Crohn Disease 

  • Author: Priya Rangasamy, MD; Chief Editor: Julian Katz, MD   more...
 
Updated: Jun 16, 2011
 

Background

Crohn disease is an idiopathic, chronic, transmural inflammatory process of the bowel that often leads to fibrosis and obstructive symptoms and can affect any part of the gastrointestinal tract from the mouth to the anus. This condition is believed to be the result of an imbalance between proinflammatory and anti-inflammatory mediators. Approximately 30% of Crohn disease cases involve the small bowel, particularly the terminal ileum, another 30% involve only the colon, and 40% involve both the small bowel and colon.[1]

The characteristic presentation of Crohn disease is abdominal pain and diarrhea, which may be complicated by intestinal fistulization, obstruction, or both. Unpredictable flares and remissions characterize the long-term course of this illness.[2, 3, 4] (See Clinical Presentation)

Once considered rare in the pediatric population, Crohn disease is recognized with increasing frequency in children of all ages and has become one of the most important chronic diseases that affect children and adolescents. In addition to the common GI symptoms of diarrhea, rectal bleeding, and abdominal pain, children often experience growth failure, malnutrition, pubertal delay, and bone demineralization. Other problems in the pediatric population include psychological issues that occur in children and adolescents. The unique problems encountered in the pediatric population necessitate a medical approach that promotes clinical improvement and reverses growth failure with minimal toxicity. (See Treatment and Management.)

The preferred imaging examinations are plain radiography, double-contrast barium enema examination, and single-contrast upper GI series with small bowel follow-though or enteroclysis with computed tomography (CT) and double-contrast evaluation of the small bowel. Laboratory data for Crohn disease are nonspecific and are of value principally in assisting with management. Endoscopic visualization and biopsy are essential in the diagnosis of Crohn disease. Upper GI endoscopy may be used to diagnose gastroduodenal disease and is recommended for all children regardless of the presence or absence of upper GI symptoms. (See Workup.)

Despite extensive workup, 10% of patients with isolated Crohn colitis have an indeterminate colitis, with features of both Crohn disease and ulcerative colitis. If these patients undergo long-term follow-up, small bowel disease characteristic of Crohn disease ultimately develops. (See Diagnosis.)

The general goals of treatment for Crohn disease are to achieve the best possible clinical, laboratory, and histologic control of the inflammatory disease with the least adverse effects from medication; to permit the patient to function as normally as possible; and, in children, to promote growth with adequate nutrition. (See Treatment and Management.)

Therapy is typically administered in a step-up approach. Patients with mild disease are treated with 5-aminosalicylic acid (5-ASA), antibiotics, and nutritional therapy. If no response occurs or if disease is more severe than initially thought, corticosteroid and immunomodulatory therapy with 6-mercaptopurine (6-MP; Purinethol) or methotrexate (Folex PFS, Rheumatrex) is attempted. Finally, biologic and surgical therapies, at the tip of the treatment pyramid, are used.[5] (See Medications.)

Surgery plays an integral role in controlling symptoms and treating complications of Crohn disease. Because of the high rate of disease recurrence after segmental bowel resection, the guiding principle of surgery is preservation of intestinal length and function.[2] (See Treatment and Management.)

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Pathophysiology

Chronic inflammation from T-cell activation leading to tissue injury is implicated. After activation by antigen presentation, unrestrained responses of helper lymphocytes type 1 (Th1) predominate in Crohn disease because of defective regulation. Th1 cytokines such as interleukin (IL)–12 and tumor necrosis factor (TNF)–alpha stimulate the inflammatory response. Inflammatory cells recruited by these cytokines release nonspecific inflammatory substances, including arachidonic acid metabolites, proteases, platelet activating factor, and free radicals, which result in direct injury to the intestine.

Microscopically, the initial lesion starts as a focal inflammatory infiltrate around the crypts, followed by ulceration of superficial mucosa. Later, inflammatory cells invade the deep mucosal layers and, in that process, begin to organize into noncaseating granulomas. The granulomas extend through all layers of the intestinal wall and into the mesentery and the regional lymph nodes. Neutrophil infiltration into the crypts forms crypt abscesses, leading to destruction of the crypt and atrophy of the colon. Chronic damage may be seen in the form of villous blunting in the small intestine as well. Ulcerations are common and are often seen on a background of normal mucosa. Although granuloma formation is pathognomonic of Crohn disease, its absence does not exclude the diagnosis.[6] (See the images below.)

