Diagnosis of gout

Gout

Gout

Gout - rheumatic pathology caused by the deposition of crystals of uric acid salts - urate in the joints, then in the kidneys. The gout clinic is characterized by recurrent and progressive attacks of arthritis with intense pains and the formation of tofusi - gouty nodules, leading to deformity of the joints. In the future, the kidneys are affected, urolithiasis and kidney failure may develop. For the diagnosis of gout, synovial fluid is studied for the presence of urates, X-ray examination of the affected joints. Treatment of gout is aimed at stopping inflammation( NSAIDs, glucocorticoids), reducing the level of uric acid in the blood, normalizing nutrition.

Gout

At the heart of the pathogenesis of gout are metabolic disorders caused by a violation of the regulation of purine metabolism in the body and leading to the accumulation of uric acid and its derivatives - acid urate salts. Increased concentration of uric acid( hyperuricemia) in blood plasma and urate deposition is a consequence of their increased synthesis and decrease in urinary excretion. Urine microcrystals accumulate in the articular cavities with the development of gouty inflammation, as well as in the kidneys, causing nephropathy.

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Gout usually affects patients after 40 years, while in men it is detected 20 times more often than in women.

Gout classification

In the gout clinic, there are different renal, metabolic and mixed forms. The renal form of gout is characterized by a decrease in the excretion of uric acid, the metabolic - by the excess of its formation;a mixed form combines moderate disorders of synthesis and removal of uric acid from the body.

Depending on the reasons leading to the development of the disease, gout may be primary or secondary. Primary gout is often due to genetic defects and hypofunction of enzymes involved in the exchange of purines and excretion of urinary salts. Gout development factors include excessive and monotonous eating patterns, increased consumption of meat and alcohol, and a low-activity lifestyle. Secondary gout is a consequence of other diseases - renal pathology with a violation of their functions, blood diseases( leukemia, lymphoma, polycythemia), psoriasis, drug therapy with cytostatics, saluretic drugs and other drugs.

The clinical classification distinguishes seven forms of gout flow: a typical( classic) attack of acute gouty arthritis, polyarthritis for infectious-allergic type, subacute, rheumatoid-like, pseudo-reflagious, periarthritic and malosymptomatic variants.

Symptoms of gout

In the gout clinic, there are 3 phases: premorbid, intermittent and chronic.

The premorbid phase is characterized by asymptomatic uricemia and is not yet a gout. At the laboratory level, hyperuricemia is detected in 8-14% of adults. The intermittent phase of gout is characterized by episodes of attacks of acute arthritis, alternating with asymptomatic periods. To the manifestations of chronic gout form the formation of gouty nodules( tofusov), chronic course of gouty arthritis, extraarticular manifestations in the form of kidney damage( in 50-70% of clinical cases).

A classic attack of acute gouty arthritis develops in 50-80% of patients. Typically a sudden start, more often at night. The primary attack of gout is often provoked by alcohol, fatty foods, trauma, hypothermia. The attack of gout is characterized by severe pain in the area of ​​the metatarsophalangeal joint of the first toe, febrile syndrome, swelling of the joint, gloss and hyperemia of the skin above it, a violation of the function of the joint. After 3-10 days, the attack of gout subsides with the disappearance of all signs and the normalization of functions. Repeated gouty attack can develop after several months and even years, but each time the intervals between attacks are shortened. In men, the primary attack of gout occurs more often as a monoarthritis with lesion of the foot joints, in women - oligo- and polyarthritis involving the joints of the hand.

Polyarthritis for infectious-allergic type in gout develops in 5% of patients. This form of gout is characterized by migraine pain in multiple joints, rapid regression of signs of inflammation, as in the case of the clinic of infectious-allergic polyarthritis.

The subacute variant of the gout current is characterized by the typical localization of pain in the first metatarsophalangeal joint and moderately expressed signs of lesion. In subacute gout in young patients, the development of mono- or oligoarthritis of medium and large joints is possible.

The rheumatoid-like form of gout is distinguished by primary interest in the joints of the hands in the form of mono- or oligoarthritis.

In pseudo-reflux-type gout, monoarthritis of various locations with inflammation of the joint and paranasal tissues, fever are observed. At the clinic, this option resembles the course of phlegmon or acute arthritis.

Malosymptomnoe variant of the gout current is characterized by poorly expressed, worn out symptoms - a small pain, weak flushing of the skin in the affected area.

For the periarthritic form of gout, the lesion of the bursa and tendons( often calcaneal) is prone to damage to the joints. In the future, the phenomena of chronic gouty polyarthritis with lesions of the joints of the legs, their defoguration and stiffness;deformation of articular tissues, bony proliferation;contractures, a crunch in the knee and ankle joints, incomplete dislocation of the fingers. Against this background, gout attacks continue with the possible development of gouty status - non-subsiding exacerbation of arthritis with chronic inflammation of the parasynthetic tissues due to their infiltration with salts. As a result of severe gout attacks, patients lose their ability to work and physical activity.

