephritis. This disease of kings occurs with a predominance of hematuria and active progression towards chronic kidney failure (CRF).

From all of the above, it should be logically concluded that the 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

The disease of kings, as gout is often called, can also be detected by other methods. So, in 1963, at an international symposium, several criteria for diagnosing pathology were developed.

Its development is evidenced by symptoms: tophi, an increase in the level of uric acid in the blood, acute pain attacks, usually occurring unexpectedly and so quickly passing, the presence of uric acid salt crystals in the joint fluid and tissues (diagnosed by chemical examination or microscopic).

The doctor can make the 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 you know, cannot be an early sign. For this reason, this symptom is not informative enough 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;
tofus was confirmed by polarizing microscopy, chemical analysis;
the presence of at least 6 of the 12 radiological and laboratory symptoms listed below (maximum inflammation 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 lesions of the tarsal joint, absence of pathological microorganisms in the culture of the articular fluid, hyperuricemia, subcortical cystic ulcers detected by X-ray).

The disease of kings and treatment

If during the studies the preliminary diagnosis was confirmed, then in this case 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:

sharp attack;
interictal period;
chronicle.

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

Physicians distinguish three main tasks when treatment is carried out:

withdrawal of symptoms;
relapse prevention;
preventing the transition of the disease into a chronic form.

Treatment of gout will be of high quality only if the prescriptions of the doctor are strictly followed. Diet plays an important role in this matter. Without a well-scheduled diet, treatment will not be successful.

Supplement the treatment 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 a change 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 musculoskeletal apparatus of the spine, as well as for tissue healing after injuries.

Degenerative-dystrophic spondylosis of the spine is observed mainly in the elderly, 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;
vascular permeability disorders;
Deposits in the wall of arteries of cholesterol plaques;
Multiple ruptures of muscles and ligaments;
Metabolic diseases.

With heart disease, microcirculation is disturbed, so the spine experiences a lack of oxygen. Against this background, even with minimal damage to the ligaments, their multiple ruptures are formed. Initially, repair occurs due to overgrowth of damaged areas with non-functional fibrous (connective) tissue.

If the process exists for a long time, salts of the calcium mineral (Ca) are deposited at the break points. They are clearly visible on the x-ray. Osteophytes irritate the nerve receptors of the musculoskeletal apparatus, and "aching" pain appears.

Violation of vascular permeability is accompanied by multiple small hemorrhages. If they appear in the small capillaries of the musculoskeletal system of the spine, inflammation occurs in the tissues. Bone "thorns" arise during the long-term existence of the process.

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

In metabolic diseases (for example, gout), soft tissue ossification may appear primarily as a result of an excess of chemical compounds. With gout, uric acid accumulates in the ligaments, which causes damage to them. 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.

Usually spondylosis exists 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 another, and vice versa.

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

Spondylosis of the 1st degree has no pronounced clinical symptoms. Insignificant damage to the musculoskeletal apparatus with it in rare cases causes aching pain. True, there is a specificity of the disease depending on the localization.

Degenerative-dystrophic spondylosis in the cervical region is dangerous not so much because of the pain syndrome as the likelihood of impaired blood supply to the brain. In the transverse processes of the cervical vertebrae passes the vertebral artery, which supplies 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 in 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.

Asymptomatic spondylosis of the thoracic spine of the 1st degree proceeds, since the mobility of the area is “fixed” by the ribs. A small displacement of the vertebrae with this form does not lead to infringement of the nerve fibers and serious compression of the vessels.

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

More pronounced symptoms of spondylosis are observed with the localization of bone osteophytes 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, spondylosis of the 2nd degree in the lumbar region forms:

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

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

Neurological symptoms

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

Neurological symptoms in spondylosis:

Bechterew's disease is a pain syndrome on the side of the lesion when lifting up a healthy leg. It appears due to the mobility of the damaged nerve fiber;
Symptom Lasegue - pain when lifting up the legs. The syndrome disappears when the leg is straightened in the knee joint. When lifting the leg up to an angle of 30 degrees, pressure on the nerves increases, so the pain intensifies;
Neri - when bending the head, lumboischialgic pains are observed;
Bragarda - with a positive symptom of Lasegue, the pain syndrome increases with dorsiflexion of the foot;
Wasserman - when the leg is extended, pain occurs in the knee joint;
Matskevich - in the position on the stomach, pain increases when the leg is bent in the knee joint.

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

The heart rate increases;
Increases blood pressure;
There is colicky pain in the chest when turning the body;
Difficulty breathing.

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

Headache and dizziness;
Spasmodic contractions of the shoulder muscles;
The impossibility of raising your hand up;
Difficulty bending the head forward and backward.

What is observed with spondylosis of 1 and 2 degrees in the lumbar spine:

Aching pain in the back, buttocks and lower limbs;
Increased urination and impaired defecation;
Loss of sensation in the skin of the legs;
Violation of the blood supply in 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 following changes are compensatory in order to reduce the depreciation pressure on the spinal column when walking and lifting loads:

Limitation of the mobility of the spinal column;
Decreased flexion amplitude of the back;
Difficulties with maximum inclinations to the sides;
Forced posture to compensate for pain (ischialgic scoliosis).

