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Idiopathic inflammatory bowel disease.

Idiopathic chronic inflammatory bowel disease - Crohn's disease and ulcerative colitis. The latter in Russian-language literature is designated as ulcerative colitis.

Crohn's disease is an inflammatory disease involving all layers of the intestinal wall in the process and is characterized by an intermittent (segmental) nature of the lesion of various parts of the gastrointestinal tract. The consequence of transmural inflammation is the formation of fistulas and abscesses. The disease has a diverse clinical picture with various intestinal and extraintestinal manifestations and complications. A complete cure is not possible.

Ulcerative colitis is a lesion of the mucous membrane of the colon, which is localized mainly in its distal parts. Changes initially occur in the rectum, then sequentially spread in the proximal direction and in about 10% of cases capture the entire colon. Cure can be achieved after total colectomy.

Crohn's disease and ulcerative colitis are clinically more similar to each other than to differences.

Epidemiology. The incidence of idiopathic inflammatory bowel disease varies widely in different countries - from 0.05 to 13.2 per 100 thousand people. The prevalence of ulcerative colitis and Crohn's disease has common patterns. In northern countries, such as England, Sweden, Norway, the United States, the highest incidence is observed. In contrast, incidence rates are low in southern Europe, Asia, the Middle East, South Africa and Australia. This suggests that environmental factors influence the occurrence of these diseases. In Russia, systematic studies on the incidence of idiopathic inflammatory bowel disease until 1996 were not conducted. In the Moscow region, for example, the incidence of Crohn's disease was 2.7, and ulcerative colitis - 20.1 per 100 thousand people.

The results of epidemiological studies indicate a widespread increase in the frequency of idiopathic inflammatory bowel disease, especially Crohn's disease. So, for example, in Iceland in the period 1970–79. to 1980–89 the incidence of ulcerative colitis increased 2 times, Crohn's disease - 3 times, in Denmark Crohn's disease increased 6 times. In general, over the past 30 years, the incidence of idiopathic inflammatory bowel disease has increased 5 times. However, it is difficult to judge the true incidence rate, as patients with these sufferings turn to doctors late and the correct diagnosis is made after 2-5 or more years from the onset of the disease.

All age groups, from infants to old people, suffer from idiopathic inflammatory bowel disease, but most often young people are from 15 to 30 years old. For Crohn’s disease, the age peak is considered to be 20–29 years old, for ulcerative colitis - 20–40 years. The second age peak in incidence occurs in 60–80 years. The bimodal distribution of morbidity is associated with various etiological factors - genetic in young and environmental factors in the elderly. It is possible that the elderly idiopathic inflammatory bowel disease eliminates ischemic colitis.

It is believed that ulcerative colitis equally often affects men and women. On the contrary, around the world there is a slightly higher incidence of Crohn's disease among women, with a ratio of 1: 1.8.

So, young age, severe course with frequent lifelong disability, widespread increase in morbidity make the problem of idiopathic inflammatory bowel diseases extremely urgent.

The etiology of idiopathic inflammatory bowel disease is still unknown. There are only numerous theories. Infectious, immune, vascular, genetic theories, as well as the influence of environmental factors are discussed.

The most interesting was the infectious theory, since it was understood that chronic inflammation should be supported by some pathogen. The modern concept of the role of an infectious agent suggests the following possible mechanisms of its participation: a persistent infection, an immune response to the intestinal microflora with altered properties, increased permeability of the mucous membrane for bacterial metabolites (violation of the barrier function of the mucous membrane), an altered immune response to normal intestinal microflora.

As a persistent agent, mycobacterium tuberculosis was first of all assumed - the similarity of the clinic, localization and complications. However, convincing evidence could not be obtained. Another causative agent associated with the occurrence of Crohn's disease is measles virus, since in Sweden, after several measles epidemics, an increase in the incidence of Crohn's disease has been noted. It was possible to trace that infection with measles virus in the prenatal and neonatal period causes a number of immunological disorders, which leads to granulomatous vasculitis and mesenteric vessel microthrombosis with the formation of subsequently microinfarcts, which are sometimes a prelude to Crohn's disease. Moreover, pathogen antigens were sometimes found in granulomas. However, most authors consider measles infection rather than as an etiological factor in Crohn's disease, but as one of the nonspecific trigger moments in the development of idiopathic inflammatory bowel diseases. Antigens of other bacteria (Escherichia coli, Listeria monocitogenesis, Klebsiella pneumoniae) were found only in foci of necrosis, but not in granulomas. These findings indicate secondary infection of ulcers and reject the etiological role of these pathogens. Patients with idiopathic inflammatory bowel disease show intestinal microflora with altered virulence - increased adhesion, increased hydrophobicity, increased production of epithelial toxins, immunomodulating peptides, mucin-degrading enzymes, hyaluronidase, heat shock proteins, superantigens.

