For quotation: Svetlova M.S. X-ray method in the diagnosis of joint diseases // RMZh. Medical Review. 2014. No. 27. S. 1994
Joint diseases are widespread among the population throughout the world. Diagnosis of most of them involves not only the assessment of clinical manifestations and laboratory test data, but also the use of imaging techniques, primarily radiography. Despite the rapid development in recent years of such modern medical imaging methods as magnetic resonance imaging, X-ray computed tomography, and the expansion of ultrasound diagnostic capabilities, radiography remains the most common method for diagnosing and monitoring the effectiveness of treatment of joint diseases. This is due to the availability of this method, ease of research, cost-effectiveness and sufficient information content.
X-ray examination is essential for establishing the diagnosis of the disease and should be used, whenever possible, in every patient with joint damage. In this case, several radiological techniques (methods) can be used: radiography, tomography, X-ray pneumography. X-rays of joints make it possible to determine the condition of not only the osteochondral elements that make up the joint, but also the soft periarticular tissues, which is sometimes important for diagnosis. When performing radiographs of joints, it is mandatory to take a picture of the joint in at least 2 projections (frontal and lateral) and compare the affected and healthy paired joints. Only under these conditions, on the basis of an x-ray, can one reliably judge the condition of the joint.
It must be borne in mind that at the initial stage of the disease, radiography does not reveal any pathological symptoms. The earliest radiological sign of inflammatory diseases of the joints is osteoporosis of the epiphyses of the bones that make up the joint. In the presence of osteoporosis, the spongy substance of the epiphyses appears more transparent on the radiograph, and against its background the contours of the bone, formed by a more dense cortical layer, which in the future may also undergo thinning, stand out sharply. Osteoporosis (both diffuse and focal) develops most often in acute and chronic inflammatory diseases of the joints. With degenerative-dystrophic lesions of the joints in the early stages, osteoporosis is not observed, so this sign may have differential diagnostic value in such cases. In the later stages of arthrosis, moderate osteoporosis may be observed, combined with cystic bone restructuring.
Degenerative-dystrophic forms of joint diseases are characterized by compaction of the bone substance of the subchondral layer of the epiphyses (end plates of the articular surfaces). This compaction develops as the articular cartilage degenerates and its buffering function decreases (as a compensatory phenomenon). With the complete disappearance of cartilage, but with preservation of mobility in the joint, which usually occurs with arthrosis, a more pronounced and more widespread sclerosis of the bone is determined on the x-ray. On the contrary, with loss of joint function, thinning of the subchondral layer of the epiphyses is observed, even with preserved cartilage.
An important radiological sign is a change in the X-ray joint space, reflecting mainly the condition of the articular cartilage. Widening of the joint space can be observed with large effusions in the joint cavity or with thickening of the articular cartilage, which occurs, for example, with Perthes disease. Much more often there is a narrowing of the joint space due to degenerative changes, destruction or even complete disappearance of cartilage. A narrowing of the X-ray joint space always indicates a pathology of the articular cartilage. It can occur both in long-term inflammatory and dystrophic lesions of the joints, progressing with the course of the disease, and thus has no differential diagnostic value. Complete disappearance of the joint space is observed in inflammatory diseases in the event of the development of bone ankylosis. During degenerative processes, the joint space never completely disappears.
The condition of the articular surfaces of the epiphyses has significantly greater differential diagnostic significance. Inflammatory diseases of the joints are characterized by destructive changes in the articular surfaces and, above all, the presence of marginal bone defects - the so-called usurs. Uzures are most often located on the lateral parts of the articular surfaces, from where pannus (granulation tissue) “creeps” onto the articular cartilage.
In recent years, in the diagnosis of joint lesions, importance has been attached to cystic reorganization of bone tissue, which can be observed in both inflammatory and degenerative processes.
Despite some common radiographic signs, each joint disease has its own radiographic picture. There is quite a lot of data in the literature about the possibilities of X-ray diagnosis of osteoarthritis, rheumatoid arthritis (RA) and much less information about the features of the X-ray picture of ankylosing spondylitis (AS), psoriatic arthritis (PA), gout, i.e. those diseases that are often encountered in practice doctors in their daily work.
So, AS, or ankylosing spondylitis, is an inflammatory disease that affects the spine, sacroiliac joints and peripheral joints. For radiological examination of patients with suspected AS, it is necessary to perform radiographs of the sacroiliac joint and spine. When examining the sacroiliac joint, it is recommended to take 3 photographs: 1 - in a direct projection and 2 - in an oblique one (right and left, at an angle of 45o). When examining the spine, radiography is required in direct and lateral, and sometimes in oblique projections.
Radiological symptoms are the most important and early sign of 2-sided sacroiliitis. At first, one joint may be changed; after a few months, the second one is also involved in the process. The first sign of sacroiliitis is the blurring of the bone edges that form the joint; the joint space appears wider. Later, marginal erosions appear, the contours of the articular surfaces look “eaten away”, uneven, and the joint space narrows. In parallel, periarticular sclerosis develops, followed by ankylosis and obliteration of the joint. In most cases, the characteristic x-ray picture develops only 2 years after the onset of the disease, but sometimes after 3-4 months. It is possible to detect early signs of sacroiliitis.
Another important sign is a characteristic lesion of the intervertebral joints - blurring of the articular plates, and then narrowing of the joint space. As a result, ankylosis forms and the joint space is not visible. In this case, there are no marginal osteophytes, the joint space does not change, and neoarthrosis does not form. This sign, in combination with 2-sided symmetrical sacroiliitis, makes it possible to confidently diagnose AS.
Characteristic of AS is the formation of bone bridges (syndesmophytes) between adjacent vertebrae due to ossification of the peripheral parts of the intervertebral discs. First of all, they arise at the border of the thoracic and lumbar spine on the lateral surface. With the widespread formation of syndesmophytes in all parts of the spine, the “bamboo stick” symptom appears.
Less specific radiological signs of spinal damage in AS include:
- formation of erosions at the junction of the fibrous ring with the vertebra, especially in the anterior sections;
- square shape of the vertebra (on the lateral radiograph);
- ossification of the longitudinal ligaments, which appears on the x-ray in the frontal projection in the form of longitudinal strips, and in the lateral projection the ossification of the anterior longitudinal ligament is clearly noticeable;
- vertebral ankylosis, which, as a rule, forms first in the anterior parts of the spine (Fig. 1).
