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Ulcerative Colitis is classified as a disease that is known as one of the inflammatory bowel diseases. Inflammation in this condition affects the superficial mucosa layer of the colon; the large intestine, there is always rectum involvement and a continuation along the colon with a clear distinction between those areas that are healthy and those that are affected (Sephton, 2009). Symptoms include watery and possibly bloody diarrhea, as well as mucus and pus in various amounts. Abnormal abdominal sounds may be heard in the abdominal quadrants upon auscultation and be accompanied by abdominal pain. Fever, pain in the joints, weight loss, and GI bleeding may also accompany nausea and vomiting (Board, ADAM & National Center for Biotechnology Information, 2012)
Though the exact cause is unknown there are many research studies that have been able to suggest with scientific validation the possibility of many factors, causes and contributions to the disease. One research study conducted in 2006 suggested that there was a significant genetic contribution that factored in those more susceptible to those with an inflammatory bowel disease (Satsangi,2006) Studies at the molecular level have identified and determined genetic susceptibility to ulcerative colitis. Of course this discovery is able to provide new insight into the pathogenicity of the disease and disease process.
Risk factors usually include those in poor health and it is a higher risk between the ages of 15-30 and then resurfaces between the ages of 50-70. Family history and Jewish ancestry are also implicated though family history may be linked to genetics and studies in these areas are able to provide stronger links between this family history and the prevalence of the disease. Breastfeeding, appendectomy, and smoking are also associated risks (Head, and Jurenka, 2003).
Normal system functions appear to be prohibited by ââ‚¬Ëœincreases in certain inflammatory mediators, oxidative stress signs, deranged colonic milieu, decreased oxidation of short chain fatty acids, increased intestinal permeability, an increase in the production of sulfides, and decreased methylation,ââ‚¬â„¢ (Head, and Jurenka, 2003). Certain cytokines along with anti-oxidant levels as well as the presence of bacteria interfere with normal system functions. These systematic functional abnormalities each contribute to symptoms of ulcerative colitis. For example increased oxidative stress is manifested in the intestinal mucosa of patients. Bowel lesions are much more evident when the bacteria concentration is highest, likely contributing to bloody stools and abdominal pains.
Conventional treatments include antibiotics, corticosteroids, amino salicylates, and immune modulators. Corticosteroids are most often used during acute phases. Preventative measures to avoid flare ups during times of remission usually involve behavioral changes. It is commonly advised that nutrient deficits be checked for and corrected as UC is associated with several. Vitamin A, vitamin E, vitamin C, vitamin K, folic acid, calcium, iron, zinc, selenium and magnesium are all important elements are any deficiencies should be balanced though many if not all of these factor in any disease that has immune system implications as a causative factor. Special diets depending on chemistry results can be prescribed for prevention along with in some cases the use or probiotics in the diet. Specific nutrients are also thought to play roles in prevention.
Major areas of ongoing research in ulcerative colitis involve genetics factors and genetic markers that are predictive of the disease. Protein tyrosine phosphatase non-receptor type 2 identified as a genome increasing susceptibility for UC (Brand, 2012). Despite this knowledge its phenotypic effects are unclear and being researched. Phenotypic effects are those effects that are observable due to the presence of this genome.
One Korean study concluded that there was no association between the genomes TNFSF15 and IL23R in a Korean research group. This genome has been mentioned in reports and research findings among Caucasians though findings and conclusions have been inconsistent. Though the TNFSF15 genome for some reason shows a small association with UC it is in Caucasian male patients only (Kyuyoung, 2011).
A third research study identified that UC shares many susceptibility genes with Crohnââ‚¬â„¢s disease, which is good cause for further study as they are both irritable bowel syndromes and understanding the different genomes present in each case allows for a better understanding of the pathogenicity of the disease as well as being better prepared to treat and prevent the disease. (Leonard, 2010). Genetic association discovered through research highlights the importance of alterations in barrier function and cell specific innate responses.
Studies suggest that UC is less extensive at later stages of life though symptoms are more likely to begin with more severe initial onsets of the disease. Severe episodes risk the development of toxic mega-colon associated with a higher rate of fatality. Due to age and general health surgery is not often initially elected in elderly patients; despite this as surgical intervention and medical therapy has improved mortality rates among elderly patients have improved. These patients are at a higher risk for complications from UC and must be more closely monitored (Nikolaos, 2001).
Though UC is an illness that can be disabling it is possible to live with this chronic disease, minimizing flare ups. The diagnosis itself of UC is as non-traumatic as possible though it can be difficult as UC mimics many other conditions. One should expect blood testing, occult stool samples which will check for the presence of blood and mucous and the ultimate in diagnosing UC which is through sigmoidoscopy and colonoscopy which are each used to view the interior condition of the colon.
Those who have been diagnosed with UC are recommended to have a colonoscopy with biopsy every 1 to two years depending on how long they have been diagnosed with an irritable bowel disease and which side of the colon has primarily been affected. Those with no history of bowel disease are recommended to have a colonoscopy at certain intervals after the age of 50 to screen for colorectal cancer.