Ulcerative Colitis 

  • Author: Marc D Basson, MD, PhD, MBA, FACS; Chief Editor: Julian Katz, MD   more...
 
Updated: Dec 23, 2011
 

Background

Ulcerative colitis is one of the 2 major types of inflammatory bowel disease (IBD), along with Crohn disease. Unlike Crohn disease, which can affect any part of the gastrointestinal tract, ulcerative colitis characteristically involves the large bowel (see the images below).

Ulcerative colitis as visualized with a colonoscopUlcerative colitis as visualized with a colonoscope. Single-contrast enema study in a patient with totaSingle-contrast enema study in a patient with total colitis shows mucosal ulcers with a variety of shapes, including collar-button ulcers, in which undermining of the ulcers occurs, and double-tracking ulcers, in which the ulcers are longitudinally orientated.

The exact etiology of ulcerative colitis is unknown, but the disease appears to be multifactorial and polygenic. Proposed causes include environmental factors, immune dysfunction, and a likely genetic predisposition. Some have suggested that children of below-average birth weight who are born to mothers with ulcerative colitis have a greater risk of developing the disease. (See Etiology.)

Histocompatibility human leukocyte antigen (HLA)–B27 is identified in most patients with ulcerative colitis, although this finding is not causally associated with the condition and the finding of HLA-B27 does not imply a substantially increased risk for ulcerative colitis. Ulcerative colitis might also be influenced by diet, although diet is thought to play a secondary role. Food or bacterial antigens might exert an effect on the already damaged mucosal lining, which has increased permeability.

Ulcerative colitis is a lifelong illness that has a profound emotional and social impact on affected patients.

Grossly, the colonic mucosa appears hyperemic, with loss of the normal vascular pattern. The mucosa is granular and friable. Frequently, broad-based ulcerations cause islands of normal mucosa to appear polypoid, leading to the term pseudopolyp (see the image below).

Inflamed colonic mucosa demonstrating pseudopolypsInflamed colonic mucosa demonstrating pseudopolyps.

The bowel wall is thin or of normal thickness, but edema, the accumulation of fat, and hypertrophy of the muscle layer may give the impression of a thickened bowel wall. The disease is largely confined to the mucosa and, to a lesser extent, the submucosa. Muscle-layer and serosal involvement is very rare; such involvement is seen in patients with severe disease, particularly toxic dilatation, and reflects a secondary effect of the severe disease rather than primary ulcerative colitis pathogenesis. Early disease manifests as hemorrhagic inflammation with loss of the normal vascular pattern; petechial hemorrhages; and bleeding. Edema is present, and large areas become denuded of mucosa. Undermining of the mucosa leads to the formation of crypt abscesses, which are the hallmark of the disease. (See Clinical Presentation.)

The diagnosis of ulcerative colitis is best made with endoscopy and mucosal biopsy for histopathology. Laboratory studies are helpful to exclude other diagnoses and assess the patient's nutritional status, but serologic markers can assist in the diagnosis of inflammatory bowel disease. Radiographic imaging has an important role in the workup of patients with suspected inflammatory bowel disease and in the differentiation of ulcerative colitis from Crohn disease by demonstrating fistulae or the presence of substantial coexisting more proximal small bowel disease in a patient who turns out to actually have Crohn disease. (See Workup.)

The initial treatment for ulcerative colitis includes corticosteroids, anti-inflammatory agents, antidiarrheal agents, and rehydration (see Medication ). Surgery is considered if medical treatment fails or if a surgical emergency develops. (See Treatment and Management.)

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Anatomy

Ulcerative colitis extends proximally from the anal verge in an uninterrupted pattern to involve part or the entire colon. The rectum is involved in more than 95% of cases; some authorities believe that the rectum is always involved in untreated patients. Rectal involvement occurs even when the rest of the colon is spared.

Ulcerative colitis occasionally involves the terminal ileum, as a result of an incompetent ileocecal valve. In these cases, which may constitute as many as 10% of patients, the reflux of noxious inflammatory mediators from the colon results in superficial mucosal inflammation of the terminal ileum, called backwash ileitis.[1, 2] About 30 cm of the terminal ileum is usually affected.

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Pathophysiology

A variety of immunologic changes have been documented in ulcerative colitis. Subsets of T cells accumulate in the lamina propria of the diseased colonic segment. In patients with ulcerative colitis, these T cells are cytotoxic to colonic epithelium. This change is accompanied by an increase in the population of B cells and plasma cells, with increased production of immunoglobulin G (IgG) and immunoglobulin E (IgE).[3]

Anticolonic antibodies have been detected in patients with ulcerative colitis. A small proportion of patients with ulcerative colitis have smooth muscle and anticytoskeletal antibodies.

