From Big Medical Encyclopedia

GOUT (grech, podagra a trap, a rheumatic onychalgia) — the disease caused by the disturbances of purine exchange leading to increase in level of uric acid in blood and to adjournment of urates in fabrics.

The first classical description of clinic of P. belongs to T. Sydenham (1683). In 1848 Garrod (A. V. of Garrod) for the first time pointed to P.'s communication with increase in level uric to - you in blood (hyperuricemia), and in 1899 Freydvelter (M. of Freudwelter) found crystals of urates in joint liquid of sick Items.

By data epidemiol, researches, P. suffers from 0,04 to 0,37% of adult population. The item makes 0,1 — 5,8% of total number of rheumatic diseases. The disease develops hl. obr. at men (93 — 98% of cases) also begins more often at the age of 35 — 50 years.

Allocate primary and secondary P. Pervichnaya P. secondary P. — one of displays of other diseases or a consequence of use of nek-ry pharmaceuticals is an independent disease, and.

The etiology

is the cornerstone of P. increase in level uric to - you in blood — a ginerurikemiya (see. Lithemia ), various origin can have edges. Allocate two main reasons it: increase in synthesis and (or) disintegration of purine bases (see. Purine exchange ), being a source of education uric to - you and being a part nucleinic to - t (a so-called metabolic hyperuricemia, or metabolic gout), and delay of removal uric to - you with urine (a so-called renal ginerurikemiya, or renal gout). Perhaps also a combination of the specified factors.

Assume that disturbances of activity of the enzymes which are taking part in process of education uric to - you from purine bases or in mechanisms of removal of urates are kidneys an origin of primary P. Sos.Toyaniye of the separate enzymes regulating metabolism of urates at sick P. studied insufficiently. Only two fermental defects which are followed only by a hyperuricemia and P. are known: increase in activity of a fosforpbozilpiro-fosfatsintetaza and partial deficit гипоксантингуанинфосфорибо-зилтрансферазы. Both enzymes take part in metabolism purine osn0vany, their defects are genetically caused; only males are ill. Genetic factors have essential value in development primary the Item. According to Rikkevart (And. Byckewaert, 1978), is available for Vg of patients with this form P. the relative having the same disease, and the ginerurikemiya is found in members of families of sick P.

Secondary P.'s reasons, also as well as, more intensive can be primary, than normal, exchange nuklershovy to - t (and according to purine bases) that is noted at myeloid leukemia and other myeloproliferative diseases, hemoglobinopathies, inborn heart diseases which are followed by a hyperglobulia, psoriasis, use of inosine and cytostatic drugs and also delay of removal of urates with urine (at chronic renal nedostatochnostp, lead poisoning, prolonged treatment by diuretic drugs). Carry P. at Lesh's syndrome to secondary — Naykhana — the disease caused inborn full (or almost full) absence гипоксантингуанинфосфорибозил-трансферазы and shown also neurologic and mental disorders.

A pathogeny

the Major pathogenetic factor — a ginerurikemiya (more than 7 mg / 100 ml uric to - you in blood for men and more than 6 mg / 100 ml for women); the hyperuricemia exceeding 9 mg / 100 ml in 90% of cases is followed a wedge, P. V manifestations P.'s pathogeny the factors promoting crystallization also matter uric acid (see): dominance in fabrics almost insoluble uric to - you over more its easily soluble salts — urates (see); acid pH values of fabrics, increase uric to - you, the blood connected with globulins. In P.'s pathogeny exogenous factors have a certain value: excess use of the products rich with purine bases (meat, bean, etc.), and also greasy food and alcohol.

The brightest symptom of P. — acute arthritis (see. Arthritises ) — develops owing to adjournment in a joint cavity of the uratovy microcrystals capable to activate Hageman's factor (see. Hemorrhagic diathesis ), components of a complement, a kinina that leads to increase in vascular permeability (see) and to inflow of neutrophils. Phagocytosis of crystals is followed by release of lizosomalny enzymes therefore develops inflammation (see).

The pathogeny another often meeting a wedge, P.'s manifestations — damages of kidneys is various. In one cases, at development so-called at military, or gouty, a nephropathy, the long hyperuricemia has major importance. Crystals of urates are postponed at the same time preferential in an interstitium of kidneys and tubules. In other cases, at development of an urolithiasis (see. Urolithiasis ), pathogenetic value has, first of all, the increased allocation uric to - you with urine.

