Chronic enteritis - Causes

Chronic enteritis is a polyetiological disease. It can often be the outcome of acute enteritis, but it can also develop independently. Infection pathogens play a significant role in the development of the disease, although some researchers believe that functional disorders are most often observed after acute intestinal infections, which is difficult to agree with.

Past acute intestinal infections

According to research, past intestinal infections are the cause of chronic enteritis in approximately 33-40% of patients. Chronic enteritis develops after dysentery, salmonellosis, staphylococcal infection. In the last decade, great importance has been attached to yersinia, campylobacter, proteus, pseudomonas aeruginosa, viruses, in particular rotavirus, as well as protozoal and helminthic invasion (lamblia, roundworm, strongyloides, broad tapeworm, opisthorchiasis, cryptosporidia). It has been established, for example, that many parasites with a long-term invasion disrupt the absorption function of the small intestine and can lead to the development of malabsorption syndrome. Past enterovirus infections can also play a certain role.

In case of massive invasion, chronic enteritis may be caused by Giardia. People who are carriers of HLA-A1 and B12 antigens are most susceptible to Giardia invasion.

Alimentary factor

Dry food, overeating, consumption of food with an unbalanced composition (i.e. mainly carbohydrate and poor in vitamins), abuse of spices and hot seasonings play a certain role in the development of chronic enteritis. It should be noted, however, that the above-mentioned alimentary errors are not, naturally, the main etiological factors. Rather, they predispose to the development of this disease.

Alcohol abuse

Alcohol can cause dysfunction of the mucous membrane, have a toxic effect on it and contribute to the development of chronic enteritis.

Allergy

The most important allergenic effect is food allergy. "Food allergy is the clinical manifestation of increased sensitivity of the body to food products, depending on the immune reaction of food antigens with the corresponding antibodies or sensitized lymphocytes."

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

Exposure to toxic and medicinal substances

Chronic enteritis can develop as a result of exposure to toxic substances (arsenic, lead, mercury, zinc, phosphorus, etc.), as well as with long-term use of many medications (salicylates, indomethacin, corticosteroids, immunosuppressants, cytostatic drugs, some antibiotics with long-term or uncontrolled use).

Ionizing radiation

Ionizing effects on the small intestine cause the development of radiation enteritis. This is possible during radiation therapy of malignant tumors of the abdominal cavity and small pelvis.

Ileocecal valve insufficiency

The ileocecal valve prevents regurgitation of the contents of the large intestine into the small intestine. Its barrier function increases sharply 2-3 hours after eating. The cecum plays a major role in maintaining the function of the ileocecal valve. It protects the ileocecal valve from excessive hydraulic pressure, acting as a kind of "air vent". Normally, the length of the cecum is 8-10 cm. With its congenital insufficient development (in 6% of people), ileocecal insufficiency appears.

The formation of the cecum is completed by the age of 4. Its congenital insufficiency can thus manifest itself early and ileocecal valve insufficiency can occur already in early childhood. With ileocecal valve insufficiency, the contents of the large intestine are thrown into the small intestine during straining, defecation, and increased pressure in the large intestine - this is the main reason for the development of reflux enteritis.

According to Ya. D. Vitebsky, there are congenital and acquired, as well as relative and absolute ileocecal insufficiency. With relative insufficiency, the valve remains open only at high pressure in the colon; with absolute insufficiency, the valve gapes constantly.

Insufficiency of the major duodenal papilla

When the large duodenal papilla is insufficient, bile leaks out of digestion into the small intestine, which contributes to the development of enteritis and diarrhea (bile acids stimulate the motor function of the intestine).

Past gastrointestinal surgeries

The development of chronic enteritis is facilitated by gastrectomy or gastric resection, vagotomy, application of gastroenteroanastomosis, intestinal resection. The development of postoperative intestinal adhesions is also important.

Intestinal malformations

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

Ischemia of the small intestinal wall

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

Causes causing the development of secondary chronic enteritis

Secondary chronic enteritis develops in diseases of the digestive organs (peptic ulcer of the stomach and duodenum, chronic hepatitis, liver cirrhosis, diseases of the biliary tract, pancreas), kidney diseases with the 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, intestinal motility disorders, disruption of not only the function of the digestive glands, but also immunological homeostasis, microcirculation, changes in intestinal microflora, and genetic factors play a significant role. Structural and functional disorders of the small intestinal mucosa are facilitated by congenital and acquired changes in the metabolism of the intestinal wall, and disruption of the neurohormonal regulation of the regenerative processes of its mucosa.

In the process of chronicization of intestinal diseases, both pathological processes in the intestine itself with the occurrence of dysbacteriosis, and disorders of the functions of a number of digestive organs, metabolic and immunological shifts that can support intestinal disorders are of great importance.

When studying the mechanisms of chronicity of small intestine diseases, it was found that they have common features in various nosological forms. Among these mechanisms, the most important are changes in the microbial flora and disorders of digestion, motility and the digestive-transport conveyor associated with the proliferation of bacteria in the small intestine, which contributes to the occurrence of disorders of all types of metabolism, especially protein and fats.

The main pathogenetic factors of chronic enteritis are the following.

Inflammation and disruption of physiological regeneration of the small intestinal mucosa

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

Modern gastroenterologists believe that the greatest significance in the pathogenesis of this disease is played by dystrophic changes and disruption of physiological regeneration of the small intestinal mucosa. Chronic enteritis is characterized by crypt epithelial proliferation and delayed enterocyte differentiation processes. As a result, most of the small intestinal villi are lined with undifferentiated, immature and, therefore, functionally defective enterocytes, which quickly die. These circumstances naturally contribute to the development of mucosal atrophy, maldigestion and malabsorption syndromes.

