Presentation
Patients with colitis usually present with the classic symptoms of stomach pain, diarrhoea, nausea and vomiting. The onset is insidious. Those with necrotising enterocolitis may present with perforation and shock in severe cases which may lead to death. The first sign is abdominal distension with retention followed by vomiting. Infants with allergic colitis present with vomiting, diarrhoea and with blood and mucus in stools [6].
Ulcerative colitis and Crohn’s disease are usually insidious in onset. They present with diarrhoea, occult blood in stools, weight loss and growth failure in children. Adults present with abdominal pain and diarrhoea.
Patients with pseudomembranous colitis present with abdominal cramps, profuse watery or mucoid diarrhoea, tenesmus, fever and tenderness. During the initial attack or relapse of ulcerative colitis, apthous stomatitis is often present.
Workup
Laboratory tests should be done to rule out anemia, electrolyte abnormalities and hypoalbuminaemia. There might also be leucocytosis, thrombocytosis and elevated ESR and C-reactive protein. Liver function tests should be done as well. Elevated levels of alkaline phosphatase and γ-glutamyl transpeptidase suggest the possibility of primary sclerosing cholangitis.
Perinuclear antineutrophil cytoplasmic antibodies (p-ANCA) are relatively specific (60 to 70%) for ulcerative colitis. Anti–Saccharomyces cerevisiae antibodies (ASCA) are fairly specific for diagnosing Crohn’s disease. However, they are not reliable for differentiating between the two.
Abdominal X-rays are not diagnostic but can help assist for the same as it may show any abnormalities in the diseased bowel. Barium enema also helps in showing similar changes occurring in the lining of the colon.
A stool culture and microscopy can help to exclude the presence of Entamoeba histolytica and other infectious causes. A sigmoidoscopy along with a biopsy of the affected areas may also be done. Colonoscopy is not really necessary but may be done electively [7].
Treatment
Loperamide is used to treat the diarrhoea along with dietary management to relieve the symptoms [7]. Anticytokine drugs, corticosteroids are usually the drugs of choice. The symptoms of colitis can be improved if raw fruits and vegetables are avoided thus, also lessening the trauma to the inflamed colonic mucosa.
At times, it is noted that a milk and gluten free diet greatly helps reduce the symptoms thus promoting the overall well-being of the patient. Corticosteroids are tapered based on the response. Patients who cannot be withdrawn from corticosteroids are usually given azathioprine [8].
Nearly one third of patients suffering from ulcerative colitis require surgery. It has been proved that total proctocolectomy is curative and the quality and expectancy of life is restored to normal.
Prognosis
The prognosis of colitis is good if attended well. However, if diarrhoea is not treated in time, it can lead to death. It is the leading cause of mortality and morbidity in children.
Necrotising enterocolitis with pneumatosis intestinalis does not have a good prognosis as medical treatment fails in 20% of patients. 70% of children with ulcerative colitis go in to remission within 3 months of initial therapy [9].
Depending upon the duration and the extent of the disease, the risk for developing adenocarcinoma increases. Hence, surveillance colonoscopy should be performed once a year or twice a year 8-10 years after the first diagnosis. Almost all patients respond to medical treatment and stay in remission.
Etiology
The exact cause of colitis is not known. A commonly accepted hypothesis suggests that for genetically predisposed persons, exogenous factors (e.g., infectious agents, normal lumenal flora) as well as host factors (e.g., vascular supply, intestinal epithelial cell barrier function, neuronal activity) produce a state of chronically dysregulated mucosal immunity that is modified further by environmental factors like smoking. However, some studies have identified a gene (NOD2) that can complicate the situation and is involved in the affection of the terminal ileum [2].
Inflammation of the colon may also be caused due to infection, ischaemia, hypersensitivity to various allergens, or several drugs. Some evidence even suggests a genetic predisposition to colitis which includes ethnic differences, etc.
Parasitic infections are the common causes for colitis in developing countries whereas in USA, bacterial and viral infections are the main causes. Infectious colitis is caused due to bacteria like Shigella, E.coli and Salmonella.
The arteries supplying to the colon have the potential to get narrow because of atherosclerosis. When the arteries become narrow, the colon becomes inflamed because of the loss in blood supply leading to ischaemic colitis. Ulcerative colitis is an autoimmune illness. Inflammation of the colon can also occur if chemicals are instilled into it for e.g. during an enema.
Psychosocial factors may contribute to the worsening of symptoms. Stress factors are associated with an increase in colitis symptoms such as abdominal pain, diarrhoea and bleeding per rectum. IBD patients have been hypothesized to have a characteristic personality that renders them susceptible to emotional stresses. However, emotional dysfunction could also be the result of chronic illness rather than a cause.
Epidemiology
Irritable bowel disease usually affects adolescents and young adults. It is more commonly seen in males. The prevalence of ulcerative colitis in the United States is estimated to be 100-200 per 100,000 populations and the incidence of Crohn’s disease is estimated to be about 3-4 per 100,000 populations. Ulcerative colitis is highest in the United States and Northern Europe and is lowest in Japan and South Africa. Amoebic infections are highest in frequency amongst tropical climates [3].
