From Big Medical Encyclopedia

ENTERYT (enteritis; Greek enteron a gut + - itis) — the inflammatory or inflammatory and dystrophic defeat of a small bowel leading at a chronic current to an atrophy of her mucous membrane.

To divide inflammatory processes in intestines into enterita and colitis (see)

P. Obraztsov offered in 1896, it described also their main differential and diagnostic criteria. In the first third of 20 century Schmidt and Notnagel's doctrine gained distribution (A. Schmidt, To. W. H. Nothnagel) about intestinal dyspepsia to which referred the pathological processes in intestines of preferential functional character which are not followed by structural change of an intestinal wall. However intravital studying morfol. changes of a mucous membrane of a gut at various patol. processes, and also researches in the field of physiology allowed to refuse this point of view and to consider E. from positions of unity of structural and functional disturbances. In most cases at a chronic current E. the large intestine also is involved in pathological process; it formed the basis for allocation row оте^ chestvenny scientists of an independent nosological form — a chronic coloenteritis. However many gastroenterologists object to such association, believing that saving the terms «enteritis» and «colitis» underlining preferential localization of process allows to approach treatment differentially. Depending on duration distinguish acute and chronic enteritis.

Acute enteritis. Isolated acute E. it is observed rather seldom; in clinical practice the gastroenteritis, (see) or a coloenteritis usually meets.

Acute enteritis has inf more often. nature. It arises at such diseases as a typhoid (see), dysentery (see), iyersinioz (see), a salmonellosis (see), cholera (see); to cause acute E. also staphylococcus, colibacillus (enteropathogenic, including enterotoxigenic) and other bacteria can (see Toxicoinfections food). Virus E. meets less often than bacterial. Rotaviruses are its most frequent reason (see), the smaller role in developing of a disease belongs to intestinal viruses (see), to adenoviruses (see), to coronaviruses (ohm.), etc. Enteritis arises also at candidiasis (see) and other fungal infections of intestines. Major pathogenetic factors infectious acute E. strengthening of intestinal secretion and increase in permeability of an intestinal wall caused by the damaging influence inf are. the agent and his toxins on a mucous membrane of a small bowel and the changes happening in cellular membranes (see Ponosa).

Acute E. can have the allergic nature, and also result from poisoning with mushrooms, salts of heavy metals, pharmaceuticals (see Poisonings).

Acute E. happens diffusion and in this case strikes all small bowel, or process is localized in its certain department. The inflammation can be catarral, fibrinous, purulent, necrotic and necrotic - ulcer. Catarral E. it is characterized by a hyperemia and hypostasis of a mucous membrane and a submucosa, a hyperplasia of scyphoid cells, sometimes dystrophic changes of enterocytes at tops of fibers. The similar picture is observed, e.g., at a gastrointestinal form of a salmonellosis.

Fibrinous E. it is often combined with fibrinous colitis (see). The mucous membrane of a small and large intestine of a nekrotizirovan, is impregnated with the fibrinous exudate forming grayish-yellow neot-delyayushchuyusya a film (a so-called pseudomembranous coloenteritis). Own plate of a mucous membrane and submucosa are edematous, plentifully infiltrirovana leukocytes and lymphoid cells.

At purulent E. there is a diffusion treatment of a wall of a small bowel pus (phlegmon) or formation of small abscesses on site of lymphoid follicles. Such apostematous E. meets at an iyersinioza, for to-rogo defeat of preferential terminal department of an ileal gut is characteristic. At the same time in a mucous membrane accumulations neutrophylic to a gran of .gyshchit, surrounded with epithelial cells, histiocytes and lymphocytes come to light.

For necrotic E. destructive changes of a mucous membrane are inherent, at necrotic - ulcer E. also erosion and ulcers are formed. At necrotic E., the activator to-rogo is Clostridium perfringens, in initial departments of a jejunum dark red sites of a hemorrhagic necrosis form, the wall of a gut becomes sharply edematous therefore its gleam is narrowed. / the necrosis of walls and fibrinferments of arterioles Is noted. Similar morfol. changes are revealed at the ulcer and necrotic coloenteritis of newborns caused by colibacillus, at Krom are surprised the ileal, blind and ascending colon. Along with hemorrhages and ulcerations inflammatory infiltration of all layers of a wall of a gut is noted. At necrotic E., caused by staphylococcus, in a wall of a small bowel numerous superficial ulcerations are observed; microscopically the picture of an acute inflammation of a mucous membrane, its sharp plethora, extensive necrotic changes comes to light; during the coloring of drugs across Gram (see Gram a method) on a mucosal surface of a cover a set of stafilokokk find.