Histologic features of chronic colitis with crypt Histologic features of chronic colitis with crypt atrophy and branching, and lymphocytic infiltrate. Hematoxylin-eosin staining. Courtesy of Dr E. Ruchelli. Colonic granuloma in a patient with Crohn disease.Colonic granuloma in a patient with Crohn disease. Hematoxylin-eosin staining. Courtesy of Dr E. Ruchelli.

Macroscopically, the initial abnormality is hyperemia and edema of the involved mucosa. Later, discrete superficial ulcers form over lymphoid aggregates and are seen as red spots or mucosal depressions (see the image below). These can become deep, serpiginous ulcers located transversely and longitudinally over an inflamed mucosa, giving the mucosa a cobblestone appearance. The lesions are often segmental, being separated by healthy areas, and are often referred to as skip lesions.[6]

Colonoscopic image of a large ulcer and inflammatiColonoscopic image of a large ulcer and inflammation of the descending colon in a 12-year-old boy with Crohn disease.

Transmural inflammation results in thickening of the bowel wall and narrowing of the lumen. As Crohn disease progresses, it is complicated by obstruction or deep ulceration leading to fistulization by way of the sinus tracts penetrating the serosa, microperforation, abscess formation, adhesions, and malabsorption.[2]

Obstruction is caused initially by significant edema of the mucosa and associated spasm of the bowel. Obstruction is intermittent and is often reversible with conservative measures and anti-inflammatory agents. With further disease progression, the obstruction becomes chronic because of fibrotic scarring, luminal narrowing, and stricture formation.[2]

Fistulae may be enteroenteral, enterovesical, enterovaginal, or enterocutaneous. The inflammation extending through the bowel wall may also involve the mesentery and surrounding lymph nodes. Creeping fat may be seen when the mesentery wraps around the bowel surface.[2]

Serosal inflammation causes adhesions; thus, free perforations are less common in Crohn disease than in other inflammatory bowel conditions.[2]

Malabsorption can occur as a result of loss of functional mucosal absorptive surface. This phenomenon can lead to protein-calorie malnutrition, dehydration, and multiple nutrient deficiencies. Involvement of the terminal ileum may result in malabsorption of bile acids, which leads to steatorrhea, fat-soluble vitamin deficiency, and gallstone formation. Fat malabsorption, by trapping calcium, may result in increased oxalate excretion (normally complexed by calcium), causing kidney stone formation. Steatorrhea and fat-soluble vitamin deficiency may also lead to clotting abnormalities, calcium deficiency, and osteomalacia, which may progress to osteoporosis. Vitamin B-12 deficiency may also occur with ileal resection or long-standing ileal disease.[2]

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Etiology

The exact cause of Crohn disease remains unknown. Genetic, microbial, immunologic, environmental, dietary, vascular, and psychosocial factors, including smoking, oral contraceptives, and nonsteroidal anti-inflammatory agents (NSAIDs), have been implicated. It has been suggested that patients have an inherited susceptibility for an aberrant immunologic response to one or more of these provoking factors.[6] An interaction between the predisposing genetic factors, environmental factors, host factors, and triggering event is likely necessary for the disease to develop.

Studies have shown compelling evidence for an inheritable risk for the development of Crohn disease. However, classic Mendelian inheritance is not seen. Most of the genes thought to be involved in the development of the disease play a role in mucosal immunity and their products are found on the mucosal barrier epithelium.[6]

Several genes are thought to contribute to the complex phenotype. Mutations within the NOD2 gene (also known as the IBD1 gene or CARD-15-caspase activating recruitment domain) have been shown to confer susceptibility to Crohn disease. The NOD2/CARD15 gene, which is found on chromosome 16, regulates intracellular immune response to bacterial products. Approximately 25% of white children have a CARD15 mutation, compared with only 2% of black and Hispanic children. Another region that has been linked to IBD is the IBD-3 gene on chromosome 6, which is in an area that includes the human leukocyte antigen (HLA) complex. In addition, an area on chromosome 5q known as IBD-5 has been linked specifically to Crohn disease; it contains a cytokine gene cluster.[6]

An association between mutations in the IL23R gene and inflammatory bowel disease (IBD) has recently been confirmed, suggesting a major protective effect on susceptibility to Crohn disease.A predisposition to Crohn disease, specifically with ileal involvement, has been associated with a single nucleotide polymorphism (SNP) in the ATG16L1 gene, which is involved in autophagocytosis, an essential component of the innate immune response targeted toward pathogen-derived proteins.

