Gout is a rheumatic pathology caused by the deposition of crystals of uric acid salts – urates in the joints, then in the kidneys. Clinic is characterized by recurrent and progressive attacks of arthritis with intense pain and the formation of tofuses – gouty nodules that lead to joint deformation. In the future, the kidneys are affected, urolithiasis and kidney failure may develop. To diagnose gout, the synovial fluid is examined for the presence of urates, X-ray examination of the affected joints. Treatment is aimed at relieving inflammation (NSAIDs, glucocorticoids), reducing the level of uric acid in the blood, normalizing nutrition.
ICD 10
M10 Gout
Meaning
The pathogenesis is based on 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 – acidic urate salts. The increased concentration of uric acid (hyperuricemia) in the blood plasma and the deposition of urates is a consequence of their increased synthesis and a decrease in urinary excretion. Urate microcrystals accumulate in the articular cavities with the development of gouty inflammation, as well as in the kidneys, causing gouty nephropathy. Gout usually affects patients after 40 years, while in men it is detected 20 times more often than in women.
Classification
In the clinic of disease, renal, metabolic and mixed forms differ. The renal form of gout is characterized by a decrease in uric acid excretion, the metabolic form is characterized by excess of its formation; the mixed form combines moderate violations of the synthesis and removal of uric acid from the body.
Depending on the causes leading to the development of the disease, gout can be primary or secondary. Primary gout is often caused by genetic defects and hypofunction of enzymes involved in the exchange of purines and excretion of urinary salts. The factors of the development of gout include excessive and monotonous nature of nutrition, increased consumption of meat and alcohol, and a low-activity lifestyle. Secondary gout is a consequence of other diseases – kidney pathology with a violation of their functions, blood diseases (leukemia, lymphoma, polycythemia), psoriasis, drug therapy with cytostatics, saluretics and other drugs.
The clinical classification distinguishes seven forms of gout: a typical (classic) attack of acute gouty arthritis, polyarthritis of an infectious-allergic type, subacute, rheumatoid-like, pseudophlegmonous, periarthritic and low-symptom variants.
Symptoms
There are 3 phases of gout in the clinic: premorbid, intermittent and chronic.
The premorbid phase is characterized by asymptomatic uricemia and is not yet gout. At the laboratory level, hyperuricemia is detected in 8-14% of adults. The intermittent phase of gout is characterized by episodes of acute arthritis attacks alternating with asymptomatic periods. The manifestations of the chronic form of gout include the formation of gouty nodules (tofuses), the chronic course of gouty arthritis, extra-articular 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 onset, more often at night. The primary attack of gout is often provoked by alcohol, fatty foods, trauma, hypothermia. An attack of gout is characterized by the sharpest pains in the area of the metatarsophalangeal joint of the 1st toe, febrile syndrome, swelling of the joint, gloss and hyperemia of the skin above it, impaired joint function. After 3-10 days, the gout attack subsides with the disappearance of all signs and normalization of functions. Repeated gouty attack can develop after several months or even years, but each time the intervals between attacks are shortened. In men, the primary attack of gout more often occurs as monoarthritis with damage to the joints of the foot, in women – oligo- and polyarthritis involving the joints of the hand.
Polyarthritis of the infectious-allergic type with gout develops in 5% of patients. This form of gout is characterized by migrating pains in multiple joints, rapid regression of signs of inflammation, as in the case of the clinic of infectious and allergic polyarthritis. The subacute variant of the course of gout is characterized by a typical localization of pain in the first metatarsophalangeal joint and moderately pronounced signs of lesion. With subacute gout, young patients may develop mono- or oligoarthritis of medium and large joints.
The rheumatoid-like form of gout is characterized by the primary interest of the joints of the hands in the form of mono- or oligoarthritis. In the pseudophlegmonous type of gout, monoarthritis of various localization with inflammation of the joint and para-articular tissues, fever are observed. According to the clinic, this option resembles the course of phlegmon or acute arthritis. A low–symptomatic variant of the course of gout is characterized by weakly expressed, erased symptoms – slight pain, mild hyperemia of the skin in the affected area.
The periarthritic form of gout is characterized by damage to the bursae and tendons (more often calcaneal) with preserved joints. In the future, the phenomena of chronic gouty polyarthritis with damage to the joints of the legs, their defiguration and stiffness; deformities of articular tissues, bone growths; contractures, crunching in the knee and ankle joints, incomplete dislocations of the fingers are added. Against this background, gout attacks continue with the possible development of gouty status – an ongoing exacerbation of arthritis with chronic inflammation of the parasarticular tissues due to their infiltration by salts. As a result of severe attacks of gout, patients lose their ability to work and motor activity.