The disease begins sharply. Patients have a diarrhea, nausea, repeated vomiting, pains in an upper half of a stomach, the headache, sharp weakness, can raise body temperature. Patients are pale, the eyes which sank down; language dry, is laid over by a white plaque; the stomach is blown up. In the first 2 — 3 days a chair to 10 — 15 times a day, kcal plentiful (polyexcrements), watery; appetite is absent. During the involvement in process of a large intestine (coloenteritis) desires on defecation become frequent. Owing to dehydration of an organism (see) and losses of chlorides (see the Hypochloraemia) appear in hard cases muscle pains and a spasm in extremities. At patients the ABP goes down, tendency to bradycardia is noted. In hard cases in connection with development of the disseminated intravascular blood coagulation symptoms of hemorrhagic diathesis — bleeding, fibrinferments are observed (see. Hemorrhagic diathesis). Complication acute E. there can be an acute vascular insufficiency (see the Collapse).

The diagnosis is made on the basis by a wedge, pictures, data epidemiol. anamnesis, results lab. researches. At a palpation morbidity and rumbling in the field of a small bowel is noted. The oliguria, a proteinuria, a microhematuria, quite often a leukopenia, eriarotsitoz are noted. In Calais (see) a large amount of slime, undigested cellulose, grain of starch, muscle fibers are defined. Results of bacteriological and virologic researches a calla, identification of antigens of activators in urine, saliva, blood or increase of an antiserum capacity to them are of great importance.

In hard cases the research of a koagulogramma is necessary (see). Differential diagnosis is carried out with an acute appendicitis (see), is more rare with acute intestinal impassability (see Impassability of intestines), perforated stomach ulcer or a duodenum (see. Peptic ulcer), acute pancreatitis (see).

Appendicitis at adults usually proceeds without diarrhea, at children at appendicitis the diarrhea is observed more often, however the kcal does not happen plentiful and watery; pains at appendicitis are usually localized in the right ileal area and unlike acute E. signs of irritation of a peritoneum come to light. At acute intestinal impassability colicy pains in a stomach are noted, the chair is absent, the stomach is not blown up, gases do not depart, intestinal noise disappear, symptoms of irritation of a peritoneum appear, at rentgenol. a research of intestines fluid levels are defined. The strong («knife-like») abdominal pain, the expressed tension of a front abdominal wall (a «doskoobrazny» stomach), lack of a chair, a leukocytosis, availability of free gas in an abdominal cavity are characteristic of a perforated ulcer at rentgenol. research. At acute pancreatitis megalgias, usually have the surrounding character, often in connection with paresis of intestines the delay of a chair is observed, in urine and blood the level of amylase increases.

The patient appoint a bed rest, plentiful drink, mechanically and chemically sparing diet with decrease sheathe caloric contents of food, restriction of carbohydrates and fats, exclude the fresh milk, products containing cellulose, spices, a pickles, smoked products (diet No. 4) from a diet. In several days the diet is expanded (diet No. 4B), however all products are boiled or steamed in the wiped look (see clinical nutrition). At acute infectious E. (unlike colitis) antibacterial therapy is not shown. At unsharply expressed symptoms of dehydration the patient allow to drink small drinks glyukozoelektrolitny solutions; at a severe disease salt solutions enter intravenously. Use fermental drugs. At the expressed intoxication corticosteroids (parenterally, short courses), Haemodesum, Polyglucinum are shown (see. Blood-substituting liquids), plasma transfusion (see the Blood plasma), at development of a syndrome of the disseminated intravascular coagulation enter anticoagulants.