With prolonged anamnesis of gout( longer than 5-6 years) and hyperuricemia of high degree, there are specific signs - tofusi or gouty nodules, which are a cluster of urate crystals in soft tissues. Favorite sites of tofus locate are the ears, subcutaneous tissue of forearms, elbows, fingers, feet, legs, thighs. During attacks of gout, tofu can be opened with an outflow of whitish discharge.

Complications of gout

Hyperuricemia and accumulation of urate salts with gout leads to their deposition in the kidneys with the development of nephropathy;Gouty nephritis, characterized by proteinuria, microhematuria, cylindruria;arterial hypertension with the subsequent transition to chronic renal failure.

In 40% of patients there is a development of urolithiasis with renal colic at the height of a gout attack, complications in the form of pyelonephritis.

Diagnosis of gout

Patients with suspected gout are recommended to consult a rheumatologist and urologist.

General clinical analysis of blood outside the gouty attack is not changed;in the period of attack there is a neutrophilic shift to the left, an increase in ESR.A biochemical blood test with exacerbation of gout reveals an increase in uric acid, fibrin, seromucoid, sialic acids, haptoglobin, γ- and α2-globulins.

On radiography of joints, characteristic changes are revealed in chronic gouty polyarthritis. Radiological picture reveals the presence of osteoporosis, against which background the centers of enlightenment in the region of epiphyses and joints up to 2-3 cm in size are determined;with a deep neglect of the process - the destruction of the bony epiphyses with their replacement by the accumulation of urate masses. Specific signs of gout on radiographs are determined after 5 years from the manifestation of the disease.

To collect the joint fluid, puncture the joint. Microscopic analysis of synovial fluid in gout shows the presence of microcrystals of sodium urate in it. In the study of punctate tofusov crystals of uric acid are found. During ultrasound of the kidneys, urate calculi are determined.

Diagnostic gout markers are:

  • microcrystalline urates in the synovial fluid;
  • laboratory-confirmed tofusi with the deposition of crystalline urates;
  • presence of at least six of the following signs: a history of more than one acute attack of arthritis;maximum signs of inflammation of the joint in the acute phase;redness of the skin over the inflamed joint;monoarticular type of lesion;pain and swelling of the I metatarsophalangeal joint on one side;one-sided nature of the defeat of the arch of the foot;tofus-like nodules;asymmetrical swelling of the joint;hyperuricemia;X-ray-detectable subcortical cysts without erosion;lack of growth of microflora in joints of articular fluid.

Treatment of gout

The main principle of gout therapy is to control the content of uric acid by suppressing its production and accelerating excretion from the body.

A diet is prescribed that excludes consumption of fish and meat broths, meat of animals, kidneys, liver, lungs, alcohol. The diet includes a restriction on legumes and vegetables( beans, peas, beans, spinach, sorrel, radish, eggplant, asparagus, cauliflower), mushrooms, caviar, some fish species( sardines, Baltic herring, etc.).With gout, the calorie requirement is met by carbohydrate food, so patients should control their weight. In moderation, eggs, cereals, lean fish, lamb, beef can be eaten. With gout it is required to limit the salt load and intake of a sufficient volume of liquid( up to 3 liters per day).

The medical approach to gout therapy is aimed at arresting acute gouty attacks, their prevention in the future, prevention of urate deposition in the joints and kidneys.

For the reduction of gout attacks, NSAIDs( indomethacin), vegetable alkaloids( colchicine), local ointments and gels are used. As antiresidivnoy therapy for gout is appointed colchicine in small doses or antihyperuricemic drugs. The goal of treating gout is to reduce the concentration of uric acid in the blood 2 times lower than the norm required for dissolving urate crystals. To activate the excretion of uric acid, uricosuric drugs are prescribed: pro-benefic, sulphinpyrazone, azapropion, benzbeteron. The means inhibiting the production of uric acid include milurite, allopurinol.

With an atypical form of gout that occurs with the accumulation of intra-articular effusion, its puncture evacuation is performed.

Conducting sessions of extracorporeal hemocorrection is aimed at reducing the concentration of uric acid and urate salts, suppressing inflammation and reducing the dosage of the drugs taken.

Physiotherapy and spa treatment for gout is performed in the remission phase. Conducting the UFO area of ​​the joint in the acute phase in a number of cases helps to stop the onset of gout.

Prognosis for gout

Timely recognition and initiation of rational treatment gives predictably favorable results. The factors aggravating the prognosis of the gout are young( up to 30 years) age, a combination of urolithiasis and urinary tract infections, weighed somatic anamnesis( diabetes mellitus, arterial hypertension), progression of nephropathy.

Prevention of gout

The need for gout prevention should be considered in chemotherapy as well as in patients with the threat of decay and necrosis of the tumor. From the first day of the chemotherapy course, the appointment of hypo-ricerchemic drugs( allopurinol) is necessary.

