Heredity

Another problem that often affects the reproductive and affective environment of patients with IBD is the fear that their children may inherit the same disease [12]. There is a 10.5% risk that the children of a parent with IBD may develop the disease, and 10% of patients have a first-degree relative with the disease, attesting to the role of heredity and genetic susceptibility to these morbid conditions in which multifac-torial pathogenesis requires triggering factors of an environmental origin.

The modality of transmission of the genes that may cause the development of IBD is complex and cannot be explained with a mere Mendelian pattern. Studies on twins revealed that, in the case of MC, consistency is 44-50% in monozygotic twins and 0-3% in zygotic twins whereas in the case of UC, consistency is lower, at 6-14% in monozygotic twins and 0-5% in heterozy-gotic twins [12]. Some studies revealed that there is a stronger familial tendency in CD, attesting to the importance of the genetic arrangement in determining the tendency to develop the disease [12]. Recent researches [13] began to detect the chromosome regions that are probably involved in order to determine susceptibility to the disease. Some of these regions seem to be specific in CD and UC whereas others have a lower specificity. These discoveries are relevant in light of the possibility, from studying the genotype of a certain patient, of anticipating phenotypical features of the disease, distinguishing - for example, in the case of CD - types with a higher risk of fistulisation from those with a predominant tendency to form stenosis. Knowledge of a patient's genetic arrangement could help in the evaluation of risk of extraintestinal manifestations and the probability of response to medical and surgical therapy. For example, a gene was detected, called CARD 15, situated on chromosome 16, which codifies for a protein involved in the primary immune response to infections through the activation of the NF-kB. In patients with MC, mutations of this gene seem to be associated with a tendency to ileal localisation, an earlier age of onset and a higher tendency to stenosis. In the light of these considerations, it is reasonable to think that, in a more or less remote future, physicians may be able to anticipate features of the evolutive course of the disease in each patient by targeted genetic studies, optimising management by individualising medical-surgical therapy [13].

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