The clinical symptoms of various chronic diseases of the small intestine have much in common, which often leads to an erroneous interpretation of their etiology. Chronic recurrent diarrhea in combination with malabsorption syndrome and metabolic disorders of varying severity are the most typical clinical manifestations in diseases of the small intestine various etiologies. The main pathophysiological factors of chronic diarrhea are intestinal hypersecretion, an increase in osmotic pressure in the intestinal cavity, intestinal hyperexudation (exudative enteropathy), and acceleration of the transit of intestinal contents.

Intestinal hypersecretion is provoked by bacterial toxins, deconjugated bile acids, inflammatory mediators, which cause damage to the protective parietal mucous barrier of the small intestine, enterocyte membranes with the formation of inflammatory mediators and neuropeptides. Toxins and these stimuli are perceived by specific receptors on enterocyte membranes and activate the synthesis of cyclic AMP inside the cell from ATP. This contributes to a selective increase in the permeability of enterocyte membranes for water, chloride and sodium ions into the intestinal lumen, i.e. secretion, while inhibiting the absorption of sodium ions.

An increase in osmotic pressure in the intestinal cavity (osmotic diarrhea) is observed with congenital fermentopathy (lactase deficiency, celiac disease), when taking osmotic drugs (magnesium, sorbitol, lactulose), an operated stomach, short bowel syndrome, exocrine pancreatic insufficiency.

Lactase deficiency is the most common form of interstitial fermentopathy. The presence of unsplit, non-absorbable milk sugar in the intestinal lumen causes a flow of interstitial fluid from the intestinal walls into its lumen along the osmotic pressure gradient, increasing the volume of intestinal contents and its accelerated passage, osmotic diarrhea. In the colon, bacterial degradation of unsplit glucose to water and organic acids (lactic, acetic, etc.) occurs, which also stimulate the mechanoreceptors of the mucous membrane, accelerating peristalsis. At the same time, acidification of the intestinal contents is noted (pH 4.54.0). Undigested nutrients in the intestinal lumen contribute to the reproduction of opportunistic microflora, dysbiosis develops, causing deconjugation bile acids, an increase in the permeability of the protective mucosal barrier and damage to the epithelium of the intestinal mucosa due to exposure to bacterial toxins. Penetrating through damaged lipoproteins of intercellular membranes of enterocytes, macromolecules of unsplit proteins and sugars cause allergic reactions and food intolerance, which occur in 530 patients of this profile (A.M. Nogaller, 1994; V.K. Mazo, 1997). Connection atopic dermatitis with an allergic reaction deserves serious attention in determining the etiology of impaired bowel functions, taking into account the food history.

Intestinal hyperexudation exudative enteropathy can be primary (idiopathic) and secondary, resulting from changes in intestinal permeability in other enteropathies (Menetrier's disease, spruceliac, Crohn's disease, tuberculosis, Whipple's disease, radiation enteritis, intestinal lymphoma, carcinoma, abdominal form of lymphogranulomatosis, etc.) . The pathogenetic basis is the increased permeability of the intestinal mucosa with increased intake of plasma proteins (albumin, gglobulin) into its lumen through the ectatic lymphatic vessels of the intestine and their increased catabolism.

Motor functional diarrhea is characteristic of irritable bowel syndrome (IBS), thyrotoxicosis, collagenoses. The most common form of functional diarrhea, IBS, occurs with impaired functions of the small and large intestine (motility, secretion, sensitivity), which is due to a change in the balance and interaction of neurotransmitters and hormones (serotonin, motilin, enkephalins, neurotensin, cholecystokinin, somatomedin, etc.), characteristic of brain and intestinal plexuses axis: brainintestinalbrain (A.M. Ugolev, 1972, 1995; Grossman, 1982; J. Fioramonti, 1997).

Often, several pathophysiological mechanisms are involved in the complex pathogenesis of enteritis - secretory, exudative, motor, which is typical for terminal ileitis (Crohn's disease), ethanol and iatrogenic (drug) enteritis after taking antibacterial drugs, non-steroidal anti-inflammatory and laxatives, radiation damage. Consequences antibiotic therapy are manifested by dysbiosis of varying severity, secretory diarrhea. Taking broad-spectrum antibiotics (kanamycin, lincomycin, neomycin, rifampicin) causes the eradication of normal intestinal microflora and contributes to the overgrowth of clostridia that produce enterotoxins A and B, which cause swelling of the intestinal mucosa and ulceration pseudomembranous enterocolitis with severe manifestations: diarrhea, sometimes bleeding, intoxication, high fever, leukocytosis. The use of clindamycin is the main risk factor for the development of this pathology in debilitated patients. That is why this drug should only be used to treat serious infections.

NSAIDs (indomethacin, brufen, acetylsalicylic acid) inhibit the activity of cyclooxygenase (COX1) and inhibit the synthesis of prostaglandins, which affects the composition of the parietal intestinal mucus, reduces its protective properties, contributing to protein loss, the formation of ulcers, perforations, bleeding.

It should be borne in mind that long-term use of laxatives from the group of anthraglycosides (senna, buckthorn bark, rhubarb, aloe) and diphenolic laxatives (bisacodyl, oxyphenisatin) damage intercellular junctions and cell membranes, increase the permeability of the mucous membrane, desquamation of the epithelium. With prolonged use of laxatives, drug-induced diarrhea with dehydration, hypokalemia, sodium loss, and malabsorption syndrome is observed. Among the side effects described are irreversible changes in the intestinal mucosa, cancer of its various departments.

Tuberculosis of the intestine last years is not a rare diagnosis in chronic diarrhea. The most common localization is the terminal part of the small intestine. Differential diagnosis is carried out between Crohn's disease, a tumor of the intestine and tuberculosis according to the histological examination of a biopsy from the affected area. The detection of epithelioid granulomas with Pirogov-Langhans cells confirms the diagnosis of intestinal tuberculosis.

Radiation enteritis is manifested not only by dysbiosis. Radiation exposure induces chromosomal damage to the DNA of enterocytes, increases apoptosis, mucosal edema, increased mucosal permeability, and exudation of plasma proteins into the intestinal lumen.

In ischemic enteritis (atherosclerosis of the superior mesenteric artery, systemic vasculitis), a violation of mesenteric blood flow causes hypoxia of the intestinal wall, inhibition of the synthesis and activity of enzymes synthesized by enterocytes (disaccharidases, alkaline phosphatase, etc.), which causes malabsorption syndrome.

More rare forms of enteropathy are caused by variable immunodeficiency, Whipple's disease, lymphoproliferative diseases, carcinoid syndrome, hepatoma, HIV infection.

With diversity etiological factors chronic enteropathy, there is a general pattern of development of diarrheal syndrome, loss of fluid and electrolytes, disruption of the structure and function of the mucous barrier of the small intestine, and a decrease in its cytoprotective properties. However, with the complexity of the pathophysiological mechanisms of chronic diarrhea, determining its etiology is a prerequisite for the appointment of rational therapy. It should be emphasized that the term "chronic enteritis" without indicating the etiology of the disease and confirmed morphological signs inflammatory process in the intestinal mucosa is not a complete diagnosis, i.e. nosological concept (A.L. Aruin, 1994), and has not been used in the WHO nomenclature (ICD 10), in foreign literature and in clinics for more than 20 years.

However, widespread medical practice incomplete bacteriological analysis of the "disgroup" without determining Yersinia, Campylobacter, Klebsiella and other rarer microorganisms due to its truncation is not highly informative and therefore does not allow a significant category of patients to reliably exclude the bacterial etiology of enteritis. However, in this situation, only antibacterial therapy can give an antiseptic effect. In addition, in the therapeutic aspect serious problems arise due to the fact that in recent years a change in the pathogenicity and sensitivity to antibiotics of "wild" pathogens of mutant strains has been established, in contrast to previously known ones, i.e. "collection" strains. The frequent occurrence of resistant, including multidrug-resistant, forms of intestinal infections has led to a change in the clinical symptoms of these diseases, which also makes diagnosis difficult. These mutants show resistance to standard antibiotic therapy, for example, to penicillins, tetracyclines, cephalosporins, sulfamides, due to their production of exoenzyme βlactamase, which destroys the βlactam ring of penicillins and cephalosporins. That is why the use of new antiseptics Intetrix, nifuroxazide with a minimum bactericidal concentration and a wide spectrum of antibacterial action against pathogens of gastrointestinal diseases, including mutant strains, is very relevant for both acute and chronic bacterial diarrhea. A valuable property of Intetrix with good tolerance is to maintain the balance of the host's saprophytic flora and restore eubiosis.