Neurological manifestations are the loss and weakening of body reflexes. So. spondylosis of the 3rd degree can lead to a decrease in impulses in the region of the ligaments of the lower extremities. At the same time, when tapping with a neurological hammer on the patella, the knee does not rise up, as is normal.

A neurologist can identify serious spinal injuries just by looking at the patient. It detects trophic disorders:

Cyanosis of the skin of the back;
peeling of the skin;
Lowering the temperature of the skin;
Eye twitches when nerves are pinched.

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

Features of compression syndrome

Radicular compression appears during the disease, not only due to the formation of bone osteophytes, but also due to the secondary formation of intervertebral hernias. When it is present, any attempt to make a rotation of the body or movement causes acute pain, like sensations when an electric current passes through the body.

With cervical spondylosis, pain is observed in the region of the upper limb and can reach the tips of the 4th and 5th fingers. It is exacerbated by sneezing or lifting weights.

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

Cervical spondylosis is more sympathetic than radicular (as in the lumbar localization of the disease). Their peculiarity lies in the presence of a primary focus, and 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 neuropathologist.

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

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 the use of x-ray methods of examination:
Computed and magnetic resonance imaging;
Radiography of the spine in two projections.

The main stages of treatment of spondylosis:

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

Spondylosis of the 1st and 2nd degree is manifested by aching pains, 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 the treatment of the disease is therapeutic exercises. It is designed to normalize the state 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. Muscle relaxants are used to normalize muscle tone: mydocalm.

Unfortunately, if a doctor has diagnosed 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 recommendations of the doctor. Otherwise, it is difficult to prevent disability.

Definition. Gout- a disease of heterogeneous origin, characterized by the deposition of urate crystals in various tissues in the form of sodium monourate or uric acid (Bunchuk N.V., 1997).

Historical information

The term gout comes from the Latin "gutta” (drop) and reflects the idea that the disease is the result of fasting malicious infusion (drop by drop). Another name for gout is also known - “the disease of kings”.

In the history of the study of gout, the following milestones can be distinguished ( M. coher, B . Emmerson, 1994):

5th century BC - description of gout by Hippocrates ("Gout is not bald and not a eunuch");

3rd century AD - Galen : describes tophi;

1679 - Van Leeuwenhoek identifies crystals in tophi;

1798 - Wallaston: revealed the presence of uric acid in tophi;

1814 - shows the effectiveness of colchicine in gout;

1913 - Folin, Denis offer a biochemical determination of the concentration of urate in the blood serum

1936 - Prophylactic efficacy of colchicine noted;

1963 Rundles proved the effectiveness of allopurinol for the prevention of gout attacks;

1967 - Kelly revealed etiopathogenetic deficit value hypoxanthylguanine phosphoribosyl transferase (GKGFT) for the development of gout.

Prevalence

Gout mostly affects men over 40 years of age. Women get gout about 20 times less often, but after 50 years this ratio decreases slightly. The rarer development of gout in women is due to the greater excretion of urate in the urine due to the effect of estrogens.

According to an epidemiological study conducted in the 1980s in the USSR, the frequency of gout among residents over the age of 15 was 0.1%, which is higher than in Japan (0.05%), but lower than in most European countries and USA (0.5-3.5%). In certain ethnic groups of residents of Polynesia, the Philippines and New Zealand, the incidence of gout reaches 10%. A study of the dynamics of incidence in the United States showed an increase in the frequency of gout - from 1967 to 1992. 7 times. An upward trend in incidence has also been noted in other developed countries.

Etiology

The determining factor in the development of gout are different in origin disorders of uric acid metabolism(synthesis and / or excretion), leading to a persistent increase in its level in the blood - hyperuricemia . Allocate primary And secondary gout (and hyperuricemia). Secondary gout is recognized when it is one of the syndromes of another disease, in which, for one reason or another (congenital or acquired), disturbances in the metabolism of uric acid occur. For example, secondary gout due to increased formation of uric acid develops in acute and chronic leukemia, multiple myeloma, lymphoma, kidney carcinoma and other malignant tumors, hyperparathyroidism, psoriasis, hemoglobinopathies, von Willebrand disease and some other diseases. Chronic renal failure is the most common cause of secondary gout due to slow excretion of uric acid by the kidneys. The development of secondary gout is also possible with sarcoidosis, hypothyroidism, salicylates, cyclosporine, and some other drugs.

In the case of primary gout, no diseases that could cause it are found. Among patients with primary gout, those who have increased urate synthesis make up only 10%. Specific enzymatic defects are detected in these patients only in isolated cases. In the vast majority of patients with primary gout, the cause of the disease is a violation of the excretion of uric acid by the kidneys. In these patients, both isolated defects in the various phases of uric acid excretion (decreased secretion, increased reabsorption) and combined disorders can be observed.

