Crohn's disease

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Crohn's disease
The three most common sites of intestinal involvement in Crohn's disease are ileal, ileocolic and colonic.[1]
ICD-10 K50
ICD-9 555
OMIM 266600
DiseasesDB 3178
MedlinePlus 000249
MeSH D003424

Crohn's disease

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and keywords: Regional enteritis

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differential Diagnosis

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory tests | ECG | Chest X Ray |CT | MRI | Echocardiography or Ultrasound |Other imaging studies | Alternative diagnostics

Treatment

Medical therapy | Surgical options | Prevention | Financial costs| [[Crohn's disease future or investigational therapies|Future therapies]

Diagnosis

Natural History , Complications and Prognosis

Complications
Endoscopic image of colon cancer identified in the sigmoid colon (anatomy) on screening colonoscopy for Crohn's disease.

Crohn's disease can lead to several mechanical complications within the intestines, including obstruction, fistulae, and abscesses. Obstruction typically occurs from strictures or adhesions which narrow the lumen, blocking the passage of the intestinal contents. Fistulae can develop between two loops of bowel, between the bowel and bladder, between the bowel and vagina, and between the bowel and skin. Abscesses are walled off collections of infection, which can occur in the abdomen or in the perianal area in Crohn's disease sufferers.

Crohn's disease also increases the risk of cancer in the area of inflammation. For example, individuals with Crohn's disease involving the small bowel are at higher risk for small intestinal cancer. Similarly, people with Crohn's colitis have a relative risk of 5.6 for developing colon cancer.[2] Screening for colon cancer with colonoscopy is recommended for anyone who has had Crohn's colitis for eight years, or more.[3]

Individuals with Crohn's disease are at risk of malnutrition for many reasons, including decreased food intake and malabsorption. The risk increases following resection of the small bowel. Such individuals may require oral supplements to increase their caloric intake, or in severe cases, total parenteral nutrition (TPN). Most people with moderate or severe Crohn's disease are referred to a dietitian for assistance in nutrition.[4]

There are many complications that can come with Crohn's disease like: obstructions, abscesses, free perforation, and hemorrhage.[5]

Women with Inflammatory bowel disease shows that they "face a higher risk of adverse outcomes related to pregnancy, according to a report in the October issue of Gastroenterology" [2].

Prognosis

Crohn's disease is a chronic condition for which there is currently no cure. It is characterized by periods of improvement followed by episodes when symptoms flare up. With treatment, most people achieve a healthy height and weight, and the mortality rate for the disease is low. Crohn's disease is associated with an increased risk of small bowel and colorectal carcinoma.[6]

Crohn's cannot be cured by surgery, though surgery does happen with blockages, whether partial or a full blockage occurs. After the first surgery, the Crohn's usually shows up at the site of the resection though it can appear in other locations. After a resection, scar tissue builds up which causes strictures. A stricture is when the intestines becomes too small to allow excrement to pass through easily which can lead to a blockage. After the first resection, another resection may be necessary within five years of the first surgery. [3]

Many patients will have temporary stoma formations together with possible associated complications. [4]

Diagnosis

Endoscopic image of Crohn's colitis showing deep ulceration.
CT scan showing Crohn's disease in the fundus of the stomach
Crohn's disease can mimic ulcerative colitis on endoscopy. This endoscopic image is of Crohn's colitis showing diffuse loss of mucosal architecture, friability of mucosa in sigmoid colon and exudate on wall, all of which can be found with ulcerative colitis.

The diagnosis of Crohn's disease can sometimes be challenging,[7] and a number of tests are often required to assist the physician in making the diagnosis.[8] Sometimes even with all the tests the Crohn's does not show itself. A colonoscopy has about a 70% chance of showing the disease and the rest of the tests go down in percentage. Disease in the small bowel can not be seen through some of the regular tests; for example, a colonoscopy can't get there.

