Psychology Wiki
Register
Advertisement

Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual differences | Personality | Philosophy | Social |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |

Clinical: Approaches · Group therapy · Techniques · Types of problem · Areas of specialism · Taxonomies · Therapeutic issues · Modes of delivery · Model translation project · Personal experiences ·


This article needs rewriting to enhance its relevance to psychologists..
Please help to improve this page yourself if you can..


Patterns of CD.svg|
Crohn's disease
ICD-10 K50
ICD-9 555
OMIM 266600
DiseasesDB 3178
MedlinePlus 000249
eMedicine med/477 ped/507 radio/197
MeSH {{{MeshNumber}}}


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 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]

The disease was first described in 1904 by Warsaw surgeon Antoni Lesniowski. In 1932, American gastroenterologist Burrill Bernard Crohn and two colleagues described a series of patients with inflammation of the terminal ileum, the area most commonly affected.[2]. Now known by Crohn's name, the disease affects between 400,000 and 600,000 people in North America.[3] Prevalence estimates for Northern Europe have ranged from 27–48 per 100,000.[4] Crohn's disease often develops in the teenage years, though individuals in their 60s and 70s are also at increased risk.[1][5] There is a genetic component to susceptibility with highest relative risk in siblings, affecting males and females equally.

Gastro psychology
Brain animated color nevit

Specialities
Functional gastrointestinal disorder
Other disorders
Related topics

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-α, interleukin-2, and interferon γ are elevated in Crohn's disease, and are involved in mediating the inflammation.[6] [7]

Unlike the other major type of IBD, ulcerative colitis, there is no known medical or surgical cure for Crohn's disease.[8] 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.[9]

Classification[]

Distribution of CD

Distribution of gastrointestinal Crohn's disease. Based on data from American Gastroenterological Association.

Crohn's disease almost invariably affects the gastrointestinal tract. As a result, most gastroenterologists classify the disease by the affected areas. Ileocolic Crohn's disease, which affects both the ileum (the last part of the small intestine that connects to the large intestine) and the large intestine, accounts for fifty percent of cases. Crohn's ileitis, affecting the ileum only, accounts for thirty percent of cases, and Crohn's colitis, affecting the large intestine, accounts for the remaining twenty percent of cases, and may be particularly difficult to distinguish from ulcerative colitis. The disease can attack any part of the digestive tract, from mouth to anus. However, individuals affected by the disease rarely fall outside these three classifications, being affected in other parts of the gastrointestinal tract such as the stomach and esophagus.[1] Crohn's disease may also be classified by the behaviour of disease as it progresses. This was formalized in the Vienna classification of Crohn's disease.[10] There are three categories of disease presentation in Crohn's disease: stricturing, penetrating, and inflammatory. Stricturing disease causes narrowing of the bowel which may lead to bowel obstruction or changes in the caliber of the feces. Penetrating disease creates abnormal passageways (fistulae) between the bowel and other structures such as the skin. Inflammatory disease (or non-stricturing, non-penetrating disease) causes inflammation without causing strictures or fistulae.[10][11]

Symptoms[]

CD serpiginous ulcer

Endoscopy image of colon showing serpiginous ulcer, a classic finding in Crohn's disease

Many people with Crohn's disease have symptoms for years prior to the diagnosis.[12] The usual onset is between 15 and 30 years of age, with no difference between men and women. Because of the patchy nature of the gastrointestinal disease and the depth of tissue involvement, initial symptoms can be more vague than with ulcerative colitis. People with Crohn's disease will go through periods of flare-ups and remission.

Gastrointestinal symptoms

Abdominal pain may be the initial symptom of Crohn's disease. The pain is commonly cramp-like and may be relieved by defecation. It is often accompanied by diarrhea, which may, or may not, be bloody though constipation is not uncommon especially in those who have had surgery. 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.[1][5][9][13] 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.[1] 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.[5] Flatus and bloating may also add to the intestinal discomfort.[5]

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.[5] 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[1] or anal fissure. Perianal skin tags are also common in Crohn's disease.[14] 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.[15]

Systemic symptoms

Crohn's disease, like many other chronic, inflammatory diseases, can cause a variety of systemic symptoms.[1] Among children, growth failure is common. Many children are first diagnosed with Crohn's disease based on inability to maintain growth.[16] 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.[17] Fever may also be present, though fevers greater than 38.5 ˚C (101.3 ˚F) are uncommon unless there is a complication such as an abscess[1] 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 and might lose their appetite.[16] People with extensive small intestine disease may also have malabsorption of carbohydrates or lipids, which can further exacerbate weight loss.[18]

Extraintestinal symptoms

In addition to systemic and gastrointestinal involvement, Crohn's disease can affect many other organ systems.[19] Inflammation of the interior portion of the eye, known as uveitis, can cause eye pain, especially when exposed to light (photophobia). Inflammation may also involve the white part of the eye (sclera), a condition called episcleritis. Both episcleritis and uveitis can lead to loss of vision if untreated.