Medicinal enteritis is stopped by the exclusion of provoking drugs. With pseudomembranous enterocolitis, it is recommended to cancel clindamycin (lincomycin, neomycin, rifampicin) and prescribe oral vancomycin at a dose of 125,500 mg 4 times a day for 1014 days and metronidazole 250 mg 3 times a day for 1014 days, followed by probiotics.

In the treatment of ischemic enteritis, the main role is given to angioprotectors and antiplatelet agents. The effectiveness of the treatment of Whipple's disease is achieved by long-term use of antibacterial drugs: cotrimoxizole 480 mg 2 times a day (12 months), tetracycline 2 g per day for 612 months. Treatment can last up to two years. In carcinoid syndrome, regression of severe clinical manifestations (persistent diarrhea, temperature rises) is observed after long-term therapy with sandostatin.

Therapeutic tactics involves a combination of etiotropic therapy with pathogenetic. So, in case of chronic diarrhea, additional astringents, sorbents are prescribed: Smektu, bismuth preparations. Smecta increases the thickness of the intestinal mucin layer, adsorbs viruses, bacterial toxins, intestinal gases and bile acids, protecting the mucous membrane, restores the normal intestinal microflora, reduces the secretion of electrolytes, water, normalizes motility, eliminates flatulence. The protective properties of Smecta against various aggressors make it possible to consider it the drug of choice for chronic diarrhea.

According to indications, correction of metabolic disorders is carried out by parenteral administration of electrolyte mixtures, protein preparations, fat-soluble vitamins A, D, K, calcium preparations. Deficiency of intestinal enzymes (dipeptidases, disaccharidases) due to inflammation and destruction of the intestinal mucosa, it is advisable to compensate for the appointment of pancreatic enzymes. To restore the microecological system of the intestine, its stability, probiotics are prescribed. Their sanitizing effect is due to the production of antibacterial metabolites that inhibit the growth of potentially pathogenic microbes and a high ability to adhere to the mucous layer, to the intestinal epithelium. This increases the colonization anti-infective resistance of the intestinal barrier, stimulating the lymphoid apparatus, a sufficient level of secretory Ig A.

Chronic enteropathy - lesions of the small intestine of various origins, accompanied by short-term or long-term enteral insufficiency due to the absence, deficiency or dysfunction of certain intestinal enzymes. Among enteropathies, gluten, disaccharidase, exudative hypoproteinemic (Gordon's disease) and intestinal lipodystrophy (Whipple's disease) are distinguished.

Enteropathies (enzymopathies) are characterized by a deficiency of several enzymes (polyenzymopathies), which is more often observed with secondary, i.e. acquired enteropathies observed in diseases of the digestive system (primarily the small and large intestines, pancreas, etc.), endocrine pathology, immune disorders, drug and radiation exposure. Primary enzymopathies associated with a genetic defect in the synthesis of one of the intestinal enzymes.

Clinically, enteropathy is manifested mainly by a syndrome of insufficiency of digestion (maldigestia) and impaired absorption (malabsorption), as well as gastrointestinal, metabolic disorders, symptoms of disorders of other organs and systems.

celiac disease

Celiac enteropathy is a disease of the small intestine, manifested by a syndrome of insufficient absorption, the occurrence of which is caused by intolerance to one of the components of the cereal protein - gluten (gliadin) due to a congenital deficiency of the enzyme that breaks it down. Synonyms: celiac disease-sprue (from the Dutch sprue - foam, since the patient's stool sometimes resembles foam), celiac disease, idiopathic steatorrhea, non-tropical sprue. Celiac disease was described over 100 years ago by S. Gee.

The prevalence of celiac disease ranges from 1:300 in the west of Ireland, i.e. in 0.3% of the general population, and 1:1000-1:2000 in other European countries up to 1:3000, i.e. 0.03% (average 1:1000). In Estonia, for example, the frequency of the disease is 1:2700 (in 1990-1992), in Paris among the European population - 1:2000, in Sweden - 1-3.7:1000, in Ireland - 1:555, in Italy - 4.6:1000, in Austria - 1:476. Extremely rarely, celiac disease is detected in Africa, Japan and China.

In celiac disease, gluten (and its incomplete breakdown products) eventually damages the lining of the small intestine. Morphologically, there is damage or a decrease in the number of absorptive cells, flattening or disappearance of the villi, a significant increase in the number of proliferating undifferentiated crypt cells, and a noticeable elongation of the crypts. predominantly proximal sections of the small intestine.

Unfortunately, today, as many years ago, when discussing the pathogenesis of celiac disease, we can only say with full confidence that gliadin causes atrophy of the mucous membrane of the small intestine, resulting in malabsorption syndrome, which in turn leads to the development of malnutrition, rickets-like syndrome and many other metabolic disorders. However, exactly how gliadin leads to atrophy of the small intestinal mucosa is not entirely clear.

In the acute period of celiac disease, atrophic changes in the mucous membrane are revealed in the form of smoothness and complete disappearance of the version, an increase in the depth of the crypts. According to our data, the number of goblet cells decreases and they are localized mainly in the area of ​​crypts, while normally these cells are evenly distributed over the entire surface of the epithelial layer. The epithelial layer is flattened, enterocytes acquire a cubic shape, the volume of cells decreases. In enterocytes, the number of lysosomes increases and large digestive vacuoles appear. The height of microvilli is significantly reduced up to their complete disappearance. At the same time, the glycocalyx on the apical plasmolemma is well developed.

There are reports in the literature that against the background of mucosal atrophy in celiac disease, the intensity of epithelial proliferation increases by 3 times. At the same time, the total number of cells in crypts can increase by almost 5 times. The rate of enterocyte migration increases, which is considered as an adaptation in response to the accelerated destruction of cells in celiac disease. The high rate of renewal of the cell population is also confirmed by a significant increase in the concentration of ATP and GTP in combination with a moderate increase in the level of end products of the breakdown of purines in the mucous membrane of the small intestine during the manifestation of the disease. The rate of endogenous cholesterol synthesis in enterocytes in celiac disease in the remission phase is increased, but is suppressed by the administration of gliadin, which may also be associated with hyperregenerative processes in the mucosa. Thus, a complex of changes in the mucous membrane of the small intestine can be referred to as hyperregenerative atrophy.

With the introduction of gliadin in the diet of children with celiac disease in remission within 3-4 days from the moment of administration, the activity of parietal enzymes, especially lactase alanine proline peptidase, clearly decreases in the intestine. In 52% of adult patients with celiac disease, a flat curve is observed during the lactose tolerance test before treatment, in 12% of the violations persist after treatment. With a differentiated hydrogen test, only 67.5% of patients could tolerate 10-12.5 g of lactose, i.e. as much as is contained in 200-250 ml of cow's milk. This indicates lactose intolerance in celiac disease.

The permeability of the intestinal mucosa according to the lactulose-rhamnose test and the test with polyethylene glycol increases against the background of the administration of gluten to children with celiac disease in remission.

All available data indicate a fairly rapid damage to the mucous membrane of the small intestine, although practitioners are well aware of the presence of a significant, sometimes calculated in months (1-2 months on average), latent period between the first introduction of gliadin into the diet and the appearance of clinical signs diseases.

It was shown that when prescribing the III fraction of gliadin, the deepening of the crypts of the small intestine is detected already after 24 hours. . According to other researchers, as early as 2.5 hours after loading with gluten in patients with celiac disease in remission, a decrease in the height of the version, an increase in the number of intraepithelial lymphocytes, a decrease in surface area and the ratio of vein / crypt are noted, and electron microscopy reveals violations of the microvilli, an increase in the endoplasmic reticulum, an increase in lysosomes in the apical part of enterocytes. According to a study with the determination of the level of alpha-2-microglobulin in the perfusate, this time is 60-90 minutes.