The forecast depends on a cause of illness. More often acute E. in several days comes to an end with an absolute recovery. In some cases transition of acute process in chronic is noted.

Prevention comes down to the prevention and timely treatment of intestinal infections.

Acute enteritis at children proceeds as well as at adults, medical and preventive events are held by the same principles.

Chronic enteritis. In domestic medicine chronic enteritis is allocated in an independent nosological form, abroad carry to chronic enteritis only a disease Krone (see Krone a disease). According to the classification offered in 1975 by A. V. Frol-kis, chronic enterita divide depending on an etiology, preferential localization of process, morphological features of a mucous membrane, weight a wedge, manifestations, the nature of functional disturbances.

Etiology and pathogeny. Chronic infectious enteritis arises after the postponed acute intestinal infections — dysentery, salmonellosis, infections caused by nek-ry pathogenic strains of colibacillus (see), enteroviruses (see. Intestinal viruses), etc. During development of chronic process in intestines the activator usually loses the pathogenetic value and ceases to be sowed from a calla. At the same time the main role in development patol. process get nonspecific factors and especially dysbacteriosis (see). Exception are iyersiniya (enterokolitny, pseudotuberculous is more rare), to-rye continue to be sowed from a calla of the patient even at hron. course of process.

Damages of intestines can be the cause of chronic parasitic enteritis at parasitic diseases — a lambliasis (see), an amebiasis (see), a balanthidiasis (see), a strongyloidosis (see), helminthosis!: (see), etc.

Chronic E. can arise owing to poisoning with mercury, zinc, at long alcohol intake (toxic enteritis), and also as a result of endogenous intoxication, napr, at uraemia (see).

Emergence chronic E. the hl can be caused also by effect of medicines (medicamentous enteritis). obr. the antibacterial drugs causing development of dysbacteriosis. In this case damage of both a thin, and large intestine (a pseudomembranous coloenteritis) is connected with impact on a mucous membrane of intestines of a sporiferous bacterium of Clostridium difficile steady against antibiotics.

Chronic E. develops as a result of a sensitization of intestines to this or that allergen (allergic enteritis). Its emergence is more often it is connected with food allergy (see), for example at children at intolerance is protein of cow's milk. To chronic E. an allergic etiology carry also eosinophilic enteritis (gastroenteritis) developing at allergic reaction to food stuffs and to nek-ry intestinal parasites (ascarids, lyambliya, etc.).

Chronic E. it can be caused by ionizing radiation (beam enteritis); it often occurs at patients with malignant new growths of an abdominal cavity and bodies of a small pelvis after performing radiation therapy by it.

Emergence chronic E. it can be caused by anomalies of development of intestines (inborn megacolon), change of its form as a result patol. process (the acquired megacolon), and also commissural processes in an abdominal cavity (so-called mechanical enteritis). Structural changes and functions of intestines depend in this case on expressiveness of a coprostasis.

Chronic E. can develop after an enterectomy in connection with adaptation changes of the remained part of a small bowel that is connected with increase in number of the absorbing cells and an intensification of processes of absorption in the functioning sites of a mucous membrane. At a resection of the considerable site of a small bowel of compensation of digestive and vsasyvatelny functions completely does not occur in this connection the sprue develops (see Malabsorption a syndrome). The resection to 40% of a small bowel at preservation of a duodenum, a distal part of an ileal gut and the ileocecal valve usually is followed by good compensation while removal of a distal part of an ileal gut and the ileocecal valve leads to the expressed malabsorption. The same processes are the cornerstone of the enteritis developing during the imposing by it-noilealnogo of an anastomosis, which is often applied abroad to treatment of obesity.

Reason chronic E. there can be also an ischemia of a wall of a small bowel (ischemic enteritis) most often arising because of atherosclerosis or as a result of an inflammation of mezenterialny vessels (see the Mesentery).

Allocate secondary (symptomatic) chronic enteritis, to-ry usually arises at diseases of other departments of the alimentary system (a stomach, a liver, a pancreas), and also at pathology of various bodies and systems (endocrine diseases, collagenoses, etc.). Big role in development patol. process in this case play disturbances of nervous and humoral control of activity of intestines, the frustration caused by loss of functions of other links of process of digestion have a certain value (gastric digestion, receipt in intestines bilious to - t).