Crohn's disease is associated with a type of rheumatologic disease known as seronegative spondyloarthropathy. This group of diseases is characterized by inflammation of one or more joints (arthritis) or muscle insertions (enthesitis). The arthritis can affect larger joints such as the knee or shoulder or may exclusively involve the small joints of the hand and feet. The arthritis may also involve the spine, leading to ankylosing spondylitis if the entire spine is involved or simply sacroiliitis if only the lower spine is involved. The symptoms of arthritis include painful, warm, swollen, stiff joints and loss of joint mobility or function.

Crohn's disease may also involve the skin, blood, and endocrine system. One type of skin manifestation, erythema nodosum, presents as red nodules usually appearing on the shins. Erythema nodosum is due to inflammation of the underlying subcutaneous tissue and is characterized by septal panniculitis. Another skin lesion, pyoderma gangrenosum, is typically a painful ulcerating nodule. Crohn's disease also increases the risk of blood clots; painful swelling of the lower legs can be a sign of deep venous thrombosis, while difficulty breathing may be a result of pulmonary embolism. Autoimmune hemolytic anemia, a condition in which the immune system attacks the red blood cells, is also more common in Crohn's disease and may cause fatigue, pallor, and other symptoms common in anemia. Clubbing, a deformity of the ends of the fingers, may also be a result of Crohn's disease. Finally, Crohn's disease may cause osteoporosis, or thinning of the bones. Individuals with osteoporosis are at increased risk of bone fractures.[4]

Complications
Colorectal cancer endo 2

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 and 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.[20] Screening for colon cancer with colonoscopy is recommended for anyone who has had Crohn's colitis for eight years, or more.[21]

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.[22]

Cause[]

NOD2 CARD15

Schematic of NOD2 CARD15 gene, which is associated with certain disease patterns in Crohn's disease

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[23] and with susceptibility to certain phenotypes of disease location and activity.[24]

Recently, research has indicated that Crohn's disease has a strong genetic link. [1] In earlier studies, only two genes were linked to Crohn's, scientists now believe there are over eight genes that show genetics play a crucial role in the disease, although environmental factors also are involved. For example, smoking raises one's risk.

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.[25] 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,[26] 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".[27] Oral contraceptives have also shown an association with the development of Crohn's disease.[28]

Abnormalities in the immune system have often been invoked as being causes of Crohn's disease. It has been hypothesized that Crohn's disease involves augmentation of the Th1 of cytokine response in inflammation.[29] Also, as the colon is rich in bacteria, many infectious agents have been suggested as causes of Crohn's disease. For example, some scientists suspect that Mycobacterium avium subsp. paratuberculosis is involved, in part because it causes a very similar disease, Johne's disease, in cattle. [30]

Pathophysiology[]

File:Crohn's transmural path.jpg

H and E section of colectomy showing transmural inflammation.

At the time of colonoscopy, biopsies of the colon are often taken in order to confirm the diagnosis. There are certain characteristic features of the pathology seen that point toward Crohn's disease. Crohn's disease shows a transmural pattern of inflammation, meaning that the inflammation may span the entire depth of the intestinal wall.[1] Grossly, ulceration is an outcome seen in highly active disease. There is usually an abrupt transition between unaffected tissue and the ulcer. Under a microscope, biopsies of the affected colon may show mucosal inflammation. Transmural inflammation results in formation of lymphoid aggregates throughout the wall of the colon. This inflammation is characterized by focal infiltration of neutrophils, a type of inflammatory cell, into the epithelium. This typically occurs in the area overlying lymphoid aggregates. These neutrophils, along with mononuclear cells, may infiltrate into the crypts leading to inflammation (crypititis) or abscess (crypt abscess). Granulomas, aggregates of macrophage derivatives known as giant cells, are found in 50% of cases and are most specific for Crohn's disease. The granulomas of Crohn's disease do not show "caseation", a cheese-like appearance on microscopic examination that is characteristic of granulomas associated with infections such as tuberculosis. Biopsies may also show chronic mucosal damage as evidenced by blunting of the intestinal villi, atypical branching of the crypts, and change in the tissue type (metaplasia). One example of such metaplasia, Paneth cell metaplasia, involves development of Paneth cells (typically found in the small intestine) in other parts of the gastrointestinal system.[31] This section is a stub. You can help by adding to it.