Necrotizing enterocolitis is commonly seen in newborns with very low birth weight. Pre-term infants are susceptible to it as well. IBD is also more commonly seen in children aged 5-16 years. It either occurs between the ages of 15-25 years or 50-80 years. The prevalence of irritable bowel disease is more amongst the European Jewish people of Ashkenazi descent [4].
Pathophysiology
In colitis (ulcerative colitis and Crohn’s disease), activated CD4 cells of the lamina propria and peripheral blood secrete inflammatory cytokines. Some activate other inflammatory cells such as macrophages and B cells.
They act indirectly and recruit other inflammatory leukocytes, mononuclear cells and lymphocytes from the peripheral vasculature into the colon via interactions between homing receptors on leukocytes (e.g., α4β7 integrin) and addressins on vascular endothelium (e.g., MadCAM1). CD4 T cells are of two major types: TH1 cells [interferon (IFN) γ, tumor necrosis factor (TNF)] and TH2 cells (IL-4, IL-5, IL-13). TH1 cells appear to induce transmural granulomatous inflammation that resembles Crohn’s disease, and TH2 cells appear to induce superficial mucosal inflammation resembling Ulcerative Colitis. The TH1 cytokine pathway is initiated by interleukin-12, an important cytokine in the pathogenesis of mucosal inflammation [5].
Once initiated, the immune inflammatory response is perpetuated as a consequence of T cell activation. A sequence of inflammatory mediators acts to extend the response. Inflammatory cytokines, such as Interleukins 1 & 6, Tumour Necrosis Factor alpha have diverse effects on tissue. They promote collagen production, fibrogenesis, production of other inflammatory mediators and activation of tissue metalloproteinases. They activate the chain of coagulation in surrounding blood vessels (e.g., increased production of von Willebrand’s factor).
In colitis, the activity of the cytokines is dysregulated, resulting in the imbalance between the pro-inflammatory and anti-inflammatory mediators.
Exogenous factors may have an as yet undefined infectious etiology. The immune response to a specific organism could be expressed differently, depending upon the genetic makeup of a particular individual. Multiple pathogens (e.g., Salmonella, Shigella sp., Campylobacter sp.) may initiate colitis by triggering an inflammatory response that the mucosal immune system cannot control.
Prevention
Colitis, especially the inflammatory bowel variant is difficult to prevent at the present time because the likely causes are hereditary or an auto-immune response to an unknown stimulus. However, infectious colitis is an ailment caused due to the lack of proper hygiene, lack of clean drinking water and sanitation. This can be prevented if proper care is taken. As ischaemic colitis is caused due to the narrowing of the blood vessels supplying the colon, taking care of other types of circulatory problems such as peripheral vascular diseases and stroke can also reduce the risk for ischaemic colitis [10].
Summary
Colitis is a term used to indicate the inflammation of the colon. Colitis could be associated with enteritis which is the inflammation of the intestine and proctitis which is the inflammation of the rectum.
Crohn’s disease, ulcerative colitis and indeterminate colitis are three idiopathic disorders associated with inflammation of the intestinal lining [1].
Colitis can cause pain, diarrhoea and bleeding from the rectum. Patient’s suffering from colitis and inflammatory bowel diseases are at high risk of developing colorectal cancer.
Patient Information
Colitis is a term used to indicate inflammation of the colon. It is usually seen in adolescents and young adults. There is no known cause for colitis although some studies attribute it to hereditary factors and the fact that colitis is an auto-immune disease. Infective colitis is caused by micro-organisms such as E.coli, Salmonella and Shigella and this is the type of colitis that can be prevented by maintaining a clean environment with proper hygiene and sanitation. The other variants of colitis such as ulcerative colitis and Crohn's disease cannot be prevented because of their auto immune nature.
Colitis presents with symptoms such as abdominal pain, bowel dysfunction and bleeding. Daily stress can also affect the intestine causing an aggravation of the symptons. It is diagnosed with the help of lab-tests and X-rays which may show abnormalities in the bowel. A biopsy will show changes in the mucosal lining. Psychosocial support and education about the illness to the family will help in achieving positive long term goals where treatment is concerned.
References
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- Hugot JP, Chamaillard M, Zouali H et al. Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn’s disease. Nature. 2001 May 31;411(6837):599-603.
- Higuchi LM. Epidemiology and diagnosis of inflammatory bowel disease in children and adolescents. UpToDate. 2005;12.3. Last accessed: Dec 12, 2013.
- Hou JK, El-Serag H, Thirumurthi S. Distribution and Manifestations of Inflammatory Bowel Disease in Asians, Hispanics, and African Americans: A Systematic Review. Am J Gastroenterol. 2009 Aug; 104(8):2100-9
- Friedman S, Rubin H, Bodian C et al. Screening and surveillance colonoscopy in chronic Crohn’s colitis: Results of a Surveillance Program Spanning 25 Years. Clin Gastroenterol Hepatol. 2008;6(9):993-98.
- Bousvaros A, Leichtner A. Overview of the management of Crohn's disease in children and adolescents. UpToDate. 2005;13.2. Last accessed: Mar 12, 2014.
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- Kornbluth A, Sachar DB. Ulcerative colitis practice guidelines in adults. Am J Gastroenterol. 1997:92:204-11.
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