Involvement of the hip and knee joints in the process is manifested by a narrowing of the joint space; erosions are rarely detected. The joints of the hands and feet are very rarely affected. X-rays reveal erosions that are very similar to those in RA, but osteoporosis is mild, and the changes are often asymmetrical. Erosion and sclerosis can be detected in the sternocostal and sternoclavicular joints, and ankylosis can sometimes be observed in the pubic symphysis. With a long course in the area of the wings of the pelvic bones and on the ischial tuberosities, small exostoses can be detected - “spiny pelvis”.
Thus, the following radiological stages can be distinguished during AS:
a) radiological signs of the disease are not visible on a traditional radiograph;
b) signs of sacroiliitis are revealed, i.e., blurring of the subchondral layer of the joints is noted; initially a slight expansion, and then a narrowing of the joint space; signs of formation of erosions and osteophytes appear in the joints of the spine;
c) ankylosis of the sacroiliac joints and the “bamboo stick” symptom; joint spaces in the intervertebral joints are not visible; signs of osteoporosis;
d) the spine has the appearance of a tubular bone, the discs and all ligaments ossify, and bone atrophy occurs.
PA is a fairly common disease of the musculoskeletal system, combined with skin lesions of psoriasis. The X-ray picture of PA has a number of features. Thus, osteoporosis, characteristic of many joint diseases, in PA is clearly observed only at the onset of the disease and in the mutilating form.
Radiological manifestations of arthritis of the distal interphalangeal joints are quite typical. This is an erosive asymmetric process, in which proliferative changes are simultaneously detected in the form of bone growths at the bases and tips of the phalanges, periostitis.
Erosion, having arisen at the edges of the joint, subsequently spreads to its center. In this case, the apices of the terminal and middle phalanges are worn down with simultaneous thinning of the diaphyses of the middle phalanges, and the second articular surface is deformed in the form of a concavity, which creates the radiological symptom “pencils in a glass”, or “cup and saucer”.
Characterized by the proliferation of bone tissue around erosions and osteolysis of the distal phalanges. One bone is often pushed into another like a telescope (“telescopic” finger).
In polyarthritis that occurs without damage to the end joints, the x-ray picture may resemble RA with marginal erosions of the epiphyses and bone ankylosis of the joints, however, the development of ankylosing process in several joints of the same finger is considered pathognomonic for PA.
The mutating form of PA, as mentioned above, is manifested by severe osteolytic changes in the constituent joints of the bones. Not only the epiphyses, but also the diaphyses of the bones of the joints involved in the pathological process are subject to resorption. Sometimes the lesion affects not only all the joints of the hands and feet, but also the diaphyses of the bones of the forearm (Fig. 2).
X-ray changes in the spine in patients with PA include:
- osteoporosis of the vertebrae;
- paraspinal ossifications;
- ankylosis and erosion of intervertebral joints;
- deformation of the vertebrae;
- syndesmophytes;
- reduction in the height of intervertebral discs;
- multiple osteophytosis (lateral, anterior, posterior angles of the vertebrae);
- sharpening and elongation of the edges of the uncovertebral joints;
- Schmorl's hernia.
Damage to the spine and sacroiliac joints during radiographic examination can be detected in 57% of patients, most of whom have no clinical signs of sacroiliitis and spondyloarthritis. In other words, spondyloarthritis occurs latently, which must be kept in mind when examining the patient. Sacroiliitis is most often 1-sided, although a 2-sided symmetrical process with ankylosis of the sacroiliac joints is also observed, as in true AS.
Thus, radiological signs that help distinguish PA from other inflammatory rheumatic diseases of the joints are as follows:
- asymmetry of damage to the joints of the hands;
- arthritis on radiographs may be without periarticular osteoporosis;
- isolated damage to the distal interphalangeal joints of the hands with no changes or slight changes in other small joints of the hands;
- axial damage to 3 joints of one finger;
- transverse lesions of the joints of the hands at the same level (1- or 2-sided);
- destruction of the terminal phalanges (acroosteolysis);
- terminal narrowing (atrophy) of the distal epiphyses of the phalanges of the fingers and metacarpal bones;
- cup-shaped deformation of the proximal part of the phalanges of the fingers together with the terminal narrowing of the distal epiphyses - the “pencil in a glass” symptom;
- bone ankylosis, especially of the proximal and distal interphalangeal joints of the hands;
- multiple intra-articular osteolysis and destruction of the epiphyses of bones with multidirectional deformations of the joints (arthritis mutilans);
- inflammatory changes in the sacroiliac joints - sacroiliitis (usually unilateral asymmetrical or bilateral, perhaps the absence of sacroiliitis);
- changes in the spine (asymmetrical syndesmophytes, paravertebral ossifications).
Gout is a systemic disease associated with impaired purine metabolism, deposition of urate in articular and/or periarticular tissues and inflammation developing in connection with this.
In acute arthritis, specific changes are not detected on radiographs. X-ray changes characteristic of gout usually develop no earlier than 3 years from the onset of the disease. At the same time, signs of destruction, degeneration and regeneration can be observed.
Gout is characterized by intraosseous cyst-like formations of various sizes, caused by tophi, which can be located inside the joint, but, what is especially noteworthy, next to it and even at some distance. Chronic gouty arthritis may be accompanied by cartilage destruction (narrowing of the joint space) and the development of marginal bone erosions. The so-called “piercer symptom” - marginal bone erosions or cyst-like formations of regular shape with clear, sometimes sclerotic contours - is rarely observed in gout and is not specific for it. More typical for this disease is the pronounced destruction that occurs over time not only of the subchondral portion of the bone, but also of the entire epiphysis and even part of the diaphysis (intra-articular osteolysis). In this case, a significant expansion of the “eaten away” articular parts of the bones and a sharpening of their edges can be observed. Bone ankylosis in gout has been described, but is extremely rare (Fig. 3).
The localization of radiological changes is always peculiar in gout. Typically, the most pronounced pathology is found in the joints of the feet (primarily in the joints of the big toes) and hands. Rare but known sites of radiological changes in gout include the shoulder, hip, sacroiliac joints and spine. It is important to note that destructive joint changes or intraosseous cysts are considered a sign of “tophus” gout.
Bone changes in gout rarely decrease with specific therapy; over time, they may even increase slightly. Tophi located in soft tissue can also be detected by radiography, especially if they become calcified, which is uncommon.
Thus, in the diagnosis of joint diseases, without a doubt, the x-ray method should be used, especially in the daily practice of a primary care doctor, since each of the diseases has its own x-ray signs characteristic only of it. Knowledge of the features of the X-ray picture of arthritis can certainly help the practitioner in making the correct diagnosis.