Prevention of new exacerbations of gout depends on compliance with water-salt regime, diet, body weight control. In the presence of relatives suffering from gout, other family members are advised to monitor the level of uric acid.

krasotaimedicina.ru

Gout

Gout

Gout is a rheumatic pathology caused by the deposition of crystals of uric acid salts - urates in the joints, then in the kidneys. The gout clinic is characterized by recurrent and progressive attacks of arthritis with intense pains and the formation of tofusi - gouty nodules, leading to deformity of the joints. In the future, the kidneys are affected, urolithiasis and kidney failure may develop. For the diagnosis of gout, synovial fluid is studied for the presence of urates, X-ray examination of the affected joints. Treatment of gout is aimed at stopping inflammation( NSAIDs, glucocorticoids), reducing the level of uric acid in the blood, normalizing nutrition.

Gout

The pathogenesis of gout is caused by metabolic disorders caused by a violation of the regulation of purine metabolism in the body and leading to the accumulation of uric acid and its derivatives - acid urate salts. Increased concentration of uric acid( hyperuricemia) in blood plasma and urate deposition is a consequence of their increased synthesis and decrease in urinary excretion. Urine microcrystals accumulate in the articular cavities with the development of gouty inflammation, as well as in the kidneys, causing nephropathy.

Gout usually affects patients after 40 years, while in men it is detected 20 times more often than in women.

Gout classification

In the gout clinic, renal, metabolic and mixed forms are distinguished. The renal form of gout is characterized by a decrease in the excretion of uric acid, the metabolic - by the excess of its formation;a mixed form combines moderate disorders of synthesis and removal of uric acid from the body.

Depending on the reasons leading to the development of the disease, gout may be primary or secondary. Primary gout is often due to genetic defects and hypofunction of enzymes involved in the exchange of purines and excretion of urinary salts. Gout development factors include excessive and monotonous eating patterns, increased consumption of meat and alcohol, and a low-activity lifestyle. Secondary gout is a consequence of other diseases - renal pathology with a violation of their functions, blood diseases( leukemia, lymphoma, polycythemia), psoriasis, drug therapy with cytostatics, saluretic drugs and other drugs.

The clinical classification distinguishes seven forms of gout flow: a typical( classic) attack of acute gouty arthritis, polyarthritis of the infectious-allergic type, subacute, rheumatoid-like, pseudo-reflagious, periarthritic and malosymptomatic variants.

Symptoms of gout

In the gout clinic, there are 3 phases: premorbid, intermittent and chronic.

The premorbid phase is characterized by asymptomatic uricemia and is not yet a gout. At the laboratory level, hyperuricemia is detected in 8-14% of adults. The intermittent phase of gout is characterized by episodes of attacks of acute arthritis, alternating with asymptomatic periods. To the manifestations of chronic gout form the formation of gouty nodules( tofusov), chronic course of gouty arthritis, extraarticular manifestations in the form of kidney damage( in 50-70% of clinical cases).

A classic attack of acute gouty arthritis develops in 50-80% of patients. Typically a sudden start, more often at night. The primary attack of gout is often provoked by alcohol, fatty foods, trauma, hypothermia. The attack of gout is characterized by severe pain in the area of ​​the metatarsophalangeal joint of the first toe, febrile syndrome, swelling of the joint, gloss and hyperemia of the skin above it, a violation of the function of the joint. After 3-10 days, the attack of gout subsides with the disappearance of all signs and the normalization of functions. Repeated gouty attack can develop after several months and even years, but each time the intervals between attacks are shortened. In men, the primary attack of gout occurs more often as a monoarthritis with lesion of the foot joints, in women - oligo- and polyarthritis involving the joints of the hand.

Polyarthritis for infectious-allergic type in gout develops in 5% of patients. This form of gout is characterized by migraine pain in multiple joints, rapid regression of signs of inflammation, as in the case of the clinic of infectious-allergic polyarthritis.

The subacute variant of the gout current is characterized by a typical localization of pain in the first metatarsophalangeal joint and moderately expressed signs of lesion. In subacute gout in young patients, the development of mono- or oligoarthritis of medium and large joints is possible.

The rheumatoid-like form of gout is distinguished by primary interest of the joints of the hands in the form of mono- or oligoarthritis.

In pseudo-reflux-type gout, monoarthritis of various locations with inflammation of the joint and paranasal tissues, fever is observed. At the clinic, this option resembles the course of phlegmon or acute arthritis.

Malosymptomny variant of the gout current is characterized by a mild, worn out symptomatology - a small pain, weak flushing of the skin in the affected area.