Of particular importance is the determination of that peptide fragment of gliadin or that peptide bond that is responsible for the damage to the gastrointestinal tract.

With intraluodenal administration of a synthetic analogue of A-gliadin corresponding to the sequence of amino acid residues 206-217, patients with celiac disease in the remission phase developed characteristic morphological changes in the mucous membrane and a decrease in disaccharidase activity was observed, which was absent with the administration of gliadin to healthy people.

It is assumed that N-terminal and C-terminal fragments of A-gliadin may be responsible for the formation of celiac disease. Peptide fragments corresponding to amino acid sequences 3-21, 31-49, and 202-220 of the A-gliadin molecule were synthesized. Fragment 31-49 causes morphological changes in the small intestine during jejunal perfusion.

In a "toxicity" study on tissue culture of enterocytes from patients with celiac disease, it was found that 4 of the 7 gliadin derivatives studied significantly inhibited the growth of enterocytes. The amino acid sequences -pro-ser-gln-gln- and -gln-gln-gln-pro- were common to all. These sequences are absent in non-toxic cereal peptides. Interestingly, the first sequence is homologous to positions 8-12 of the E1 b protein sequence of adenovirus 12, although it differs by 1 amino acid (-pro-ser-gln-cys-). Rice prolamine also contains moderate amounts of glutamine and proline with the sequences -gln-gln-leu-leu-pro-phe- and -gln-gln-gln-gln-gln-phe-, but rice does not cause celiac disease.

Evidence suggests that some features of the small intestinal mucosa of patients with celiac disease predispose to gliadin exposure. These may be: 1) the inability of brush border enzymes, in particular dipeptidases, to cleave the above bonds or polypeptides, followed by a direct action of gliadin on the epithelium (dipeptidase theory), 2) sensitization of the mucous membrane to gliadin, when the epithelium becomes the target of an immunological process (immunological theory ), 3) congenital features of the receptor apparatus of epitheliocytes, contributing to damage to the epithelium (receptor theory), 4) features of the receptor apparatus of the epithelial cell, prepared by some viruses (viral theory). Finally, a combination of the listed features is possible. All of these options will be discussed in turn below.

Some authors attribute the disease to a reduced activity of dipeptidases in the brush border of enterocytes, which do not fully cleave proline from the gliadin molecule. Uncleaved gliadin, in turn, has a “toxic” effect on the mucous membrane of the small bear. At the same time, other studies have shown that the activity of a number of proline peptidases in the jejunum in celiac disease does not differ significantly from that in healthy people. Contradictory research data do not allow a definitive conclusion. Unfortunately, these studies have not been continued in recent years, but the dipeptidase theory cannot be completely ruled out as an independent one.

Number of cells producing immunoglobulins (Ig) of classes A, M and G in the mucous membrane of the small intestine, with celiac disease in the active stage is significantly increased compared to that in healthy people; in patients on the agliadin diet (AGD), intermediate values ​​are noted. These changes occur in parallel with the in vitro production of IgA IgM, IgC, slgA in mucosal culture from biopsy specimens from the same patients. In celiac disease, there is an increased number of cells in the small intestine that produce antigliadin antibodies (AGA). IgA-secreting cells predominate, while IgC- and IgM-secreting cells are few. Most likely, AGA are secondary markers of the process, but do not have a damaging effect on the epithelium of the small intestine. AGA production is also possible in healthy people; it increases significantly in patients with celiac disease, especially if AGD is not observed. Moreover, in patients with celiac disease, an increased production of antibodies to casein, lactoglobulin and ovalbumin was revealed (in 36-78% of cases). It cannot be ruled out that the reason for this is the increased permeability of the mucous membrane against the background of the atrophic process and the activation of the production of antibodies to other nutritional components is also associated with this.

When loaded with gluten, the number of intraepithelial lymphocytes increases. Being high in the active stage of celiac disease, it decreases against the background of compliance with AGA and increases again with exercise. In celiac disease in remission, the administration of gluten leads to an increase in the number of T-lymphocytes after 2 hours.

In healthy people, about 95% of intraepithelial lymphocytes express heterodimeric receptors consisting of alpha and beta chains. They are carried by CD4+ or CD8+ cells. 5% of T cells carry similar receptors consisting of gamma and delta chains. It is assumed that the latter cells are cytotoxic, producing interleukin-2, and are able to independently recognize the antigen. Activated T cells produce lymphokines that can damage the epithelium, increase mucosal permeability while stimulating crypt epithelial proliferation, which has been shown in tissue culture. We are talking, first of all, about gamma-interferon, and interleukin-1, interleukin-2 and tumor necrotizing factor do not possess these properties. Identification of IEL in celiac disease has shown that in the active stage of the disease or after the administration of gliadin to patients on AHD, the number of T-cells expressing gamma or delta receptors in the mucosa significantly increases. Most of them (90%) do not carry CD8 receptors. It was shown that against the background of gluten loading, the number of T-cells bearing receptors for interleukin-2 (CD25+ cells) increased from 2.8 to 10% after 24 hours and up to 10.8% after 48 hours. These cells were represented mainly by CD4+ and CD8+ cells. In addition, the number of pan-HLA-class II+ macrophages, CD68+ cells, increased. Significantly higher levels of interleukin-2 receptors were shown on blood lymphocytes with a significant correlation with CD4+ but not CD8+ lymphocytes.

When discussing the immunological theory of the pathogenesis of celiac disease, it is important to determine whether the identified immune changes are primary or are the result of mucosal damage. On the one hand, it is impossible to exclude the primary feature of the immune response. An atopic reaction is ruled out, since the corresponding IgE is not detected in celiac disease. The rate of development of the effect suggests the presence of a type III immunological reaction (like the Arthus phenomenon), especially since an increase in the content of IgM cells in the mucosa, the presence of circulating immune complexes in the blood, the complement fixation reaction, and the ability of gluten to stimulate complementary activity according to an alternative way. In light of the peculiarities of the IEL composition, which were discussed in detail above, a type IV immunological reaction cannot be completely excluded either. On the other hand, it has been shown that almost all immunological findings are not strictly specific for celiac disease, but can be observed in other diseases characterized by damage to the small intestine and be a manifestation of the inflammatory process. Indeed, even in healthy people, cells producing AGA are found in the intestinal wall, and gliadin causes an increase in the number of IEL and a decrease in xylose absorption. As a result of damage to the mucous membrane of the small intestine, its permeability may increase, which leads to the entry of large protein molecules through the epithelial layer and the development of a local immune response with an increase in the number of IEL, stimulation of B cells and production of antibodies, including antigliadin ones. Most likely, the identified shifts reflect only the mechanism of damage to the mucous membrane of the small intestine, the final link in the pathogenesis of the disease, but not its fundamental principle.

In this regard, a combination of dipeptidase and immunological theories seems quite likely: as a result of dipeptidase deficiency, undercleaved gliadin causes damage to the mucous membrane and stimulates the immune response.

It was found that in patients with celiac disease in the blood increased titers of antibodies to adenovirus type 12, which decrease against the background of AHD as the condition of patients improves. On this basis, a hypothesis was put forward about the role of viruses in the pathogenesis of celiac disease, which is also unconvincing. Most likely, if viruses play any role in the pathogenesis of celiac disease, then it is secondary. This is indicated by the fact that the level of antibodies to adenoviruses in the blood decreases against the background of AHD without any specific treatment and virus infection is secondary to damage to the small intestinal mucosa, although the subtle mechanisms of this infection have not been established.