Persistent long-term hyperuricemia is a mandatory and main condition for the development of gout. In those who develop primary gout, hyperuricemia reaches its maximum severity by the age of 25, while the average age of patients with gout is approximately 47 years. The incidence of gout in individuals with hyperuricemia averages 2.7-12% and depends on the level of hyperuricemia. The development of primary gout requires a combination of hyperuricemia with such acquired factors in adulthood as the consumption of large amounts of foods rich in purines, alcohol, overweight, which increase the already existing disorders of uric acid. There is a well-known aphorism: "Partners of hyperuricemia are friends of abundance."

Alcohol is one of the important factors contributing to the development of hyperuricemia. Mechanism hyperuricemic The effect of alcohol is presumably associated with an increase in the content of lactic acid, which makes it difficult for the kidneys to excrete urates ( J. Cameron et al ., 1981). In addition, alcohol contributes to the formation of urates, increasing the rate of ATP breakdown. Beer contains a significant amount guanosine-purine base, which becomes an additional load ( R. Janson, 1999).

It is widely believed that there is a direct relationship between a high level of uric acid in the blood and a person’s intelligence, about a special predisposition to the development of gout in men who have achieved success in life and have leadership qualities ( J. Wyngaarden, W Kelly , 1976). For example, Isaac Newton, Michelangelo, Benjamin Franklin, Charles Darwin suffered from gout.

The source of uric acid is purine bases (adenine and guanine) - components of nucleic acids (both endogenous and, to a much lesser extent, supplied with food), as well as purine nucleosides from which ATP is formed, and similar compounds. The metabolism of purine bases is regulated by several enzymes. Currently, the presence of two enzymatic defects has been proven, which are accompanied by a sharp increase in the synthesis of uric acid and the development of gout already in childhood: deficit hypoxanthine-guanine phosphoribosyl transferase (HCGFT) and increased activity of 5-phosphoribosyl-1-synthetase. These enzymes are controlled by genes associated with the X chromosome, so males are more likely to get sick.

It is well known that gout is often inherited: cases of this disease in relatives occur, according to various sources, in 6-81% of patients, and hyperuricemia is found in 25-27% of relatives of patients with primary gout. A six-generation family with gouty arthritis and progressive nephropathy has been described in Japan ( M. Yokota et al., 1991).

Information about the change in the main complex histocompatibility very little in patients with gout. A weak association of gout with HLA B 14 (B. Cassium et al., 1994).

Pathogenesis

If the content of uric acid in the blood or tissue fluid is more than 0.42 mmol / l (at a temperature of 37 0 C), there is a danger of urate crystallization. It remains unclear why some people with higher uremia do not develop either gouty arthritis or tophi. With a decrease in temperature, the crystallization of uric acid is facilitated, which explains the predominant deposition of urate crystals in avascular tissues (articular cartilage and cartilage of the auricles), in a relatively poor blood-supplied structures (tendons, ligaments) or relatively poorly blood-supplied anatomical areas (in particular, in the feet). The favorite onset of gout is from the metatarsophalangeal joints of the big toes, possibly due to the fact that it is in them that degenerative-dystrophic changes in the cartilage occur earlier and most often, which predisposes to the deposition of urates.

A gout attack is associated with the formation of sodium urate crystals ( M. Cohen et al ., 1994). The crystals are “coated” with a protein shell, as a result of which they have the ability to initiate inflammatory reactions.Ig G , adsorbed on crystals, reacts withFc-receptors of inflammatory cells, activating them, and apolipoprotein B, also included in the protein shell of urates, inhibits phagocytosis and cellular immune response. Thus, urates stimulate the production of chemotaxis factors, cytokines (interleukins 1,6,8 and tumor necrosis factor), prostaglandins, leukotrienes and oxygen radicals by neutrophils, monocytes and synovial cells. Cytokines cause an influx of neutrophils into the joint cavity, in addition, the complement system and the release of lysosomal enzymes by neutrophils are activated.

The very fact of the appearance of urate crystals in the joint cavity, apparently, is not enough for the onset of arthritis, since urate crystals are often found in the synovial fluid during the interictal period of gout (in about 52-58% - in the knee and first metatarsophalangeal joints).

self-passingthe nature of inflammation in the joint with gout is determined by the ability of phagocytes to digest crystals and the release of a number of anti-inflammatory factors, in particular platelet growth factor - beta. The predominant development of arthritis in gout at night is explained by the fact that tissue hydration decreases at rest and an increase in the concentration of uric acid in the joint fluid occurs.

Uric acid lithiasis approximately 40% of patients with gout precede articular manifestations. Hyperuricemia has an important pathogenetic significance in the development of urolithiasis, but plays an even greater role hyperuricosuria . With the release of less than 700 mg of uric acid per day, urolithiasis is observed in 21% of patients, and with the release of 1100 mg / day or more - in 50% of patients ( T.-F. Ju, A . b. Gutman, 1987). Other predisposing factors include impaired solubility of uric acid due to acidic urine. Stone formation is also facilitated by urinary stasis (congenital anomalies of the urinary tract, prostatic hypertrophy, etc.) and its infection.

