Crohn’s disease (also known as regional enteritis) is a chronic, episodic, inflammatory condition of the gastrointestinal tract characterized by transmural inflammation (affecting the entire wall of the involved bowel) and skip lesions (areas of inflammation with areas of normal lining in between). Crohn’s disease is a type of inflammatory bowel disease (IBD) and can affect any part of the gastrointestinal tract from mouth to anus; as a result, the symptoms of Crohn’s disease can vary between affected individuals. The main gastrointestinal symptoms are abdominal pain, diarrhea, which may be bloody, and weight loss.
Crohn’s disease can also cause complications outside of the gastrointestinal tract such as skin rashes, arthritis, and inflammation of the eye. (1) Crohn’s disease affects between 400,000 and 600,000 people in North America(2). Prevalence estimates for Northern Europe have ranged from 27–48 per 100,000 (3). Crohn’s disease often develops in the teenage years, though individuals in their 60s and 70s are also at increased risk. There is a genetic component to susceptibility, affecting males and females equally. The disease may be triggered by environmental factors.
Although the cause of Crohn’s disease is not known, it is widely believed to be an autoimmune disease. The condition occurs when the immune system contributes to damage of the gastrointestinal tract by causing inflammation. Many cytokines in the Th1 classification, including TNF-? , interleukin-2, and interferon ? are elevated in Crohn’s disease, and are involved in mediating the inflammation. Unlike the other major type of IBD, ulcerative colitis, there is no known medical or surgical cure for Crohn’s disease. Instead, a number of medical treatments are utilized with the goal of putting and keeping the disease in remission.
These include steroid medications, immunomodulators (such as azathioprine and methotrexate), and newer biological medications, such as infliximab. The disease was named after Burrill Bernard Crohn, an American gastroenterologist. In 1932, Crohn and two colleagues first described a series of patients with inflammation of the terminal ileum, the area most commonly affected in Crohn’s disease. symptoms Abdominal pain may be the initial symptom of Crohn’s disease. The pain is commonly crampy and may be relieved by defecation. It is often accompanied by diarrhea, which may be bloody.
The nature of the diarrhea in Crohn’s disease depends on the part of the small intestine or colon that is involved. Ileitis typically results in large-volume watery feces. Colitis may result in a smaller volume of feces of higher frequency. Fecal consistency may range from solid to watery. In severe cases, an individual may have more than 20 bowel movements per day and may need to awaken at night to defecate. Visible bleeding in the feces is less common in Crohn’s disease than in ulcerative colitis, but may be seen in the setting of Crohn’s colitis. Bloody bowel movements are typically intermittent, and may be bright or dark red in colour.
In the setting of severe Crohn’s colitis, bleeding may be copious. Flatus and bloating may also add to the intestinal discomfort. Symptoms caused by intestinal stenosis are also common in Crohn’s disease. Abdominal pain is often most severe in areas of the bowel with stenoses. In the setting of severe stenosis, vomiting and nausea may indicate the beginnings of small bowel obstruction. Crohn’s disease may also be associated with primary sclerosing cholangitis, a type of inflammation of the bile ducts. Peri-anal discomfort may also be prominent in Crohn’s disease.
Itchiness or pain around the anus may be suggestive of inflammation, fistulization or abscess around the anal area or anal fissure. Perianal skin tags are also common in Crohn’s disease. Fecal incontinence may accompany peri-anal Crohn’s disease. At the opposite end of the gastrointestinal tract, the mouth may be affected by non-healing sores (aphthous ulcers). Rarely, the esophagus, and stomach may be involved in Crohn’s disease. These can cause symptoms including difficulty swallowing (odynophagia upper abdominal pain, and vomiting. Crohn’s disease, like many other chronic, inflammatory diseases, can cause a variety of systemic symptoms.
Among children, growth failure is common. Many children are first diagnosed with Crohn’s disease based on inability to maintain growth. As Crohn’s disease may manifest at the time of the growth spurt in puberty, up to 30% of children with Crohn’s disease may have retardation of growth. Fever may also be present, though fevers greater than 38. 5 ? Care uncommon unless there is a complication such as an abscess Among older individuals, Crohn’s disease may manifest as weight loss. This is usually related to decreased food intake, since individuals with intestinal symptoms from Crohn’s disease often feel better when they do not eat.
People with extensive small intestine disease may also have malabsorption of carbohydrates or lipids, which can further exacerbate weight loss. CAUSE: The exact cause of Crohn’s disease is unknown. However, genetic and environmental factors have been invoked in the pathogenesis of the disease. Mutations in the CARD15 gene (also known as the NOD2 gene) are associated with Crohn’s disease and with susceptibility to certain phenotypes of disease location and activity. Many environmental factors have also been hypothesized as causes or risk factors for Crohn’s disease.