Emergence of inflammatory process in a small bowel is promoted by a hypovitaminosis, defective food; the intestinal dysbacteriosis leading to development of structural disturbances of a mucous membrane of a small bowel is of great importance. About existence of dysbacteriosis at chronic E. irrespective of its etiology change of microbic structure a calla testifies: sharp reduction of number or disappearance of bifidobacteria, dominance of stafilokokk, a protea, fungi, emergence of virulent properties in nek-ry intestinal microbes — colibacillus, enterococci. A certain role in development of chronic process in a small bowel at enteritis of any etiology belongs to an allergy (see). The proof of it is increase at patients chronic E. an antiserum capacity to intestinal microbes, to a nek-eye to foodstuff, to tissues of intestines, positive skin tests (see. Allergy diagnostic tests), positive provocative tests (see), etc. As a result of action of antibodies and sensibilized lymphocytes on a mucous membrane of a small bowel there is a damage and death of epithelial cells owing to what its function is broken. Sometimes development of a disease is connected with insufficiency of immune system (deficit of immunoglobulins of a class A). In some cases, napr, at genetically determined enzymopathies (see), genetic factors — hereditarily the caused deficit of intestinal enzymes, first of all disaccharidases (lactase, etc.), leading to disturbances of digestion with the subsequent development of structural disturbances of a small bowel matter.

Children have origins the same diseases, as at adults, however more often it is connected with the postponed intestinal infection. More prematurity of a disease is promoted by defects of enzymatic structures of a mucous membrane of a small bowel, immune disturbances. Refer defeat to risk factors went. - kish. a path at relatives, a hypotrophy and an unstable chair at the child at early age, ekssudativnokataralny diathesis.

Pathological anatomy. Depending on preferential localization pthe rotsess is distinguished by a jejunitis, an ileitis and the most often found total chronic enteritis. Patomorfol. changes are characterized by signs of a chronic inflammation, disturbances of regeneration and a mucosal atrophy. At the long course of process the atrophy of fibers (hyper regenerator is more often) is usually combined with a hyperplasia of crypts. A subtotal or total hyper regenerator mucosal atrophy at E., as a rule, confirms a gluten disease (see). At microscopic examination of a fiber of a small bowel are thickened, shortened, sometimes are spliced among themselves; crypts are usually extended. More rare, napr, at beam E., there is a hyporegenerative atrophy, at a cut there is a shortening of both fibers, and crypts. Cells of an intestinal epithelium are flattened; their cytoplasm contains many RNA; kernels have the spindle-shaped form, are displaced to a surface of cells. At chronic E. acceleration of cellular proliferation with a simultaneous delay of differentiation of epithelial cells is noted what confirm existence of the not completely differentiated cells located on surfaces of fibers, and also increase in the field of crypts of quantity of the cells synthesizing DNA and the expansion of a generative zone revealed at an autoradio graphic research. At an electronic mik-roskopicheskom a research reveal deformation, shortening, depression and uneven swellings of microvillis of epithelial cells with a border — the changes which are morfol. substrate of disturbances of absorption and membrane digestion. Considerably infiltration of own plate of a mucous membrane lymphoid increases and plasmocytes (at eosinophilic enteritis — eosinophils), the large number of lymphocytes is between cells of an intestinal epithelium. In cytoplasm of lymphocytes by means of an immunofluorescence (see) and others immunomorfo logical methods reveal A, M, G immunoglobulins, significant increase in the cells supporting IgG (see Immunoglobulins).

