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  • Title: The epidemiology and the pathogenesis of inflammatory bowel disease.
    Author: Karlinger K, Györke T, Makö E, Mester A, Tarján Z.
    Journal: Eur J Radiol; 2000 Sep; 35(3):154-67. PubMed ID: 11000558.
    Abstract:
    The etiology of inflammatory bowel disease (IBD) is still unknown. However, a satisfactory solution cannot be far away. IBD actually encompasses two diseases, i.e. Crohn's disease (CD) and ulcerous colitis (UC). These diseases resemble each other so closely that they cannot be distinguished even pathologically, but differ from each other sufficiently to regard them as independent entities. Epidemiological observations may be helpful in identifying the true causative factors of this evasive disease. Geographically, the prevalence of the disease has a slope from North to South and, to a lesser degree, from West to East. The Western-Eastern discrepancy can be attributed to a difference in Western life styles. The incidence of the disease has been increasing world-wide of late, but its spread has been slowing down in highly affected countries. Racial and ethnic relations in different populations and immigration studies offer interesting data which can reflect genetic, inherited, environmental and behavioural factors. The disease seems to have a characteristic racial-ethnic distribution: the Jewish population is highly susceptible everywhere, but its prevalence in that population nears that of the domestic society in which they live. In Hungary, the Roma (Gypsies) have a considerably lower prevalence than the average population. This can be attributed to a genetic or environmental influence. According to age, the onset of the disease occurs more often in the second or the third decade of life, but there also is another peak in the 60s. Regarding sexual distribution, there is a slight preponderance of colitis ulcerosa in men and of Crohn's disease in women. It may correspond to the stronger auto-immune affection in the process of Crohn's disease. Environmental factors and behavioural influences also are investigated. Diet, the role of the early ages, smoking habits and the influence of hormonal status and drugs are viewed as useful contributing factors in the manifestation of the disease. Genetic studies show that one-fourth of IBD patients have an affected family member. HLAB27 histocombatibility also plays an important, but not determining role in the development of the disease. Genetic factors seem to have a stronger influence in Crohn's disease than ulcerative colitis. The existence of multiple sclerosis-IBD families may reflect the common genetic background or the similar microbial effect as well. A great number of bacterial and viral factors has been suspected of being infectious factors in IBD, mostly in CD. Mycobacteria, Yersinia, Campylobacter, Clostridium, Clamidias, etc. as well as bacteria and some viruses such as herpes and rotavirus and the primary measles virus. None of them has been proven as a real and exclusively pathogenic factor. Immunological background has an important function in the manifestation of the disease. If an individual has a genetic susceptibility to infections, the down regulation of an inflammation in the bowel wall does not occur in a proper way. This initiates the auto-immune process which is a self-increasing cycle. Extra-intestinal manifestations of IBD are of high importance because they can not only follow intestinal symptoms, but precede them by years. Hepatic and biliary disturbances (primary sclerosing cholangitis), are the most serious complications. Mucocutaneous manifestations can be the first appearance of the main disease (in the mouth). Auto-immune consequences (erythema nodosum) or complications caused even by the therapy can occur. Ocular and musculoskeletal manifestations supposedly have the same genetic background and often precede the intestinal symptoms. Considering the epidemiological, genetic and immunological data, we can conclude that ulcerative colitis and Crohn's disease are heterogeneous disorders of mutifactorial etiology in which hereditary (genetic) and environmental (microbial, behaviour) factors interact to produce the disease.
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