Literature
1. Nasonov E.L. Clinical recommendations. Rheumatology. M.: GEOTAR-Media, 2008.
2. Kishkovsky A.N., Tyutin L.A., Esinovskaya G.N. Atlas of placements for X-ray examinations. L.: Medicine, 1987.
3. Lindenbraten L.D., Korolyuk I.P. Medical radiology (basics of radiation diagnostics and radiation therapy). 2nd ed., revised. and additional M.: Medicine, 2000.
4. Agababova E.R. Differential diagnosis of seronegative arthritis // Ter. archive. 1986. T. 58. No. 7. P. 149.
5. Zedgenidze G.A. Clinical radiology. M., 1984.
6. Nasonova V.A., Astapenko M.G. Clinical rheumatology. M., 1989.
7. Sidelnikova S.M. Questions of pathogenesis, diagnosis and differential diagnosis of seronegative spondyloarthritis // Ter. archive. 1986. T. 58. No. 6. P. 148.
8. Badokin V.V. Rheumatology. M.: Litterra, 2012.
9. Molochkov V.A., Badokin V.V., Albanova V.I. and others. Psoriasis and psoriatic arthritis. M.: Partnership of Scientific Publications KMK; Authors' Academy, 2007.
Gout is a chronic progressive disease caused by a disorder of purine metabolism, characterized by an increased (normal for adult women - 150-350 µmol/l; for adult men - 210-420 µmol/l) level of uric acid in the blood (hyperuricemia), with subsequent deposition of urates in articular and/or periarticular tissues. Detection of hyperuricemia is not sufficient to establish a diagnosis, since only 10% of individuals who suffer from this disease have gout. Almost 95% of people diagnosed with gout are men between 40 and 50 years of age, although the disease is noted to be “getting younger.”
The rest are menopausal women. Gout has increasingly become accompanied by individual diseases such as obesity, hypertriglyceridemia (increased levels of neutral fats in the blood) and insulin resistance (impaired amount of insulin in the blood). We can conclude that gout is not a cause, but a consequence of metabolic disorders in the body. There are two types of gout: primary and secondary. Primary gout is a hereditary disease (11-42% of cases), which is associated primarily with a predisposition to hyperuricemia, which is transmitted in an autosomal dominant manner.
The cause of primary gout is the impaired activity of enzymes that are involved in the formation of uric acid from purine bases or in the mechanisms of urate excretion by the kidneys. And the causes of secondary gout are renal failure, blood diseases accompanied by increased catabolism (processes aimed at destroying substances in the body), and the use of a number of medications (diuretics, salicylates, etc.).
Lesions
The main function of the kidneys is filtration and absorption 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 900-1600 mg, and about 60% of this amount is replaced daily by new formation due to the breakdown of nucleotides and erythroblasts and the synthesis of nitrogen-containing compounds.
With prolonged hyperuricemia (with increased formation of uric acid in the body), adaptive reactions develop to reduce the level of uric acid in the blood. This occurs due to an increase in kidney activity and the deposition of urates in the soft tissues of cartilage. The clinical symptom of gout is associated precisely with the deposition of uric acid crystals in soft tissues. Although the mechanism of urate deposition is not fully understood, there are two main factors:
- Insufficient vascularization (permeated with blood vessels) of tissues such as tendons and cartilage, in which there is an increased concentration of urates.
- Local temperature, serum pH, and the presence of substances that retain urate in the fluid (proteoglycans) all affect the rate of sedimentation of uric acid salts. Increased diffusion of water from the joint increases the concentration of crystallized urate.
It has been proven that complete dissolution of uric acid salts occurs at pH = 12.0-13.0 (strongly alkaline solution), which in reality exists inside the human body. Hypothermia of peripheral joints (ankles, phalanges of fingers) promotes accelerated crystallization of urates and the formation of microtophi. With a high concentration of microcrystals in tissues (joint cartilage, bone epiphyses, etc.), the formation of micro- and macrotophus begins. Sizes range from millet grain to chicken egg. The accumulation of urates leads to cartilage destruction. Next, uric acid salts begin to be deposited in the subchondral bone (the foundation for cartilage, providing its trophism) with its destruction (the radiological name is a puncture symptom).
Uric acid also accumulates in the kidneys (gouty kidney or gouty nephropathy). All patients with gout have affected kidneys, so renal failure is considered not as a complication, but as one of the visceral (internal) manifestations of the disease. Gouty kidney (nephropathy) may manifest itself in the form of urolithiasis, interstitial nephritis, glomerulonephritis or arteriolonephrosclerosis.
Gout symptoms
- a symptom of severe pain in one or more joints - the intensity of the pain increases over several hours;
- a symptom of swelling or burning, as well as redness of the skin in sore joints and limbs;
- sometimes a symptom of slight fever;
- a symptom of returning pain, which occurs with prolonged gouty arthritis;
- a symptom of the formation of hard white lumps under the skin (tophi);
- symptom 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 increased amounts of uric acid in the body and/or the passage of urate stones with or without attacks of colic. This period can be quite long. The onset of attacks of the first gouty crisis indicates that the disease has begun to actively develop.
Gouty arthritis
During the intermittent period, acute attacks of gouty arthritis alternate with asymptomatic intervals between them. Long-term hyperuricemia and exposure to provoking factors (drinking alcohol, prolonged fasting, eating foods rich in purines, trauma, taking medications, etc.) lead to nocturnal acute attacks of gouty arthritis in 50-60% of cases. The onset of the attack is a sharp pain in the first metatarsophalangeal joint of the leg (big toe). The affected area quickly swells, the skin becomes hot from a sudden rush of blood, the swelling tightens the skin, which affects pain receptors. Shiny, tense, red skin soon becomes bluish-purple, which is accompanied by peeling, fever, and leukocytosis. There is a dysfunction of the joint, the attack is accompanied by fever. Other spherical joints, foot joints, and, somewhat less frequently, ankle and knee joints are also affected.
Less commonly affected are the elbow, wrist and hand joints; extremely rare - shoulder, sternoclavicular, hip, temporomandibular, sacroiliac and spinal joints. Acute gouty bursitis (inflammation of the mucous bursae, mainly of the joints) is known; the prepatellar (located under the skin in front of the kneecap) or ulnar bursa is usually affected. Under the influence of synovitis (inflammation of the synovial membranes of the joint), the joints become deformed, the skin at the site of inflammation becomes tense, shiny, stretched, and when pressed, the dimple disappears. The boundaries of hyperemia (poor circulation) are unclear, bordered by a narrow strip of pale skin. This picture is observed from 1-2 to 7 days, then local inflammatory processes decrease, but the pain can sometimes continue at night. Gouty arthritis begins to go away after a few days with proper treatment. First, the redness of the skin disappears, its temperature normalizes, and later the pain and swelling of the tissues disappear. The skin wrinkles, there is abundant pityriasis-like peeling and local itching. Sometimes gout-specific tophi appear. The early stages of intermittent gout are characterized by rare recurrences of attacks (1-2 times a year). But the longer the disease progresses, the more often the symptoms of gouty arthritis return, becoming longer lasting and less acute.