Infectious agents such as Mycobacterium paratuberculosis, Pseudomonas species, and Listeria species have all been implicated in the pathogenesis of Crohn disease, suggesting that the inflammation seen with the disease is the result of a dysfunctional, but appropriate, response to an infectious source.[6]

Interleukins and TNF-alpha have also been implicated in the disease process. Crohn disease is characterized by a Th-1 cellular immune response pattern that leads to production of IL-12, TNF-alpha, and interferon gamma (IFN-gamma). TNF-alpha has been shown to play a critical role in the inflammation in this disease. Increased production of TNF-alpha by macrophages in patients with Crohn disease results in increased concentrations of TNF-alpha in the stool, blood, and mucosa.[7]

Environmental influences such as tobacco use seem to have an effect on Crohn disease. Smoking has been shown to double the risk of Crohn disease, whereas the risk of developing ulcerative colitis is lower in people who smoke than in those who have never smoked.[6, 8] It has been suggested that a diet high in fatty foods may increase the risk for Crohn disease.[9] Concerns about the measles vaccine and the development of the disease have been proven unfounded.[10] Although appendectomy has been suggested to be protective in ulcerative colitis, it is not a protective factor in Crohn disease.[11]

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Epidemiology

United States statistics

The prevalence of Crohn disease in the United States is approximately 7 cases per 100,000 population.[2] The incidence and the prevalence of Crohn disease (especially the colonic subset) seem to have increased steadily over the last 5 decades, mainly in northern climates. Urban areas may have a higher prevalence of IBD than rural areas.[2, 3] Upper socioeconomic classes are thought to have a higher prevalence than lower socioeconomic classes, a fact likely influenced by increased access to health care, although genetic and environmental factors may play a role.[2, 12]

The age of onset of Crohn disease has a bimodal distribution. The first peak occurs between age 15 and 30 years, and the second peak occurs between age 60 and 80 years. However, most cases begin before age 30 years, and approximately 20-30% of all patients with Crohn disease are diagnosed before age 20 years. A greater proportion of colonic and distal Crohn disease has been diagnosed in older patients, whereas younger patients have predominantly ileal disease.[2] Among children, Crohn disease is reported to be more common in whites than in blacks and rare in Asian and Hispanic children.

Data on the racial incidence of Crohn disease seem to show that the condition is uncommon in nonwhites in underdeveloped regions; however, this is not applicable to nonwhites in urban settings, where the rate may even exceed that of whites.[2] Rates are higher in people of Jewish descent, particularly Ashkenazi Jews and Jews of middle European origin, compared with Sephardic or eastern European Jews.[13]

The rate of Crohn disease in women is 1.1-1.8 times higher than that in men. There is a reverse pattern with pediatric IBD, with a higher rate in boys than in girls. In the United States, the pediatric male-to-female ratio in 2003 was 1.6:1.

International statistics

Incidence rates in Europe range from 0.7-9.8 cases per 100,000 persons. In both Europe and North America, higher incidence rates have been characterized in more northern latitudes.[2] [3] Rates in Asia range from 0.5-4.2 per cases 100,000 persons. The lowest recorded rates of new cases appear to be in South Africa (0.3-2.6 cases per 100,000 population) and Latin America (0-0.03 cases per 100,000 population), respectively.[2] [3]

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Prognosis

Crohn disease usually has a chronic, indolent course regardless of the site of involvement. Studies have estimated ranges from no increased risk to up to a 5-fold increased risk of death. A 15-year survival rate of 93.7% has been reported for the general population, but the risk of death and complications in Crohn disease increases with the duration of the illness. Over time, 10% of patients will be disabled by their disease.[2]

As the disease progresses, medical therapy can become less effective. In the first year after diagnosis, the relapse rate approaches 50%, with 10% of patients having a chronic relapsing course.[2] Most patients develop complications that require surgery, but Crohn disease frequently recurs after surgery.[2] Patients with proximal small bowel disease have a higher risk of mortality compared with those who have ileal or ileocecal disease. The excess mortality may be ascribed to complications of Crohn disease.[2] The leading cause of disease-related death is GI tract cancer, including colorectal and small bowel adenocarcinoma, lymphomas, and squamous cell carcinomas arising in association with a chronic fistula to the skin. Some studies have also shown an association between Crohn disease and respiratory cancers.[2]

Acute Crohn disease, which is often discovered during laparotomy for suspected appendicitis, has an excellent prognosis. The acute episode is treated conservatively, and two thirds of patients may not have subsequent evidence of regional enteritis.[2]

Although Crohn disease is a chronic condition with recurrent relapses, appropriate medical and surgical therapy helps patients to have a reasonable quality of life, with an overall good prognosis and extremely low risk of fatal outcome.[2]

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Patient Education

Education of patients and their families is encouraged and is extremely important in the treatment process. Useful education materials can be obtained by contacting the Crohn's and Colitis Foundation of America

For excellent patient education resources, visit eMedicine's Crohn Disease Center and Esophagus, Stomach, and Intestine Center.