Diagnosis[]

CD colitis

Endoscopic image of Crohn's colitis showing deep ulceration.

CT scan gastric CD

CT scan showing Crohn's disease in the fundus of the stomach

CD colitis 2

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,[12] and a number of tests are often required to assist the physician in making the diagnosis.[5] 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.[32]

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.[33]The utility of capsule endoscopy for this, however, is still uncertain.[34]

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.[33][35] 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.[36]

CT and MRI scans are useful for evaluating the small bowel with enteroclysis protocols.[37]They are additionally useful for looking for intra-abdominal complications of Crohn's disease such as abscesses, small bowel obstruction, or fistulae.[38] 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[39]

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.[40] Erythrocyte sedimentation rate, or ESR, and C-reactive protein measurements can also be useful to gauge the degree of inflammation.[41] Testing for anti-Saccharomyces cerevisiae antibodies (ASCA) and anti-neutrophil cytoplasmic antibodies (ANCA) has been evaluated to identify inflammatory diseases of the intestine[42] and to differentiate Crohn's disease from ulcerative colitis.[43]

Comparison with ulcerative colitis[]

The most common disease that mimics the symptoms of Crohn's disease is ulcerative colitis, as both are inflammatory bowel diseases that can affect the colon with similar symptoms. It is important to differentiate these diseases, since the course of the diseases and treatments may be different. In some cases, however, it may not be possible to tell the difference, in which case the disease is classified as indeterminate colitis.[9][1][5]

Comparisons of various factors in Crohn's disease and ulcerative colitis
Crohn's disease Ulcerative colitis
Terminal ileum involvement Commonly Never
Colon involvement Usually Always
Rectum involvement Seldom Usually[44]
Involvement around the anus Common[45] Seldom
Bile duct involvement No increase in rate of primary sclerosing cholangitis Higher rate[46]
Distribution of Disease Patchy areas of inflammation Continuous area of inflammation[44]
Endoscopy Deep geographic and serpiginous (snake-like) ulcers Continuous ulcer
Depth of inflammation May be transmural, deep into tissues[45][1] Shallow, mucosal
Fistulae Common[45] Seldom
Stenosis Common Seldom
Autoimmune disease Widely regarded as an autoimmune disease No consensus
Cytokine response Associated with Th1 Vaguely associated with Th2
Granulomas on biopsy Can have granulomas[45] Granulomas uncommon[44]
Surgical cure Often returns following removal of affected part Usually cured by removal of colon
Smoking Higher risk for smokers Lower risk for smokers[44]

Treatment[]

Main article: Treatment of Crohn's 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.[45]

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. Re-operation rates were 31% and 27%, respectively, indicating that strictureplasty is a safe and effective treatment for selected patients. PMID 8918424

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.[47]

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.

Due to one of the symptoms of the disease; that is, skip lesions (shown on imaging scan) that can appear anywhere from the mouth to the anus, dietician follow up may be essential in patients receiving multiple surgical operations.[How to reference and link to summary or text]

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

  1. REDIRECT Template:Who  

This template name redirects to {{who}} which may be edited using [edit|https://psychology.fandom.com/wiki/Template:Who?action=edit edit].

See also
  1. :category:Redirects
  2. :Category:Redirects from other template
  3. Wikipedia:Redirects
  4. Wikipedia:Template messages/Redirect pages


This section is a stub. You can help by adding to it.

Epidemiology[]

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.[48][49] Crohn's disease is more common in northern countries, and shows a higher preponderance in northern areas of the same country.[50] 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.[48] It also has a higher incidence in Ashkenazi Jews.[9]

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][5] It is rare in early childhood. There is no association with gender, social class or occupation.[How to reference and link to summary or text] Parents, siblings or children of people with Crohn's disease are 3 to 20 times more likely to develop the disease.[51] Twin studies show a concordance of greater than 55% for Crohn's disease.[52] This section is a stub. You can help by adding to it.