Clinical picture total chronic E. irrespective of an etiology of a disease it is characterized by the symptoms caused by disturbance of functions of intestines (an enteral syndrome). In total wedge, manifestations chronic E. divide on local and the general. Local intestinal symptoms first of all are frustration of a chair. The diarrhea is usually observed. Unlike chronic colitis a chair less frequent (as a rule, to 4 — 6 times a day). The lock is less often observed (the chair can be and normal). The quantity a calla is increased; excrements liquid or kashitseobrazny, chartreuse color; in Calais the remains of undigested food with the naked eye are visible, the steatorrhea is noted (see). Patients are disturbed by the abdominal murmur, a meteorism (see) which are especially expressed in the second half of day — in the period of the greatest activity of digestive processes. The meteorism quite often is followed by pain in heart, heartbeat, an asthma. Patients complain of feeling of completeness and a raspi-raniye in a stomach after food, an abdominal pain (in a navel, sometimes on all stomach, at an ileitis — in the right ileal area), intensity to-rykh increases at height of digestion; at accession of mezenterialny lymphadenitis of pain become constants, amplify at an exercise stress. The specified intestinal frustration depending on dominance of fermentative or putrefactive processes can be expressed in various degree (see Digestion, pathology).

The general symptoms are defined by extent of disturbance of intestinal absorption (see Maljabsorbtion a syndrome), and also disorder of functions of other departments of the alimentary system involved in patol. process. At patients increased fatigue, decrease in working capacity, weight loss, a loss of appetite up to its total loss is noted (in some cases appetite is increased). There are trophic frustration in the form of a xeroderma, a hair loss, fragility of nails. In hard cases dehydration is observed (see Dehydration of an organism). The metabolism (proteins, fats, carbohydrates, vitamins, electrolytes) is broken. As a result of disturbance of absorption and loss of proteins of a blood plasma through an intestinal wall the syndrome of an exudative enteropathy (a hypoproteinemia, hypostases, ascites, exhaustion develops up to a cachexia). The lack of vitamins leads to frustration of a nervous system (a spasm, paresthesia, etc.), to damage of an oral cavity (an atrophy of nipples of language, a crack, an erosion of language, a glossitis, stomatitis, etc.), to increase in permeability of capillaries and strengthening of bleeding, to osteoporosis and fractures of bones. At chronic E. quite often there are damages of skin — dermatitis, a hyperkeratosis, eczema, neurodermatitis, etc. Disorders of electrolytic exchange are shown by dryness of mucous membranes, tachycardia, decrease in intestinal motility, etc. Disturbance of absorption of iron can become the reason of an iron deficiency anemia (see).

At chronic E. there are endocrine frustration, the defeat of gipofizarnonadpochechnikovy system which is shown hypotonia, a hyperpegmentation, decrease in sexual function is more often observed.

At patients chronic E. disturbance of functions of other digestive organs is possible. Damage of a stomach is shown by oppression of secretion, pains in epigastric area, dispeptic frustration; at gastroscopy symptoms of gastritis, sometimes atrophic come to light (see Gastroscopy). During the involvement in process of a pancreas are observed morbidity at its palpation, symptoms of pancreatitis (see). Increase and abnormal liver function is quite often noted, at a biopsy find dystrophic changes of hepatocytes. At patients with chronic E. the phenomena reminding a dumping syndrome (weakness, heat and feeling of rush of blood to the head, heartbeat, dizziness, perspiration, face reddening, nausea, the plentiful department of dense saliva arising right after food) or the hypoglycemic syndrome which is shown in several hours after food sharp weakness, the dizziness, apathy, pallor cold then, a fever, a sonitus can be observed (see P ostgastrorezek-tsionny complications).

The functional dumping syndrome, infrequent chair (1 — 3 time a day), the plentiful, kashitseobrazny, clay excrements smearing a toilet bowl — the «fat diarrhea» caused by accumulation in intestines not absorbed fat to - t are characteristic of a jejunitis. At also pour (more often an ileotyphlitis) more frequent chair (to 6 — 8 times a day), watery, foamy excrements — the «bilious diarrhea» connected with accumulation bilious to - t in final departments of a small bowel is noted; more expressed, than at defeat of proximal departments of a small bowel electrolytic disturbances; pains are localized preferential in the right ileal area, at a palpation consolidation of a final piece of an ileal gut, the stretched humming caecum is noted. At an ileotyphlitis the syndrome of insufficiency of the ileocecal valve quite often develops — the gaping of an ileocecal opening caused by stretching of the gate of the ileocecal valve gases and intestinal contents at the same time occurs a pelting of contents of a caecum in an ileal gut (reflux enteritis).