In addition, see eMedicine's patient education articles, Crohn Disease in Children and Teens, Crohn Disease, Crohn Disease FAQs, Inflammatory Bowel Disease, and Irritable Bowel Syndrome.

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Contributor Information and Disclosures
Author

Priya Rangasamy, MD  Fellow, Department of Gastroenterology/Hepatology, University of Connecticut Health Center

Priya Rangasamy, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Coauthor(s)

Yung-Hsin Chen, MD  Staff Physician, Department of Radiology, Nassau University Medical Center

Yung-Hsin Chen, MD is a member of the following medical societies: American Roentgen Ray Society, Radiological Society of North America, and Society of Skeletal Radiology

Disclosure: Nothing to disclose.

Marcy L Coash, DO  Staff Physician, Department of Internal Medicine, University of Connecticut

Marcy L Coash, DO is a member of the following medical societies: American Medical Student Association/Foundation and American Osteopathic Association

Disclosure: Nothing to disclose.

Spencer B Gay, MD  Professor of Radiology, Director of Body Computed Tomography, Department of Radiology, University of Virginia Health Sciences Center

Disclosure: Nothing to disclose.

John L Haddad, MD  Clinical Associate Professor, Department of Radiology, Weill Medical College of Cornell University; Director of Body MRI, Department of Radiology, Methodist Hospital in Houston

John L Haddad, MD is a member of the following medical societies: American College of Radiology, American Medical Association, and Radiological Society of North America

Disclosure: Nothing to disclose.

Eugene C Lin, MD  Consulting Radiologist, Virginia Mason Medical Center; Clinical Assistant Professor of Radiology, University of Washington School of Medicine

Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine

Disclosure: Nothing to disclose.

Dermot PB McGovern, MD, PhD, MRCP  Director of Translational Medicine, Inflammatory Bowel and Immunobiology Research Institute; Associate Professor of Medicine, David Geffen School of Medicine, UCLA, Cedars-Sinai Medical Center

Dermot PB McGovern, MD, PhD, MRCP is a member of the following medical societies: American Gastroenterological Association, American Society of Human Genetics, British Society of Gastroenterology, and Royal College of Physicians of the United Kingdom

Disclosure: UCB Honoraria Consulting; UCB Honoraria Speaking and teaching; Salix Honoraria Speaking and teaching; UCB Grant/research funds Other; Prometheus Consulting fee Consulting

Gil Y Melmed, MD  Director, Clinical Trials, Inflammatory Bowel Disease Center, Cedars-Sinai Medical Center; Assistant Clinical Professor of Medicine, David Geffen School of Medicine at UCLA

Gil Y Melmed, MD is a member of the following medical societies: American College of Gastroenterology and American Gastroenterological Association

Disclosure: Amgen Consulting fee Consulting; Shire Honoraria Speaking and teaching; Proctor and Gamble Honoraria Speaking and teaching; UCB Consulting fee Consulting; Centocor Consulting fee Consulting; Prometheus Labs Honoraria Speaking and teaching

David I Weltman, MD  Consulting Staff, S & D Medical, LLP; Director, Department of Radiology, Southside Hospital

David I Weltman, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Association of Program Directors in Radiology, New York County Medical Society, and Radiological Society of North America

Disclosure: Nothing to disclose.

George Y Wu, MD, PhD  Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine

George Y Wu, MD, PhD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, American Medical Association, American Society for Clinical Investigation, and Association of American Physicians

Disclosure: Springer Consulting fee Consulting; Gilead Consulting fee Review panel membership; Gilead Honoraria Speaking and teaching; Bristol-Myers Squibb Honoraria Speaking and teaching; Springer Royalty Review panel membership

Dahua Zhou, MD  Staff Physician, Department of Radiology, Nassau University Medical Center

Dahua Zhou, MD is a member of the following medical societies: Radiological Society of North America

Disclosure: Nothing to disclose.