For the periarthritic form of gout, lesions of the burs and tendons( often calcaneal) are common, with joint joints. In the future, the phenomena of chronic gouty polyarthritis with lesions of the joints of the legs, their defoguration and stiffness;deformation of articular tissues, bony proliferation;contractures, a crunch in the knee and ankle joints, incomplete dislocation of the fingers. Against this background, gout attacks continue with the possible development of gouty status - non-subsiding exacerbation of arthritis with chronic inflammation of the parasynthetic tissues due to their infiltration with salts. As a result of severe gout attacks, patients lose their ability to work and physical activity.

With prolonged anamnesis of gout( longer than 5-6 years) and hyperuricemia of high degree, there are specific signs - tofusi or gouty nodules, which are a cluster of urate crystals in soft tissues. Favorite sites of tofus locate are the ears, subcutaneous tissue of forearms, elbows, fingers, feet, legs, thighs. During attacks of gout, tofu can be opened with an outflow of whitish discharge.

Complications of gout

Hyperuricemia and accumulation of urate salts with gout leads to their deposition in the kidneys with the development of nephropathy;Gouty nephritis, characterized by proteinuria, microhematuria, cylindruria;arterial hypertension with the subsequent transition to chronic renal failure.

In 40% of patients there is a development of urolithiasis with renal colic at the height of a gout attack, complications in the form of pyelonephritis.

Diagnosis of gout

Patients with suspected gout are advised by a rheumatologist and urologist.

General clinical analysis of blood outside the gouty attack is not changed;in the period of attack there is a neutrophilic shift to the left, an increase in ESR.A biochemical blood test with exacerbation of gout reveals an increase in uric acid, fibrin, seromucoid, sialic acids, haptoglobin, γ- and α2-globulins.

On radiography of joints, characteristic changes are revealed in chronic gouty polyarthritis. Radiological picture reveals the presence of osteoporosis, against which background the centers of enlightenment in the region of epiphyses and joints up to 2-3 cm in size are determined;with a deep neglect of the process - the destruction of the bony epiphyses with their replacement by the accumulation of urate masses. Specific signs of gout on radiographs are determined after 5 years from the manifestation of the disease.

For articular fluid, joint puncture is performed. Microscopic analysis of synovial fluid in gout shows the presence of microcrystals of sodium urate in it. In the study of punctate tofusov crystals of uric acid are found. During ultrasound of the kidneys, urate calculi are determined.

Diagnostic gout markers are:

  • microcrystalline urates in the synovial fluid;
  • laboratory-confirmed tofusi with the deposition of crystalline urates;
  • has at least six of the following signs: a history of more than one acute attack of arthritis;maximum signs of inflammation of the joint in the acute phase;redness of the skin over the inflamed joint;monoarticular type of lesion;pain and swelling of the I metatarsophalangeal joint on one side;one-sided nature of the defeat of the arch of the foot;tofus-like nodules;asymmetrical swelling of the joint;hyperuricemia;X-ray-detectable subcortical cysts without erosion;lack of growth of microflora in joints of articular fluid.

Treatment of gout

The main principle of gout therapy is to control the content of uric acid by suppressing its production and accelerating excretion from the body.

A diet is prescribed that excludes consumption of fish and meat broths, meat of animals, kidneys, liver, lungs, alcohol. The diet includes a restriction on legumes and vegetables( beans, peas, beans, spinach, sorrel, radish, eggplant, asparagus, cauliflower), mushrooms, caviar, some fish species( sardines, Baltic herring, etc.).With gout, the calorie requirement is met by carbohydrate food, so patients should control their weight. In moderation, eggs, cereals, lean fish, lamb, beef can be eaten. With gout it is required to limit the salt load and intake of a sufficient volume of liquid( up to 3 liters per day).

The medical approach to gout therapy is aimed at arresting acute gouty attacks, their prevention in the future, prevention of urate deposition in the joints and kidneys.

For the reduction of gout attacks, NSAIDs( indomethacin), vegetable alkaloids( colchicine), local ointments and gels are used. As antiresidivnoy therapy for gout is appointed colchicine in small doses or antihyperuricemic drugs. The goal of treating gout is to reduce the concentration of uric acid in the blood 2 times lower than the norm required for dissolving urate crystals. To activate the excretion of uric acid, uricosuric drugs are prescribed: pro-benefic, sulphinpyrazone, azapropion, benzbeteron. The means inhibiting the production of uric acid include milurite, allopurinol.

At an atypical form of gout, which proceeds with the accumulation of intra-articular effusion, its puncture evacuation is performed.

Conducting sessions of extracorporeal hemocorrection is aimed at reducing the concentration of uric acid and urate salts, suppressing inflammation and reducing the dosage of the drugs taken.

Physiotherapy and spa treatment for gout is performed in the remission phase. Conducting the UFO area of ​​the joint in the acute phase in a number of cases helps to stop the onset of gout.

Prognosis for gout

Timely recognition and initiation of rational treatment gives predictably favorable results. The factors aggravating the prognosis of the gout are young( up to 30 years) age, a combination of urolithiasis and urinary tract infections, weighed somatic anamnesis( diabetes mellitus, arterial hypertension), progression of nephropathy.