It cannot be ruled out that the "toxicity" of gliadin (whole or its fragments) is associated with the presence on the surface of epitheliocytes of some abnormal receptors that gliadin binds to, causing cell damage. Receptor mechanisms, no doubt, are involved in the formation of some symptoms of celiac disease. In particular, from these positions it is possible to explain the immediate strengthening of the intestinal continent when wheat flour mixed with barium slurry is administered to the patient in the course of an X-ray examination, which was once used to diagnose celiac disease. It has also been shown that in vitro acetylglucosamine and its oligomers introduced into the system prevent damage to tissue culture cells obtained from a patient with celiac disease. This made it possible to make an assumption about the disturbed composition of glycoproteins on the surface of the patient's epithelium.

New hypotheses have emerged at the intersection of receptor and immunological theories.

As you know, genetic factors play an important role in the development of celiac disease. The mode of transmission is probably autosomal dominant with incomplete penetrance. Among the closest relatives of the patient, filed by histological examination, the incidence of the disease varies from 2 to 12%. In identical twins, the concordance for celiac disease is approximately 70%, in HLA-identical individuals - up to 30%. On average, 14% of parents of patients with celiac disease themselves have latent celiac disease. The mechanisms leading to the formation of AGA and damage to the small intestinal mucosa are inherited relatively independently. The ability to produce AGA can be defined as features immune system, and high permeability of the mucous membrane for large protein molecules in combination with insufficient activity of proteases of the parietal layer in the small intestine. On the other hand, non-selective hyperpermeability occurs in patients with active celiac disease, which is most likely associated with significant mucosal damage.

A relationship has been established between celiac disease and some antigens of the class II HLA system. Class II major histocompatibility complex - polymorphic membrane glycoproteins that provide functional interaction of cells in the process of immune response. They are encoded on the short arm of chromosome 6 as products of the HI-A-D region and consist of heterodimers of non-covalently linked chains. 15 different subclasses of this class have been identified and 9 respectively grouped in DP , DQ, DR-groups according to the position and similarity of genes. Since these glycoproteins are located on the surface of macrophages, T- and B-cells and perform receptor functions, it can be assumed that they are responsible for the recognition of "toxic" gliadin fractions, triggering a complex of immunopathological processes. In patients with celiac disease, the most common haplotypes are DR3, DR7, DQW2. The DQW2 haplotype in Northern Europe is found in more than 90°/o of patients with celiac disease (72% of the general population). Antigens DR3 and DR7 were detected in 80 and 50°/o, respectively, of patients with celiac disease, and the combination - in 34°/o (among the general population, respectively, 26, 20 and T/o). The risk of developing celiac disease is 11:5:60. Overall, only 10% of celiac patients in Europe have neither DR3 nor DR7 genes. In relatives of patients with celiac disease, DR3 occurs in 55-60% of cases. The DR.3 heterodimer consists of DQ a 1 0501 and DQ b 1 0202 monomers located on the same chromosome (cis position), while DR5 includes DQ a 1 0501, and DR7 contains DQ b I 0202. Thus , DR5/DR7 heterozygotes contain the same combination of monomers located, however, on different chromosomes (trans position). This feature combines two haplotypes that are most common among patients with celiac disease.

The receptor-immunological theory could answer many questions regarding the pathogenesis of celiac disease, especially in the light of recent data obtained from the study of the characteristics of the genotype of patients. Since haplotypes DR3 and DR5/DR7 are associated with the presence on the surface of B-lymphocytes, activated T-cells, enterocytes and macrophages of receptors for gliadin or its fragments, which are involved in the presentation of gliadin to T-helpers, the presence of abnormal receptors determines an inadequate response of the immune system to gliadin with damage to the mucous membrane of the small intestine. This point of view, partly confirmed by experimental work, can become a link between all other theories of the development of celiac disease. This does not exclude the importance of dipeptidase deficiency, which can facilitate the access of uncleaved gliadin to these receptors. However, since not all patients with celiac disease have one of these haplotypes, the question may arise either about the presence of unknown similar haplotypes, or about the heterogeneity of celiac disease, or about the unreliability of the proposed hypothesis.

Clinical symptoms in children. Celiac disease manifests itself after the introduction of gliadin-containing foods into the diet. Very often this product is semolina, which is usually introduced into the diet at the age of 4-6 months, therefore, in the classical case, the manifestation of celiac disease occurs at the 6-8th month of life. In some cases, gliadin-containing products, including some artificial feeding formulas, may be introduced earlier than indicated, which suggests a correspondingly early manifestation of the disease. From this follows the need for a thorough history taking of a child with malabsorption syndrome and knowledge of the composition of modern foods. On the other hand, in many children, the manifestation of celiac disease occurs late, sometimes 5-6 months or more after the first introduction of gliadin-containing foods into the diet, sometimes after infectious disease(intestinal infection, SARS), but often for no apparent reason. Previously, such celiac disease was called secondary, considering that it is not congenital, but acquired. Currently, there is a point of view that all cases of celiac disease have a congenital basis, and the timing of manifestation is associated with the degree of severity of the underlying defect and, consequently, with the compensatory capabilities of the intestine. The infectious process in this case is not a cause, but a provoking factor. Thus, the timing of the manifestation of celiac disease varies widely, but, according to our observations, the maximum frequency occurs at the age of 6 months to 2 years.

Typical features celiac disease in children are frequent mushy profuse stools with a grayish tint, weight loss, abdominal enlargement, subsequently - lag in psychomotor development. The first three symptoms may appear simultaneously or in any order, making it difficult timely diagnosis diseases. The severity of symptoms also fluctuates, and quite significantly. In this regard, celiac disease should be excluded during the differential diagnosis in all cases of malabsorption syndrome of unknown origin.

Clinical manifestations in adults are highly variable. In a severe course of the disease, when the entire small intestine is involved in the pathological process, a pronounced, untreatable, often life-incompatible syndrome of total malabsorption develops. Patients with limited lesions, including only duodenum and proximal jejunum may not have gastrointestinal symptoms. They may only have anemia due to iron deficiency and/or folic acid, vitamin B 12, as well as signs of bone demineralization.

Persistent diarrhea with polyfaeces, watery or semi-formed stools, light brown or gray, or greasy, often frothy, with a characteristic fetid, rancid odor. Some patients have constipation. Severe flatulence, pain around the navel, loss of appetite, weight loss, burning and soreness of the tongue.

The skin is dry, the nails are dull, crumble, the hair is brittle, it falls out easily. Fingers "drum sticks", nails - "watch glasses". Hypoproteinemic edema.

Palpation of the abdomen is painful in the umbilical region.

Relationship of exacerbation of the disease with the inclusion in the diet of food products from wheat, rye, oats, barley, containing gluten.

The disappearance of the symptoms of the disease with a gluten-free diet.

The natural course of untreated celiac disease is characterized by alternating periods of exacerbation and remission. The disease can begin in infancy when foods containing gluten are introduced. If treatment is not started, the symptoms are observed throughout childhood, but during adolescence they often decrease or disappear completely. In 30-40 years, the symptoms of the disease usually resume.

In a number of patients, the manifestations of the disease are virtually absent, and the diagnosis is difficult until they reach middle and even old age. Asymptomatic course of the disease in adults is possible.

Laboratory data

1. KLA: anemia. 2.BAK: hypoproteinemia, hypocalcemia, decreased iron content. 3.Coprocytogram: steatorrhea, pieces of undigested food. 4. Decrease in the content of aminopeptidase in the intestinal juice.

Survey program

1. Identification of the connection between the exacerbation of the disease and the gluten-free diet and the effect of the gluten-free diet. 2. OA of blood, urine, feces. 3.BAK: total protein, protein fractions, iron. 4.Coprocytogram. 5.Gliadinotolerant test - after taking gliadin (350 mg/kg of body weight), the content of glutamine in the blood increases by 40% or more.