Each time, the intervals between attacks of the disease shorten and cease to be asymptomatic, and blood tests can reveal an increased content of uric acid. This is an indicator that the disease is becoming chronic. Chronic gout is described by the occurrence of tophi and/or chronic gouty polyarthritis. The disease develops 5-10 years after the first attack and is characterized by chronic inflammation of the joints and periarticular (periarticular) tissues, the appearance of tophi (subcutaneous deposits of uric acid crystals), as well as combined damage to the joints (polyarthritis), soft tissues and internal organs (usually the kidneys) .
The location of tophi is different: it can be the ears, the area of the elbow joints, hands, feet, Achilles tendons. The presence of tophi indicates a progressive inability of the body to remove uric acid salts at a rate equal to the rate of their formation.
Chronic tophi gout
When gouty arthritis develops for quite some time, the formation of tophi occurs everywhere: in cartilage, in internal organs and bone tissue. Subcutaneous or intradermal formations consisting of monocrystals of sodium urate in the area of the fingers and toes, knee joints, elbows and ears are a sign that gouty arthritis has entered the chronic stage. Sometimes ulcers can be noted on the surface of the tophi, from which spontaneous discharge of a white pasty mass is possible. The formation of tophi in the bone space is called a puncture or break symptom, which can be diagnosed using x-rays.
Nephrolithiasis (kidney stone disease) in gout occurs due to the deposition of urate in the kidneys, forming stones. The more actively hyperuricemia progresses and the rate of crystal deposition increases, the greater the likelihood that tophi formations will appear in the early stages of the disease. This is often observed against the background of chronic renal failure in elderly women taking diuretics; in some forms of juvenile gout, myeloproliferative diseases (associated with disruption of brain stem cells) and post-transplantation (cyclosporine) gout. Typically, the presence of tophi of any localization is combined with chronic gouty arthritis, in which there is no asymptomatic period, and is accompanied by polyarthritis (multiple joint damage).
General diagnostics
Gout is a disease that is difficult to diagnose in the early stages, since most of the time it is asymptomatic, and during periods of acute attacks its course resembles reactive arthritis. Therefore, an important part of the diagnosis of gout is an analysis of the level of uric acid in the blood, in daily urine and the clearance (speed of purification) of uric acid.
During an attack, laboratory acute-phase reactions are detected; a urine test may show slight proteinuria, leukocyturia, and microhematuria. Deterioration in the concentrating ability of the kidneys according to the Zimnitsky test indicates the presence of asymptomatic interstitial nephritis (inflammation of the kidneys) with the gradual development of nephrosclerosis (overgrowth of connective tissue in the kidneys). In the synovial fluid there is a decrease in viscosity, high cytosis, and the needle-like structure of sodium urate crystals is visible under a microscope. Morphological examination of the subcutaneous tophi reveals, against the background of dystrophic (degrading) and necrotic changes in tissue, a whitish mass of sodium urate crystals, around which a zone of inflammatory reaction 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; isolated tophi are observed.
Moderate gout is characterized by more frequent (3-5 times a year) exacerbation of the disease, which progresses in 2-4 joints at once, moderate skin and joint destruction, multiple tophi are observed and kidney stone disease is diagnosed. 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 not very informative. The radiological phenomenon typical of late gout is quite well known - the “punch” symptom. This is a defect in the bone on which the joint rests, can be 5 mm in diameter or more, located in the middle part of the base of the diaphysis (the middle part of the long tubular bones) or in the head of the phalanx, most often the first metatarsophalangeal joint. But as information accumulated, it became clear that a situation is more often observed when radiographic changes are not detected in patients with gouty arthritis.
Manifestation of the punch symptom
It is necessary to note a number of points that make the radiological symptoms of the punch significant. The pathomorphological (i.e., internal structure different from the norm) substrate of this x-ray phenomenon is intraosseous tophi, which is similar to a cystic (having a separate wall and cavity) formation, due to the fact that uric acid salt crystals do not retain x-rays. The identified “puncher” determines the stage of the disease as chronic tophi. It is worth noting that identification of tophi of any location is a direct indication for starting anti-gout therapy. In general, the “puncture” symptom in patients with primary gout is a late sign and is associated with a long course of the disease and chronic arthritis.
On the other hand, an early radiological sign of gout is a reversible diffuse thickening of soft tissues during an acute attack due to the fact that during inflammatory processes there is a rush of blood and deposition of solid crystalline forms in areas of edema. In this case, local thinning of the bone substance (transient arthritis) can be detected, and as the disease progresses, destructive processes in this area can also occur. X-ray manifestations: initially, erosion can form along the edges of the bone in the form of a shell or shell with overhanging bone edges, with clearly defined contours, which is very typical for gouty arthritis, in contrast to rheumatoid arthritis, tuberculosis, sarcoidosis, syphilis, leprosy. Erosion processes can be detected both in the joint itself and outside it.
With intra-articular localization of tophi, destructive processes begin from the edges and, as they develop, move towards the center. Extra-articular erosions are usually localized in the cortical layer of the metamyphyses (from the medulla of the edges of the long tubular bone) and the diaphysis of the bones. Most often, this erosion is associated with close adjacent soft tissue tophi and is defined as round or oval marginal 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-ray images resemble “rat bites.” Asymmetrical erosions with destruction of cartilage are typical; bone ankylosis (fusion of articular surfaces) is rarely formed. If calcium is present in the tophi structures, then X-ray positive inclusions can be detected, which sometimes stimulate chondromas (a tumor consisting of cartilage tissue). The joint space width of the affected joints usually remains normal until the late stages of gouty arthritis. These changes can mimic osteoarthritis (joint degradation), but in some cases both conditions occur.
Stages of joint damage
- tophi in the bone adjacent to the joint capsule and in deeper layers, rarely - manifestations of soft tissue compaction - gouty arthritis is just developing;
- large tophi formations near the joint and small erosions of the articular surfaces, increasing compaction of the periarticular soft tissues, sometimes containing a certain amount of calcium - gouty arthritis manifests itself in acute attacks;
- severe erosion on at least 1/3 of the surface of the joint, complete aseptic resorption of all articular tissues of the epiphysis, significant compaction of soft tissues with calcium deposits - chronic gouty arthritis.