History[]

Inflammatory bowel diseases were described by Giovanni Battista Morgagni (1682-1771), by Polish surgeon Antoni Leśniowski in 1904 (leading to the use of the eponym "Leśniowski-Crohn disease" in Poland) and by Scottish physician T. Kennedy Dalziel in 1913.[53]

Burrill Bernard Crohn, an American gastroenterologist at Mount Sinai Hospital, described fourteen cases in 1932, and submitted them to the American Medical Association under the rubric of "Terminal ileitis: A new clinical entity". Later that year, he, along with colleagues Leon Ginzburg and Gordon Oppenheimer published the case series as "Regional ileitis: a pathologic and clinical entity".[2]

See also[]


References[]

  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 Hanauer, Stephen B. (March 1996). Inflammatory bowel disease. New England Journal of Medicine 334 (13): 841-848. PMID 8596552.
  2. 2.0 2.1 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
  3. 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. PMID 11856078.
  4. 4.0 4.1 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. PMID 16863561. Cite error: Invalid <ref> tag; name "Bernstein" defined multiple times with different content
  5. 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7 Gopal, Latha, Senthil Nachimuthu Crohn Disease. eMedicine. URL accessed on 2006-07-02.
  6. Pallone F, Monteleone G. Regulatory cytokines in inflammatory bowel disease.. Aliment Pharmacol Ther 10 Suppl 2: 75-9; discussion 80. PMID 8899105.
  7. Romagnani S (1999). Th1/Th2 cells.. Inflamm Bowel Dis 5 (4): 285-94. PMID 10579123.
  8. Al-Ataie, M Bashar, Vishwanath N Shenoy Ulcerative colitis. eMedicine. URL accessed on 2006-07-02.
  9. 9.0 9.1 9.2 9.3 Podolsky, Daniel K. (August 2002). Inflammatory bowel disease. New England Journal of Medicine 346 (6): 417-29. PMID 12167685.
  10. 10.0 10.1 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. 12.0 12.1 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. PMID 11151877.
  13. Mueller, M. H., M. E. Kreis, M. L. Gross, H. D. Becker, T. T. Zittel & E. C. Jehle (August 2002). Anorectal functional disorders in the absence of anorectal inflammation in patients with Crohn's disease. British Journal of Surgery 89 (8): 1027-31. PMID 12153630.
  14. Taylor B, Williams G, Hughes L, Rhodes J (1989). The histology of anal skin tags in Crohn's disease: an aid to confirmation of the diagnosis. Int J Colorectal Dis 4 (3): 197-9. PMID 2769004.
  15. Fix, Oren K., Jorge A. Soto, Charles W. Andrews and Francis A. Farraye (December 2004). Gastroduodenal Crohn's disease. Gastrointestinel Endoscopy 60 (6): 985. PMID 15605018.
  16. 16.0 16.1 Beattie, R.M., N. M. Croft, J. M. Fell, N. A. Afzal and R. B. Heuschkel (May 2006). Inflammatory bowel disease. Archives of Disease in Childhood 91 (5): 426-32. PMID 16632672.
  17. Büller, H.A. (February 1997). Problems in diagnosis of IBD in children. The Netherlands Journal of Medicine 50 (2): S8-S11. PMID 9050326.
  18. O'Keefe, S. J. (1996). Nutrition and gastrointestinal disease. Scandinavian Journal of Gastroenterology Supplement (220): 52-9. PMID 8898436.
  19. Danese, Silvio, Stefano Semeraro, Alfredo Papa, Italia Roberto, Franco Scaldaferri, Giuseppe Fedeli, Giovanni Gasbarrini, Antonio Gasbarrini (December 2005). Extraintestinal manifestations in inflammatory bowel disease. World Journal of Gastroenterology 11 (46): 7227-7236. PMID 16437620.
  20. 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.
  21. 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.
  22. 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.
  23. Ogura Y, Bonen DK, Inohara N, et al. A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease. Nature. 2001 May 31;411(6837):603-6.
  24. Cuthbert A, Fisher S, Mirza M, et al. (2002). The contribution of NOD2 gene mutations to the risk and site of disease in inflammatory bowel disease.. Gastroenterology 122 (4): 867-74. PMID 11910337.
  25. Sakamoto N, Kono S, Wakai K, et al. (2005). Dietary risk factors for inflammatory bowel disease: a multicenter case-control study in Japan.. Inflamm Bowel Dis 11 (2): 154-63. PMID 15677909.
