Chronic non-ulcer colitis: pathogenesis

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 effects of infection, drugs, toxic and allergic factors.
2. Violation of the immune system, in particular, a decrease in the protective functions of the gastrointestinal immune system. Lymphoid tissue of the gastrointestinal tract serves as the first line of specific protection against microorganisms; most Ig-producing cells of the body (B-lymphocytes and plasmocytes) are in the L. Propria of the intestine. The presence of local immunity, the optimal synthesis of the intestinal wall of immunoglobulin A, lysozyme is a reliable protection against infection and prevents the development of an infectious inflammatory process in the intestine. With chronic enteritis and colitis, the production of the intestinal wall of immunoglobulins (primarily IgA), lysozyme, decreases, which contributes to the development of chronic colitis.
3. The development of the sensitization of the patient's organism to the intestinal microflora and microorganisms in other foci of infection plays an important role in the pathogenesis of chronic colitis. In the mechanism of development of microbial allergies, the changes in the properties of the automicroflora, the increase in the permeability of the intestinal mucosa for microbial antigens, and the food allergy are important.
4. Autoimmune disorders also play a role in the development of chronic colitis (mainly in severe its course). AM Nogaller (1989), M. Kh. Levitan (1981) proved the presence of sensitization to antigens of the mucous membrane of the colon and the production of antibodies to the altered epithelium of the intestinal wall.
5. Involvement of the intestinal nervous system in the pathological process leads to disruption of the motor function of the intestine and contributes to the development of trophic disorders of the mucous membrane of the large intestine.
6. Dysbacteriosis is the most important pathogenetic factor of chronic colitis, which supports the inflammatory process in the mucosa of the colon.
7. Violation of the secretion of gastrointestinal hormones, biogenic amines, prostaglandins. Violation of the function of the gastrointestinal endocrine system contributes to disorders of motor function of the intestine, development of dysbacteriosis, aggravation of the inflammatory process in the intestinal mucosa, disorders of secretory, excretory function of the colon. In particular, with chronic colitis, the absorption of water in the right side of the colon decreases, the absorption and secretion of water and electrolytes in the left part are disturbed.

Among biogenic amines, an important role belongs to serotonin. It is known that in the phase of exacerbation of chronic colitis, hyperserotoninemia is observed. Its severity correlates with the characteristics of the clinic. So, hyperserotoninemia is combined with diarrhea, hypoxerotonemia - with constipation. A high serotonin level contributes to the development of dysbacteriosis, especially colonization in the intestine of the hemolytic E. Coli.

Pathomorphology

In chronic colitis, the inflammatory process in the mucosa of the large intestine is combined with its degenerative-dystrophic changes, and with prolonged course of the disease, mucosal atrophy develops.

Chronic colitis without atrophy of the mucous membrane in the period of exacerbation is characterized by the fact that the mucous membrane is full-blooded, with pinpoint hemorrhages and erosions. Histological examination of the mucosa reveals lymphoid-plasmocyte infiltration of L. Propria, an increase in the number of goblet cells.

Chronic atrophic colitis is characterized by the smoothness of the folds, the granularity of the mucosa, it has a pale gray color. At a microscopic examination, flattening of villi, decrease in crypts and number of goblet cells is noted. Lymphoid-plasmocyte infiltration of the propria of the mucous membrane is characteristic.

Periodic exacerbations of this form of colitis can 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 crypt is flattened. Another type of atrophic colitis is deep cystic colitis . In this case, intestinal glands or tubular structures are revealed in the submucosal layer of the intestine, in the enlarged lumen of which the exudate is visible. To chronic colitis it is customary to refer only the diffuse form of deep cystic colitis, and consider the local form as a complication of a "solitary ulcer."

Recently, a peculiar form of chronic colitis has been described, in which thickening of the subepithelial layer due to collagen is noted - this is called collagen colitis . Collagen colitis electron microscopically in the basal membrane reveals collagen, microfibrils, amorphous protein and immunoglobulins. Some authors believe that the disease is based on nonspecific inflammation with a distortion of collagen synthesis, others that it has an autoimmune character, because it combines with other autoimmune diseases (thyroid gland, joints) and is based on the "disease" of perichriptal fibroblasts that acquire a structure myofibroblasts.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10],