Diets high in sweet, fatty or refined foods may play a role. A retrospective Japanese study found that those diagnosed with Crohn’s disease had higher intakes of sugar, fat, fish and shellfish than controls prior to diagnosis. A similar study in Israel also found higher intakes of fats (especially chemically modified fats) and sucrose, with lower intakes of fructose and fruits, water, potassium, magnesium and vitamin C in the diets of Crohn’s disease sufferers before diagnosis, and cites three large European studies in which sugar intake was significantly increased in people with Crohn’s disease compared with controls.
Smoking has been shown to increase the risk of the return of active disease, or “flares”. Oral contraceptives have also shown an association with the development of Crohn’s disease. The diagnosis of Crohn’s disease can sometimes be challenging, and a number of tests are often required to assist the physician in making the diagnosis. Endoscopy A colonoscopy is the best test for making the diagnosis of Crohn’s disease as it allows direct visualization of the colon and the terminal ileum, identifying the pattern of disease involvement.
During the procedure, the gastroenterologist can also perform a biopsy, taking small samples of tissue for laboratory analysis which may help confirm a diagnosis. As 30% of Crohn’s disease involves only the ileum, cannulation of the terminal ileum is required in making the diagnosis. Finding a patchy distribution of disease, with involvement of the colon or ileum but not the rectum, is suggestive of Crohn’s disease, as are other endoscopic stigmata.
Wireless capsule endoscopy is a technique where a small capsule with a built-in camera is swallowed, the camera takes serial pictures of the entire gastrointestinal tract and is passed in the patient’s faeces. It has been used in the search for Crohn’s disease in the small bowel, which cannot be reached with colonoscopy or gastroscopy. The utility of capsule endoscopy for this, however, is still uncertain. Radiologic tests A small bowel follow-through may suggest the diagnosis of Crohn’s disease and is useful when the disease involves only the small intestine.
Because colonoscopy and gastroscopy allow direct visualization of only the terminal ileum and beginning of the duodenum, they cannot be used to evaluate the remainder of the small intestine. As a result, a barium follow-through x-ray, wherein barium sulfate suspension is ingested and fluoroscopic images of the bowel are taken over time, is useful for looking for inflammation and narrowing of the small bowel Barium enemas, in which barium is inserted into the rectum and fluoroscopy used to image the bowel, are rarely used in the work-up of Crohn’s disease due to the advent of colonoscopy.
They remain useful for identifying anatomical abnormalities when strictures of the colon are too small for a colonoscope to pass through, or in the detection of colonic fistulae. CT and MRI scans are useful for evaluating the small bowel with enteroclysis protocols. They are additionally useful for looking for intra-abdominal complications of Crohn’s disease such as abscesses, small bowel obstruction, or fistulae. Magnetic resonance imaging (MRI) are another option for imaging the small bowel as well as looking for complications, though it is more expensive and less readily available Blood tests
A complete blood count may reveal anemia, which may be caused either by blood loss or vitamin B12 deficiency. The latter may be seen with ileitis because vitamin B12 is absorbed in the ileum. Erythrocyte sedimentation rate, or ESR, and C-reactive protein measurements can also be useful to gauge the degree of inflammation. Testing for anti-Saccharomyces cerevisiae antibodies (ASCA) and anti-neutrophil cytoplasmic antibodies (ANCA) has been evaluated to identify inflammatory diseases of the intestine and to differentiate Crohn’s disease from ulcerative colitis. TREATMENT: Treatment is only needed for people exhibiting symptoms.
The therapeutic approach to Crohn’s disease is sequential: to treat acute disease, and then to maintain remission. Treatment initially involves the use of medications to treat any infection and to reduce inflammation. This usually involves the use of aminosalicylate anti-inflammatory drugs and corticosteroids, and may include antibiotics. Surgery may be required for complications such as obstructions or abscesses, or if the disease does not respond to drugs within a reasonable time. Once remission is induced, the goal of treatment becomes maintenance of remission, avoiding flares.
Because of side-effects, the prolonged use of corticosteroids must be avoided. Although some people are able to maintain remission with aminosalicylates alone, many require immunosuppressive drugs. Surgery is generally reserved for complications of Crohn’s disease, or when disease that resists treatment with drugs is confined to one location that can be removed. Surgery is often used to manage complications of Crohn’s disease, including fistulae, small bowel obstruction, colon cancer, small intestine cancer and fibrostenotic strictures, when strictureplasty (expansion of the stricture) is sometimes performed.
