Chronic enteritis: causes

Chronic enteritis is a polyethological disease. Often, it can be the outcome of acute enteritis, but it can also develop independently. Infectious agents play an important role in the onset of the disease, although some researchers believe that after acute intestinal infections, functional disorders are most often observed, which is difficult to accept.

Postponed acute intestinal infections

According to the research, the intestinal infections transferred cause the development of chronic enteritis in approximately 33-40% of patients. Chronic enteritis develops after the transferred dysentery, salmonellosis, staphylococcal infection. In the last decade, Yersinia, Campylobacteria, Proteus, Pseudomonas aeruginosa, viruses, in particular rotavirus, as well as protozoal and helminthic invasion (lamblia, ascarids, strongyloids, wide ribbons, opisthorchia, cryptosporidia) have become of great importance . It is established, for example, that many parasites with long-lasting invasion disrupt the absorption function of the small intestine and can lead to the development of the syndrome of impaired absorption. A role can also be played by the transferred enterovirus infections.

With massive invasion, the cause of chronic enteritis may be Giardia. Lamblias infections are most susceptible to persons - carriers of HLA-A1 and B12 antigens.

Alment factor

In the development of chronic enteritis, nutrition, dry eating, overeating, the use of unbalanced food (ie predominantly carbohydrate and poor vitamins), the abuse of spices, spicy seasonings are of particular importance. It should be noted, however, that these alimentary errors are not, of course, the main etiological factors. They tend to predispose to the development of this disease.

Alcohol abuse

Alcohol can cause malfunction of the mucosa, have a toxic effect on it and contribute to the development of chronic enteritis.

Allergy

The most important among the allergenic effects is food allergy. "Food allergy refers to the clinical manifestations of hypersensitivity to food products, depending on the immune response of food antigens with the appropriate antibodies or sensitized lymphocytes."

The most common allergogenic products are cow's milk, fish, chocolate, eggs, etc.

Exposure to toxic and medicinal substances

Chronic enteritis can develop due to exposure to toxic substances (arsenic, lead, mercury, zinc, phosphorus, etc.), as well as long-term use of many drugs (salicylates, indomethacin, corticosteroids, immunosuppressants, cytotoxic drugs, some antibiotics for prolonged or uncontrolled use).

Ionizing radiation

Ionizing effect on the small intestine causes the development of radiation enteritis. This is possible with radiation therapy of malignant tumors of the abdominal cavity, small pelvis.

Insufficiency of the ileocecal valve

The ileocecal valve prevents regurgitation of the contents of the colon into a thin one. 2-3 hours after eating, its barrier function is dramatically increased. In the preservation of the function of the ileocecal valve, the large role is played by the cecum. It protects the ileocecal valve from excessive hydraulic pressure, being a kind of "vent". Normally, the length of the cecum is 8-10 cm. In case of an inadequate development of it (in 6% of people) ileocecal insufficiency appears.

The formation of the cecum ends at 4 years of age. Congenital inferiority of it can, therefore, appear early and the inadequacy of the ileocecal valve can occur already in early childhood. When the ileocecal valve is inadequate, the contents of the large intestine are thrown into the small intestine during straining, defecation, and increased pressure in the colon - this is the main cause of the development of reflux enteritis.

According to Ya.D. Vitebsky, congenital and acquired, as well as relative and absolute ileocecal insufficiency are isolated. With relative failure, the valve remains open only at high colonic pressure; at absolute - the valve gap continuously.

Insufficiency of the large duodenal nipple

When the large duodenal nipple is insufficient, the outflow of bile out of digestion to the small intestine occurs, which promotes the development of enteritis, diarrhea (bile acids stimulate the motor function of the intestine).

Postponed operations of the gastrointestinal tract

The development of chronic enteritis is promoted by gastroectomy or resection of the stomach, vagotomy, the imposition of gastroenteroanastomosis, resection of the intestine. The development of postoperative intestinal adhesions is also important.

Bowel anomalies

The development of chronic enteritis is promoted by megacolon, congenital changes in the shape of the small intestine.

Ischemia of the wall of small intestine

Ischemic changes of various nature in the wall of the small intestine contribute to the violation of regeneration of the small intestine mucosa, the development of inflammatory-dystrophic changes in it.

The causes of the development of secondary chronic enteritis

Secondary chronic enteritis develops in diseases of the digestive organs (stomach ulcer and duodenal ulcer, chronic hepatitis, liver cirrhosis, bile duct diseases, pancreas), kidney diseases with development of chronic renal failure (uremic enteritis); systemic diseases of connective tissue; eczema; psoriasis; endocrine diseases (thyrotoxicosis, diabetes mellitus); diseases of the circulatory and respiratory organs; immunodeficiency states.