Forecast of the consequences of gout
With timely recognition and treatment of gout, unpleasant consequences or development into a chronic form of the disease can be avoided. Unfavorable factors that influence the degree of development of the disease: age under 30 years, persistent hyperuricemia exceeding 0.6 mmol/l (10 mg%), persistent hyperuricosuria exceeding 1100 mg/day, the presence of urolithiasis in combination with a urinary tract infection; progressive nephropathy, especially in combination with diabetes mellitus and arterial hypertension. Life expectancy is determined by the development of renal and cardiovascular pathologies. In conclusion, it is worth noting that gout is a difficult to diagnose systemic disease, the symptoms of which are varied and often overlap with various other diseases.
Only in 10% of cases can a doctor immediately diagnose gout, since its early form is sluggish, almost asymptomatic. That is why it is important to monitor diseases that have obvious external manifestations (pain or deformation of any part of the body), and the condition of the blood. Blood is an indicator of a person's condition. Timely diagnosis of gout will allow you to choose the most effective treatment method. And if the final diagnosis was made only at a late stage, then, in order to be able to move normally (gout affects the joints, deforming them), only surgical intervention and a long rehabilitation period will help, without a guarantee that the disease will not return again. Be healthy!
Be sure to consult your doctor before treating any illness. This will help take into account individual tolerance, confirm the diagnosis, ensure the correctness of treatment and eliminate negative drug interactions. If you use prescriptions without consulting your doctor, it is entirely at your own risk. All information on the site is presented for informational purposes and is not a medical aid. All responsibility for use lies with you.
Hippocrates also described this disease and gave it a name. In Greek “podos” means “foot”, “agro” means “trap”. This type of foot trap was considered a disease of kings. And indeed, paradoxically, the higher a person’s standard of living, the greater the chance of contracting this unpleasant disease. It has long been noted that during times of war and economic crisis, almost no one gets gout. Among men, gout is much more common, which allows women to say that the stronger sex leads an idle lifestyle.
Content:X-ray of gout on big toe
What's so bad about gout?
Jokes aside, it’s worth explaining that gout is a consequence of high levels of uric acid in the blood. It is formed by the breakdown of proteins and is a white powder, poorly soluble in water. When uric acid is poorly excreted from the body, it begins to deposit in the joints. There are people prone to crystal formation. They are also susceptible to gout.
Gout is most common on the big toe. It is believed that such a disease begins precisely from this joint, because degenerative-dystrophic changes in cartilage most often occur here. This causes great suffering. Men fall into the trap after 40 years of age, and women are at risk of developing gout after menopause. There is no way to get rid of gout, so to suppress it, you need to change your lifestyle.
In addition to the joints of the legs, gout can affect the elbows, wrists and other joints. Sometimes it also affects internal organs. Changes can be observed in the nervous and cardiovascular systems. The skin, digestive organs and vision are affected.
You can only find out about gout after an attack. It is accompanied by severe pain and immobility of the joint. As the disease progresses, attacks become more frequent and increase in duration. Gout usually predominates at night.
Types and symptoms of gout
An attack of gout can occur after a festive feast with an abundance of meat and alcohol. Everything comes very unexpectedly, most often during sleep:
- joint swelling,
- redness,
- temperature,
- chills,
- warming up of the joint
- “sheet syndrome”, when it hurts even from contact with bed linen.
Gout on the thumb - poster with description
Gout can attack several joints at once, completely immobilizing a person for a couple of days. And then suddenly it goes away in an instant, and the symptoms no longer appear. But gout does not go away forever. At this point, it is important to follow a protein-free diet. This is a feature of gouty arthritis - spontaneity, with no symptoms observed between attacks. If precautions are not followed and treatment is ignored, the time interval between attacks is reduced, the attacks themselves lengthen and new joints are affected.
A common type of gout is tophi. Tophi are nodular formations of crystals in the subcutaneous tissue, they are painless. Their favorite areas on their feet are:
- Achilles tendon area,
- foot joints,
- extensor surfaces of the thigh,
- extensor surfaces of the leg.
There are primary and secondary gout. Primary occurs with a genetic predisposition as a result of an inherited metabolic disorder. Secondary gout develops as a result of diseases of the endocrine system, kidneys, cardiovascular system, and alcoholism. Lying for a long time due to injury, or taking certain medications for a long time also increases the risk of gout.
Pronounced swelling of the big toe
Ears can show gout. They are usually strewn with the same subcutaneous nodules. And if you open such a nodule, there will be white powder there. In addition to visualization, blood and urine tests are taken, and in severe cases, an x-ray is also taken. An X-ray photo shows the process of destruction of the joint.
Consequences
If gout is not treated, and this is sometimes done by people who have it in a sluggish form, then blood pressure may increase, kidney failure may occur, and stones may form. Gout leads to joint deformation, the development of arthrosis, and sometimes destruction. Patients with gout are “doomed” to eat mainly plant foods, no jellied meat, if meat, then only lean and boiled. Meat broths are strictly prohibited. When cooked, purines from meat pass into the broth, and they contribute to the formation of uric acid.
It is necessary to completely give up coffee, chocolate, sardines in oil, mushrooms, and alcohol. You should try to eat foods that have diuretic properties: plums, cherries, tea. You should also part with extra pounds. Whatever one may say, you will have to lead a healthy lifestyle.
How is gout treated?
You should get used to the idea that gout, a foot disease, is ineradicable. Therefore, you have to live, deceiving and subordinating her to your conditions. If we have already more or less figured out the lifestyle and diet, then we should indicate what the drug treatment is aimed at:
- relief of gout attack,
- release of uric acid crystals,
- limiting foods that produce uric acid,
- reduction of urea crystallization due to the supply of large amounts of water.
The doctor may suggest extracorporeal hemocorrection. It is interesting because it serves as an alternative to drug treatment, in which many drugs have serious side effects. This method consists of taking blood plasma from the patient, which is subjected to special treatment, as a result of which uric acid crystals fall out. When plasma is filtered, these crystals are removed and it is returned without salts or acid back into the patient's body.
The procedure is very effective and safe. With a repeated procedure, all excess uric acid is removed. This eliminates the cause of gout. If you are overweight, it is recommended to follow a diet under the supervision of a doctor. The fact is that sudden weight loss leads to the formation of uric acid and causes a gout crisis.