Otherwise, and for other complications, resection and anastomosis – the removal of the affected section of intestine and the rejoining of the healthy sections – is the surgery usually performed for Crohn’s disease (e. g. , ileocolonic resection). Neither type of surgery cures Crohn’s disease, as recurrence often reappears in previously unaffected areas of the intestine. Small intestine transplants are experimental, and are usually only performed when there is a risk of short bowel syndrome due to repeated resection surgeries. Diet and lifestyle
There is no evidence that diet causes or cures Crohn’s disease, but many people with Crohn’s disease note that certain foods improve or worsen their symptoms. Fish oil has been found to be effective in reducing the chance of relapse in less severe cases. REFERENCE: 1) • Hanauer, Stephen B. (March 1996). “Inflammatory bowel disease”. New England Journal of Medicine 334 (13): 841-848. PMID 8596552. Retrieved on 2006-11-10. 2) • Loftus, E. V. , P. Schoenfeld, W. J. Sandborn (January 2002). “The epidemiology and natural history of Crohn’s disease in population-based patient cohorts from North America: a systematic review”.
Alimentary Pharmacology & Therapeutics 16 (1): 51-60. DOI:10. 1046/j. 1365-2036. 2002. 01140. x. PMID 11856078. 3) • Bernstein, Charles N. (July 2006). “The Epidemiology of Inflammatory Bowel Disease in Canada: A Population-Based Study”. The American Journal of Gastroenterology 101 (7): 1559–1568. DOI:10. 1111/j. 1572-0241. 2006. 00603. x. PMID 16863561. 4) • Gopal, Latha; Senthil Nachimuthu (2006-05-23). Crohn Disease. eMedicine. Retrieved on 2006-07-02. 5) • Pallone F, Monteleone G. “Regulatory cytokines in inflammatory bowel disease. “. Aliment Pharmacol Ther 10 Suppl 2: 75-9; discussion 80. PMID 8899105 6) • Romagnani S (1999).
“Th1/Th2 cells. “. Inflamm Bowel Dis 5 (4): 285-94. PMID 10579123. 7) • Al-Ataie, M Bashar; Vishwanath N Shenoy (2005-10-04). Ulcerative colitis. eMedicine. Retrieved on 2006-07-02. 8) • Podolsky, Daniel K. (August 2002). “Inflammatory bowel disease”. New England Journal of Medicine 346 (6): 417-29. PMID 12167685 Retrieved on 2006-07-02 9) • Crohn BB, Ginzburg L, Oppenheimer GD. “Regional ileitis: a pathologic and clinical entity. ” Mt Sinai J Med 2000 May;67(3):263-8. PMID 10828911 10) • Gasche C, Scholmerich J, Brynskov J, D’Haens G, Hanauer S, Irvine E, Jewell D, Rachmilewitz D, Sachar D, Sandborn W, Sutherland L (2000).
“A simple classification of Crohn’s disease: report of the Working Party for the World Congresses of Gastroenterology, Vienna 1998”. Inflamm Bowel Dis 6 (1): 8-15. PMID 10701144 11) • Dubinsky MC, Fleshner PP. (2003). “Treatment of Crohn’s Disease of Inflammatory, Stenotic, and Fistulizing Phenotypes. “. Curr Treat Options Gastroenterol 6 (3): 183-200. PMID 12744819 12) • Pimentel, Mark, Michael Chang, Evelyn J. Chow, Siamak Tabibzadeh, Viorelia Kirit-Kiriak, Stephan R. Targan, Henry C. Lin (December 2000). “Identification of a prodromal period in Crohn’s disease but not ulcerative colitis”.
American Journal of Gastroenterology 95 (12): 3458-62. DOI:10. 1111/j. 1572-0241. 2000. 03361. x PMID 11151877 13) • Hara, Amy K. , Jonathan A. Leighton, Russell I. Heigh, Virender K. Sharma, Alvin C. Silva, Giovanni De Petris, Joseph G. Hentz and David E. Fleischer (January 2006). “Crohn disease of the small bowel: preliminary comparison among CT enterography, capsule endoscopy, small-bowel follow-through, and ileoscopy”. Radiology 238 (1): 128-34. DOI:10. 1148/radiol. 2381050296 PMID 16373764 14) • Triester, Stuart L. , Jonathan A. Leighton, Grigoris I. Leontiadis, Suryakanth R. Gurudu, David E. Fleische, Amy K.