Pathological anatomy

Fig. 1. Microdrug of synovial fluid at gout: crystals of a needle form.
Fig. 1. Microdrug of a gouty tofus from area of an elbow joint: adjournment of urates in the form of the amorphous masses and crystals, on the periphery — cellular reaction with participation of multinucleate cells and development of rough fibrous fabric; coloring hematoxylin-eosine; x 200.

At P. there is an adjournment of crystals of urates in joint cartilages, an epiphysis of bones, circumarticular fabrics, kidneys and other bodies. Microscopic changes depend on extent of defeat and prevalence of process. Deposits of crystals infiltrirut surrounding fabrics, forming gouty nodes — tofusa — with development in the periphery of granulyatsionno-cicatricial fabric (tsvetn. fig. 1). Deposits of crystals on the surface of a joint cartilage have an appearance of whitish spots in the beginning, then the joint surface looks as covered with gypsum. For gistol, drugs fix researches in absolute alcohol or in mix of formalin and absolute alcohol since crystals of urates are dissolved in formalin. Microscopically crystals of urates have the form of straight lines, curves and S-shaped fine needles (fig. 1) up to 0,06 cm long which are located in the form of beams, glybok and disks. Deposits of urates cause a local necrosis of fabrics. Around this site inflammatory reaction with infiltrate from histiocytes, lymphoid, plasmocytes and a large number of the colossal cells containing fagotsitirovanny crystals develops. Around inflammatory infiltrate the fibrous capsule can be formed. Adjournment of urates in a synovial membrane leads to emergence synovitis (see), the long current to-rogo (chronic P.) is characterized by development of granulyatsionny fabric in the form of the pannus causing destruction of a joint cartilage, subchondral department of a bone and in rare instances an anchylosis of a joint (see. Anchylosis ).

In subchondral department of a bone where urates are laid, there are secondary changes as microfractures to formation of fibrous and bone callosities, development of cysts and osteosclerosis (see).

Patol, process in kidneys at P. is two types. Preferential adjournment of urates in an interstitium and an epithelium of tubules leads to development of an abacterial inflammation — pyelonephritis (see) — and to the subsequent sclerosis of renal fabric. The second type of damage of kidneys is characterized by adjournment of crystals of urates in collective renal tubules, a renal pelvis, and also ureters and a bladder, prp it formation of stones and the subsequent development of pyelonephritis is possible. Outcome patol. process in both cases there can be a so-called gouty contracted kidney.

A clinical picture

Allocate three stages of a typical course of a disease: bessilshtomny hyperuricemia, intermittent and chronic. The asymptomatic hyperuricemia can proceed for years; symptoms of arthritis, damage of kidneys and uric system are absent. The beginning of an intermittent stage consider the first attack of arthritis (or emergence of an urolithiasis). It is characterized by hl. obr. periodic developing of the acute arthritis which is coming to the end every time with full remission. In many cases it is possible to reveal the factors provoking an attack: alcohol abuse, rich with purine bases or greasy food, injury of a joint, general physical and neuroemotional overwork, operative measures, hypokinesia, use of some pharmaceuticals (purine derivatives, diuretic, etc.). At nek-ry patients the attack is preceded by the prodromal phenomena: various psychoemotional disturbances (depression, aggression, euphoria), dyspepsia and dysuria, etc. The picture of a gouty attack is very characteristic, especially in the first years of a disease. Suddenly, is more often at night, the acute arthritis (as a rule, monoarthritis) affecting usually joints of feet, especially often metatarsophalangeal joints of the first fingers develops. Also other localization is possible, however: the ankle, knee joint, is more rare joints of brushes. Rather quickly pain syndrome reaches considerable intensity and even more amplifies at the most insignificant movements in a joint. Note the expressed puffiness of fabrics and the dermahemia over a joint getting a bit later a cyanochroic shade. To morning of pain abate a little, but by next night increase again. In the subsequent their intensity considerably decreases, and in 2 — 3 weeks they disappear completely. Also other phenomena of arthritis are stopped several days later; there comes, as a rule, full the wedge, remission. The gouty attack can be followed by a fever, fervescence, perspiration, excitement, tachycardia, arterial hypertension. The subsequent attacks of gout arise usually through rather wide interval of time (1 — 2 years), but then gradually become frequent. Usually at each attack one any joint is surprised, 2 — 3 joints are more rare. Extraarticular localization of an acute gouty inflammation is much less often observed (dermatitis, a tendovaginitis, a bursitis, a miositis, pharyngitis, tonsillitis, a nephropathy, etc.). Wedge, symptomatology at the same time very polimorfna. The gouty nature of extraarticular manifestations is confirmed by existence in this area of tofus or a therapeutic effectiveness of colchicine. The usual duration of an intermittent stage of Item 6 — 8 years.