Big toe bandage
Folk remedies for gout
A patient suffering from gout can do a lot to improve his condition himself. Treatment with folk remedies is quite effective. Elderly people who do not have enough financial resources for good leather and soft shoes, which gout does not like, say that foil brings relief. It is placed on the bump under the sock before putting on your shoes. And nothing hurts!
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The disease inevitably progresses, causes pathological changes in internal organs and threatens disability. Correct examination allows you to avoid a false diagnosis and slow down the progression of the disease.
Criteria for diagnosing gout
Joint diseases have similar symptoms, have a hidden course and inevitably become chronic. This significantly complicates the differentiation of ailments and prevents timely treatment. In 1961, the global medical community defined general diagnostic criteria for gout:
- increased concentration of uric acid in the blood, urine, joint fluid;
- a history of sudden attacks of acute arthritis lasting up to 1-2 days;
- detection of uric acid crystals, urates in soft tissues, articular cavity;
- visual detection of salt deposits – .
The detection of two or more criteria from the above list serves as a valid basis for diagnosing gout. American scientists expanded this list to 12 points:
- excess content of uric acid and salts;
- pathological absence of microflora in the synovial fluid;
- the presence of non-erosive subcortical cysts on x-rays;
- a medical history of 2 or more attacks of gouty arthritis;
- the acute phase during attacks is observed on the first day;
- prolonged inflammation in the metatarsophalangeal joint on the legs;
- unilateral form of damage to the joints on the foot;
- asymmetric type of joint damage;
- signs of arthritis in one joint of the foot;
- hyperemia (redness) of the skin in the joint area;
- confirmed presence of tophi;
- damage to one metatarsophalangeal joint.
Note!
The diagnosis of gout is made when six of these criteria are met or uric acid and urate crystals are detected in the tophi (or synovial fluid).
Clinical picture and external examination
When making a diagnosis, collecting data for anamnesis plays an important role. By studying the medical history, the doctor receives valuable information for identifying the disease. To diagnose gout, it is necessary to distinguish it from similar diseases (rheumatism,). During an external examination, the following facts are established:
- time of appearance and duration of the first symptoms;
- change in the appearance of the joint - swelling, redness, deformation;
- the presence of surgical operations, injuries, pathologies;
- complicated heredity and predisposition;
- the patient's lifestyle, habits.
Note!
The clinical picture of a chronic, long-term disease often has a pronounced, clearly identifiable character. An experienced specialist is able to determine gout without tests, guided by his own experience, skills and knowledge. However, most often a preliminary diagnosis is made, which requires confirmation and justification by an appropriate examination.
Features of differential diagnosis
At the first signs of damage to the joints on the legs, a rheumatologist, surgeon, or traumatologist is required. After studying the clinical picture, the doctor decides what tests need to be taken for gout. Differential diagnosis allows you to accurately determine the causes of the disease based on the results of laboratory tests of blood, urine, and instrumental examination.
Laboratory tests
The first stage in diagnosing any disease is laboratory testing of blood and urine. The analysis results indicate changes in the composition and rheological properties of liquids. These data suggest the cause and patterns of development of the disease. To identify gout you will need:
- results of general blood and urine tests;
- data from their biochemical study;
- results of studying the composition of joint fluid;
- study of the contents of tophi.
General blood test results
A constant excess of uric acid and crystallization of urates is accompanied by metabolic disorders and inflammatory processes in the joints. These factors inevitably lead to changes in the chemical composition of fluids in the body. Blood test indicators for gout according to general parameters:
- increased proportion of neutrophils;
- change in leukocyte formula;
- decrease in the number of lymphocytes;
- increase in erythrocyte sedimentation rate (ESR).
Note!
At the initial stage of gout, there may be no deviations from the norm in a general blood test.
Features of biochemical blood analysis
With a complete biochemical blood test, the value of various indicators is established. Their specific change and ratio suggests the presence of gout and determines the degree of neglect.
Established and generally accepted standards for blood parameters:
| Tests for gout (indicator) | Children (1-14 years old) | Men | In women |
|---|---|---|---|
| Total protein value | 48-82 g/l | 64-83 g/l | |
| Albumin content | 33-55 mg/l | 33-50 mg/l | |
| C-reactive protein content | None | up to 0.5 g/l | |
| Creatinine value | 35-110 µm/l | 63-115 µm/l | 54-97 µm/l |
| Meaning of uric acid | 0.15-0.28 µmol/l | 0.13-0.21 µmol/l | 0.16-0.41 µmol/l |
| Calcium value | 0.94-1.16 mmol/l | 1.04-1.27 mmol/l | 2.14-2.5 mmol/l |
| Total bilirubin value | 17- 67 µmol/l | 3.5-20.7 µmol/l | 3.41-17.0 µmol/l |
| High Density Lipoprotein Cholesterol Value | 0.9-1.9 mmol/l | 0.7-1.83 mmol/l | 0.9-2.2 mmol/l |
| Low-density lipoprotein cholesterol value | 1.6-3.5 mmol/l | 2.1-4.7 mmol/l | 1.91-4.5 mmol/l |
The results of a biochemical blood test for uric acid in gout are overestimated. For self-diagnosis and establishment of hyperuricemia, increased levels of C-reactive protein, sialic acids, and fibrin are taken into account. If dysfunction of the kidneys or urinary system is suspected, the value of bilirubin, prothrombin, and liver enzymes is studied.
Results of a general urine test
With hyperuricemia, there is an increase in the level of uric acid, urate in the urine, crystallization of salts in the urinary tract, kidneys, and bladder. General analysis is effective with concomitant. Based on the results of a urine test for gout, the following is determined:
- increased concentration of uric acid;
- alkaline pH>7 at the late stage of gout;
- deviation in color due to changes in composition;
- the presence of urate crystals in the dry residue of urine;
- detection of protein molecules (albumin);
- small amounts of blood, epithelium.
Study of synovial fluid
An important step in the differential diagnosis of gout in the legs is the study of articular (synovial) fluid. Its composition is close to blood plasma, differing in the content of hyaluronic acid. The norm is the presence of cholesterol, cells (synovocytes, lymphocytes, monocytes, neutrophils). By puncture, synovial fluid is extracted from the joint cavity for bacteriological and bacterioscopic examination. Changes in its indicators indicate gout:
- violation of color, density, viscosity;
- the appearance of turbidity, mucin clots;
- deviation from the norm pH=7.3 to 7.6;
- detection of erythrocytes, leukocytes;
- the appearance of phagocytes, destroyed cells;
- study of synoviocytogram;
- crystals of urates, phosphates.