With a long history of gout (longer than 5-6 years) and hyperuricemia of a high degree, specific signs appear – tofuses or gouty nodules, which are an accumulation of urate crystals in soft tissues. The favorite areas of localization of topuses are the auricles, subcutaneous tissue of the forearms, elbows, fingers, feet, shins, thighs. During gout attacks, topuses can be opened with a whitish discharge coming out.
Complications
Hyperuricemia and accumulation of urate salts in gout leads to their deposition in the kidneys with the development of nephropathy; gouty nephritis, characterized by proteinuria, microhematuria, cylindrical; arterial hypertension with subsequent transition to chronic renal failure.
In 40% of patients, the development of urolithiasis with renal colic at the height of a gout attack, complications in the form of pyelonephritis is noted.
Diagnostics
Patients with suspected gout are recommended to consult a rheumatologist and a urologist. The general blood test outside the gouty attack has not been changed; during the attack, there is a neutrophil shift of the leukocyte formula 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.
According to the radiography of the joints, characteristic changes are detected in chronic gouty polyarthritis. The X-ray picture reveals the presence of osteoporosis, against which foci of enlightenment in the area of the epiphyses and joints up to 2-3 cm in size are determined; with deep neglect of the process, destruction of bone epiphyses with their replacement by accumulation of urate masses. Specific signs of gout on radiographs are determined after 5 years from the manifestation of the disease.
To take articular fluid, a joint puncture is performed. Microscopic analysis of synovial fluid in gout shows the presence of sodium urate microcrystals in it. When examining the material obtained by biopsy of tofuses, uric acid crystals are detected. During ultrasound of the kidneys, urate concretions are determined.
Diagnostic markers of gout are:
- microcrystalline urates in synovial fluid;
- laboratory-confirmed topuses with deposition of crystalline urates;
the presence of at least six of the following signs: the presence in the anamnesis of more than one acute attack of arthritis; maximum signs of joint inflammation 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 the one hand; unilateral nature of the lesion of the arch of the foot; tofus-like nodules; asymmetric swelling of the joint; hyperuricemia; radiologically detectable subcortical cysts without erosion; absence of microflora growth during back-seeding of articular fluid.
Treatment
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 the consumption of fish and meat broths, animal meat, kidneys, liver, lungs, alcohol. The diet introduces restrictions on legumes and vegetables (beans, peas, beans, spinach, sorrel, radish, eggplant, asparagus, cauliflower), mushrooms, caviar, some types of fish (sardines, Baltic herring, etc.). With gout, the need for calories is met by carbohydrate foods, so patients should control their weight. In moderation, it is allowed to eat eggs, cereals, lean fish, lamb, beef. With gout, it is necessary to limit the salt load and take a sufficient volume of fluid (up to 3 liters per day).
The medical approach to the treatment of gout is aimed at relieving acute gouty attacks, preventing them in the future, preventing the deposition of urates in the joints and kidneys. NSAIDs (indomethacin), vegetable alkaloids (colchicine), local ointments and gels are used to relieve gout attacks. Colchicine in small doses or antihyperuricemic drugs are prescribed as anti-relapse therapy for gout. The goal of gout treatment is to lower the concentration of uric acid in the blood by 2 times below the norm required for the dissolution of urate crystals. To activate the excretion of uric acid, uricosuric drugs are prescribed – probenecid, sulfinpyrazone, azapropazone, benzbromarone. Allopurinol is one of the agents that inhibit the production of uric acid.
With an atypical form of gout, occurring with an accumulation of intra-articular effusion, its puncture evacuation is performed. Extracorporeal hemocorrection sessions are aimed at reducing the concentration of uric acid and urate salts, suppressing inflammation and reducing the dosage of medications taken. Physiotherapy and spa treatment for gout is carried out in the remission stage. Conducting a UVI of the area of the joint concerned in the acute phase in some cases helps to stop the gout attack that has begun.
Prognosis and prevention
Timely recognition and the beginning of rational treatment gives prognostically favorable results. Factors aggravating the prognosis of gout are young (up to 30 years old) age, a combination of urolithiasis and urinary tract infections, a burdened somatic history (diabetes mellitus, hypertension), progression of nephropathy.
The need to prevent gout should be taken into account during chemotherapy, as well as in patients with the threat of tumor decay and necrosis. From the first day of the course of chemotherapeutic treatment, it is necessary to prescribe hypouricemic drugs (allopurinol). Prevention of new exacerbations of gout depends on compliance with the water-salt regime, diet, body weight control. If there are relatives suffering from gout, other family members are advised to monitor the level of uric acid.