Kidney damage in gout can be presented urate nephropathy, for which the deposition of monosodium urate crystals in the interstitial tissue is typical. Of primary importance in its origin is chronic hyperuricemia. The deposition of microtophi in the interstitium predisposes to arterial hypertension. Another type of kidney damage is characterized by the formation and deposition of uric acid crystals in the collecting ducts, calyces, pelvis, or ureter. Since both types of kidney damage in gout are often detected in one patient, this division is conditional.

Pathological picture

During acute gouty arthritis, urate crystals are found in the superficial layer of the synovial membrane. Synovitis is nonspecific. Histopathological changes include fibrin deposits, synovial cell proliferation, and marked neutrophilic leukocyte infiltration. Even in the early stages, infiltration by lymphocytes and plasma cells can be seen. Tophi in the synovial membrane are usually observed in patients with repeated attacks of gout. In tophi, there is a large accumulation of urate crystals, surrounded by granulomatous tissue containing giant multinucleated cells. In some cases, over time, tophi can calcify and even ossify. Joint damage in chronic gout is characterized by significant destruction of cartilage, and often subchondral bone, changes in tendons, ligaments and synovial bags.

Clinical picture

It is customary to count the onset of gout from the first attack of arthritis, although before that, on average 10 years earlier, 10-40% of patients develop one or more renal colic caused by urate lithiasis.

There is a classic description of a typical gout attack: “The victim goes to bed and falls asleep in good health. Around two in the morning she wakes up with pain in her big toe, less often in her heel or ankle. This pain is similar to that which occurs when a joint is dislocated, another part of the patients compares the pain with the feeling of cold water pouring on the joint. This is followed by chilliness and a feeling of trembling with low temperature. The pain, which is mild at first, gradually becomes intense. After a while, the attack peaks, bones, ligaments of the metatarsus and tarsus are involved. Now - this is an incredible tension of the ligaments and the feeling that the latter are torn to pieces - this is already a gnawing pain. So a refined and cheerful person, stricken with a disease, sleeps off his feet. He can't put on heavy night clothes, he can't walk around the room, everything gets on his nerves.

The night passes in torment, without sleep, the patient constantly changes position, which leads to constant pain in the joints and worsening of the attack. From this time on, all efforts aimed at relieving pain by changing the position of the trunk or limbs remain in vain ”( J. Wyngaarten et al.,1976).

With gout, acute and chronic arthritis is distinguished.

Acute arthritis. For the first "attack" of gout in men, monoarthritis and predominant damage to the joints of the foot are typical. Acute arthritis of the joints of the big toe during the entire period of the disease is observed in almost all patients, but during the first attack of gout it is observed only in 50%. Less typical for gout is inflammation of the elbow and wrist joints. Oligo- or polyarthritis at the onset of gout in men is not typical, but is typical for women. Another feature of gout in women is the more frequent involvement of the joints of the hands. In both men and women, the first to be affected with gout are those joints that were previously changed for some reason. It is known, for example, the involvement of the distal interphalangeal joints of bones altered due to osteoarthritis.

In classic cases, suddenly, often at night or early in the morning, a sharp pain develops in one joint, usually in the lower limb. The pain quickly, within a few hours, increases to intolerance, there is a pronounced swelling of the affected joint, usually accompanied by reddening of the skin over it. Movement in the inflamed joint becomes almost impossible, as well as support on the affected limb. The pain is significant even without movement, often its intensification is caused even by a light touch of the joint with a blanket. Pain, swelling of the joint and hyperemia of the skin over it can be so pronounced that they resemble phlegmon. During an attack of gout, moderate fever, leukocytosis, and an increase in ESR are often noted.

A characteristic feature of gouty arthritis is the spontaneous (without treatment) complete regression of symptoms in a few hours or more often in a few days.

The course of untreated gout is very variable. The most characteristic is the constant increase in the "attacks" of arthritis, a tendency to their more protracted nature. In rare cases, there is a clinical course of gout with an almost complete absence of light intervals between attacks of arthritis and the rapid development of tophi.

The development of acute gouty arthritis is facilitated by any abrupt changes in the content of uric acid in the blood, both upward and downward, and the latter, perhaps even to a greater extent. Acute gouty arthritis can be triggered by trauma, exercise, emotional stress, sudden changes in diet (both overeating and fasting), drinking alcohol, bleeding, infections, myocardial infarction, surgery (usually after 3-4 days), certain drugs (diuretic, mainly thiazide, vitamin B 12, allopurinol, chemotherapeutic anticancer drugs, intravenous heparin, cyclosporine, administration of protein drugs), as well as radiation therapy.

Allocate atypical forms of gout(V.A. Nasonova, M.G. Astapenko, 1989): rheumatoid-like, pseudophlegmonous, polyarthritic(migratory), subacute form, asthenic, periarthritic a form with localization of the process in the tendons and bursae (most often in the calcaneal tendon) with intact joints.