X-ray examination
For chronic and advanced forms of gout, radiography is prescribed. The method is effective for diagnosing diseases on the legs, establishing the stage of the disease and detecting complications. X-ray reveals irreversible changes in the structure of bones and cartilage of the affected joints. Typical radiological signs of gout:
| Research elements | Picture in the picture | Pathological processes |
|---|---|---|
| Soft tissues (muscles, membranes) | Local dimming with blurred outline. | Tissue compaction due to inflammation, crystallization of urates. |
| Joint bones | Visual deformation of the bone surface, detection of an overhanging edge or swelling of the edge, areas with darkening. | Erosion, destruction of the bone surface, cartilage, crystallization of urates around and inside the bones. |
| Joints | A symptom of a puncture in gout is light-colored areas with a diameter of 0.3-3 cm on an x-ray of the diseased joint. | Formation of intraosseous tophi, destruction of bone tissue at the late stage of gout. |
Other diagnostic methods
To establish the diagnosis of gout, modern diagnostic methods are used in medicine. They identify additional signs of the disease that are used to confirm the diagnosis:
- Ultrasound, tomography (computer, magnetic resonance) - during the period of exacerbation, they are used to detect narrowing of the interarticular space, inflammation, hardening of soft periarticular tissues, joint deformation, pathology in the kidneys and ureter;
- Biopsy is a detailed study of intra-articular fluid to determine excess uric acid in the synovial fluid in the problem joint.
How to prepare for tests
There are known cases of false blood test results for gout, biased results of urine and joint fluid tests. The reliability and information content of laboratory research increases with proper preparation for the delivery of biological material:
- 3 days before the tests, follow a strict diet - exclude foods prohibited for gout;
- 10 hours before, stop taking vitamin C;
- do not take diuretic medications for 24 hours;
- do not engage in sports for 3 days;
- All tests are taken on an empty stomach, early in the morning.
Following these rules eliminates the possibility of distorting test results and making an erroneous diagnosis.
Gout- a disease associated with a disorder of purine metabolism, characterized by an increase in the level of uric acid in the blood (hyperuricemia) and the deposition of urate in the articular and/or periarticular tissues. Detection of hyperuricemia is not enough to establish a diagnosis, because only 10% of people with hyperuricemia have gout. The most common causes are decreased excretion or increased production of uric acid. Chronic gout is characterized by the formation of tophi.
Code according to the international classification of diseases ICD-10:
- M11.1
Etiology
. Overproduction of uric acid at a normal level of its excretion is noted in 10% of patients. Primary overproduction is associated with.. defects in the enzymatic system for the synthesis of uric acid.. increased activity of 5-phosphoribosyl-1- synthetase.. deficiency of hypoxanthine-guanine phosphoribosyl transferase.. with storage diseases glycogen (types 1, 3, 5, 7).. Secondary hyperproduction is caused by.. increased cell breakdown during alcoholism, myeloproliferative diseases, chronic hemolysis, psoriasis or antitumor chemotherapy.. increased purine catabolism during alcoholism, tissue hypoxia, excessive physical exertion. exposure to drugs: cytostatic immunosuppressants, cyanocobalamin, fructose.
. Impaired uric acid excretion (uric acid excretion less than 700 mg/day) is observed in 90% of patients. May be associated with... diseases leading to a decrease in urate clearance: renal failure, dehydration, acidosis, hyperparathyroidism, hypothyroidism, hyperaldosteronism, eclampsia, hypoestrogenemia... the action of drugs: diuretics, alcohol, small doses of acetylsalicylic acid, caffeine, diazepam, diphenhydramine, ascorbic acid, lead.
Reasons
Genetic aspects. The activity of phosphoribosyl pyrophosphate synthetase 1 (311850, PRPS1 gene, Xq22 q24) is controlled by the X chromosome, so only males are affected.
Pathogenesis gouty attack. As a result of prolonged hyperuricemia, microtophi (clusters of crystals) are formed in the synovial membrane and cartilage. Due to injury, increased temperature in the joint, or changes in the concentration of uric acid in the blood or synovial fluid, the microtophi are destroyed and the crystals are released into the joint cavity. Synovial cells produce IL-1, IL-6, IL-8, which act as chemoattractants for neutrophils. Immunoglobulins and complement components opsonize (envelop) urates, stimulating the phagocytic activity of neutrophils. The phagosomes of neutrophils that have absorbed the crystals merge with lysosomes, and lysosomal enzymes destroy the protein shell of the crystals. The crystals damage neutrophils, and lysosomal enzymes released into the synovial cavity trigger inflammation.
Symptoms (signs)
Clinical picture(by stages of flow)
. Asymptomatic hyperuricemia is elevated blood uric acid levels in the absence of clinical signs of crystal deposition (i.e., no arthritis, tophi, nephropathy, or urate stones).
. Acute gouty arthritis is the second stage and the first manifest form of gout - sudden onset arthritis with severe pain. A typical attack most often affects one joint on the legs, and in 50% of patients the first metatarsophalangeal joint is affected. Most gout attacks occur at night and occur with a rapid increase in erythema and temperature around the joint, swelling and pain. Inflammation can spread to soft tissues, forming the clinical picture of cellulite or phlebitis. Severe cases are accompanied by an increase in body temperature. The usual duration of an attack is several days, less often several weeks. After an attack, the joint returns to its normal shape. In some cases, a polyarticular variant is also possible.
. The interictal period - the third stage of gout - occurs after the end of the first attack and can be interrupted by the next acute attack.. Repeated monoarticular attacks. In 7% of patients, after the first episode of gout, no repeated attacks are noted. However, in 62%, repeated attacks occur during the first year of illness. In typical cases, during the interictal period, patients do not complain, but if the patient does not receive treatment, then each subsequent attack is more severe and the interictal period is shortened. Disease progression. Over time, the attacks become more severe and take on the character of polyarthritis. Some patients quickly develop chronic gouty arthritis, with virtually no remissions; in such cases, differential diagnosis is made with rheumatoid arthritis.
. Chronic gouty arthritis (chronic tophi gout) occurs if left untreated; it is considered the final stage of gout. Tophus form clusters of urate crystals surrounded by inflammatory cells and fibrous masses. Tophi are dense, mobile, cream or yellowish in color with the release of chalky contents when ulcerated. Typical localization of tophi: auricle; over the affected joints; subchondral parts of the articular surfaces; on the extensor surface of the forearm; in the elbow area; over the Achilles and hamstring tendons.
. Kidney damage: nephrolithiasis, tubulo-interstitial nephritis.
