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Chronic non-ulcerative colitis - Pathogenesis

 
, medical expert
Last reviewed: 04.07.2025
 
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The main pathogenetic factors of chronic colitis are the following:

  1. Direct damage to the mucous membrane of the colon under the influence of etiological factors. This applies primarily to the influence of infection, drugs, toxic and allergic factors.
  2. Impaired immune system function, in particular, decreased protective functions of the gastrointestinal immune system. The lymphoid tissue of the gastrointestinal tract serves as the first line of specific defense against microorganisms; most Ig-producing cells of the body (B-lymphocytes and plasma cells) are found in the intestinal L. propria. The presence of local immunity, optimal synthesis of immunoglobulin A and lysozyme by the intestinal wall is a reliable defense against infection and prevents the development of infectious and inflammatory processes in the intestine. In chronic enteritis and colitis, the production of immunoglobulins (primarily IgA) and lysozyme by the intestinal wall decreases, which contributes to the development of chronic colitis.
  3. The development of sensitization of the patient's organism to the intestinal automicroflora and microorganisms located in other foci of infection plays an important role in the pathogenesis of chronic colitis. Changes in the properties of the automicroflora, increased permeability of the intestinal mucosa for microbial antigens, and food allergies are important in the mechanism of development of microbial allergy.
  4. Autoimmune disorders also play a certain role in the development of chronic colitis (mainly in its severe course). A. M. Nogaller (1989), M. Kh. Levitan (1981) proved the presence of sensitization to antigens of the colon mucosa and the production of antibodies to the modified epithelium of the intestinal wall.
  5. Involvement of the intestinal nervous system in the pathological process leads to disruption of the intestinal motor function and contributes to the development of trophic disorders of the colon mucosa.
  6. Dysbacteriosis is the most important pathogenetic factor of chronic colitis, supporting the inflammatory process in the mucous membrane of the colon.
  7. Impaired secretion of gastrointestinal hormones, biogenic amines, prostaglandins. Impaired function of the gastrointestinal endocrine system contributes to disorders of the intestinal motor function, development of dysbacteriosis, aggravation of the inflammatory process in the intestinal mucosa, disorders of the secretory, excretory function of the colon. In particular, in chronic colitis, water absorption in the right half of the colon decreases, and absorption and secretion of water and electrolytes in the left section are impaired.

Among biogenic amines, serotonin plays a significant role. It is known that hyperserotoninemia is observed in the acute phase of chronic colitis. Its severity correlates with the clinical features. Thus, hyperserotoninemia is combined with diarrhea, hyposerotoninemia - with constipation. High levels of serotonin contribute to the development of dysbacteriosis, especially colonization of hemolytic E. coli in the intestine.

Pathomorphology

In chronic colitis, the inflammatory process in the mucous membrane of the large intestine is combined with regenerative-dystrophic changes, and with a long-term course of the disease, atrophy of the mucous membrane develops.

Chronic colitis without mucosal atrophy during the exacerbation period is characterized by the mucosa being full-blooded, with point hemorrhages and erosions. Histological examination of the mucosa reveals lymphoid-plasmacytic infiltration of L. propria, an increase in the number of goblet cells.

Chronic atrophic colitis is characterized by smoothed folds, granularity of the mucous membrane, it has a pale-gray color. Microscopic examination reveals flattening of the villi, a decrease in crypts and the number of goblet cells. Lymphoid-plasmocytic infiltration of the proper plate of the mucous membrane is characteristic.

Periodic exacerbations of this form of colitis may result in the development of superficial cystic colitis . In this case, the crypts are cystically stretched due to the accumulation of a large amount of mucus in them, and the epithelium lining the crypts is flattened. Another type of atrophic colitis is deep cystic colitis . In this case, intestinal glands or tubular structures are detected in the submucosal layer of the intestine, in the expanded lumen of which exudate is visible. Only the diffuse form of deep cystic colitis is usually classified as chronic colitis, and the local form is considered a complication of a "solitary ulcer".

Recently, a specific form of chronic colitis has been described, in which thickening of the subepithelial layer is observed due to collagen - this is the so-called collagenous colitis . In collagenous colitis, collagen, microfibrils, amorphous protein and immunoglobulins are detected in the basement membrane using an electron microscope. Some authors believe that the disease is based on non-specific inflammation with a distortion of collagen synthesis, others - that it has an autoimmune nature, since it is combined with other autoimmune diseases (thyroid gland, joints) and is based on a "disease" of pericryptal fibroblasts, which acquire the structure of myofibroblasts.

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