Prevention of gout

The need for gout prevention should be considered in chemotherapy, as well as in patients with the threat of decay and necrosis of the tumor. From the first day of the chemotherapy course, the appointment of hypo-ricerchemic drugs( allopurinol) is necessary.

Prevention of new exacerbations of gout depends on compliance with water-salt regime, diet, body weight control. In the presence of relatives suffering from gout, other family members are advised to monitor the level of uric acid.

krasotaimedicina.ru

GOVERNMENT

GOU VPO TVERSKAYA GMA ROSZDRAVA

Department of Faculty Therapy

Head of the department is Professor V.V.Chernin

PODAGRA

Supervisor: Professor of the Department Julia G.S.

Tver 2006

PURPOSE OF THE SESSION: As a result of studying the topic, the student must learn to diagnose gout with the indication of a specific form, outline a survey plan, make differential diagnosis and choose the tactics of treating a patient with this disease.

OBJECTIVES:

As a result of mastering the topic, the student must know :

  • Gout definition;

  • Metabolism of uric acid in the body;

  • Epidemiology of gout;

  • Methods of laboratory and instrumental gout diagnostics;

  • Differential diagnostic criteria for gout.

Based on the received data, should be able to :

  • Collect complaints and anamnesis in patients with gout;

  • Conduct a clinical examination of the patient;

  • Interpret the results of additional survey methods;

  • To diagnose a patient with gout;

  • Carry out a differential diagnosis with other diseases;

  • Prescribe treatment;

  • Give advice on the prevention of disease.

BASIC TERMS: gout, uric acid, uric acid metabolism, uric acid clearance, sodium urate, hyperuratemia, hyperuria, acute arthritis attack, visceral gout, gouty nephropathy, tofusi, gouty condition, uricosuricas, uricostatics, basic gout therapy.

INFORMATION ON THEME

Gout is a disease that is based on a violation of purine metabolism with excess deposition of uric acid salts in the tissues, which leads to damage to the joints, kidneys and other internal organs.

Prevalence of gout is 0.1%( in the US - 1.5%).Among rheumatic diseases, it accounts for up to 5%.Mostly men are sick at the age of 35-60 years. Gout in women in the general group of patients is 2-3%, develops after the onset of menopause and proceeds relatively easily, less often in childbearing age it is hard with joint and kidney damage.

Classification of gout
  1. On the etiology: 1.1.Primary.1.2.By secondary pathway: 2.1.Metabolic.2.2.Renal.2.3.Mixed.

  2. Periods of development: 3.1.Premorbid.3.2.Intermittent.3.3.Chronic gout.

  3. Current: 4.1.Lung.4.2 The average gravity.4.3.Heavy.

Primary gout( idiopathic, essential) is an independent disease. Characterized as a hereditary and familial anomaly of purine metabolism, determined by several genes.

Secondary gout is a manifestation of other diseases( myeloleukemia, psoriasis, CRF, hemoglobinopathies, congenital heart diseases with erythrocytosis) or consequence of the use of medications( riboxin, cytostatics, saluretics).

The metabolic type is dominated by the synthesis of uric acid. It occurs in 60% of patients.

In renal type( 10% of patients) uric acid excretion is decreased.

Mixed type( 30% of patients) moderately increased the synthesis of uric acid and decreased its excretion by the kidneys.

Urinary acid exchange

In humans, uric acid is the final product of cleavage of purines. Stocks of uric acid in the body are in the norm 1000 mg at a refresh rate of 650 mg / day. The source of uric acid formation are purine compounds that come with food or are formed in the body during the exchange of nucleotides. Urinary acid is secreted mainly by the kidneys. Therefore, it is important to know its clearance - the amount of blood that can be cleared in the kidneys from excess uric acid. In plasma, uric acid is contained in the form of free urate sodium.

In healthy people, the uric acid clearance is 6-9 ml / min, the daily uraturia is 1.8-3.6 mMol( 300-600 mg).Normal indicators of uric acid blood: for men 0,3-0,42 mMol / l, for women 0,24-0,36 mMol / l.

The content of uric acid above the norm is regarded as hyperuricemia. For a long time, hyperuricemia may be asymptomatic and only a few years later the clinical picture of gout develops.

There are 3 types of hyperuricemia similar to types of gout:

  1. metabolic - high uraturia and normal uric acid clearance;

  2. renal - low uraturia and uric acid clearance;

  3. mixed - normal or decreased urethra and normal uric acid clearance.

Etiology of gout

Primary gout often reveals genetically determined defects in enzymes involved in the metabolism of purines: a decrease in the activity of hypoxanthine-guanine phosphoribosyltransferase( GGFRT) and adenine phosphoribosyl pyrophosphate synthetase, which leads to an increase in the synthesis of uric acid. With a genetic defect, there are also disorders from the enzyme systems of the kidneys, where excretion of uric acid takes place. The deficiency or absence of most enzymes with gout is associated with sex and is mainly found in men.