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. Occasionally, the colonoscope can travel past the terminal ileum but it varies from patient to patient. 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,[1] 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.[9]

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.[10]The utility of capsule endoscopy for this, however, is still uncertain.[11]

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.[10][12] 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.[13]

CT and MRI scans are useful for evaluating the small bowel with enteroclysis protocols.[14]They are additionally useful for looking for intra-abdominal complications of Crohn's disease such as abscesses, small bowel obstruction, or fistulae.[15] 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[16]

Images shown below are courtesy of RadsWiki and copylefted

  • Abdominal x-ray of a patient with Crohn disease

    Abdominal x-ray of a patient with Crohn disease

  • Pseudosacculations in Crohn's disease

    Pseudosacculations in Crohn's disease

  • Pseudosacculations in Crohn's disease

    Pseudosacculations in Crohn's disease

  • Pseudosacculations in Crohn's disease

    Pseudosacculations in Crohn's disease

  • Active Crohn's disease CT

    Active Crohn's disease CT

  • Active Crohn's disease MRI

    Active Crohn's disease MRI

  • Active Crohn's disease MRI

    Active Crohn's disease MRI

  • Active Crohn's disease small bowel series

    Active Crohn's disease small bowel series

  • Comb sign in Crohn's disease

    Comb sign in Crohn's disease

Blood tests

A complete blood count may reveal anemia, which may be caused either by blood loss or [[Cyanocobalamin|vitamin BTemplate:Ssub]] deficiency. The latter may be seen with ileitis because vitamin BTemplate:Ssub is absorbed in the ileum.[17] Erythrocyte sedimentation rate, or ESR, and C-reactive protein measurements can also be useful to gauge the degree of inflammation.[18] It is also true in patient with ilectomy done in response to the complication. Another cause of anaemia is anaemia of chronic disease, characterized by its microcytic and hypochromic anaemia. There are reasons in anaemia, including medication in treatment of inflammatory bowel disease like azathioprine can lead to cytopenia and sulfasalazine can also result in folate malabsorption, etc. Testing for anti-Saccharomyces cerevisiae antibodies (ASCA) and anti-neutrophil cytoplasmic antibodies (ANCA) has been evaluated to identify inflammatory diseases of the intestine[19] and to differentiate Crohn's disease from ulcerative colitis.[20]

Epidemiology and Demographics

Crohn's disease affects between 400,000 and 600,000 people in North America.[21] Prevalence estimates for Northern Europe have ranged from 27–48 per 100,000.[22] Crohn's disease tends to present initially in the teens and twenties, with another peak incidence in the fifties to seventies, although the disease can occur at any age.[1][8]

The incidence of Crohn's disease has been ascertained from population studies in Norway and the United States and is similar at 6 to 7.1:100,000.[23][24] Crohn's disease is more common in northern countries, and shows a higher preponderance in northern areas of the same country.[25] The incidence of Crohn's disease in North America is 6:100,000, and is thought to be similar in Europe, but lower in Asia and Africa.[23] It also has a higher incidence in Ashkenazi Jews.[26]

Crohn's disease has a bimodal distribution in incidence as a function of age: the disease tends to strike people in their teens and twenties, and people in their fifties through seventies.[1][8] It is rare in early childhood. There is no association with gender, social class or occupation. Parents, siblings or children of people with Crohn's disease are 3 to 20 times more likely to develop the disease.[27] Twin studies show a concordance of greater than 55% for Crohn's disease.[28]

Risk Factors

Although the cause of Crohn's disease is not known, it is believed to be an autoimmune disease that is genetically linked. The highest relative risk occurs in siblings, affecting males and females equally. Smokers are three times more likely to get Crohn's disease.

Unlike the other major type of IBD, ulcerative colitis, there is no known medical or surgical cure for Crohn's disease.[29] Instead, a number of medical treatments are utilized with the goal of putting and keeping the disease in remission. These include 5-aminosalicylic acid (5-ASA) formulations (Pentasa capsules, Asacol tablets, Lialda tablets, Rowasa retention enemas), steroid medications, immunomodulators (such as azathioprine, mercaptopurine (6-MP), and methotrexate), and newer biological medications, such as infliximab (Remicade) and adalimumab (Humira).[26]Also in January 2008 the U.S. Food and Drug Administration approved a new biologic known as natalizumab (Tysabri) for both induction of remission and maintenance of remission in moderate and severe Crohns Disease.