Celiac disease is often accompanied by secondary metabolic disorders. All types of metabolism suffer, primarily protein. On the one hand, malabsorption itself can lead to significant protein deficiency, on the other hand, damage to the mucous membrane of the small intestine often leads to the development of secondary exudative enteropathy. As a result of severe hypoproteinemia and hypoalbuminemia, protein-free edema develops, up to anasarca. Malabsorption of calcium and vitamin D leads to the development of osteoporosis and the formation of rickets-like deformities of the skeletal system. Lipid and carbohydrate malabsorption affects energy metabolism. Formed polyhypovitaminosis. Lactase deficiency often accompanies celiac disease, there is bloating and rumbling in the abdomen after drinking milk, the stool becomes frothy and acquires a sour smell. An inevitable consequence of any trouble in the intestines is intestinal dysbacteriosis, in connection with which greens and mucus can be found in the stool. Finally, against the background of celiac disease, food allergy, including intolerance to cow's milk proteins. In the absence of treatment, there is a lag in psychomotor development, children, especially those of the 1-2nd year of life, lose their acquired skills, become apathetic.

The lack of clear knowledge about the pathogenesis of celiac disease does not allow the development of a rigorous diagnostic program. The diagnosis is made on the basis of clinical manifestations, anamnesis data, endoscopic and histological studies of the small intestine mucosa and the detection of AGA in the blood. Endoscopically in the jejunum in many patients with celiac disease, transverse striation of the folds is detected, however, this symptom is not absolute and, in rare cases, can occur with some other diseases of the small intestine.

Histologically, atrophy of the mucous membrane of the small intestine, flattening of the epithelium, deepening of the crypts and increased mitotic activity are determined.

The level of IgA class AGA increases in early dates diseases; against the background of treatment, they quickly disappear within 1-2 months. AGA of the IgC class appear later than IgA and their level may remain elevated for 6-12 months even with adequate therapy. For reliable serological diagnosis definition of AGA of both classes is necessary.

An additional examination method can be a stool lipidogram, which will clarify the nature and severity of steatorrhea, will allow to differentiate pancreatic damage, characterized by increased excretion of triglycerides with feces, from intestinal damage with increased excretion of non-esterified fatty acids. The xylose test makes it possible to generally assess the degree of malabsorption of monosaccharides using xylose as an example. The determination of carbohydrates in feces allows you to establish the severity of lactase deficiency. However, it should be emphasized that these methods are auxiliary in nature, their results may indicate the presence of celiac disease, but they cannot definitively confirm the diagnosis.

Due to the difficulties of diagnosis, back in 1969, the European Society of Gastroenterologists and Nutritionists (ESPGAN) proposed the following criteria for celiac disease: 1) persistent intolerance to gliadin, 2) atrophy of the small intestine mucosa develops in the active phase of the disease, 3) against the background of AHD, the mucous membrane is restored, 4) repeated introduction of gliadin into the diet leads to the development of atrophy of the small intestine mucosa. This procedure for diagnosing celiac disease can be applied in doubtful cases. Attention should be paid to the need to comply with all parts of the protocol. In particular, one cannot focus only on the positive effect of AHD, since it can be observed not only in celiac disease, but also in many other intestinal diseases.

Erased and atypical cases of celiac disease cause particular difficulties for diagnosis. The severity of pathological changes and, consequently, the symptoms of the disease can vary widely, and in practice there are cases when children are in a critical situation already 2 months after the manifestation of celiac disease. On the other hand, there are cases when children with the manifestation of the disease in the 1st-2nd year of life lived up to 9-10 years without treatment. In the latter case, severe secondary metabolic disorders develop, which may even come to the fore and mask the symptoms of the underlying disease. Most often this concerns violations of phosphorus-calcium metabolism with the development of severe rickets-like syndrome, bone deformity and short stature. There are cases of severe hypocalcemia with the development of convulsive syndrome, in connection with which there were suspicions of epilepsy.

In atypical cases, celiac disease is manifested by any individual symptom. Even such a classic sign as diarrhea may be absent or mild. We observed a case of celiac disease, which manifested as diffuse osteoporosis, and the only symptom was pain in the legs. Short stature may also be the only sign of this disease. In these cases, the diagnosis is confirmed histologically and serologically.

The mainstay of treatment for celiac disease is strict adherence to a gluten-free diet (AGD). All cereals should be excluded from the diet, except for rice, buckwheat, corn, as well as foods that may contain them, including sausages, sausages, and some canned food. Usually the diet is supplemented with the exclusion of lactose and allergens.

Soy formulas or mixtures based on casein hydrolyzate can be prescribed for children of the 1st year of life. good effect gives the introduction to the diet of fats based on medium chain triglycerides, which are broken down and absorbed in the intestine much more easily than conventional long chain ones. AGD is complemented by post-syndromic therapy. Strict adherence to the diet with timely initiation of treatment allows for the normal development of the child. Currently, it is considered proven that celiac disease requires lifelong dieting, since a departure from it is not only fraught with a possible exacerbation of the process, but significantly increases the risk of developing malignant neoplasms, including intestinal lymphomas.

Correction of metabolic disorders in patients with celiac disease depending on the severity of malabsorption syndrome

The doctor can exercise serological control over the diet according to the dynamics of AGD, especially IgA, as well as histological control during control biopsies - to restore the mucous membrane of the small intestine. In patients who strictly adhered to a gluten-free diet, the average content of antibodies to the -fraction of gliadin in IgA does not exceed the norm and IgG is moderately increased in half of the patients.

In the case of strict adherence to the diet and adequate additional therapy children with celiac disease do not lag behind their peers either in physical or mental development.

Disaccharidase-deficient enteropathies

Decreased activity or absence of one or more congenital or acquired disaccharidases leads to impaired digestion of disaccharides and the development of disaccharide-associated conditions.

Etiology and pathogenesis. In the intestinal mucosa, 6 disaccharidases were isolated by chromatography:

Only monosaccharides can be absorbed.

The most common deficiency lactase(milk intolerance) - in 15-20% of adult residents of Northern and Central Europe and 75-100% of the indigenous peoples of Africa, America, East and Southeast Asia, invertases(sucrose intolerance) trehalase(mushroom intolerance) cellobiase(intolerance to foods high in fiber). Unsplit disaccharides are not absorbed and serve as a substrate for the active reproduction of bacteria in the small and large intestine. Under the influence of bacteria, disaccharides decompose with the formation of three-carbon compounds, CO 2 , hydrogen.

Clinic. Disaccharidazodeficient enteropathies are divided into primary (hereditary) and secondary, arising from diseases of the gastrointestinal tract or taking certain medicines(neomycin, progesterone, etc.).

Primary disaccharidase-deficient enteropathies

Lactase deficiency is inherited in an autosomal recessive manner. Genetically determined lactase deficiency usually occurs at the age of 3 to 13 years (less often - up to 20 years). Lactase intolerance runs in families. Congenital deficiency of disaccharidases for a certain time can be compensated. At the same time, a long-term deficiency of enzymes that break down disaccharides leads to morphological changes in the intestinal mucosa, a “breakdown” of compensation.

The most common symptoms of hereditary disaccharide-associated enteropathy are a feeling of fullness, bloating, loud rumbling, transfusion, osmotic diarrhea, manifested by severe watery diarrhea that occurs 30 minutes to several hours after ingestion of an intolerable disaccharide. With percussion of the abdomen - a pronounced tympanitis. There is polyfecal matter, feces have an acidic environment.

Acquired (secondary) disaccharidase-deficient enteropathies develop especially often in patients with chronic enteritis (in 80%), ulcerative colitis, Crohn's disease. The clinic - as in the primary, is characterized by the manifestation of symptoms of fermentative dyspepsia.

In the diagnosis of disaccharidase-deficient enteropathies, a test is usually used, which consists in ingesting 50 g of the corresponding disaccharide with the determination of blood sugar, which does not increase significantly during the disease (no more than 1.1 mmol / l after taking lactose). The pH of faeces, lactic acid in feces, disaccharides in feces and urine are also determined.

Treatment. The main method of treatment is a diet with the exclusion of intolerable disaccharides. With lactase deficiency, milk and dairy products are excluded, except for calcined cottage cheese. In the absence of effect - enzyme preparations, astringents and carminatives.

Exudative hypoproteinemic enteropathy (Gordon's disease)

Exudative hypoproteinemic enteropathy (hypercatabolic hypoproteinemia, protein diarrhea, intestinal lymphangiectasia, disease, or Gordon's syndrome) is characterized by increased loss of plasma proteins in the feces.