Chronic gout. It is characterized by the development of certain permanent manifestations of the disease: tophi(significant accumulations of urate crystals) of various localization, chronic arthritis, kidney damage or urolithiasis. From the first "attack" of the disease to the development of chronic gout, an average of 11.6 years passes (from 3 to 42 years). The rate of progression of the disease depends on the severity of hyperuricemia and kidney damage.

The most frequent localization of subcutaneous or intradermal located visible during direct examination tophi- in the area of the fingers and toes, knee joints, protrusions on the ulnar surface of the forearms, as well as synovial bags (especially the elbows), tendons and auricles. Tophi are often concentrated around persistently altered joints. Sometimes the skin over the tophus can ulcerate, while their contents are spontaneously released, which have a pasty consistency and white color. It should be noted that intraosseous tophi, found only on radiographs, can often develop earlier than subcutaneous ones. There are known clinical descriptions of tofus lesions of the spine, compression of the spinal cord, changes in the myocardium, heart valves, conduction system, various structures of the eye and larynx. In very rare cases, tophi are determined before the development of gouty arthritis.

Joint damage . Chronic arthritis and gout can involve a variable number of joints. The small joints of the hands and feet are often affected. Articular syndrome may include destructive signs, deformity and stiffness joints. Infiltration of articular tissues with urates is accompanied by an inflammatory reaction of the tissues surrounding the joint.

An X-ray examination helps to assess changes in the joints in detail. Gout is characterized by intraosseous cystic formations of various sizes, caused by tophi. Chronic gouty arthritis may be accompanied by cartilage destruction (narrowing of the joint gap) and the development of marginal bone erosions. Over time, pronounced destruction is noted not only subchondral part of the bone, but also the entire epiphysis and even part of the diaphysis ( intra-articular osteolysis). At the same time, there is a significant expansion of the “corroded” articular sections of the bones and sharpening of their edges. The so-called “punch” symptom is marginal bone erosion or cystic formations of the correct form with clear, sometimes sclerosed contours - observed in gout infrequently and nonspecific. Bone ankylosis in gout is extremely rare. X-ray changes are most pronounced in the joints of the feet (primarily in the joints of the thumbs) and hands. More rare localization of radiographic changes in gout are the shoulder, hip, sacroiliac joints and spine. Bone changes in gout rarely improve with specific therapy. Tophi located in soft tissues can also be detected by X-ray, especially if they are calcified.

Main x-ray signs of gout summarized in Table 1.

Table 1.

X-ray signs of gout
( M. Cohen and B. Emmerson , 1994)

sign

Characteristic

soft tissues

Seal

Eccentric darkening due to tophi

Bones/joints

The articular surface is clearly presented

Juxta-articular no osteoporosis

erosion

A) "punch"

B) marginal sclerosis

B) overhanging edge ( overhanging edges)

Kidney damage. Factors favoring the development of nephropathy in gout are uricosuria over 700 mg/day. diuresis and decrease Ph urine (X. Kappen, 1990). Massive "excretion" of uric "acid" can lead to damage to the tubular apparatus of the kidneys and, secondarily, to the interstitium of the kidneys. Later, damage to the glomeruli may occur with the development immunocomplex jade. Gout is characterized by a predominance of disorders of tubular functions (especially a violation of the concentration function) over a decrease in glomerular. The most common sign of renal dysfunction in gout is mild proteinuria, which occurs in 20-40% of patients with gout and may be intermittent. The more pronounced the clinic of articular gout, the more significant the damage to the kidneys. With tofus gout, proteinuria, slight disturbances in the concentration function and a decrease in glomerular filtration are observed. Over time, changes in the kidneys gradually increase. Among the clinical manifestations of gout, it is nephropathy that most often determines the prognosis of the disease. Approximately 10% of patients with gout die of kidney failure. With the development of severe renal failure, there is a tendency to infrequent development of acute arthritis. Hemodialysis also leads to a decrease in articular "attacks".

According to Shukurova S.M. (1997), echolocation of the kidneys revealed changes in 75.4% of cases. Stones were determined with the greatest frequency (in 1/3 nephrolithiasis was bilateral). In 23% of cases, changes in the pelvicalyceal segments and calculi were simultaneously detected, which, in combination with leukocyturia, made it possible to discuss the diagnosis of concomitant pyelonephritis. Kidney cysts were determined in only 13% of patients.

Accompanying illnesses. Common diseases associated with gout include obesity, arterial hypertension, hyperlipidemia, impaired glucose tolerance (metabolic syndrome), and coronary heart disease.

According to epidemiological studies, approximately 78% of gout patients are over 10% overweight, and 57% are over 30% (Brochner-K. Morteus, 1984). Reduced glucose tolerance is found in 7-74% of patients with gout, although diabetes mellitus develops infrequently.

Hypertriglyceridemiaobserved in 50-75% of patients with gout, and hyperuricemia in 82% of patients with hypertriglyceridemia. Especially often this type of hyperlipidemia in gout is observed in patients who abuse alcohol. Although a number of patients with gout also have hypercholesterolemia, several studies have shown no correlation between uricemia and cholesterol levels.