Fig. 2. Lower extremities of the patient with gout: chronic arthritis of metatarsophalangeal joints of the first fingers, the thickening of soft tissues is visible.

The beginning hron, stages of a disease carry by the time of emergence hron, a gouty inflammation of joints, formation of a tofus or emergence of a gouty nephropathy. Hron, gouty arthritis is characterized by a resistant inflammation of one or several joints. Over time restriction of mobility in a joint is possible. Quite often in the affected joint tofusa therefore circumarticular fabrics are thickened (fig. 2) that can break even more mobility in a joint are postponed. In some cases in connection with ossifluence (see) rough deformation of a joint, and sometimes noticeable shortening of the bones forming it is noted. For hron, gouty polyarthritis (see) asymmetry of damage of joints is characteristic.

Hypodermic tofusa happen from several millimeters to 2 — 3 cm in size and more in the diameter. Tofusa of the smaller sizes if they are located close to the surface of skin, look as the yellowish-whitish educations translucent through skin and sometimes raising epidermis. At deeper hypodermic localization of a tofusa have an appearance of knotty, round, tuberiform educations dense, sometimes a chondroid consistence. Usually tofusa are painless, but at an aggravation of local inflammatory process morbidity, a softening of a tofus, a hyperemia of integuments over it can be noted. Sometimes integrity of the last is broken, and through the formed defect contents of a tofus — white pasty weight — comes to light. The sizes of the npfi node it decrease, and in nek-ry cases it disappears completely. Tofusa can have various localization, but more often they are located in auricles and an extensor surface of joints.

Hron, damage of kidneys — the second for frequency and predictively the most serious manifestation of the Item. The first type a porazheiiya of kidneys — uratny, or gouty, a nephropathy — is characterized by preferential defeat of an interstitium and renal tubules and the hl is shown. obr. a small and non-constant albuminuria (see. Proteinuria ), a cylindruria and a leukocyturia, and also arterial hypertension (see. arterial hypertension ). Feature of a gouty nephropathy is what it is usually long proceeds asymptomatically or has insignificant non-constant symptomatology and progresses usually slowly. At 17 — 25% of sick P. it is noted chronic renal failure (see).

The second type of damage of kidneys (and other departments of uric system) is characterized by formation of uratny stones. The urolithiasis is observed at 10 — 25% of patients of primary P. and twice more often at secondary P. Primerno at 1/3 patients the urolithiasis can precede attacks of arthritis. Frequency of formation of stones in uric system at P. correlates with expressiveness of a hyper uricosuria. The urolithiasis develops at a half of patients, at to-rykh allocation uric to - you with urine make 1 g and more in days. A wedge, manifestations same, as at an urolithiasis of other etiology; feature is the frequent asymptomatic current.

In some cases P., hl. obr. at patients secondary, developed against the background of hematologic diseases at treatment of cytostatic drugs, and at primary P.'s patients at sharp increase in level uric to - you, can develop an acute renal failure. It results from massive precipitation of crystals of uric acid in collective tubules of kidneys p ureters.

The atypical current of primary P. is characterized by frequent attacks of acute arthritis already at early stages of a disease, bystry development hron, arthritis, damage of joints of upper extremities. Such course of primary gout is observed rather seldom. At the same time the similar course of a disease is typical for secondary gout.

Lesh's syndrome — Naykhana, one of manifestations to-rogo is P., is observed only at boys (aged from 6 months up to 16 years). At this syndrome note umstvennuvz backwardness, an agressive behavior, aspiration to mutilation, the expressed choreoathetosis (see. Athetosis ), spastic cerebral paresis (see. Paralyses, paresis ), anemia, the expressed hyperuricemia, an urolithiasis and, as a rule. chronic arthritis.

Primary P. is often accompanied by obesity, atherosclerosis and its complications, a diabetes mellitus, allergic diseases.

