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Accordance that inflammation microenvironment indicates infiltration of

   Accordance with textbooks, inflammatory bowel diseases (IBD) is chronic inflammation circumstances of the small intestine and colon. The major subtypes of IBD are ulcerative colitis (UC) and Crohn’s disease (CD). Notwithstanding similar features, UC and CD can be differentiated based on their clinical demonstration such as histopathology, symptoms and affected areas. Crohn’s disease is associated with whole gastrointestinal tract while UC is correlated with colon and rectum. Although the clinical cause of IBD is unknown, neither environmental agents comprise infection, toxin, radiation, ischemia nor genetically element are denied.

   The UC was demonstrated in 1859 by Walks. It presents itself by clinical manifestations such as abdominal pain, bloody diarrhea, mucus in the stool and weight loss. The colon chronic inflammation is commonly shallow and frequently commences by rectum that inflammation microenvironment indicates infiltration of lymphocytes and granulocytes in inflammatory tissues, edema, crypt obstruction, and ulceration. Rectum bounded inflammation is named proctitis while not extended inflammation into descending colon is known as left-sided colitis.

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   In 1913, an accurate description of the Crohn’s disease was by Dalziel for the first time. Eventually in 1932 CD’s pathology was categorized as a chronic disease by Crohn and his colleagues. CD can affect any area of the gastrointestinal tract from the mouth to rectum. Under acute conditions, it may lead to gut obstruction. The terminal ileum is the most prevalent encountered place in the patients. CD clinical symptoms are almost close to UC. It clinically presents with abdominal pain, diarrhea, and weight loss. As it is mentioned, in acute stages, abdominal mass, intestinal obstruction or fistula occurs. Inflammation is demonstrated by button segmental excrescences, abscesses, fistulas, fissures and intestinal obstruction. Microenvironment indicates lymphoid assimilation, migration of inflammatory cells and epithelioid granuloma.

   Although there are no solid reasons why and how the IBD appears, researchers agree on the involvement of both the incognito environmental agents and immune system in IBD incidence rate. Some bacterium, parasites, and viruses have been investigated for IBD. Other factors such as smoking, nutrition, blood transfusions, the oral contraceptive pill, socioeconomic situation are proposed as IBD risk factors. The infection hypothesis proffers some unknown pathogens cause IBD and the immune system solely responses consequently. Some strong evidence presented smoking as the strongest risk factor which exacerbates IBD symptoms. Fast development of CD is often accompanied by smoking.

   Representation of an abnormal immune response to a normal stimulus is base of IBD immunological perspective. Irregular increased immune cells number in the lamina propria, cellular and humoral immune activation, effective treatment with steroids and immunosuppressive agents and intestinal mucosal immune function are reasons why IBD is categorized as an autoimmune disease. The immunological hypothesis in spite of the infection hypothesis suggests whom IBD is an eccentric immune response to a usual stimulus with considering to genetic background. The most important immunodeficiency in IBD is related to the T cell response.


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