Children have chronic clinical manifestations E. generally are defined by extent of disturbance of absorption in a small bowel. Along with above the listed symptoms at many children note selective or a cissa (children eat chalk, the earth). Early there are general symptoms in the form of emotional lability, increased fatigue, lag in the weight and growth. The age of the child is less, the general frustration develop quicker.

Process proceeds with aggravations and remissions. Depending on features of a course of process mark out three severity of chronic enteritis. At the easy course of chronic enteritis (the I degree) the wedge, manifestations are expressed unsharply, local intestinal symptoms prevail. At chronic

E. moderately severe (And degrees) both intestinal symptoms, and the general frustration are noted. At a heavy current chronic E. (The III degrees) the general condition of patients, in a wedge considerably suffers, to a picture the general symptoms prevail. It is noticed that at the persons living in areas with hot climate, symptoms of a disease are more expressed; in a temperate climate the disease is often characterized erased a wedge, a picture.

Diagnosis chronic E. put on the basis of the anamnesis, a wedge, pictures, data of comprehensive examination of the patient. At diagnosis it is necessary to consider a combination of local intestinal symptoms to the general. The stomach is blown up, and swelling is more expressed in its average departments; at a palpation morbidity is determined by the course of a large intestine, and also at the left and slightly higher than a navel (Porges's point). At a palpation of a blind and sigmoid gut loud rumbling, sometimes «capotement» (Obraztsov's symptom) is observed. At the accompanying mesadenitis morbidity at a palpation in ileocecal area of a knutra from a caecum comes to light, and also above and to the left of a navel (a cross symptom of Shternberg). At insufficiency of the ileocecal valve local swelling in the right ileal area and morbidity in the field of the ascending colon is defined at its palpation from top to down towards a caecum. For identification of disturbance of absorption use various load tests; disturbance of digestive function of a small bowel is revealed by determination of content of enzymes and their activity in intestinal juice, homogenate of the mucous membrane received by means of an enterobiopsiya and washouts from it (see Intestines, methods of a research). At chronic E. the hypoproteinemia, a disproteinemia, a hypochilesterinemia are observed. In Calais find fat, fat to - you, the changed muscle fibers, undigested cellulose. Make an intestinoskopiya for identification of inflammatory, dystrophic and atrophic changes of a mucous membrane of a small bowel (see), an aim biopsy and morfol. a research of the received material. Rentgenol. the research is of secondary importance.

The differential and diagnostic characteristic of chronic enteritis and nek-ry diseases of intestines is presented in the table.

Treatment chronic E. complex. Food is of great importance. Food during the periods of the expressed aggravations shall be most mechanically and himi-

the cheska sparing, to contain the increased amount of proteins and limited amount of carbohydrates and fats, it is necessary to exclude the products rich with cellulose, whole milk, smoked products, hot and salty dishes (diet No. 4); sodium chloride is limited to 8 — 10 g a day. In

2 — 5 days the diet is gradually expanded, increase amount of the consumed fats and carbohydrates (diet No. 4B), during the subsiding of an aggravation appoint the full-fledged diet containing the increased amount of protein, enough carbohydrates and fats (a diet of N ° 4B), however food shall remain sparing for a long time (see clinical nutrition). According to indications (at an exacerbation of a disease, the accompanying defeat of bilious ways) carry out medicinal therapy. Apply antibacterial agents — antibiotics of a broad spectrum of activity, streptocides (Salazopyridazinum, Biseptolum), derivatives of a 8-sksikhinolin (Intestopanum, Enteroseptolum, Mexasum), drugs of a nitro-furan row (furasolidone, the truck donin), etc. At dysbacteriosis appoint also biol. drugs (kolibakterin, bifidumbacterium, bifikol, laktobakterin, bacteriophage, etc.). For the purpose of impact on immune processes use antihistaminic drugs (Suprastinum, Pipolphenum, etc.), at heavy E. with the expressed digestive disturbances and absorptions — steroid hormones (Prednisolonum on 20 — 40 mg a day within 5 — 7 days with the subsequent transition to maintenance doses on 5 — 10 mg a day). Apply methyl to stimulation of metabolic processes -