Microscopically, acute and chronic inflammatory infiltrate of the lamina propria, crypt branching, and villous atrophy are present in ulcerative colitis. Microscopic changes also include inflammation of the crypts of Lieberkühn and abscesses. These findings are accompanied by a discharge of mucus from the goblet cells, the number of which is reduced as the disease progresses. The ulcerated areas are soon covered by granulation tissue. Excessive fibrosis is not a feature of the disease. The undermining of mucosa and an excess of granulation tissue lead to the formation of polypoidal mucosal excrescences, which are known as inflammatory polyps or pseudopolyps.

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Etiology

The exact etiology of ulcerative colitis is unknown, but certain factors have been found to be associated with the disease, and some hypotheses have been presented. Etiologic factors potentially contributing to ulcerative colitis include genetic factors, immune system reactions, environmental factors, nonsteroidal anti-inflammatory drug (NSAID) use, low levels of antioxidants, psychological stress factors, a smoking history, and consumption of milk products.

Genetics

The current hypothesis is that genetically susceptible individuals have abnormalities of humoral and cell-mediated immunity and/or generalized enhanced reactivity against commensal intestinal bacteria and that this dysregulated mucosal immune response predisposes to colonic inflammation.[4]

A family history of ulcerative colitis (observed in 1 in 6 relatives) is associated with a higher risk for developing the disease. Disease concordance has been documented in monozygotic twins.[5] Genetic association studies have identified multiple loci, including some that are associated with both ulcerative colitis and Crohn disease; one recently identified locus is also associated with susceptibility to colorectal cancer.[6]

Chromosomes are thought to be less stable in patients with ulcerative colitis, as measured with telomeric associations in peripheral leukocytes.[7] This phenomenon may also contribute to the increased cancer risk. Whether these abnormalities are the cause or the result of the intense systemic inflammatory response in ulcerative colitis is unresolved.

Immune reactions

Immune reactions that compromise the integrity of the intestinal epithelial barrier may contribute to ulcerative colitis. Serum and mucosal autoantibodies against intestinal epithelial cells may be involved. The presence of antineutrophil cytoplasmic antibodies (ANCA) and anti– Saccharomyces cerevisiae antibodies (ASCA) is a well-known feature of inflammatory bowel disease.[8, 9, 10, 11, 12]

In addition, an immune modulatory abnormality has been assumed to be responsible for the lower incidence of ulcerative colitis in patients who have undergone previous appendectomy. The incidence of previous appendectomy is lower in patients with ulcerative colitis (4.5%) than in control subjects (19%), and a further protective effect is observed if the appendectomy was performed before the patient was 20 years of age.[13] Also, patients in whom appendectomy was performed for inflammatory disorders (eg, appendicitis or mesenteric adenitis) seem to have a lower incidence of ulcerative colitis than patients who undergo appendectomy for other disorders such as nonspecific abdominal pain.[14]

Environmental factors

Environmental factors also play a role. For example, sulfate-reducing bacteria, which produce sulfides, are found in large numbers in patients with ulcerative colitis, and sulfide production is higher in patients with ulcerative colitis than in other people. Sulfide production is even higher in patients with active ulcerative colitis than in patients in remission. The bacterial microflora is altered in patients with active disease.[15] A decrease in Klebsiella species is seen in the ileum of patients relative to controls. This difference disappears after proctocolectomy.

NSAID use

Nonsteroidal anti-inflammatory drug (NSAID) use is higher in patients with ulcerative colitis than in control subjects, and one third of patients with an exacerbation of ulcerative colitis report recent NSAID use. This finding leads some to recommend avoidance of NSAID use in patients with ulcerative colitis.[16]

Other etiologic factors

Other factors that may be associated with ulcerative colitis include the following:

  • Vitamins A and E, both considered antioxidants, are found in low levels in as many as 16% of children with ulcerative colitis exacerbation.[17]
  • Psychological and psychosocial stress factors can play a role in the presentation of ulcerative colitis and can precipitate exacerbations.[14]
  • Smoking is negatively associated with ulcerative colitis. This relationship is reversed in Crohn disease.
  • Milk consumption may exacerbate the disease.
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Epidemiology

United States statistics

In the United States, about 1 million people are affected with ulcerative colitis.[18, 19] The annual incidence is 10.4-12 cases per 100,000 people. The prevalence rate is 35-100 cases per 100,000 people. Ulcerative colitis is 3 times more common than Crohn disease.

Ulcerative colitis occurs more frequently in whites than in African Americans or Hispanics. The incidence of ulcerative colitis is reported to be 2-4 times higher in Ashkenazi Jews. However, population studies in North America do not completely support this assertion.