Arterial hypertension is noted in ¼-½ of patients with gout. This may be due to decreased renal blood flow. Obesity may be an important link between arterial hypertension and hyperuricemia. In turn, hyperuricemia is detected in 22-38% of patients with arterial hypertension. It is assumed that an increase in the level of uric acid in the blood may be an indicator of damage to the vessels of the kidneys (or renal tubules) in arterial hypertension.

It is noted that young patients with coronary heart disease often have hyperuricemia. More than half of the causes of death in patients with gout are cardiovascular diseases.

Diagnostics. The most common criteria for the diagnosis of gout, adopted at the international symposium in Rome (1961):

Hyperuricemia- uric acid in the blood more than 0.42 mlmol/l in men and more than 0.36 mlmol/l in women

Presence of gouty nodules (tophi)

Detection of urate crystals in synovial fluid or tissues

A history of acute arthritis accompanied by severe pain that began suddenly and subsided in 1-2 days

/ The diagnosis of gout is considered reliable if any two signs

Later, S. Wallace et al. (1974), also proposed to take into account the peculiarities of the course of gouty arthritis - unilateral lesion I metatarsophalangeal joint, accompanied by redness and pain, the maximum development of symptoms on the first day, asymmetric changes in the joints on the x-ray, the absence of flora when sowing the joint fluid.

In an acute attack of gout, an increase in the level of uric acid in the blood is usually noted, but the normal value of this indicator is no exception. Of greatest value in the diagnosis of gout is polarizing microscopy of synovial fluid and other tissues (for example, tophi), in which it is possible to detect characteristic urate crystals that have a needle-like shape, and most importantly, peculiar distinctive light-optical properties - negative birefringence and a number of others. The main diagnostic value is the detection of intracellular crystals, and their extracellular location may be accompanied by asymptomatic hyperuricemia (5%) or chronic renal failure (approximately 20%). The sensitivity of this study is 69%, the specificity is about 97% ( C. Gordon et al ., 1989). The threshold concentration of urate crystals in the synovial fluid, still available for identification, is about 10 µg/ml. There are cases of acute arthritis in gout, when using polarizing microscopy, urate crystals were not detected due to their small size, but were detected by electron microscopy. Errors are possible in the presence of other crystals in the synovial fluid, in particular lipid ones. It is especially easy to identify urate crystals in superficially located tophi using polarizing microscopy.

It is important to determine the daily excretion of uric acid in the urine. Normally, after a 3-day restriction of purines in the diet, 300-600 mg (1.8-3.6 ml mol) of urates are excreted, and with normal nutrition - 600-900 mg. It is advisable to conduct this study before dieting and 7 days after it (meat, meat soups and sauces, poultry, fish, legumes, oatmeal, tea, coffee, cocoa, alcohol are excluded). Initially and in dynamics simultaneously determine the volume of urine, Ph urine, uric acid and creatinine levels in the blood. It has been established that with an increase in the daily excretion of urate in the urine of more than 1100 mg, the risk of kidney damage is 50%.

The therapeutic effect of colchicine is of particular importance in the diagnosis of acute gouty arthritis. However, it should be borne in mind that a striking effect with gout is not always observed and, conversely, with pyrophosphate arthropathy and calcifying tendonitis colchicine can be very effective.

Treatment

Treatment of gout involves a differentiated strategy depending on the stage of the disease - an acute attack or an interictal period, a tofus form.

Allocate main tasks in the treatment of goutPanrotsky J., 1996):

End an acute attack as soon as possible;

- Prevent relapse.

Prevent or reduce the manifestations of chronic gout, primarily the formation of kidney stones and tophi.

In a number of gout patients with relatively low hyperuricemia and infrequently recurrent arthritis, measures such as dietary restrictions, weight loss, refusal to drink beer and strong alcoholic beverages can bring a significant therapeutic effect and should be tried before prescribing drugs, but even very strict a low-purine diet can reduce uricemia by no more than 0.06 mlmol / l, and daily uricosuria by no more than 200-400 mg, which is clearly not enough in most patients. Dietary recommendations include the exclusion of broths and sauces, the restriction of meat and fish products, legumes, strong coffee and tea, and alcohol. The amount of proteins is reduced to 1 g / kg, fat - less than 1 g / kg, the need for calories is satisfied mainly due to carbohydrates. A slight increase in the amount of fluid you drink (up to 2-3 liters per day), regular visits to the bath or sauna are useful, which contributes to the extrarenal excretion of uric acid. It is also important to control the maintenance of normal body weight and blood pressure, glucose and blood lipids. An important place in the treatment of gout is occupied by the education of the patient, the purpose of which is to understand the role of various factors that positively and negatively affect his disease.

Before choosing a therapy, each patient with gout should be properly examined. The magnitude and persistence of hyperuricemia and daily uricosuria, kidney function and the state of the urinary tract should be analyzed, the stage of the disease and concomitant diseases should be determined.

