Introduction
Ulcerative colitis is a highly adverse condition that might lead to serious complications in a patient. It is a chronic inflammatory disease of the intestine that causes ulcers in the lining of the colon; however, it may spread to other parts of the intestines as well (National Institute of Diabetes and Digestive and Kidney Diseases [NIDDK], 2014). The current paper discusses the potential causes of this disease, focusing mainly on genetic factors that may increase its risk.
Causes of the Disorder
Generally speaking, it is not certain which factors exactly may serve as a cause of ulcerative colitis (NIDDK, 2014). It is believed that genetic and environmental factors may play this role (NIDDK, 2014). It is noteworthy that ulcerative colitis may also be described as an autoimmune disease (NIDDK, 2014). As for the genetic causes of this disorder, it is known that incidence of ulcerative colitis is higher than average in relatives (in monozygotic twins, in particular) than in randomly selected individuals; also, certain ethnicities suffer from this disease more often than others (NIDDK, 2014; Nussbaum, McInnes, & Willard, 2007). It is also assumed that the chance of developing ulcerative colitis may be increased, although slightly, by environmental factors such as taking NSAIDs, oral contraception, or antibiotics, having a diet high in fats, and some others (NIDDK, 2014).
Genetic Origins of the Disorder, and Considerations for Practice and Patient Education
On the whole, it is stated that ulcerative colitis may have a genetic etiology (Nussbaum et al., 2007, p. 250). Ulcerative colitis is one of the two main types of inflammatory bowel disease, along with Crohn disease (Nussbaum et al., 2007). It has been discovered that both these disorders display significant family clustering, as well as greatly increased rates of concordance in monozygotic twins, but the inheritance patterns of these diseases are not Mendelian, which allows for concluding that they are caused by several genetic factors rather than by a single gene (Nussbaum et al., 2007, p. 250). It is also stressed that in one study, there was a concordance rate of only 6% for ulcerative colitis in monozygotic twins, but that in dizygotic twins, no concordance was observed for ulcerative colitis (as cited in Nussbaum et al., 2007, p. 251).
This allows for a number of considerations pertaining to medical practice when it comes to dealing with ulcerative colitis. Nowadays, no cure for ulcerative colitis exists (Cleynen et al., 2016). Therefore, it is only possible to take steps aimed at managing this condition. It is stated that five main types of medications may be utilized on their own or in combination so as to address this disorder, namely, corticosteroids, anti-inflammatory drugs, immune modulators, antibiotics, and/or mixed inflammatory-immune modulators (Nussbaum et al., 2007, p. 251). When it comes to the conclusions which may be made from the inference that ulcerative colitis has a complex inheritance, it should be noted that patients whose relatives suffer from this disorder need to be treated as being under greater than average risk of developing this condition, but that such a risk is lower than it would have been for children of parents with this condition if the inheritance patterns were Mendelian.
As for patient education, it should be observed that individuals who have a history of ulcerative colitis in their family ought to undergo patient education so that it would be explained to them that they may be at a greater than average risk of developing this condition, which means that they need to take steps aimed at avoiding environmental factors that may stimulate the development of this disease (Nussbaum et al., 2007, p. 251). For instance, these patients might be advised to have a diet which is not too high in fats, and avoid taking oral contraceptives too often (NIDDK, 2014).
The Gene Mutation of the Disease
According to Cleynen et al. (2016), genetic research has found that in genes, there exist nearly 163 susceptibility loci for inflammatory diseases of the bowels, most of which are shared by ulcerative colitis and Crohn’s disease. Thus, on the whole, it is problematic to analyze the gene mutation of ulcerative colitis or to state how the mutation occurs due to the fact that it is unknown which genes exactly lead to this disorder (Cleynen et al., 2016). As for whether the disease is acquired or inherited, it is stressed that ulcerative colitis has strong genetic contribution (Nussbaum et al., 2007, p. 251), and it is possible to speculate that these genetic factors are hereditary, but whether the condition develops also depends on other factors.
Does Chromosomal Analysis Indicate Risk for Ulcerative Colitis?
As has been discussed above, it is unknown which genes exactly are associated with ulcerative colitis (Cleynen et al., 2016). Therefore, it is possible to conclude that chromosomal analysis cannot currently be employed in order to identify whether a patient faces a higher than average risk for developing ulcerative colitis. However, other factors, such as a history of this disorder in the family, may be indicative of such a risk (Nussbaum et al., 2007).
Conclusion
On the whole, it should be stressed that ulcerative colitis is a highly adverse condition the etiology of which is not certain. Nevertheless, such phenomena as significant family clustering, large rates of concordance among monozygotic twins, and non-Mendelian inheritance patterns indicate that this disease may be caused by complex genetic factors. In addition, scholars conclude that certain environmental factors might also contribute to the development of this chronic disorder.
References
Cleynen, I., Boucher, G., Jostins, L., Schumm, L. P., Zeissig, S., Ahmad, T.,…Lees, C. W. (2016). Inherited determinants of Crohn’s disease and ulcerative colitis phenotypes: A genetic association study. The Lancet, 387(10014), 156-167. Web.
National Institute of Diabetes and Digestive and Kidney Diseases. (2014). Ulcerative colitis. Web.
Nussbaum, R., McInnes, R. R., & Willard, H. F. (2007). Thompson and Thompson genetics in medicine (7th ed.). Philadelphia, PA: Saunders Elsevier.