The diagnosis

the Diagnosis is considered reliable at detection of deposits of urates in fabrics. Are among characteristic signs of P.: 1) strengthening of urates in joint liquid; 2) the acute arthritis which is characterized by suddenness of emergence, localization in metatarsophalangeal joints of the first fingers, bystry development of local hypostasis, the sharp morbidity expressed by a dermahemia and bystry approach (in 1 — 3 week) full remission; 3) an exacerbation of arthritis in connection with the use of the food rich with purine bases, fats, alcohol or use of the pharmaceuticals leading to a hyperuricemia (inosine, diuretic, etc.); 4) the hyperuricemia exceeding norm on 2 mg / 100 ml; 5) tofusa. The combination of 2 — 3 specified signs (in the presence of a hyperuricemia) allows with sufficient definiteness to make

to P. Kroma of the specified symptoms a certain value in diagnosis symptoms of «punch» and «inflation of bone edge» have the diagnosis rentgenol, (see below); the debut of a disease is aged more senior than 35 years; frequent detection in urine of precipitated calcium superphosphates of urate connections; P.'s presence at blood relatives.

Radiological damage of joints at P. is characterized by existence of bone changes which arise only at chronic gouty arthritis and, as a rule, in many years after an onset of the illness. Nevertheless, data rentgenol. researches in cases atypical a wedge, P.'s currents can be an important diagnostic character.

Fig. 3. Roentgenogram of foot (at the left; and its increased fragment — the I finger (on the right) at chronic gouty arthritis: typical destructive changes of a bone tissue in metatarsophalangeal joints; destruction of cortical bone substance in the field of a head of the I plusnevy bone — a symptom of «inflation of bone edge» (it is specified by an arrow).
Fig. 4. The roentgenogram of a brush (at the left) and its increased fragment — the II finger (on the right) at chronic gouty arthritis: increase in volume of soft tissues in proximal interphalangeal and metacarpophalangeal joints, destructive changes of these joints (are specified by shooters).

At P. find changes of joints and an epiphysis of bones, hl. obr. in the form of the centers of an enlightenment of a rounded or oval shape (intra bone tofusa), from several millimeters to 2 — 3 cm in the diameter. Localization of changes corresponds to localization of arthritis, most often it is bones of a metatarsus and a brush. If tofus occupies almost all thickness of a bone, on the roentgenogram the unstructured site of depression is visible. At long existence gouty tofus it is accurately delimited from the thin sclerous border which is not changed a bone tissue and on the roentgenogram has the round «stamped» form (a symptom of «punch»). The quantity of intra bone tofus fluctuates from one to several; sometimes they merge among themselves in larger conglomerate. Large nodes, increasing, afterwards can destroy cortical substance of a bone — a symptom of «inflation of bone edge» (fig. 3). At far come destructive changes the integrity of a joint surface of a bone (fig. 4) is broken.

Considerable bone destruction sometimes complicates differential diagnosis of gouty arthritis and other arthritises, hl. obr. pseudorheumatism (see). However and in these cases it is possible to note characteristic of P. swelling of the thinned cortical substance and the yacheistost of the drawing formed by borders of several next tofus. At an arrangement of a gouty tofus near the joint surface of a bone semicircular defect of a bone is formed. Because of it the extent of a joint surface of the affected bone appears less in comparison with not changed joint surface of an opposite bone of this joint. At P. development of the circumarticular osteoporosis which is one of characteristic rentgenol, signs of the majority of other arthritises is not observed.

At hron, the course of joint process the reparative phenomena — substitution of defect again formed bone tissue, formation of osteophytes at edges of joint surfaces of the bones creating a typical picture of the secondary deforming osteoarthrosis develop (see. Arthroses ).

At a heavy current of P. there is a sharp deformation of joints both because of destruction, and because of the mutual shift of bones of a joint. Seldom or never process comes to an end with formation of a bone anchylosis.

Differential diagnosis carry out with pseudogout (see), a pseudorheumatism (see), rheumatic polyarthritis (see Rheumatism), septic arthritis (see. Arthritises ), traumatic periarthritis (see), arthrosis (see), calcification (see), thrombophlebitis (see), an erysipelatous inflammation (see. Ugly face ), phlegmon (see), etc.


Treatment is directed to stopping of bad attacks and normalization of metabolism of urates, decrease in contents uric to - you in blood.