However, the normal intestinal flora and its metabolites (endotoxins, chemotactic peptides) under certain conditions support chronic inflammation in the intestine, which results in a violation of the barrier function of the mucous membrane.
And there may be an altered immune response to the normal intestinal flora - antiepithelial antibodies cross-react with bacterial epitopes are found in areas of accumulations of anaerobic flora. This leads to the development of chronic inflammation and damage to the intestinal mucosa. The inflammatory process, in turn, is accompanied by activation of the local immune system: when idiopathic inflammatory bowel diseases are activated, intraepithelial lymphocytes produce a significant amount of IgG (in healthy animals, IgA predominates). It has now been established that these antibodies are directed against the cytoplasmic proteins of the intestinal microflora. Therefore, the aggravation, and sometimes the debut of idiopathic inflammatory bowel diseases, is associated with a breakdown in tolerance to normal intestinal microflora.

A significant increase in idiopathic inflammatory bowel disease in recent years is due primarily to environmental factors. The most studied are smoking, oral contraceptives, dietary factors, and the use of antibiotics. It has been shown that the incidence of idiopathic inflammatory bowel disease in smokers is 2 times higher than in non-smokers, and the dose-dependent effect of smoking was also revealed - the higher the intensity of smoking, the higher the risk of Crohn's disease. In children of smoking parents, nonspecific ulcerative colitis develops 2 times more often and Crohn's disease 5 times more often. The alleged pathophysiological mechanism includes impaired formation of mucus in the intestine, weakening of rectal blood flow, immunological effects (a violation of the ratio of T-helpers and T-suppressors and cytokine production has been detected).

A number of authors associate idiopathic inflammatory bowel disease with oral contraceptives. In this case, the mechanism of influence has not been deciphered, but it is believed that estrogens may contribute to the emergence of microthrombi, which underlie pathological changes, especially in Crohn's disease.

The reliability of the influence of dietary factors on the occurrence of idiopathic inflammatory bowel diseases has not been proven. However, it is believed that the consumption of fats, in particular long-chain triglycerides, correlates with the incidence of idiopathic inflammatory bowel disease. The role of omega-3 fatty acids, which are metabolized by immunoregulatory leukotrienes and prostaglandins, is discussed. In the experience of using elementary diets in patients with idiopathic inflammatory bowel disease, it was possible to cause long-term remissions.

An increase in the incidence of idiopathic inflammatory bowel disease occurs in parallel with the widespread use of antibiotics. Data from population studies confirm an increased risk of idiopathic inflammatory bowel disease in people who received antibiotics. It is known that antibiotics alter the biological properties of the intestinal flora, and in individuals with a genetic predisposition to idiopathic inflammatory bowel disease, their manifestation while taking antibiotics is possible.

Genetic factors. There are numerous factors proving the genetic condition of Crohn's disease and ulcerative colitis. We studied genetic markers, including blood groups, the state of secretors, alpha1-antitrypsin - no correlation with idiopathic inflammatory bowel disease was detected. Some susceptibility to idiopathic inflammatory bowel disease of individuals with genes encoding 6 and 7 pairs of chromosomes was found.

Considering that the ability of the immune system to regulate inflammation is genetically determined, in patients with idiopathic inflammatory bowel disease, gene markers involved in the regulation of the immune response were studied. We studied the relationship of idiopathic inflammatory bowel diseases with genes I and II of the HLA histocompatibility system. The connection of Crohn's disease with the DRB1 allele in Europeans has been proven. In contrast, the HLA DPB1 allele is extremely rare in patients with Crohn's disease and is possibly protective against this disease. For ulcerative colitis, association with HLA - DR2 (85%) and HLA-DO1wl (96%) is characteristic.

Given the central role of cytokines in modulating the immune response, attempts have been made to identify mutations or polymorphisms in genes encoding cytokines. The association of Crohn's disease with a specific haplotype of tumor necrosis factor (TNF) microsatellites has been proven. In the pericentromeric region of the 16th chromosome, loci were discovered that predisposed to the development of Crohn's disease. It is in these loci that genes are located that determine the structure of the adhesion molecule - sialoforin, receptors for interleukin-4 and the C3 component of complement. Finally, the presence of family cases of idiopathic inflammatory bowel diseases, a high risk of developing them in relatives of the first degree of kinship with patients with Crohn's disease (3.9%, which is 13 times higher than in the control population) confirm a genetic predisposition to these diseases. In addition, there is a high incidence of idiopathic inflammatory bowel disease in mono- and dizygotic twins.

There are numerous data indicating a violation of cellular and humoral immunity in patients with idiopathic inflammatory bowel disease. In addition to hypergammaglobulinemia and IgG overproduction, all patients with ulcerative colitis and Crohn's disease have antibodies to the cytoplasmic antigens of neutrophils and monocytes - ANCA (antineutrophilic cytoplasmic antibodies). In Crohn's disease, they are found in 27% of patients, and in ulcerative colitis - in 70%. Typically, ANCA is found in systemic vasculitis, primary sclerosing cholangitis (82%), i.e. with diseases with severe immune disorders. Their presence in idiopathic inflammatory bowel diseases leaves the question open - either we are talking about a pathological process directly associated with an immune phenomenon, or the immune response is secondary to the developed lesions.

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