Specialty Editor Board

Waqar A Qureshi, MD  Associate Professor of Medicine, Chief of Endoscopy, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine and Veterans Affairs Medical Center

Waqar A Qureshi, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

BS Anand, MD  Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Bruce Buehler, MD  Professor, Department of Pediatrics and Genetics, Director RSA, University of Nebraska Medical Center

Bruce Buehler, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine, American Academy of Pediatrics, American Association on Mental Retardation, American College of Medical Genetics, American College of Physician Executives, American Medical Association, and Nebraska Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD  Clinical Professor of Medicine, Drexel University College of Medicine

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Kathleen M Raynor, MD, Priyankha Balasundaram, MD, and Senthil Nachimuthu, MD, FACP, to the development and writing of the source articles.

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Colonoscopic image of a large ulcer and inflammation of the descending colon in a 12-year-old boy with Crohn disease.
Histologic features of chronic colitis with crypt atrophy and branching, and lymphocytic infiltrate. Hematoxylin-eosin staining. Courtesy of Dr E. Ruchelli.
Colonic granuloma in a patient with Crohn disease. Hematoxylin-eosin staining. Courtesy of Dr E. Ruchelli.
Postoperative photograph depicts the incisions used for laparoscopic ileocolectomy in a 14-year-old male adolescent with obstruction of the terminal ileum. Note the 2-cm incision in the right lower abdomen through which the specimen was extracted and the extracorporeal anastomosis performed. The 12-mm umbilical incision is nicely hidden in the depths of the umbilicus. A 5-mm incision is visible in the left lower abdomen, and another is in the left suprapubic region just above the top of the pants.
On this laparoscopic photograph, the mesentery of the terminal ileum is being coagulated with a sealing device (LigaSure; Valley Lab, Boulder, Colo). Note that the ligation of the mesentery proceeds near the border of the ileum rather than at the base of the mesentery.
Image obtained during upper GI series with a small bowel follow-through shows narrowing and irregularity in the distal ileum in a 16-year-old male adolescent with Crohn disease.
Crohn disease. Aphthous ulcers. Double-contrast barium enema examination in Crohn colitis demonstrates numerous aphthous ulcers.
Crohn disease. Crohn colitis. Double-contrast barium enema study demonstrates marked ulceration, inflammatory changes, and narrowing of the right colon
Crohn disease. Cobblestoning. Spot view of the terminal ileum from a small bowel follow-through study demonstrates linear longitudinal and transverse ulcerations that create a cobblestone appearance. Also, note the relatively greater involvement of the mesenteric side of the terminal ileum and the displacement of the involved loop away from the normal small bowel secondary to mesenteric inflammation and fibrofatty proliferation.
Crohn disease of the terminal ileum. Small bowel follow-through study demonstrates the string sign in the terminal ileum. Also, note pseudodiverticula of the antimesenteric wall of the terminal ileum, secondary to greater distensibility of this less-involved segment of the wall.
Crohn disease. Spot view of the terminal ileum from a small bowel follow-through study demonstrates the string sign, consistent with narrowing and stricturing. Also, note a sinus tract originating from the medial wall of the terminal ileum and the involvement of the medial wall of the cecum.
Crohn disease. Enterocolic fistula. Double-contrast barium enema study demonstrates multiple fistulous tracts between the terminal ileum and the right colon adjacent to the ileocecal valve, the so-called double-tracking of the ileocecal valve.
Crohn disease. Active small bowel inflammation. CT scan demonstrates small bowel wall thickening, mesenteric inflammatory stranding, and mesenteric adenopathy.
MRI of an inflamed terminal ileum in a 10-year-old girl with Crohn disease.
MRI of a small abscess on the right side of the anal sphincter in a 9-year-old boy with Crohn disease.
Table. Characteristics Differentiating Crohn Disease and Ulcerative Colitis
Characteristic
Crohn diseaseUlcerative colitis
DistributionEntire GI tractColon only, although gastritis recognized
Skip lesionsContinuous involvement proximally from rectum
PathologyFull thicknessMucosa only
Granulomas (30%)No granulomas
RadiologyEntire GI tractColon only
Skip lesionsContinuous involvement proximally from rectum
Fistulae, abscesses, fibrotic stricturesMucosal disease only
Cancer riskIncreasedEstimated 1% per year starting 10 years after diagnosis
Presentation
Crohn diseaseUlcerative colitis
BleedingOccasionalVery common
ObstructionCommonUncommon
FistulaCommonNone
Weight lossCommonUncommon
Perianal diseaseCommonRare
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