The most effective remedy of treatment of acute gouty arthritis is K0LHITs1Sh. The mechanism of effect of colchicine at P. consists in suppression of phagocytosis of uratovy crystals neutrophils, increase in solubility of urates in plasma and their excretion. Usually appoint 0,5 mg of colchicine every 2 hour, but no more than 4 mg in the first two days, with the subsequent dose decline. Duration of a course 6 — 8 days. Colchicine can cause the toxic phenomena from outside went. - kish. a path that limits its use. Apply to stopping of acute gouty arthritis also non-steroidal anti-inflammatory drugs: Butadionum (0,45 — 0,6 g a day), indometacin (0,15 g a day), Voltarenum (0,15 g a day). They are less toxic, than colchicine. Therapeutic effect of these drugs at a bad gouty attack is shown in 24 — 72 hours. Also intra joint introduction of a hydrocortisone is possible (25 — 50 mg in one joint). In addition to pharmaceuticals, at a bad attack absolute rest, an exception of food of the products rich with purine bases, and plentiful alkaline drink is necessary.

For normalization of urate exchange appoint practically during all life a diet with the limited content of purine bases and fats. Meat or fish are resolved by 3 — 4 times a week in the boiled-down look. Meat soups, meat of young animals, kidneys, a liver, bean, alcohol, strong tea and coffee are prohibited. Recommend plentiful alkaline drink (2 — 2,5 l a day).

The pharmaceuticals reducing contents uric to - you in blood, are divided on urikodep-ressivny (oppressing synthesis uric to - you) and uricosuric (increasing release of uric acid with urine).

The choice of drug of this or that group depends on what form P. takes place in this case: metabolic (urikode-pressivny means are shown) or renal (uricosuric means are shown), and also from a condition of kidneys (in the presence of a gouty nephropathy and an urolithiasis uricosuric means are contraindicated).

The most widespread Uri-kodepressivnym means is Allopyrinolum (mplurit) inhibiting enzyme to a ksantinokspdaz which turns hypoxanthine into xanthine, and the last — in uric to - that. Allopyrinolum apply in a dose 200 — 600 mg a day; decrease in contents uric to - you in blood is noted in 1 — 3 week. In 6 — 8 weeks at most of patients there occurs permanent normalization of a lithemia then appoint maintenance doses of drug: 100 — 200 mg a day. Allopyrinolum is contraindicated at the expressed renal failure. Aethamidum, derivatives of coumarone belong to urikozurp-chesky means antu-wounds, probenetsid (benemid) (benziodaron, benzbromaron). Probenetsid apply 0,5 g 2 — 4 times a day, anturan — on 100 — 600 mg a day. Benziodaron on 300 mg a day, benzbromaron — on 100 mg a day. These drugs have the expressed uricosuric effect, and derivatives of coumarone also small urikodepressivny action. Aethamidum is appointed on 2,8 g a day (2 cycles for 7 —-10 days with a week break 3 — 4 times a year). It possesses weak uricosuric action. The lack of uricosuric means is that they can promote formation of stones in uric ways.

The general principle of purpose of the means reducing contents uric to - you in blood, are following: at first select a dose of drug, allows to normalize edges or to considerably reduce contents uric to - you in blood, then (usually in several months) pass to the supporting dosages (1/2 — 1/4 initial). Already within half a year permanent decrease in a lithemia, an urezheniye or disappearance of attacks of P., reduction or a full rassasyvaniye of tofu of owls is caused by correctly picked up antigouty treatment. However in the first months of treatment increase of attacks of P. owing to mobilization of urates from depot (tofus) is possible. In these cases appoint small doses of colchicine (1 mg a day).

To treatment and prevention of aggravations of P. apply also (usually as addition to drug treatment) a fiziobalneoterapiya (see. Balneoterapiya , Balneotherapy ). For prevention of attacks of the item recommend hydropathic procedures: rubdowns or douches, souls, including Charcot's douche, underwater shower massage, contrast bathtubs, and also general mineral bathtubs (radonic 40 — 120 nkyuri/l, sulphidic 100 — 150 mg/l, chloride sodium, iodine-bromine). Especially well proved radonic bathtubs (see. Radon waters ), having direct uricosuric effect. At chronic arthritis apply mud applications (see. Mud cure ), and also parafinoozokeri treatment. Widely use intake slabompneralizovan-ny M1sheralnykh waters, imeyuptsy sh; fir-tree pH values (Borjomi, to Sairma, Luzhanskaya No. 1 and No. 2, Kvasov's Glade, etc.) which promote an oshchelachivaiiya of internal environment of an organism, thereby slowing down adjournment of urates in fabrics. Besides, mineral waters strengthen removal uric to - you with urine. Appoint to drink t 35-40 water ° on 0,5 — 2 glasses three times a day. Time of reception of water is defined depending on secretory function of a stomach.