Treatment of asymptomatic hyperuricemia . To address the issue of treatment tactics, the results of determining the daily excretion of uric acid in the urine are of primary importance. When a persistent hyperuricosuria more than 900 mg per day, which is not eliminated by a low-purine diet, the question of the constant use of allopurinol should be considered. If the daily excretion of uric acid in the urine is not increased, then anti-gouty drugs are not indicated and a low-purine diet, weight loss and other preventive measures are of primary importance in the treatment.

Management of acute gouty arthritis usually administered with colchicine or non-steroidal anti-inflammatory drugs (NSAIDs). It is believed that colchicine is able to eliminate the symptoms of acute gouty arthritis in about 80% of patients within 48 hours after the start of therapy. In the case of using the drug in the first few hours after the onset of an attack, the effectiveness increases to 90%. The physician prescribing colchicine must be aware of the patient's comorbidities. Colchicine (Colchicum - Dispert,Solvay Pharma) is administered orally, at an initial dose of 0.5 mg (in accordance with the recommendations of other authors - 1 mg). Then, every hour, an additional 0.5 mg of the drug is prescribed (or 1 mg of the drug every 2 hours) until the arthritis is completely relieved or until diarrhea (vomiting) appears, but not less than 6-8 mg per day. The dose of the drug should be reduced with a decrease in creatinine clearance below 50-60 ml / min. In most patients, the effect is already noted from 0.5 mg of colchicine and becomes distinct by 12 hours of treatment. For more than one day, colchicine is usually not used to treat a gout attack. Perhaps parallel use in acute gouty arthritis of colchicine in small doses (0.5 mg 2 times a day) and NSAIDs. Sometimes, when oral colchicine cannot be administered, for example, after surgery, the drug is used intravenously.

Among NSAIDs, preference is given to drugs with a rapid onset of action and the most active in anti-inflammatory respect: diclofenac sodium and phenylbutazone, but not acetylsalicylic acid. Diclofenac sodium at the first appointment, it is prescribed orally at a dose of 50-100 mg or intramuscularly at a dose of 75 mg. Phenylbutazone (butadione) - at a dose of 0.3 g. Then, if necessary, every 2-3 hours, NSAIDs are repeated: diclofenac sodium at a dose of 25-50 mg up to 200 and even 400 mg per day, and phenylbutazone - up to 0.6 g in 3-4 doses. Due to frequent adverse reactions (edema, arterial hypertension, gastrointestinal disorders, hematological disorders), phenylbutazone is almost never used. For the relief of acute gouty arthritis, ibuprofen at a dose of 2,000-3,200 mg / day can also be used, taking into account the good tolerability of the drug. For all NSAIDs, the same principle remains as for colchicine - the earliest possible appointment at a sufficiently high initial dosage.

An acute attack of gout can be stopped by injecting into the inflamed joint glucocorticosteroids, having previously evacuated the synovial fluid, as well as prescribing these drugs orally (prednisolone 20-40 mg for 3-4 days) or intramuscularly. This method of treatment should be resorted to if colchicine or NSAIDs are ineffective or poorly tolerated.

Treatment anti-gouty means ( allopurinol, benzbromarone) is carried out only after the relief of gouty arthritis, usually not earlier than after 3 weeks.

Treatment of frequently recurrent gouty arthritis. With absence hyperuricosuria, signs of kidney damage and urolithiasis There are two possible approaches to treatment.

The issue of starting specific therapy is resolved positively with a significant severity of uricemia (more than 0.6 mlmol / l) and the presence of tophi. In this situation, it is possible to use both allopurinol and uricosuric funds.

The dose of allopurinol is selected individually. Most often, it is recommended to start treatment with the appointment of 0.3-0.4 g of the drug per day, once. Sometimes a smaller dose is enough. The effectiveness of treatment is monitored by repeated determination of the level of uric acid in the blood. The desired level of this indicator is less than 0.36 mlmol / l (in men), and the ideal level is within the range of 0.24-0.3 mlmol / l. It must be borne in mind that the dissolution of urates in the extracellular fluid and tissues occurs only if the uricemia is less than 0.42 mlmol / l. Usually, under the influence of allopurinol, the level of uric acid decreases after 24-48 hours and normalizes when an adequate dose is selected after 4-14 days. The selection of a maintenance dose of allopurinol is carried out so as to ensure not only a stable normal level of uricemia, but also to prevent recurrence of arthritis and kidney damage. Resorption of subcutaneous tophi is observed no earlier than after 6-12 months of continuous allopurinol therapy. In this situation, the choice between allopurinol and uricosuric drugs are administered empirically.

probenecidappoint an initial dose of 0.25 g 2 times a day. Uricosuric The effect of the drug develops after 30 minutes. After 3-4 days, with insufficient reduction in uricemia, every 1-2 weeks increase the dose of the drug by 0.5 g. The disadvantage of the drug is often developing resistance to treatment.

Treatment sulfinpyrazone start with a dose of 0.05 g, appointing it 2 times a day. The first dose of the drug is recommended to be taken as early as possible in the morning, and the last - as late as possible in the evening. After 3-4 days, in the absence of a sufficient decrease in the level of uric acid in the blood, the daily dose sulfinpyrazone gradually, every week, increase by 0.1 g. But not more than 0.8 g / day, increasing the number of doses during the day to 3-4. Usually the maintenance dose of the drug is 0.3-0.4 g / day.