The development of gout is facilitated by:

  • excess food( prolonged overeating, monotonous meat food);

  • use of alcoholic beverages( especially beer, dry grape wines);

  • sedentary lifestyle;

  • sharp dehydration.

The most common cause of secondary gout is kidney disease with kidney failure, blood diseases accompanied by cell decay and hyperuricemia, extensive psoriasis due to the renewal of epidermal cells and the formation of purines from the cell nucleus, the taking of certain medications.

Pathogenesis of gout
At the heart of the disease is a violation of the metabolism of uric acid. There are 3 phases of pathogenesis:
  1. hyperuricemia and urate accumulation in the body;

  2. deposition of urate in tissues;

  3. acute gouty inflammation.

Due to the increased biosynthesis of urates and a decrease in urinary excretion, hyperuricemia and accumulation of urate in the body occur. This leads to increased excretion of uric acid by the kidneys and the deposition of urates in the tissues. The deposition in the articular cavity of urate microcrystals induces acute gouty inflammation by activation of Hageman factor, the components of the compliment, kinins. Increases vascular permeability, the influx of neutrophils. Phagocytosis of the crystals is accompanied by the release of lysosomal enzymes, resulting in the development of local inflammation. The urate crystals are also deposited in the interstitium of the kidneys, which leads to the development of gouty nephropathy.

The clinical picture of gout

In the the premorbid period develops gout and there is only hyperuricemia that proceeds asymptomatically. In the , the intermittent period causes an alternation of acute attacks of arthritis with asymptomatic interstitial gaps. To chronic gout is characterized by tofus, chronic gouty arthritis, extraarticular manifestations of gout.

The onset of the disease has 7 options:

  1. A typical acute attack( classic).

  2. Subacute form is characterized by minor pain and mild exudative phenomena.

  3. Rheumatoid-like variant with primary lesion of small joints of wrist, wrist joint or mono-oligoarthritis in protracted flow.

  4. Pseudophlhematose form is manifested by monoarthritis with pronounced inflammatory phenomena in the joint and surrounding tissues with high body temperature, chills, leukocytosis, increased ESR.The clinic is similar to phlegmon or acute infectious arthritis.

  5. Gout with volatile pain can debut as a migrating polyarthritis with rapid reverse development of inflammatory phenomena, which resembles an infectious allergic polyarthritis.

  6. Malosymptomatic form( asthenic) occurs with an erased clinic and subacute flow( a small pain without swelling, occasionally mild hyperemia).

  7. Periartritic form with localization of the process in tendons and bursa in intact joints.

The first clinical manifestation of gout is an attack of acute arthritis , developing suddenly, amid overall health. Sometimes prodromal phenomena can occur for 1-2 days: general malaise, chills, unpleasant sensations in the joint, indigestion, insomnia. Provoking factors of an acute attack of gout are often a violation of diet( overeating, alcohol abuse), trauma and microtrauma( long walking, narrow shoes), mental and physical stress, hypothermia, infection( flu, sore throat), changing weather, taking diuretics or other medications, increasing the content of uric acid.

The classic clinical picture of an acute gouty attack is very characteristic. Suddenly, usually at night, there are very severe pains, most often in the metatarsophalangeal joint of the big toe, less often in the joints of the arch of the foot, ankle, knee joint, very rarely in the wrist, elbow, joints of the hand, spine. Hip joints are always intact. The affected joint swells noticeably, becomes hot, with bright skin flushing( dark red or bluish-purple).These phenomena reach a maximum within a few hours, accompanied by fever, chills, leukocytosis, increased ESR.Excruciating pains intensify at the slightest contact of the diseased joint with the blanket, causing complete immobility of the limb. After 5-6 days, signs of inflammation gradually subside, and in the next 5-10 days, the function of the joint is fully restored, blood changes are normalized. The patient feels completely healthy.

Subsequently, acute attacks are repeated with typical symptoms with no symptoms of arthritis between the attacks. As the disease progresses, interictal periods decrease, the duration of exacerbations increases. Monoarticular damage, characteristic of the first years of the disease, is replaced by the phenomena of migrating polyarthritis.

After 3-5 years of the presence of the disease, nodules specific for gout( tofusi ) appear, representing urate deposits surrounded by connective tissue. They are mainly localized on the auricles, elbows, feet, fingers of the hands, in the calcaneal tendon, in the bags of the elbow joints, on the extensor surface of the forearms, hips, shins, on the forehead, in the region of the cartilaginous septum of the nose. Nodules have various sizes, painless and often unnoticeable to the patient. Sometimes tofusi soften, spontaneously open with the formation of fistulas, through which a whitish mass( microscopically consisting of sodium uric acid crystals) is released. Fistulas rarely become infected, which is due to the bactericidal action of the contents. Tofusi are an indicator of the duration and severity of the disturbance of uric acid metabolism.