Hara, Russell I. Heigh, Arthur D. Shiff, and Virender K. Sharma (May 2006). “A meta-analysis of the yield of capsule endoscopy compared to other diagnostic modalities in patients with non-stricturing small bowel Crohn’s disease”. The American Journal of Gastroenterology 101 (5): 954-64. DOI10. 1111/j. 1572-0241. 2006. 00506.. PMID 16696781 15) • Dixon, P. M. , M. E. Roulston and D. J. Nolan (January 1993). “The small bowel enema: a ten year review”. Clinical Radiology 47 (1): 46-8. DOI:10. 1016/S0009-9260(05)81213-9 PMID 8428417 16) • Carucci, L. R. , M. S. Levine (march 2002). “Radiographic imaging of inflammatory bowel disease”.
Gastroenterology Clinics of North America 31 (1): 93-117. PMID 12122746 17) • Rajesh, A. , D. D. T. Maglinte (January 2006). “Multislice CT enteroclysis: technique and clinical applications”. Clinical Radiology 61 (1): 31-9. DOI:10. 1016/j. crad. 2005. 08. 006. PMID 16356814 18) • Zissin, Rivka, Marjorie Hertz, Alexandra Osadchy, Ben Novis and Gabriela Gayer (February 2005). “Computed Tomographic Findings of Abdominal Complications of Crohn’s Disease—Pictorial Essay (PDF). Canadian Association of Radiologists Journal 56 (1): 25-35. PMID 15835588 Retrieved on 2006-07-02 19) • MacKalski, B. A. , C. N. Bernstein (May 2005).
“New diagnostic imaging tools for inflammatory bowel disease”. Gut 55 (5): 733-41. DOI:10. 1136/gut. 2005. 076612. PMID 16609136 20) • Goh, Jason, C. A. O’Morain (February 2003). “Review article: nutrition and adult inflammatory bowel disease”. Alimentary Pharmacology & Therapeutics 17 (3): 307-20. DOI:10. 1046/j. 1365-2036. 2003. 01482. x. PMID 12562443 21) • Chamouard, Patrick, Zoe Richert, Nicolas Meyer, Gabriel Rahmi, Rene Baumann (2006 April). “Diagnostic Value of C-Reactive Protein for Predicting Activity Level of Crohn’s Disease”. Clinical Gastroenterology and Hepatology. DOI:10. 1016/j. cgh. 2006. 02. 003 PMID 16630759.
Epub ahead of print 22) • Kaila, B. , K. Orr and C. N. Bernstein (December 2005). “The anti-Saccharomyces cerevisiae antibody assay in a province-wide practice: accurate in identifying cases of Crohn’s disease and predicting inflammatory disease”. The Canadian Journal of Gastroenterology 19 (12): 717-21. PMID 16341311. Retrieved on 2006-07-02 23) • Israeli, E. , I. Grotto, B. Gilburd, R. D. Balicer, E. Goldin, A. Wiik and Y. Shoenfeld (September 2005). “Anti-Saccharomyces cerevisiae and antineutrophil cytoplasmic antibodies as predictors of inflammatory bowel disease”. Gut 54 (9): 1232-6. DOI:10. 1136/gut. 2004. 060228.
PMID 16099791. 24) • Kornbluth, Asher, David B. Sachar (July 2004). “Ulcerative Colitis Practice Guidelines in Adults (PDF). American Journal of Gastroenterology 99 (7): 1371-1385. DOI:10. 1111/j. 1572-0241. 2004. 40036. x. PMID 1523368 Retrieved on 2006-11-08 25) • Hanauer, Stephen B. , William Sandborn (March 1 2001). “Management of Crohn’s Disease in Adults” (PDF). American Journal of Gastroenterology 96 (3): 635-643. DOI:10. 1111/j. 1572-0241. 2001. 03671. x PMID 11280528. Retrieved on 2006-11-08 26) • Broome, Ulrika, Annika Bergquist (February 2006). “Primary sclerosing cholangitis, inflammatory bowel disease, and colon cancer”.
Seminars in Liver Disease 26 (1): 31-41. DOI:10. 1055/s-2006-933561. PMID 16496231. 27) • Cohen LB. Re: Disappearance of Crohn’s ulcers in the terminal ileum after thalidomide therapy. Can J Gastroenterol 2004; 18(2): 101-104. Can J Gastroenterol. 2004 Jun;18(6):419. PMID 15230268. 28) • Surgery for Crohn’s Disease. Crohn’s and Colitis Foundation of America (March 2006). Retrieved on 2006-06-08 29) • A Belluzzi, C Brignola, M Campieri, A Pera, S Boschi, and M Miglioli (June 1996). “Effect of an Enteric-Coated Fish-Oil Preparation on Relapses in Crohn’s Disease”. New England Journal of Medicine 334 (24): 1557-60