  26. Reif S, Klein I, Lubin F, Farbstein M, Hallak A, Gilat T (1997). Pre-illness dietary factors in inflammatory bowel disease.. Gut 40 (6): 754-60. PMID 9245929.
  27. Cosnes J (2004). Tobacco and IBD: relevance in the understanding of disease mechanisms and clinical practice.. Best Pract Res Clin Gastroenterol 18 (3): 481-96. PMID 15157822.
  28. Lesko S, Kaufman D, Rosenberg L, et al. (1985). Evidence for an increased risk of Crohn's disease in oral contraceptive users.. Gastroenterology 89 (5): 1046-9. PMID 4043662.
  29. Cobrin GM, Abreu MT. Defects in mucosal immunity leading to Crohn's disease. Immunol Rev. 2005 Aug;206:277-95. PMID 16048555
  30. Naser SA, Collins MT. Debate on the lack of evidence of Mycobacterium avium subsp. paratuberculosis in Crohn's disease. Inflamm Bowel Dis. 2005 Dec;11(12):1123. PMID 16306778
  31. Crawford JM. "The Gastrointestinal tract, Chapter 17". In Cotran RS, Kumar V, Robbins SL. Robbins Pathologic Basis of Disease: 5th Edition. W.B. Saunders and Company, Philadelphia, 1994.
  32. Lee, S. D., R. D. Cohen (march 2002). Endoscopy in inflammatory bowel disease. Gastroenterology Clinics of North America 31 (1): 119-32. PMID 12122727.
  33. 33.0 33.1 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. PMID 16373764.
  34. 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. PMID 16696781.
  35. 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. PMID 8428417.
  36. 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.
  37. Rajesh, A., D.D.T. Maglinte (January 2006). Multislice CT enteroclysis: technique and clinical applications. Clinical Radiology 61 (1): 31-9. PMID 16356814.
  38. 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. Canadian Association of Radiologists Journal 56 (1): 25-35. PMID 15835588.
  39. MacKalski, B. A., C. N. Bernstein (May 2005). New diagnostic imaging tools for inflammatory bowel disease. Gut 55 (5): 733-41. PMID 16609136.
  40. Goh, Jason, C. A. O'Morain (February 2003). Review article: nutrition and adult inflammatory bowel disease. Alimentary Pharmacology & Therapeutics 17 (3): 307-20. PMID 12562443.
  41. Chamouard, Patrick, Zoe Richert, Nicolas Meyer, Gabriel Rahmi, René Baumann (2006 April). Diagnostic Value of C-Reactive Protein for Predicting Activity Level of Crohn's Disease. Clinical Gastroenterology and Hepatology. PMID 16630759. Epub ahead of print
  42. 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.
  43. 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. PMID 16099791.
  44. 44.0 44.1 44.2 44.3 Kornbluth, Asher, David B. Sachar (July 2004). Ulcerative Colitis Practice Guidelines in Adults. American Journal of Gastroenterology 99 (7): 1371-1385. PMID 15233681.
  45. 45.0 45.1 45.2 45.3 45.4 Hanauer, Stephen B., William Sandborn (March 1 2001). Management of Crohn's Disease in Adults. American Journal of Gastroenterology 96 (3): 635-643. PMID 11280528.
  46. Broomé, Ulrika, Annika Bergquist (February 2006). Primary sclerosing cholangitis, inflammatory bowel disease, and colon cancer. Seminars in Liver Disease 26 (1): 31-41. PMID 16496231.
  47. Hiatt, Robert A., K. R. Abrams, J. Mayberry (August? 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.
  48. 48.0 48.1 Hiatt, Robert A., Leon Kaufman (November 1988). Epidemiology of inflammatory bowel disease in a defined northern California population. Western Journal of Medicine 149 (5): 541-6. PMID 3250100.
  49. Moum, B., M. H. Vatn, A. Ekbom, E. Aadland, O. Fausa, I. Lygren, N. Stray, J. Sauar, T. Schulz (April 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.
  50. Shivananda, S., J. Lennard-Jones, R. Logan, N. Fear, A. Price, L. Carpenter and M. van Blankenstein (November 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.
  51. 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.
  52. 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
  53. Kirsner JB. Historical aspects of inflammatory bowel disease. J Clin Gastroenterol. 1988 Jun;10(3):286-97. PMID 2980764

External links[]

General Information


Organizations


This page uses Creative Commons Licensed content from Wikipedia (view authors).
Advertisement