Etiology and pathogenesis. About 100 cases of primary exudative hypoproteinemic enteropathy have been described. The secondary form of the disease is often found - with Menetrier's disease (giant hypertrophic gastritis), chronic enteritis, celiac disease, Crohn's disease, Whipple's disease, intestinal lymphoma, abdominal LGM, nonspecific ulcerative colitis, condition after resection of the stomach and intestines, sarcoidosis, intestinal amyloidosis, liver cirrhosis, nephrotic syndrome, hypogammaglobulinemia, severe circulatory failure, milk allergy, radiation sickness, SLE.

It has been proven that under physiological conditions, the body loses about 1/3 of the total amount of protein produced in it every day through the digestive tract, and partly this is the unchanged blood plasma protein. The reason for the development of exudative hypoproteinemic enteropathy is unclear. There is increased protein catabolism and loss of plasma proteins (albumin, -globulin) through the ectatic lymphatic vessels of the intestine.

Clinic. Primary exudative hypoproteinemic enteropathy often occurs in young people. At first, the disease proceeds latently due to the compensatory enhancement of the protein-synthetic function of the liver.

Signs of the syndrome: a sharp decrease in the protein content in the blood serum (up to 30-40 g / l, primarily due to a decrease in albumin, hypoproteinemic edema). The syndrome of exudative enteropathy is more often combined with the syndrome of malabsorption.

With exudative enteropathy, lymphoproliferative diseases, primary and secondary lymphangiectasia, lymphangiomatosis, and also in some patients with Whipple's disease, the mucous membrane has a greasy appearance, whitish deposits are visible on its surface, resembling snow flakes, the folds are sharply thickened. As a result of edema, the intestinal lumen sharply narrows, the endoscope (11 mm) barely passes into the lumen. These changes are explained by lymphostasis.

The general name of non-inflammatory chronic bowel disease that develops as a result of fermentopathy (enzymopathy) or congenital anomalies in the structure of the intestinal wall.

Enzymopathy or enzymopathy the general name of diseases or pathological conditions that develop due to the absence or violation of the activity of any enzymes (enzymes).

Distinguish between congenital (primary) and acquired (secondary) ) enteropathy associated with a decrease in the activity of key enzymes that ensure digestion and absorption of nutrients (food components).

Acquired (secondary) enzymopathies develop against the background of inflammatory or degenerative changes in the mucous membrane of the small intestine.

Classification of congenital enteropathies

Diseases associated with congenital absence or deficiency of enzymes.

Congenital deficiency of disaccharidases.

Disaccharidase deficiency- this is a violation of the digestion and absorption of disaccharides (lactose, sucrose, trehalose, maltose and isomaltose), due to a deficiency of the corresponding intestinal enzymes (lactase, sucrase, trehalase, maltase and isomaltase).

Disaccharidase deficiency develops in the pathology of the small intestine and is associated with a decrease in the activity of enzymes produced by enterocytes. Intestinal disaccharidases break down food disaccharides into monosaccharides, which are absorbed into the blood. Violation of membrane hydrolysis leads to the formation in the intestinal cavity of a large amount of unsplit and non-adsorbed substances, which contribute to an increase in osmotic pressure in the intestinal lumen. Increased osmotic pressure, in turn, increases the secretion of fluid and motor activity of the intestine, causing the appearance of the main clinical symptom all fermentopathies - diarrhea.

Clinical manifestations of various types of disaccharidase deficiency are practically the same. The difference is only in what foods cause the symptoms of the disease. The severity of clinical manifestations of fermentopathy and the severity of malabsorption depend on the degree of enzyme deficiency and the content of carbohydrates hydrolyzed by it in the food taken.

congenital lactase deficiency.

Congenital deficiency of sucrase (isomaltase).

Congenital trehalase deficiency.

Congenital deficiency of enterokinase (enteropeptidase).

Congenital peptidase deficiency - Celiac disease (celiac disease).

Diseases associated with congenital absence or deficiency of transport carriers. They are extremely rare.

Syndrome of malabsorption of monosaccharides.

Insufficiency of absorption of monosaccharides (glucose, galactose and fructose) is due to defects in transport systems - carrier proteins of the brush border of epithelial cells of the small intestine. In most cases, these defects are congenital (primary monosaccharide malabsorption) and are inherited in an autosomal recessive manner.

The process of absorption of glucose and galactose occurs with the participation of the same carrier proteins, therefore, in the presence of their defect, malabsorption of both monosaccharides occurs.

In fructose malabsorption disorders, there is a defect in another transport system, so primary fructose malabsorption develops regardless of the presence or absence of malabsorption of glucose and galactose.

In severe lesions of the small intestine (chronic enteritis, celiac enteropathy), secondary (acquired) insufficiency of absorption of monosaccharides may develop.

Glucose and galactose intolerance.

fructose intolerance.

Amino acid malabsorption syndrome - congenital malabsorption:

Tryptophan malabsorption is Hartnup's disease.

Malabsorption of methionine.

Low's syndrome.

Cystinuria, lysinuria, immunoglycinuria, etc.

Lipid malabsorption syndrome:

Abetalipoproteinemia.

Malabsorption of bile acids.

Vitamin malabsorption syndrome:

Violation of the absorption of vitamin B 12.

Folic acid malabsorption.

Mineral malabsorption syndrome:

Acrodermatitis enteropathic.

Primary hypomagnesemia.

Menkes syndrome.

primary hemochromatosis.

Familial hypophosphatemic rickets.

Electrolyte malabsorption syndrome:

Congenital chloride.

Lethal familial diarrhea.

Classification of secondary malabsorption

Absorption disorders against the background of inflammatory diseases:

Acute and chronic enteritis.

Crohn's disease .

Diverticulitis. Amyloidosis of the small intestine.

Resection of the small intestine.

Surgical anastomoses of the small intestine.

malabsorption due to coronary disease digestive organs.

Absorption disorders due to diseases of the hematopoietic system:

Clinical manifestations of celiac disease

Ø Typical ("classic") form - develops at any age, manifests

severe diarrhea with polyfaeces, steatorrhea, anemia, malabsorption syndrome with metabolic disorder inherent in malabsorption syndrome II-III severity. Occurs infrequently today 10-30% all cases of celiac disease.

Ø The atypical form (the most common) is characterized by the predominance of extraintestinal manifestations in the clinical picture of the disease (for example, hemorrhagic syndrome, anemia, endocrine disorders) without or with mild clinical manifestations of gastrointestinal lesions; detected in individuals with associated pathology, in groups

Ø Latent form - proceeds subclinically (in 5-10% of all cases of the disease), is detected incidentally. It is characterized by the absence of clinical manifestations of the disease with - possibly - increased titers of antibodies specific for celiac disease in individuals with a corresponding genetic predisposition. The mucous membrane of the small intestine is still, as a rule, morphologically unchanged. Atrophy and clinical manifestations of the disease may occur in response to an intense gluten load.

Typical clinical manifestations "classic" celiac disease are:

Ø diarrhea (with a frequency of up to ten times a day) and a change in its nature - liquid, mushy of various shades (more often greenish) polyfecal, steatorrhea, fetid, frothy

Ø Malabsorption

Ø abdominal pain (indistinctly localized), severe bloating, feeling of discomfort

Ø loss of appetite up to anorexia

Ø weight loss

Ø mucosal damage oral cavity- aphthae, glossitis

The gold standard in the diagnosis of celiac disease is endoscopy with biopsy and serodiagnosis: antigliadin antibodies, IgA antibodies to endomysium, antireticulin antibodies

Malabsorption - (from lat. malus - bad and lat. absorptio - absorption) - loss of one or many nutrients entering the digestive tract due to deficiency

their absorption in the small intestine.

1. The primary develops with a genetically determined enzymopathy: fructose intolerance, glucose-galactose intolerance, malabsorption of many amino acids (Hartnup's disease), malabsorption of vitamin B12 or folic acid.