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

The intestine is the most important organ of immunity. The small intestine contains the following components of the immune system:

• intraepithelial T- and B-lymphocytes (located between the epithelial cells of the mucous membrane);
• B- and T-lymphocytes of the proper layer of the mucous membrane of the small intestine, among B-lymphocytes, those predominantly producing IgA predominate;
• Peyer's patches in the submucosal layer containing B-lymphocytes (50-70%) and T-lymphocytes (11-40%);
• solitary lymphoid follicles - in the mucous and submucous layers. They contain T- and B-lymphocytes, macrophages.

An important element of the immune system of the gastrointestinal tract is the secretory immunoglobulin system. All classes of immunoglobulins are present in the intestinal contents, but the most important is IgA. It is synthesized by plasma cells of the proper layer of the mucous membrane of the small intestine.

Secretory IgA has a number of important properties:

• has high resistance to proteolytic enzymes;
• has antibody-dependent cell-mediated cytotoxicity and opsonization of phagocytosis via the Fc-a receptor
• phagocytic cells. Thus, secretory IgA takes part in the penetration of the antigen into Peyer's patch;
• does not bind complement components, 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. The anti-adhesive properties of IgA determine its antibacterial, antiviral and anti-allergenic properties.

Disruption of the immune system of the small intestine, insufficient production of y-interferon, interleukin-2 by lymphocytes, IgA deficiency contribute to the penetration of microbial antigens into the body and the development of autoimmune mechanisms, maintaining inflammatory-dystrophic processes in the mucous membrane of the small intestine. Allergic mechanisms play a certain role in the pathogenesis of chronic enteritis - the production of antibodies to intestinal bacteria (microbial allergy), antibodies to food products (food allergy), intestinal tissue elements (tissue allergy, autoimmune reactions).

Intestinal dysbacteriosis

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

Dysfunction of the gastrointestinal endocrine system

The small intestine, primarily the duodenum, produces a number of hormones that affect its functions.

• Gastrin - is produced by G-cells of the atrial part of the stomach, pancreas, proximal part of the small intestine. It has a stimulating effect on the motility of the duodenum.
• Motilin - produced by Mo cells of the upper 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. Inhibits the production of gastrin, motilin, suppresses the motor function of the intestine.
• Vasoactive intestinal polypeptide - produced in the small intestine, stomach, pancreas. Stimulates intestinal and pancreatic secretion, intestinal motility, insulin secretion, vasodilation.
• Substance P is produced in the EC cells in the cardiac and antral sections of the stomach and small intestine. It increases intestinal peristalsis, stimulates the secretion of pancreatic juice and saliva, and causes vasodilation.
• Enteroglucagon - is produced by A-cells of the proximal small intestine. Slows down the movement of contents through the small intestine. It is a "growth hormone for the gastrointestinal tract" since it is necessary to maintain normal life and reproduction (cell cycle) of gastrointestinal cells. Enteroglucagon changes the rate of cell replication, has a trophic effect, and promotes rapid restoration of the intestinal mucosa in case of various injuries.

Disruption of the functioning of the gastrointestinal endocrine system contributes to the progression of inflammatory-dystrophic changes and a decrease in the regenerative capacity of the small intestinal mucosa.

Disorders of intestinal cavity and membrane (parietal) digestion

Inflammatory-dystrophic and atrophic changes in the mucous membrane lead to a low level of enterocyte functioning, a deficiency of digestive enzymes - lactase, maltase, alkaline phosphatase, with lactase deficiency being the most pronounced. Cavity digestion is sharply reduced.

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

Parietal (membrane) digestion is significantly impaired in chronic enteritis, and along with this, the absorption function of the intestine is sharply reduced (maldigestion and malabsorption syndromes develop).

Enzyme pathologies

In chronic enteritis, especially in its long-term course, there is almost always fermentopathy. In some patients, fermentopathy may be primary, genetically determined (most often lactase deficiency), manifested or aggravated by chronic enteritis. Fermentopathy contributes to the development of maldigestion and malabsorption syndromes.

Fermentopathy is caused by a disorder of the enzyme-forming function of enterocytes, its development is facilitated by increased peroxidation in the cells of the small intestine. High activity of lipid peroxidation inhibits, first of all, the formation of lactase, maltase, and sucrase.

Changes in intestinal motor function

In chronic enteritis, the intestinal motor function is also impaired, which is facilitated by a change in the function of the gastrointestinal endocrine system. Intestinal motility is impaired by hyper- and hypomotor dyskinesia. With an increase in intestinal motility, the contact of food chyme with the intestinal mucosa decreases and a weakening of digestive processes is observed. With a decrease in intestinal motility, the movement of chyme is impaired, its stasis develops, which is accompanied by dysbacteriosis, damage to enterocyte membranes, and a violation of the precipitation of bile acids in the intestine.

Ultimately, pathogenetic factors lead to the development of malgestia and malabsorption syndromes, disturbances in protein, fat, carbohydrate, mineral, and vitamin metabolism, and severe extraintestinal disorders.

Chronic enteritis is based not only on inflammation, but also on a disturbance of physiological regeneration of the small intestinal mucosa - proliferation of crypt epithelium, cell differentiation, their "advancement" along the villi and rejection into the intestinal lumen. The process of enterocyte differentiation is delayed, as a result of which most of the villi become lined with undifferentiated, functionally incompetent epithelial cells, which quickly die. The villi become shorter and atrophy, the crypts become sclerotic or undergo cystic expansion. The stroma of the mucosa is infiltrated with plasma cells, lymphocytes, and eosinophils.

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

In chronic enteritis, the entire small intestine or one or another of its sections is affected (jejunitis, ileitis).

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