Benzbromarone (hipurik, dezurik, normurat) compares favorably with others uricosuric means of prolonged action, can be administered 1 time per day. The usual dose is 0.08-0.1 g per day, the maximum is 0.6 g.

In the treatment of gout, it is possible to use a combination of allopurinol with uricosuric means (usually sulfinpyrazone or with benzobromarone, but not with probenecid), as well as a combination of individual uricosuric funds among themselves. However, a significant “benefit” from combination therapy for gout is usually not achieved.

In primary gout, drugs are usually prescribed for lifelong daily intake, their cancellation or interruptions in treatment lead to a rapid (within 1-3 weeks) increase in the level of uric acid in the blood and the resumption of the clinical manifestations of the disease. In the first days and weeks of treatment, any antigout drugs can provoke the development of gouty arthritis. Therefore, at first, either colchicine (1.5 mg per day) or NSAIDs in average daily doses are additionally prescribed. While taking anti-inflammatory drugs, the amount of fluid you drink should be increased to 3 liters / day, so that the daily amount of urine would be at least 2 liters. It is important that diuresis is sufficient at night.

If uricemia does not reach 0.6 mlmol / l, no hyperuricosuria and tophi , for continuous use, colchicine is prescribed at a dose of 0.5-1.5 mg / day or NSAIDs in medium doses, and a low-purine diet is also recommended. The advantage of this non-specific therapy lies in the good tolerability of the drugs. placebo controlled The study showed that prophylactic administration of colchicine at a dose of 0.5 mg 2 times a day prevented arthritis relapses in 74% of patients and reduced their severity in 20%. Colchicine is generally well tolerated when taken long-term at the indicated dose.

With increased excretion of uric acid in the urine and / or in the presence of kidney damage due to urolithiasis preference is certainly given to allopurinol. Uricosuric funds are contraindicated. When choosing the dose of allopurinol in patients with reduced kidney function, it is conditionally considered that every 30 ml / min of filtered urine corresponds to a daily dose of the drug, which is 0.1 g. Allopurinol can lead to the gradual dissolution of existing urate stones, reduce the severity of gouty kidney damage, and also prevent the formation of both uric acid and oxalate stones. In the first weeks of allopurinol therapy in such patients, especially with a significant severity of kidney damage or urolithiasis, the appointment of agents that increase the solubility of uric acid in the urine is indicated. More often they use a mixture of citrate salts (magurlite, uralit- U etc.), which increases Ph -urine to alkaline values, optimum Ph is 6-7. These drugs are taken before meals, 3-4 times a day, 2-3 hours before the maximum value. Ph urine. The daily dose of citrates is usually from 6 to 18 g. Contraindications are acute and chronic renal failure and urinary tract infection. These drugs also reduce the saturation of urine with calcium oxalate, nucleation and crystal growth of this composition. The dose is selected individually, under control Ph urine. It is possible to use sodium bicarbonate for the same purpose at a dose of about 2 g per day, until alkaline values \u200b\u200bare reached. Ph urine. Rapid and effective alkalinization of urine can also be achieved with the help of the diuretic drug acetazolamide (diacarb, etc.). It is administered orally at a dose of 125-250 mg every 6-8 hours. Due to the rather sharp and rapidly advancing increase Ph urine carbonic anhydrase inhibitors (acetazolamide) are usually prescribed to patients with severe urolithiasis, when it is especially important to achieve alkalization of urine at night, as well as in acute renal failure in patients with "gouty kidney". Acetazolamide is used short-term, usually within 3-5 days. If necessary, the drug is repeated after a break of 2-3 days.

Allopurinolis the drug of choice in patients with secondary gout that develops in hematological diseases or malignant tumors of any localization during the period of active cytotoxic or radiation therapy, when the risk of developing acute gouty nephropathy sharply increases.

Treatment of "acute gouty kidney". Treatment of acute renal failure due to blockade intrarenal urine outflow with urate crystals is classified as critical and requires immediate intensive care. The patient must be urgently hospitalized. Measures are being taken to stimulate forced diuresis - intravenous administration of a large amount of fluid and the simultaneous use of saluretics in large doses (furosemide up to 2 g per day). Allopurinol is prescribed orally at a daily dose of 8 mg / kg and urine alkalizing agents (sodium bicarbonate intravenously, acetazolamide orally). The ongoing therapy is considered effective if diuresis of at least 100 ml per hour is achieved within 1-2 days. In the absence of the desired effect, hemodialysis is used.

The prognosis of gout in most cases is favorable, especially with timely recognition and rational therapy. Most predictively unfavorable factors are considered: early development of the disease (up to 30 years), persistent hyperuricemia exceeding 0.6 mlmol / l, persistent hyperuricosuria exceeding 1.100 mg / day, the presence of urolithiasis in combination with urinary tract infection, progressive nephropathy, especially in combination with diabetes mellitus and arterial hypertension.

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