2. Secondary occurs in diseases such as pancreatitis, hepatitis, gastritis, enteritis, celiac disease, colitis and certain diseases thyroid gland. It occurs much more often than primary malabsorption.

3. Sometimes it develops against the background of enzymatic deficiency, dysbacteriosis, progressive exhaustion ( anorexia, bulimia), hypovitaminosis, anemia (anemia), osteoporosis and increased intestinal motility.

Clinical picture

Symptoms of malabsorption are a reflection of metabolic disorders: protein, fat, carbohydrate, mineral, water-salt, as well as vitamin metabolism disorders.

Characterized by diarrhea that may be irregular for a number of years, but then becomes constant m. Often there are oligosymptomatic forms, in which there is a temporary rapid stool, pronounced flatulence with the release of fetid gases. Associated symptoms include: thirst, drowsiness, fatigue, apathy, muscle weakness, weight loss. The skin becomes dry, in the area of ​​​​the organs of the oral cavity, the phenomena of glossitis and stomatitis are noted. The tongue is usually bright red with flattened papillae.

In severe cases, polyfecal matter is observed - the daily amount of bowel movements exceeds 200 grams and can reach 2500 grams. . The stool is unformed, mushy or watery with a sharp

unpleasant odor, can be accelerated up to 6 times a day.

A constant symptom is steatorrhea (insufficient absorption and excretion of fats). Mineral deficiency leads to bone changes, in severe cases to osteomalacia (softening and deformation of the bones). In addition, edema, anemia occur, trophic changes in the skin and nails are clearly manifested, and muscle atrophy progresses. Fatty and protein degeneration develops in the liver, which is subsequently replaced by atrophy of the parenchyma of the organ. Decrease in body weight can reach the degree of cachexia.

Diagnostics

Includes functional absorption tests. With coproscopy, the remains of undigested food are found, in the blood test - hypoproteinemia.

Syndrome of insufficient digestion (maldigestion) is a number of signs characterizing a violation of abdominal or parietal digestion ingastrointestinaltract. Mixed forms of indigestion may also occur.

at the same time, incomplete splitting of food ingredients is noted (depending on the level of damage to the digestive canal), rapid reproduction of bacterial associations with the settlement of flora not only in the distal, but also in the proximal sections of the small intestine. Dysbacteriosis develops.

The bacterial flora is much more active than normal, participating in the fermentation of undigested nutrients, which leads to the formation of a number of toxic substances(indole, skatole, ammonia, low molecular weight fatty acids, etc.).

Toxic products of bacterial fermentation irritate the mucous membrane of the small intestine, causing increased peristalsis. After absorption and entry into the blood, they lead to general intoxication of the body.

Patients with intestinal insufficiency of food digestion present

complaints of a feeling of rumbling and transfusion in the intestines, bloating, severe flatulence, diarrhea with copious discharge of undigested feces with a sour or putrid odor.

In case of violations of abdominal digestion, scatological research methods are of great importance in the diagnosis. Steatorrhea, creatorrhea, amylorrhea are usually detected.

X-ray examination allows you to clarify the level of damage - the stomach or intestines, and in the latter case, there is an acceleration of the movement of barium suspension through the small intestine.

In order to clarify the cause of the development of maldigestion syndrome, the definition of the exocrine function of the pancreas, enterokinase and alkaline phosphatase in intestinal juice, aspiration biopsy of the small intestine mucosa.

The degree of violation of abdominal digestion is revealed in the study of the glycemic curve with a load test using a starch suspension, as well as using a radioisotope method with trioleate glycerin, sunflower or olive oil.

At bacteriological examination feces, it is necessary to identify the degree and nature of dysbacteriosis.

The diagnosis of parietal digestion disorders is determined by examining the enzymatic activity of amylase and lipase in homogenates of the small intestine mucosa. They are obtained by aspiration enterobiopsy, and the enzymes are isolated by sequential desorption.

The specific features of the glycemic curve obtained after food loads with mono- and disaccharides characterize the differences in the maldigestion syndrome with

disorders of parietal digestion from diseases associated with impaired absorption of food ingredients by the wall of the small intestine (malabsorption syndrome).

Determination of the glycemic curve during loading with polysaccharides (starch suspension) makes it possible to differentiate disorders of abdominal and parietal digestion.

At aspiration biopsy mucous membrane of the small intestine revealed a variety of atrophic or dystrophic changes in the villi, microvilli, circulatory disorders in the submucosal layer.

Course and treatment depend on the underlying disease. For the purpose of symptomatic therapy, enzyme and astringent preparations are used orally. Intestinal antiseptics.These drugs have a less detrimental effect on the symbiotic microbial flora than antibiotics. These include Intetrix, Ercefuril, Nitroxoline, Furazolidone, etc. Antibacterial drugs appointed within 10–14 days. The use of an antibiotic is justified as a backup.

Probiotics. The most widely used probiotics: Linex, Bifidumbacterin, Probifor. The course of treatment should last 1-2 months.

Enterosorbents. This group of drugs does not inhibit the normal intestinal microflora. Their disadvantage is indiscriminate sorption of conditionally pathogenic microflora and its toxins. The drugs are prescribed in short courses of 5 to 10 days. Enterosorbents are used only in the form of monotherapy, because. may inactivate the action of other drugs. These include: Filtrum, Laktofiltrum (1 tablet 3-4 times a day), Enterosgel (1 tablespoon, dissolved in 1/4 cup of water, 3 times a day).

Stimulants of the body's reactivity. To increase the reactivity of the organism in debilitated patients, it is advisable to use Gepon, Timalin, Timogen, Immunal, Immunofan and other immunostimulating agents. The course of treatment should last an average of 4 weeks. At the same time prescribe vitamins.

The term "exudative enteropathy" refers to a pathological condition characterized by the loss of blood plasma proteins through gastrointestinal tract. Usually, exudative enteropathy is accompanied by a violation of intestinal absorption (which results in a pronounced decrease in the content of blood proteins), the appearance of edema, undigested fat in the feces. Unlike other syndromes of malabsorption in exudative enteropathy, there may be no pronounced symptoms of damage to the small intestine. In rare cases, the child may lag behind in physical development.

Allocate primary and secondary forms of exudative enteropathy.

The primary forms are due to the phenomenon of lymph loss through the small intestine, which can be caused by pathological dilation of the lymphatic vessels or a generalized lesion. lymphatic system. Lymph loss can also be observed as a result of a violation of the outflow of lymph with a blockade of initially unchanged lymphatic vessels or obstructed venous outflow (for example, with heart disease).

Secondary causes of the development of exudative enteropathy, leading to a violation of the integrity of the intestinal mucosa, include a number of diseases from the gastrointestinal tract, from the kidneys, liver, and lungs. In addition, disorders of the immune system, the presence of allergic reactions, and many other diseases can play a role in the development of exudative enteropathy.

The clinical manifestations of the disease are determined by the loss of blood plasma proteins, the severity of subsequent disorders, as well as age characteristics. The allocation of a certain amount of protein through the intestines is a physiological norm. A decrease in plasma protein content occurs when the loss of protein exceeds the rate of its synthesis in the body. Due to differences in the rate of synthesis of various protein fractions, the violation of their ratio is as follows: the amount of albumin decreases and ¡ globulins in blood serum. The fibrinogen level almost always remains within the normal range. The constant loss of lymphocytes leads to a persistent absolute or relative decrease in their number, which is an important criterion for making a diagnosis. Along with protein, fats, trace elements and some vitamins are lost. Deficiency of these substances can change the clinical picture in the direction of greater or lesser severity, and in some cases may be leading (for example, convulsions against the background of a pronounced decrease in the amount of calcium in the blood).

Primary intestinal lymphangiectasia (dilation of the lymphatic vessels of the small intestine) is a special form of the syndrome that occurs with the loss of blood plasma protein. This pathology was first described in 1966. It is assumed that it is inherited in an autosomal recessive manner. However, the possibility of dominant inheritance with a high frequency of manifestation and varying degrees expression of the pathological gene.