The physiotherapy exercises are included into the general complex of treatment P. V the acute period of a disease of LFK is contraindicated. During the subsiding of the inflammatory phenomena in the affected joints to the patient appoint to lay down. gymnastics. At hron, the course of a disease moderate joint pains are not a contraindication to occupations of LFK. In this case use to lay down. gymnastics (preferential active exercises), and for the purpose of stretching of periartikulyarny fabrics passive exercises and massage apply. Thermal physiotherapeutic procedures and massage are recommended to be carried out just before to lay down. gymnastics. At the beginning of course LFK for occupations it is necessary to select physical exercises for large muscular groups of extremities and a trunk and the passive movements for sore joints (bending and extension, assignment and reduction, spinning) with perhaps full amplitude. The movements in a sore joint or joints need to be alternated to exercises for other parts of a body. In the second half of course LFK include the active movements in defeats joints, and also exercises with a gymnastic stick, maces, etc. The passive and active movements in sore joints are recommended to be carried out with a full amplitude even with considerable morbidity. Rate of movements at the beginning of the occupation slow, and then average. Number of repetitions of 10 — 15 times.

Forecast and Prevention

Forecast. Use of modern methods of treatment in most cases of P. which is not followed by a renal failure leads to remission of a disease: P.'s attacks, tofusa disappear, the lithemia decreases to datum level. At a renal failure and Lesh's syndrome — Naykhana the forecast is less favorable. Secondary P.'s forecast to a large extent is defined by success of therapy of a basic disease.

Working ability of patients significantly decreases at an aggravation of process, the expressed chronic polyarthritis, renal pathology.

Prevention includes observance of all-hygienic rules (especially concerning food). To the persons having the non-constant, but often revealed giperurikegmiya or the heredity burdened concerning P. appoint a low-purine diet with the limited content of fats.

Bibliography: Astapenko M. G. Features of clinic and diagnosis of gout in modern conditions, Rubbed. arkh., t. 52, No. 7, page 93, 1980; Astapenko M. G. and Kim D e of N - g and. Modern aspects of a pathogeny of a hyperuricemia and gout, in the same place, t. 51, L' 12, page 106, 1979, bibliogr.; To in e in K. G. Podagr, the lane with bolg., M., 1980, bibliogr.; JI e-p about r with to and y A. A. Medical physical culture at diseases of a metabolism and diseases of joints, M., 1960; Moshkov V. N. Medical physical culture in clinic of internal diseases, M., 1977; P and the X l and to E. G. Podagra, M., 1970, bibliogr.; Reynberg S.A. 'Radiodiagnosis of diseases of bones and joints, book 2, page 531, M., 1964; P about x - ying D. G. l. Radiodiagnosis of diseases of joints. A part is the general, page 143, etc., L., 1939; The Reference book on physical therapy, under the editorship of. And. N. Obrosova, M., 1976; F of e u d w e 1 t e of M. Experimentelle Untersuchungen tiber die Enstehung der Gichtknoten, Dtsch. Arch. klin. Med., Bd 69, S. 155, 1900; Garrod A. The nature and treatment of gout and rheumatic gout, L., 1859; Rod nan G. P. Gout, in book: Rheumatol, and immunol. ed. by A. S. Cohen, p. 314, N. Y., 1979; Seegmiller J. E., Rosenblo-o m F. M. a. Kelley W. M. Enzyme defect associated with a sex-linked human neurological disorder and excessive purine synthesis, Science, v. 155, p. 1682, 1967; Sydenham T. Tractatus de podagra et hydrope, L., 1683.

M. G. Astapenko, E. G. Pikhlak; V. P. Illarionov (to lay down. physical.), G. M. Mogilevsky (stalemate. An.), S. A. Sviridov (rents.), N. F. Sokolova (fizioter.).