Treatment

Main articles: Treatment of Crohn's disease and Biological therapy for inflammatory bowel disease

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.

Once remission is induced, the goal of treatment becomes maintaining remission and 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.[30]

On 14 January 2008 the U.S. Food and Drug Administration approved natalizumab (Tysabri) for both induction of remission and maintenance of remission in Crohns. Natalizumab is humanised monoclonal antibody (MAb), and the first alpha-4 antagonist in a new class of agents called selective adhesion-molecule (SAM) inhibitors. Alpha-4 integrin is required for leukocytes to adhere to the walls of blood vessels and migrate into the gut; natalizumab prevents leukocytes from doing that. Natalizumab was previously approved for multiple sclerosis. However, because it suppresses the immune system, natalizumab has been linked to a very rare adverse effect that is usually fatal if undetected. Leukocytes also protect the body from viruses, and 2 patients on natalizumab, who were also receiving other immuno-suppressive drugs (Avonex and Immuran), died of a rare brain infection, progressive multifocal leukoencephalopathy. Because of this danger, patients must be in a special monitoring program, and natalizumab is given as a mono-therapy.[31].As of late December 2007, more than 21,000 MS patients were receiving natalizumab mono-therapy without a single incidence of PML occurring.[32].

Surgery may be required for complications such as obstructions, fistulas and/or abscesses, or if the disease does not respond to drugs within a reasonable time. For patients with an obstruction due to a stricture, two options for treatment are strictureplasty and resection of that portion of bowel. According to a retrospective review at the Cleveland Clinic, there is no statistical significance between strictureplasty alone versus strictureplasty and resection specifically in cases of duodenal involvement. In these cases, re-operation rates were 31% and 27%, respectively, indicating that strictureplasty is a safe and effective treatment for selected patients with duodenal involvement.[33]

Recent studies using Helminthic therapy or Hookworms to treat Crohn's Disease and other (non-viral) auto-immune diseases seem to yield promising results.[34][35][36]