The clinical picture is dominated by massive asymmetric edema that persists for a long time, located mainly on lower limbs, as well as in body cavities (abdominal, pericardial cavities, pleural cavities), a decrease in the amount of plasma proteins, a violation of the ratio of their fractions, symptoms of dysfunction of the gastrointestinal tract, a secondary immunodeficiency state. In some children, the disease begins to manifest itself at birth. The expansion of the lymphatic vessels in Noonan syndrome is accompanied by a severe form of constantly appearing edema of the hands and feet, the toenails turn yellow, become convex, and their transverse striation appears. There are cases of a combination of expansion of the lymphatic vessels of the intestine with Di George's syndrome, underdevelopment of tooth enamel.

Diagnosis for this disease is based on the detection of a reduced number of lymphocytes in the blood, changes in the biochemical parameters of the blood. Diagnosis is possible by determining serum proteins in feces. Quantitative loss of protein in the intestine can be determined by special technically complex research methods carried out in large hospitals. The study of the state of the lymphatic system by the introduction of a contrast agent often reveals its underdevelopment. peripheral departments and a visible slowdown in the movement of lymph (up to its complete absence in some vessels). In some cases, there may be no lymph nodes near the aorta, as well as blockage of the thoracic lymphatic duct with the flow of a contrast agent into the intestinal lumen. Great diagnostic value is attached to clarifying the condition of the intestinal mucosa. An endoscopic examination of the intestine reveals the following picture: the folds of the mucous membrane of the jejunum are preserved, pale pink or pink in color with a pronounced vascular pattern, sometimes pinpoint hemorrhages, an increase in lymph nodes are determined, and a peculiar growth of the mucous membrane is also observed in the form of numerous bulges. Characteristic of the disease under consideration is the detection of histological examination pieces of the intestinal mucosa taken during endoscopic examination, dilated lymphatic vessels.

Therapeutic measures for exudative enteropathy are reduced to the intravenous administration of protein preparations, a sharp restriction of animal fats in the diet with their replacement vegetable oil. Use preparations containing fats, which are easily broken down by pancreatic enzymes without the participation of bile acids and absorbed into the body. venous system, helping to reduce the formation of lymph and facilitating its movement. Signs of the inflammatory process in the form of accelerated ESR, increased levels of circulating immune complexes dictate the need for hormonal drugs, the treatment of which can lead to the elimination of clinical manifestations of exudative enteropathy. With severe edematous syndrome, diuretics (diuretics) are needed. In addition, it is necessary to use preparations of potassium, calcium, iron and vitamins.

Intestinal enteropathy is the general name for non-inflammatory chronic bowel diseases, which are based on fermentopathy or congenital anomalies structure of the intestinal wall. Gluten enteropathy (European sprue, non-tropical sprue, adult celiac disease, idiopathic steatorrhea) is a rare hereditary disease (fermentopathy) of the intestine, characterized by the absence or reduced production of enzymes by the intestinal wall that break down gluten (gluten) - a polypeptide contained in some cereals (wheat, rye, barley, oats). The absence (or relative insufficiency) of the production of this peptidase is especially manifested in malnutrition, the predominance of cereals containing gluten in food, and intestinal infections. Products of incomplete digestion of gluten (gliadin, etc.) have a toxic effect on the intestinal wall.

Diarrhea that occurs when eating foods made from wheat, rye and barley is characteristic. With the progression of the disease, polyhypovitaminosis, disorders electrolyte balance, exhaustion. In advanced cases, chronic enteritis develops with a syndrome of insufficiency of absorption. Known assistance in differential diagnosis can be provided by samples with a load of gliadin ( rapid rise levels of glutamine in the blood after oral administration of gliadin at a dose of 350 mg / kg), the presence of signs of the disease from early childhood, exacerbation of the symptoms of the disease with a significant addition to the diet of products from wheat, rye, barley, oats, as well as the reverse development of symptoms of the disease during transfer a patient on a gluten-free diet (gluten is absent in all animal products, in corn, rice, soybeans, potatoes, vegetables, fruits, berries and other products).

Treatment in severe cases of the disease is carried out in a hospital. The patient is transferred completely to a gluten-free diet with a high content of vitamins, enveloping and astringent affinities are prescribed orally. As the condition improves, the diet is expanded, but the content of gluten-containing foods in the daily ration is left limited. Disaccharidase-deficient enteropathy - hereditary diseases caused by the absence or insufficiency of the production of disaccharidases (lactase, maltase, invertase, etc.)

), as a result of which the parietal hydrolysis in the intestine of the corresponding disaccharose-lactose, maltose, sucrose is disturbed. The type of inheritance has not been precisely established. Clinically manifested intolerance to one (or more) disaccharides and increased fermentation processes when they are taken in normal and especially in high doses; there are symptoms of fermentative dyspepsia, rumbling in the abdomen, flatulence, diarrhea, polyfecal matter with an acidic reaction of feces. Diagnosis and differential diagnosis with others chronic diseases small intestine are based on a number of specific tests: 1) improvement clinical picture diseases after exclusion from the diet of the corresponding disaccharides; 2) the study of glycemic curves after ingestion of various disaccharides-sucrose, lactose, maltose by the patient (the absence of an increase in blood sugar after taking one of the disaccharides and its increase after taking the monosaccharides included in their composition is a sign of a violation of the breakdown of this disaccharide).

Congenital intolerance to disaccharidoa usually manifests itself from childhood. However, a violation of enzyme production can also be acquired due to severe enteritis. In the latter case, a violation of the production of disaccharidases is usually combined with a violation of the production of intestinal epithelium and other enzymes. The course in most cases is not severe, but over time, with a high content of sugary substances in the diet and other unfavorable conditions, as a result of prolonged secondary irritation of the intestinal mucosa with products of increased fermentation, chronic enteritis may develop, accompanied by a syndrome of insufficiency of absorption.

Treatment. Strict adherence to a diet with the exclusion from the diet (or a sharp restriction of the content) of the corresponding disaccharide; in more severe cases - the appointment of enzyme replacement therapy. Exudative enteropathy (exudative hypoproteinemic lymphangiectasia) is a rare disease that occurs mainly in young people. Etiology, pathogenesis are not clear.

It is characterized by pathological expansion of the lymphatic vessels and increased permeability of the intestinal wall, diarrhea, significant loss of protein through the gastrointestinal tract, and hypoproteinemic edema. In severe cases, general exhaustion develops. Often hypochromic anemia, slight leukocytosis with a tendency to lymphopenia. Hypoproteinemia is noted mainly due to a decrease in the content of albumin and gamma-tobulins; hypocholesterolemia; hypocalcemia.

The content of neutral fat, fatty acids and soaps is increased in the stools. Special laboratory methods studies reveal an increased content of protein in the small intestine secretion and an increased excretion of it with feces. A radioisotope study of the excretory function of the small intestine makes it possible to determine an increase in fecal radioactivity and a rapid decrease in blood radioactivity after intravenous administration serum albumin labeled with 1131 or 51Cr, i.e.

Confirms increased loss of protein from the body through the intestines. In biopsy specimens from the intestinal mucosa, there is an expansion of the lymphatic vessels, inflammatory tissue infiltration. In the dilated lymphatic vessels and sinuses of the mesenteric lymph nodes - lipophages containing microdroplets of fat in the protoplasm. Differential diagnosis is carried out with enteritis, enterocolitis, as well as non-inflammatory disaccharidase-deficient enteropathies, sprue, celiac disease.

Enterobiopsy allows establishing the diagnosis of exudative enteropathy with certainty. The disease is chronic and slowly progressive. Patients are prone to intercurrent infections (pneumonia, purulent infections, tonsillitis, etc.).

), which can lead to their death. In severe cases, the prognosis is poor. Treatment during the period of exacerbation is carried out in a hospital. Assign a diet with a high content of protein, vitamins, fluid restriction and sodium chloride.

Plasma is transfused intravenously. Enter vitamins, with hypocalcemia - calcium preparations. With edema, diuretics are prescribed simultaneously with plasma transfusions and various protein preparations.

Attention! The described treatment does not guarantee positive result. For more reliable information, ALWAYS consult a specialist.