Laboratory data. Leukocytosis in the blood with a shift to the left and acceleration of ESR during acute attacks. Increased levels of uric acid in the blood. In 10% of cases, the concentration of uric acid in the blood is within normal limits. In the synovial fluid there are 10-60109 leukocytes/l, mainly neutrophils. The identification of needle-shaped urate crystals located intracellularly and birefringent light when examined in a polarizing microscope is of diagnostic importance. The aspirated contents of the tophi contain uric acid crystals. A study of daily uric acid excretion is carried out after a 3-day diet excluding purines.
Instrumental data. The radiograph shows pronounced erosions (a “puncture” symptom) in the subchondral zone of the bone, most often in the first metatarsophalangeal joint and in the phalanges of the fingers, but it is also possible in other joints. Periarticular osteoporosis is not typical.
Diagnostic criteria. The presence of characteristic crystalline urates in the joint fluid and/or. Tophi (proven), containing crystalline urates, confirmed chemically or by polarization microscopy. The presence of 6 of the 12 signs listed below: .. More than one attack of acute arthritis in history.. Inflammation of the joint reaches a maximum on the first day of the disease.. Monoarthritis.. Hyperemia of the skin over the affected joint.. Swelling and pain in the first metatarsus - phalangeal joint.. Unilateral damage to the first metatarsal-phalangeal joint. Unilateral damage to the joints of the foot. Suspicion of tophi. Hyperuricemia. Asymmetric swelling of the joints (radiography). Subcortical cysts without erosions (radiography). Negative results on bacteriological examination of synovial fluid.
Differential diagnosis. Infectious arthritis. Pyrophosphate arthropathy. Hydroxyapatite arthropathy. Osteoarthritis. Amyloidosis. Hyperparathyroidism. Rheumatoid arthritis.
Treatment
TREATMENT
General tactics. Diet No. 6 is prescribed. Treatment with anti-gout drugs is carried out for life in case of primary gout; in case of secondary gout, it is carried out depending on the reversibility of the situation that provokes the development of gout. Mode. In the acute period - rest.
Diet. Products, the consumption of which must be excluded.. alcoholic beverages (especially beer).. parenchymal organs of animals (liver, kidneys). Food products, the consumption of which should be limited.. fish (caviar, Baltic herring, sardines, etc.; more than large fish), crustaceans.. meat (veal, pork, poultry, broths)... some vegetables (peas, beans, mushrooms, cauliflower, asparagus, spinach).. Food products that can be consumed without restrictions.. grains (bread, porridge, bran) .. dairy products (milk, sour cream, cheese) .. all fruits and fruit juices .. fats (butter, margarine, cooking fat) .. coffee, tea, chocolate. most vegetables (potatoes, lettuce, cabbage, tomatoes, cucumbers, pumpkin, onions, carrots, beets, radishes, celery) .. sugar (but: causes weight gain!) .. spices.
Drug treatment
. Tactics for asymptomatic hyperuricemia are mainly observational. The level of uric acid excretion is examined. If it is within the normal range, it is rational to limit yourself to dietary recommendations. According to some researchers, when the normal excretion of uric acid is exceeded, it is necessary to prescribe allopurinol, but the advantage of using this drug over non-drug management of the patient has not been shown (due to the possibility of side effects from treatment, as well as its high cost).
. In the treatment of acute gouty arthritis, rest and cool wraps are very important. Colchicine plays an important role, prescribed 0.5 mg every hour until the arthritis subsides, or until side effects (vomiting, diarrhea) appear, but not less than 6-8 mg/day . To treat an acute attack of gout, colchicine is used for no more than a day.
. NSAIDs (indomethacin, ibuprofen, naproxen, piroxicam, but not salicylates) are usually used in large doses and for a short course (2-3 days). Particular caution should be exercised in case of concomitant diseases of the liver and kidneys, especially in elderly patients.
. The introduction of GC into the joint cavity in acute gouty arthritis is dangerous due to the possible presence of unrecognized septic arthritis, which debuted under the guise of gout or against its background. In addition, extreme pain in the joint due to gout makes any manipulation difficult.
. Uricostatic and uricosuric drugs are not used during an acute attack, since any fluctuations in the concentration of urate in the blood can prolong an attack of gout.
. With reduced urate excretion, preserved renal function and the absence of urinary stones, it is possible to use both uricosuric and uricostatic agents. These properties are combined by allopurinol + benzbromarone, taken 1 tablet 1 time per day. Probenecid, proposed in foreign guidelines for uricostatic purposes, is not registered in the Russian Federation. Allopurinol is considered a generally accepted uricostatic (i.e., blocking urate production) drug. Allopurinol is prescribed at a starting dose of 100 mg/day, followed by a gradual increase in dose to 300 mg/day over 3-4 weeks. If the GFR is reduced to 30-60 ml/min, the dose of allopurinol should not exceed 100 mg/day, and if the GFR is 60-90 ml/min, it should not exceed 200 mg/day.
. In cases of increased uric acid excretion in urine and/or gouty kidney damage, allopurinol is preferred. In the first weeks of allopurinol therapy in such patients, the use of agents that increase the solubility of uric acid in urine is indicated.
. In case of secondary gout against the background of hematological or oncological diseases during the period of cytotoxic or radiation therapy, allopurinol remains the treatment of choice.
The prognosis is favorable with early recognition and adequate treatment. Prognostically unfavorable factors: development of the disease before the age of 30 years, persistent hyperuricemia over 0.6 mmol/l, persistent hyperuricosuria over 1100 mg/day, the presence of urolithiasis in combination with a urinary tract infection, progressive nephropathy, especially in combination with diabetes and arterial hypertension hypertension. Hyperuricemia is a predictor of MI and death in patients with hypertension and congestive heart failure.
Age characteristics. Children and adolescents: the onset of the disease in this age group indicates the presence of inborn errors of metabolism. Elderly people: gout is usually associated with taking drugs. Premenopausal women rarely get sick.
ICD-10. M10 Gout
Application. Familial calcium gout exists in two forms (*118600, 5p, CCAL1 gene, ; chondrocalcinosis with early manifestation of osteoarthritis, *600668, 8q, CCAL2 gene, ). Clinically: arthropathy, acute intermittent arthritis, ankylosis of joints, chondrocalcinosis. Laboratory findings: calcium pyrophosphate crystals in the synovial fluid with normal serum calcium levels, decreased pyrophosphohydrolase activity in the synovial fluid. Synonyms: limited calcinosis, calcium pyrophosphate storage disease, familial articular chondrocalcinosis.
ICD-10. M11.1 Hereditary chondrocalcinosis.