the 622nd

uracil, pentoxyl having also antiinflammatory effect. For the purpose of normalization of a metabolism appoint proteinaceous drugs, vitamins, salts of calcium, magnesium, cobalt, at anemia — iron preparations. The fermental drugs (Pancreatinum, festal, panzinorm, abomin, etc.) knitting, enveloping means, and also the means contributing to normalization of digestive and vsasyvatelny function of a small bowel — the anabolic steroids stimulating the processes of membrane hydrolysis, an Euphyllinum and phenobarbital increasing activity of enzymes of membrane digestion, ephedrine, a levodopa are shown. nitrates, cholinolytic and gangliobloki-ruyushchy means. During remission by the patient mineral waters are shown (at a diarrhea appoint Yessentuki No. 4, warmed up to t ° 38 — 45 °; at a lock — Yessentuki No. 17, Bath-linsky, Slavic, etc. in the cold or warmed-up look), physiotherapeutic treatment (thermal and electro-procedures, mud cure), remedial gymnastics, a resort therapy (Yessentuki, Zheleznovodsk, Borjomi, Truskavets, Myrgorod, Arzni, Dzhermuk, Druskininkai, Feodosiy, Kraink, etc.).

Children with chronic E. are under dispensary observation. In the absence of an aggravation within 3 years they can be struck off the dispensary register.

The forecast at timely and full treatment favorable. Working capacity is lost only at the heavy recurrent course of process in connection with sharp dysfunction of intestines.


Prevention chronic E. consists in the prevention and timely treatment of acute diseases of intestines, a balanced diet.

See also Gastroenteritis, the Gastroenterocolitis.



Bibliography: Beyul E. A. and E to and with e-N and N and N. I. Chronic enterita and colitis, M., 1975, bibliogr.; Blochina I. N. and Dorofeychuk V. G. Dysbacterioses, JI., 1979; B of l South e r A. F., etc. A biopsy of a small bowel at acute intestinal infections, Riga, 1973; Gubergrits A. Ya. and Linevsky Yu. B. Diseases of a small bowel, M., 1975; Drozdov S. G. and d river Rotavirusny gastroenteritis, M., 1982; Diseases of the digestive system at children, under the editorship of B. G. Apostolov, page 70, L., 1980; 3 l and t to and N and A. R., etc.,

Nosological classification of chronic diseases of intestines, Owls. medical, No. 3, page 28, 1983; Livshits E. G. and M e d N of e T. A. Sindr of malabsorption in pediatric clinic, Riga, 1979; Pak S. G., etc. New data on a pathogeny of acute intestinal infections, Rubbed. arkh., t. 53, No. 10, page 36, 1981; F r about l ý-to and with A. V. Chronic coloenterites, L., 1975; it, Pharmacological regulation of functions of intestines, L., 1981; Frolkis A. V. and Goran-with to and I am S. V. Intestinal enzymopathies, Chisinau, 1982; BanatvalaJ. E. The role of viruses in acute diarrhoeal disease, Clin. Gastroent., v. 8, p. 569, 1979; Becker V. Malabsorption, Pathogenese und pathologische Anatomie, Z. Gastroent., Bd 13, Sonderheft, S. 189, 1975; Green-berger N. J., Arvanitakis C. H u r w i t z A. Drug treatment of gastrointestinal disorders, N. Y., 1978;

Hiibner K. Die chronisch entziindli-chen, nichtspezifischen Darmerkrankungen, Therapiewoche, Bd 27, S. 6641, 1977; Kirsner J. B. Inflammatory bowel disease, Amer. J. Gastroent., v. 69, p. 253, 1978; Rowe B. The role of Escherichia coli in gastroenteritis, Clin. Gastroent., v. 8, p. 625, 1979; Sleisenger M. H. a. Fordtran J. S. Gastrointestinal disease, Philadelphia a. o., 1978; Spezielle pathologische Anatomie, hrsg. v. W. Doerr u. a., Bd 2, T. 2, S. 1, B. u. a., 1976.

A. V. Frolkis; L. I. Aruin (stalemate. An.), Yu. G. Mukhin (ped.); author of the tab. A. V. Frolkis.