In the pathogenesis of chronic enteritis, an important role is played by motor disorders of the intestine, a violation not only of the function of the digestive glands, but also of immunological homeostasis, microcirculation, changes in the intestinal microflora, genetic factors. Structural and functional disorders of the mucous membrane of the small intestine are facilitated by congenital and acquired changes in the metabolism of the intestinal wall, the disorder of neurohormonal regulation of the regenerative processes of its mucosa.

In the process of chronic diseases of the intestine, both pathological processes in the intestine with the emergence of dysbacteriosis, as well as disorders of functions of a number of digestive organs, metabolic and immunological shifts that can support intestinal disturbances are important.

When studying the mechanisms of chronic diseases of the small intestine, it was established that they have common features with different nosological forms. Among these mechanisms, first of all, the change in the microbial flora and the digestive disorders associated with the reproduction of bacteria in the small intestine, motility and the digestive-transport conveyor, contribute to the onset of disorders of all metabolic species, especially protein and fats.

The main pathogenetic factors of chronic enteritis are the following.

Inflammation and disruption of physiological regeneration of the small intestine mucosa

In chronic enteritis, the inflammatory process develops (the stroma of the mucous membrane is infiltrated by lymphocytes, plasmocytes, eosinophils), but its intensity is not great.

Modern gastroenterologists believe that the greatest value in the pathogenesis of this disease is dystrophic changes and a violation of physiological regeneration of the mucous membrane of the small intestine. In chronic enteritis, there are phenomena of proliferation of the crypt epithelium and a delay in the processes of differentiation of enterocytes. As a result, most villi of the small intestine are lined with undifferentiated, immature and, therefore, functionally inferior enterocytes, which quickly die. These circumstances, of course, contribute to the development of mucosal atrophy, malvdigestia syndromes and malabsorption.

Disturbance of cellular and humoral immunity with the development of a secondary functional immunodeficiency state and the role of allergic mechanisms

Intestine is the most important organ of immunity. The following components of the immune system are present in the small intestine:

• intra-epithelial T- and B-lymphocytes (located between epithelial cells of the mucosa);
• B- and T-lymphocytes of their own layer of the mucous membrane of the small intestine, among the B-lymphocytes predominantly producing IgA;
• Peyer's plaques in the submucosal layer containing B-lymphocytes (50-70%) and T-lymphocytes (11-40%);
• Sollitarnymlifoidnye follicles - in the mucous and submucosal layers. They contain T- and B-lymphocytes, macrophages.

An important element of the immune system of the gastrointestinal tract is the system of secretory immunoglobulins. Intestinal contents contain all classes of immunoglobulins, but the most important is IgA. It is synthesized by the plasmatic cells of its own layer of the small intestinal mucosa.

Secretory IgA has a number of important properties:

• has a high resistance to proteolytic enzymes;
• has antibody-dependent cell-mediated cytotoxicity and opsonization of phagocytosis through the Fc-a receptor
• phagocytic cells. Thus secretory IgA takes part in the penetration of the antigen into the Pieier plaque;
• does not bind the components of complement, therefore the immune complex formed with the participation of IgA does not have a damaging effect on the intestinal mucosa;
• prevents the adhesion of microorganisms, their toxins, food and bacterial allergens to the epithelium of the intestinal mucosa, which blocks their entry into the blood. Anti-adhesive properties of IgA cause its antibacterial, antiviral and anti-allergenic properties.

Dysfunction of the immune system of the small intestine, insufficient production of γ-interferon, interleukin-2, IgA deficiency by lymphocytes promote the penetration of microbial antigens into the body and development of autoimmune mechanisms, maintenance of inflammatory-dystrophic processes in the mucosa of the small intestine. Allergic mechanisms play a role in the pathogenesis of chronic enteritis: production of antibodies to intestinal bacteria (microbial allergy), antibodies to food (food allergy), elements of intestinal tissue (tissue allergy, autoimmune reactions).

Dysbacteriosis of the intestine

In the pathogenesis of chronic enteritis, the development of dysbacteriosis is of great importance, the appearance of which is promoted by a violation of the function of the immune system of the gastrointestinal tract, as well as irrational treatment with antibiotics. Under the influence of dysbacteriosis, digestion and absorption in the small intestine are aggravated (first of all, the digestion of fats suffers). Bacterial toxins activate adenyl cyclase of enterocytes, which leads to an increase in cyclic adenosine monophosphate, a sharp increase in the permeability of the intestinal mucosa, exit into the lumen of water, electrolytes, the appearance of severe diarrhea and the development of dehydration.