See also

References

  1. ↑ 1.0 1.1 1.2 1.3
  2. ↑ Ekbom A, Helmick C, Zack M, Adami H (1990). "Increased risk of large-bowel cancer in Crohn's disease with colonic involvement". Lancet. 336 (8711): 357–9. PMID 1975343.
  3. ↑ Collins P, Mpofu C, Watson A, Rhodes J. "Strategies for detecting colon cancer and/or dysplasia in patients with inflammatory bowel disease". Cochrane Database Syst Rev: CD000279. PMID 16625534.
  4. ↑ Evans J, Steinhart A, Cohen Z, McLeod R (2003). "Home total parenteral nutrition: an alternative to early surgery for complicated inflammatory bowel disease". J Gastrointest Surg. 7 (4): 562–6. PMID 12763417.
  5. ↑ "Complications of Crohn's Disease". Retrieved 2008-01-16.
  6. ↑ Canavan, C. (2006). "Meta-analysis : colorectal and small bowel cancer risk in patients with Crohn's disease". Alimentary pharmacology & therapeutics. 23 (8): 1097–1104. ISSN 0269-2813. Retrieved 2007-05-23. Unknown parameter |month= ignored (help); Unknown parameter |coauthors= ignored (help)
  7. ↑
  8. ↑ 8.0 8.1 8.2 Gopal, Latha (2006-05-23). "Crohn Disease". eMedicine. Retrieved 2006-07-02. Unknown parameter |coauthors= ignored (help)
  9. ↑ Lee, S. D. (2002). "Endoscopy in inflammatory bowel disease". Gastroenterology Clinics of North America. 31 (1): 119–32. PMID 12122727. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  10. ↑ 10.0 10.1 Hara, Amy K. (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. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  11. ↑ Triester, Stuart L. (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. doi:10.1111/j.1572-0241.2006.00506.x. PMID 16696781. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  12. ↑ Dixon, P.M. (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. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  13. ↑ Carucci, L. R. (2002). "Radiographic imaging of inflammatory bowel disease". Gastroenterology Clinics of North America. 31 (1): 93–117. PMID 12122746. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  14. ↑ Rajesh, A. (2006). "Multislice CT enteroclysis: technique and clinical applications". Clinical Radiology. 61 (1): 31–9. doi:10.1016/j.crad.2005.08.006. PMID 16356814. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  15. ↑ Zissin, Rivka (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 2006-07-02. Unknown parameter |month= ignored (help); Unknown parameter |coauthors= ignored (help)
  16. ↑ MacKalski, B. A. (2005). "New diagnostic imaging tools for inflammatory bowel disease". Gut. 55 (5): 733–41. doi:10.1136/gut.2005.076612. PMID 16609136. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  17. ↑ Goh, Jason (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. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  18. ↑ Chamouard, Patrick (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. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help); Check date values in: |year= (help) Epub ahead of print
  19. ↑ Kaila, B. (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 2006-07-02. Unknown parameter |month= ignored (help); Unknown parameter |coauthors= ignored (help)
  20. ↑ Israeli, E. (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. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  21. ↑ Loftus, E. V. (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. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  22. ↑ Bernstein, Charles N. (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. Unknown parameter |month= ignored (help)
  23. ↑ 23.0 23.1 Hiatt, Robert A. (1988). "Epidemiology of inflammatory bowel disease in a defined northern California population". Western Journal of Medicine. 149 (5): 541–6. PMID 3250100. Retrieved 2006-07-02. Unknown parameter |month= ignored (help); Unknown parameter |coauthors= ignored (help)
  24. ↑ Moum, B. (1996). "Incidence of Crohn's disease in four counties in southeastern Norway, 1990-93. A prospective population-based study. The Inflammatory Bowel South-Eastern Norway (IBSEN) Study Group of Gastroenterologists". Scandinavian Journal of Gastroenterology. 31 (4): 355–61. PMID 8726303. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  25. ↑ Shivananda, S. (1996). "Incidence of inflammatory bowel disease across Europe: is there a difference between north and south? Results of the European Collaborative Study on Inflammatory Bowel Disease (EC-IBD)". Gut. 39 (5): 690–7. PMID 9014768. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  26. ↑ 26.0 26.1 Podolsky, Daniel K. (2002). "Inflammatory bowel disease". New England Journal of Medicine. 346 (6): 417–29. PMID 12167685. Retrieved 2006-07-02. Unknown parameter |month= ignored (help)
  27. ↑ Satsangi J, Jewell DP, Bell JI. The genetics of inflammatory bowel disease and they are sick and we too. Gut. 1997 May;40(5):572-4. PMID 9203931.
  28. ↑ Tysk C, Lindberg E, Jarnerot G, Floderus-Myrhed B. Ulcerative colitis and Crohn's disease in an unselected population of monozygotic and dizygotic twins. A study of heritability and the influence of smoking. Gut 1988 Jul;29(7):990-6. PMID 3396969
  29. ↑ Al-Ataie, M Bashar (2005-10-04). "Ulcerative colitis". eMedicine. Retrieved 2006-07-02. Unknown parameter |coauthors= ignored (help)
  30. ↑
  31. ↑ "FDA Approves Tysabri to Treat Moderate-to-Severe Crohn's Disease" (Press release). U.S. Food and Drug Administration. 2008-01-14. Retrieved 2008-01-16.
  32. ↑ .http://www.elan.com/News/full.asp?ID=1091942
  33. ↑ Ozuner G, Fazio VW, Lavery IC, Milsom JW, Strong SA (1996). "Reoperative rates for Crohn's disease following strictureplasty. Long-term analysis". Dis. Colon Rectum. 39 (11): 1199–203. PMID 8918424.
  34. ↑ British Medical Journal A proof of concept study establishing Necator americanus in Crohn’s patients and reservoir donors
  35. ↑ Daily Mail. The bloodsucking worm that fights allergies from inside your tummy 14-09-2007.
  36. ↑ How to cure your asthma or hayfever using hookworm - a practical guide. 01-05-2006.

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