Sustained changes in joints, the phenomenon of chronic polyarthritis, gradually degeneration of joints, limitation of mobility, deformation due to nodular deposits, bone proliferation, subluxation of fingers, contractures, rough crunching are gradually increasing. Ankylosis develops extremely rarely. Such patients move with difficulty, their ability to work is reduced or lost.

Against the background of chronic gouty arthritis, acute attacks of gout continue to occur. The most severe variety of their gouty status is - a continuous exacerbation of arthritis with a chronic inflammatory reaction of surrounding tissues caused by massive urate infiltration.

In the clinical picture of gout there is a lesion of other organs and systems - visceral gout. The kidneys are most often affected, the risk of affecting the heart, vessels with the development of arterial hypertension and coronary insufficiency is significant. Gout contributes to the formation of atherosclerosis, obesity, diabetes, as well as thrombosis, phlebitis, conjunctivitis, elimination gastritis, pharyngitis, etc.

Involvement in the kidney process is frequent and prognostically serious. At the heart of their defeat lies the deposition of urates in the interstitial tissue. The deposits are focal in nature, located in the interstitial tissue, the lumen of the tubules. An inflammatory reaction develops around them. There is a thickening of the walls of capillary capillaries, cell proliferation, sclerosis of glomeruli, hyaline deposits. "Gouty kidney" or gouty nephropathy is a collective concept that includes the entire kidney pathology in gout: tophus in the parenchyma of the kidney, urate stones, interstitial nephritis, glomerulosclerosis, angiosclerosis with the development of nephrosclerosis, chronic renal failure.

Gouty nephropathy is manifested by proteinuria, cylindruria, leukocyturia, attacks of renal colic, microhematuria, isostenuria, arterial hypertension. It should be remembered that gouty interstitial nephritis is more often asymptomatic, progresses slowly, is later diagnosed. An early manifestation of renal failure is a decrease in the specific density of urine.

Variants of gout current

  1. Light, when attacks of arthritis are repeated only 1-2 times a year and capture no more than two joints, there are no signs of joint destruction on the roentgenogram, there is no kidney damage, no tofus or there are individual and small ones.

  2. Medium-sized with a frequency of seizures 3-5 times a year, a lesion of 2-4 joints, moderately pronounced bone-articular destruction, multiple small tophi and the presence of kidney stone disease.

  3. Heavy with a frequency of seizures more than 5 per year, multiple joint lesions, with severe bone-joint destruction, multiple bone tofusias and the presence of severe nephropathy.

Diagnostic criteria for gout

  1. Presence of characteristic crystalline urates in articular fluid and / or

  2. Presence of tofuses( proven) containing crystalline urates, confirmed by chemical or polarization microscopy, and / or

  3. . Presence of 6 of 12 presented features:

  1. More than one acute attack of arthritis in a history of

  2. Maximuminflammation of the joint as early as the first day

  3. Monoarticular nature of arthritis

  4. Hyperemia of the skin over the affected joint

  5. Swelling or pain localized in the Iplus-phalanx joint

  6. One-sidedlesions of the joints of the foot

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Gout: causes, signs, diagnostics and prevention

  • Prevention of gout

One of the most common articular diseases is gout. This ailment is formed mainly in middle-aged men, but women also face it quite often. Completely get rid of such a disease is quite difficult, and sometimes completely impossible. Meanwhile, knowing how gout is manifested, and what activities help to reduce its symptoms, the patient can feel comfortable and not remember the presence of this disease.

IMPORTANT TO KNOW!Doctors are dumbfounded! The pain in the joints is FOREVER!Just before bedtime. .. Read on - & gt;

Gout: development process

In the official medicine, gout is also called gouty arthritis. This ailment occurs, as a rule, due to the accumulation in the joints of salts of uric acid. In a normal healthy state, it is excreted from the body through the kidneys. However, in the case of incomplete excretion or increased accumulation, this acid turns into special crystals that settle in different joints.

Moreover, these deposits can be concentrated in the skin, forming a kind of nodules. And remaining in the kidneys, they cause the formation of stones. This excessive concentration of salts causes terrible pain and inflammation. Meanwhile, the high content of uric acid does not always indicate the development of gout, so the appeal to a specialist is still inevitable.

In the vast majority of cases, gout affects the joints on the toes. However, this disease can affect and parts of the body, such as knees, elbows, hands and fingers.

Reasons for gout formation

Every disease has its causes of occurrence: gout is no exception. To date, there are several factors that contribute to the development of this disease. Among them the following variants are distinguished:

  • hereditary predisposition;
  • excessive consumption of certain types of food, including a significant amount of meat and fatty foods;
  • alcoholic beverages;
  • strong stresses( physical and emotional);
  • abuse of diuretics, aspirin;
  • is a sedentary lifestyle.

In addition, in gout disease, the causes may be hiding in the presence of other diseases. So, often problems with joints arise against a background of renal failure, as well as in case of ailments associated with blood.