Violation of the function of the gastrointestinal endocrine system

In the small intestine, mainly 12-finger, a number of hormones that influence its functions are produced.

• Gastrin - produced by G-cells of the atral part of the stomach, pancreas, proximal small intestine. Has a stimulating effect on the motility of the duodenum.
• Motilin - produced by Mo cells of the upper parts of the small intestine, enhances the motility of the small intestine.
• Somatostatin - is produced in the pancreas, cardiac part of the stomach, upper and lower parts of the small intestine. It inhibits the production of gastrin, motilin, inhibits the motor function of the intestine.
• Vasoactive intestinal polypeptide - is produced in the small intestine, stomach, pancreas. Stimulates intestinal and pancreatic secretion, intestinal motility, insulin secretion, vasodilation.
• Substance P - is produced in the EU cells in the cardiac and antral sections of the stomach, small intestine. Strengthens the peristalsis of the intestine, stimulates the secretion of pancreatic juice, saliva, causes vasodilation.
• Enteroglucagon - produced by A-cells of the proximal parts of the small intestine. Slows the movement of the contents through the small intestine. It is a growth hormone for the gastrointestinal tract, as it is necessary to maintain the normal life and reproduction (cell cycle) of the cells of the gastrointestinal tract. Enteroglucagon changes the rate of cell replication, has a trophic effect, promotes rapid recovery of the intestinal mucosa with various injuries.

The disruption of the functioning of the gastrointestinal endocrine system promotes the progression of inflammatory-dystrophic changes and a decrease in the regenerative abilities of the small intestinal mucosa.

Disturbance of intestinal cavity and membrane (parietal) digestion

Inflammatory-dystrophic and atrophic changes in the mucous membrane lead to a low level of functioning of enterocytes, a deficiency of digestive enzymes - lac gas, maltase, alkaline phosphatase, with the most expressed lactase deficiency. The cavity digestion is sharply reduced.

Along with the cavity digestion, the parietal membrane (membrane) suffers, which is carried out on the surface of the enterocytes (on the "brush border") by enzymes synthesized by the intestinal cells themselves. Membrane digestion is an important final stage in the hydrolysis of nutrients.

Pristenochnoe (membrane) digestion in chronic enteritis is significantly impaired, along with sharply reduced intestinal absorption function (maldigestia and malabsorption syndromes develop).

Fermentopathies

In chronic enteritis, especially with prolonged flow, almost always there is fermentopatin. In a number of patients, fermentopathy may be primary, genetically conditioned (most often lactase deficiency), manifested or aggravated in chronic enteritis. Fermentopathy promotes the development of syndromes of maldigestia and malabsorption.

Fermentopathy is caused by a violation of the enzyme-forming function of enterocytes, its development is promoted by the enhancement of peroxidation in the cells of the small intestine. High activity of lipid peroxidation inhibits, especially the formation of lactase, maltase, and sucrose.

Change in motor function of the intestine

In chronic enteritis, the motor function of the intestine is also impaired, which is facilitated by a change in the function of the gastoointestinal endocrine system. Disturbance of intestinal motility occurs as a type of hyper- and hypomotor dyskinesia. With increasing intestinal motility, the contact of the pituitary chyme with the intestinal mucosa decreases and the digestive processes are weakened. With a decrease in intestinal motility, the progress of the chyme is disrupted, its stasis is developing, which is accompanied by a dysbacteriosis, damage to membranes of enterocytes, a violation of the precipitation of bile acids in the intestine.

Eventually, pathogenetic factors lead to the development of syndromes of toddlers and malabsorption, to protein disorders. Fatty, carbohydrate, mineral, vitamin metabolism and expressed extraintestinal disorders.

At the heart of chronic enteritis is not only inflammation, but also a violation of the physiological regeneration of the mucosa of the small intestine-the proliferation of the crypt epithelium, the differentiation of cells, the "progression" of them along the villi and the rejection into the lumen of the intestine. The process of differentiation of enterocytes is delayed, as a result, most of the villi becomes lined with undifferentiated, functionally inconsistent epitheliocytes, which quickly die. The nares become shorter and atrophy, crypts are sclerosed or subjected to cystic enlargement. The stroma of the mucosa is infiltrated by plasma cells, lymphocytes, and eosinophils.

Based on the data of morphogenesis, chronic enteritis without mucosal atrophy and chronic atrophic enteritis are distinguished. These two forms are essentially the morphological stages (phases) of chronic enteritis, which is confirmed by repeated enterobiopsy.

In chronic enteritis, the whole small intestine or one or other of its departments (etnite, ileitis) is affected.

[1], [2], [3], [4], [5], [6], [7]