Meanwhile, it is believed that gout is a disease of well-being. After all, overeating often leads to excess body weight, followed by obesity, diabetes and hypertension are added, and finally arthritis arthritis is formed.

Kinds and symptoms of gout

To date, gout is usually classified as acute and chronic. Each species has its own characteristics, knowledge of which allows you to take the necessary measures in time and get rid of unpleasant sensations.

It is usually difficult for a person who is ignorant in medicine to identify the disease from the photo: many of them are gout, although it is fairly clearly depicted, but only a specialist can correctly diagnose it.

Acute gout

Acute progressive gout symptoms are mild, and in some cases it is completely asymptomatic and only manifests itself at times of painful outbreaks. Thus, is the only vivid manifestation of acute gout - an acute gouty attack. It is important to understand that the longer a given ailment remains without due attention from the patient, the more likely such flashes will occur.

Initially acute gout of joints is accompanied by a sharp change in mood, increased excitability, anxiety, nervousness. In addition, the patient sometimes vomits, his chair changes, heartburn occurs, taste sensations and appetite disappear. Some even have high blood pressure, shortness of breath, and pain in the heart.

The gouty arthrosis itself occurs suddenly. And, as a rule, at night. During such outburst, painful sensations increase gradually and approximately 2-3 hours reach their peak. At such moments the patient is hurt even by the weakest movements, but in the morning discomfort gradually fades.

Usually, the attack is accompanied by chills, fever, strong sweating, high blood pressure and rapid pulse. This condition can last as 2-3 days, and a week. And sometimes all the symptoms of gout go through only a couple of months. A repeated outbreak of the disease usually occurs at least 3 months later, a maximum after 20 years.

Chronic gout

Chronic gout is the next stage in the development of the disease. At this stage, uric acid is converted into specific crystals, which, accumulating, lead to the formation of chronic gouty polyarthritis.

In this case, often to this form of gout is attached to the defeat of the kidneys. The first symptoms of the chronic nature of the disease:

  • crunching when moving;
  • stiffness of the affected joint;
  • pain during exercise.

After the time has elapsed, there is a deformation of those connecting elements where inflammation is concentrated. In addition, the patient becomes quite difficult to move, and in the case of prolonged absence of correct treatment, even a complete loss of working capacity of the affected joint is possible.

With chronic gouty arthritis, certainly, there are certain painful sensations. However, unlike the acute form of the disease in this case, they are not so strong, although they can persecute the patient for several months in a row.

Diagnosis of gout

Gout disease is treated, as a rule, by several specialists. Patients with a suspicion of this ailment are recommended, first of all, to consult a rheumatologist and urologist.

Sometimes it is also necessary to consult a therapist and nephrologist. All these doctors can identify a problem with the joints, for this they send the patient to undergo a special examination.

When a diagnosis of gout blood tests is done by each patient. As a rule, it is sent for delivery of material for general clinical and biochemical research. Depending on the presence of deviations of certain indicators or their absence, the patient is assigned the following diagnostic measures.

The most informative is the result of the analysis of the joint fluid taken from the affected area - puncture. When developing gout, special microcrystals will be found. Also the patient is usually given an ultrasound of the kidneys and a radiograph of the joints.

However, it is worthwhile to know that X-ray images will be informative only in case of a neglected process or in case of chronic gouty polyarthritis. And the specific signs of gout are most often detected only after 5 years from the manifestation of the disease. But modern medicine is at a fairly high level, so timely diagnosing gout is usually not difficult.

Prevention of gout

With gout disease prevention is most often aimed at changing taste habits and lifestyle. First of all, it is necessary to substantially limit the consumption of foods rich in protein.

These include meat, fish, cauliflower, sorrel, legumes, and the like. In addition, it is necessary to completely eliminate alcoholic beverages from the diet, since they inhibit the excretion of uric acid from the body.

It is also recommended to normalize the body weight to improve metabolism and reduce the load on the joints of the legs. However, weight loss should not be sharp, you should lose weight gradually. Otherwise, it is possible to increase the uric acid in the blood, which provokes a gouty crisis.

The following factors are also classified as preventive measures:

  • sufficient fluid intake, but it is desirable that it is ordinary water, and coffee and tea should be better limited;
  • increase in motor activity, and it is more appropriate to engage in those sports that contribute to increasing the level of uric acid excretion from the body;
  • exclusion of nicotine addiction;
  • daily long-term stay in the fresh air.

Moreover, it is recommended to check the level of uric acid 2 times a year, because a slight increase in it usually is not noticed by the patient. However, sooner or later this circumstance becomes the cause of problems with joints.

In any case it is important to understand that gout in a neglected form leads to serious complications of health. It often provokes urolithiasis, cystitis, acute renal failure, wrinkling of the kidneys. Therefore, it is necessary to try to start treatment of this ailment still in the early stages.

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