Ulcerative colitis is slightly more common in women than in men. Age of onset follows a bimodal pattern, with a peak at 15-25 years and a smaller one at 55-65 years, although the disease can occur in people of any age.[20] Ulcerative colitis is uncommon in persons younger than 10 years. Two of every 100,000 children are affected; however, 20-25% of all cases of ulcerative colitis occur in persons aged 20 years or younger.

International statistics

Ulcerative colitis is more common in the Western and Northern hemispheres; the incidence is low in Asia and the Far East.

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Prognosis

Ulcerative colitis may result in disease-related mortality. However, overall mortality is not increased in patients with ulcerative colitis, as compared with the general population. An increase in mortality may be observed among elderly patients with the disease. Mortality is also increased in patients who develop complications (eg, shock, malnutrition, anemia). Evidence suggests that mortality is increased in patients with ulcerative colitis who undergo any form of medical or surgical intervention.

Involvement of the muscularis propria in the most severe cases can lead to damage to the nerve plexus, resulting in colonic dysmotility, dilation, and eventual infarction and gangrene, a condition termed toxic megacolon. This condition is characterized by a thin-walled, large, dilated colon that may eventually become perforated. Chronic disease is associated with pseudopolyp formation in about 15-20% of cases. Chronic and severe cases can be associated with areas of precancerous changes, such as carcinoma in situ or dysplasia.

The most common cause of death of patients with ulcerative colitis is toxic megacolon. Colonic adenocarcinoma develops in 3-5% of patients with ulcerative colitis, and the risk increases as the duration of disease increases. The risk of colonic malignancy is higher in cases of pancolitis and in cases in which onset of the disease occurs before the age of 15 years. Benign stricture rarely causes intestinal obstruction.

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Patient Education

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 Inflammatory Bowel Disease, Crohn Disease, and Crohn Disease FAQs.

Additional information can be found at Crohn's & Colitis Foundation of America (CCFA).

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Contributor Information and Disclosures
Author

Marc D Basson, MD, PhD, MBA, FACS  Professor, Chair, Department of Surgery, Assistant Dean for Faculty Development in Research, Michigan State University College of Human Medicine

Marc D Basson, MD, PhD, MBA, FACS is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Gastroenterological Association, Phi Beta Kappa, and Sigma Xi

Disclosure: Nothing to disclose.

Coauthor(s)

E Stanton Adkins III, MD  Clinical Associate Professor, Departments of Pediatrics and Surgery, University of South Carolina School of Medicine

E Stanton Adkins III, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Surgeons, American Medical Association, and American Pediatric Surgical Association

Disclosure: Nothing to disclose.

Kenneth Azarow, MD  Program Director, Pediatric Surgery, Children's Hospital and University of Nebraska Medical Center; Professor, Department of Surgery, Uniformed Services University of the Health Sciences

Kenneth Azarow, MD is a member of the following medical societies: American Pediatric Surgical Association

Disclosure: Nothing to disclose.

Iman Bayat, MBBS, MRCS  Principal House Officer in Surgery, Department of Surgery, Mater Health Services, Australia

Iman Bayat, MBBS, MRCS is a member of the following medical societies: Royal College of Surgeons of England

Disclosure: Nothing to disclose.

Jennifer Lynn Bonheur, MD  Attending Physician, Division of Gastroenterology, Lenox Hill Hospital

Jennifer Lynn Bonheur, MD is a member of the following medical societies: American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, New York Academy of Sciences, New York Society for Gastrointestinal Endoscopy, and Sigma Xi

Disclosure: Nothing to disclose.

John Geibel, MD, DSc, MA  Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital

John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract

Disclosure: AMGEN Royalty Consulting; ARdelyx Ownership interest Board membership

Peter W Gourlas, MD  Consulting Staff, Colorectal Unit, Princess Alexandre Hospital, Mater Adults Hospital and Greenslopes Private Hospital

Peter W Gourlas, MD is a member of the following medical societies: Royal Australasian College of Surgeons

Disclosure: Nothing to disclose.

Michael A Grosso, MD  Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital

Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons

Disclosure: Nothing to disclose.

Andre Hebra, MD  Chief, Division of Pediatric Surgery, Professor of Surgery and Pediatrics, Medical University of South Carolina College of Medicine; Surgeon-in-Chief, Medical University of South Carolina Children's Hospital

Andre Hebra, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, Children's Oncology Group, Florida Medical Association, International Pediatric Endosurgery Group, Society of American Gastrointestinal and Endoscopic Surgeons, Society of Laparoendoscopic Surgeons, South Carolina Medical Association, Southeastern Surgical Congress, and Southern Medical Association

Disclosure: Nothing to disclose.

Jodi Hirst, MBBS  Specialist Registrar in General Surgery, Mater Misericordiae Adult Hospital

Disclosure: Nothing to disclose.

Emma Igras, MBBS, FRACS  Clinical Research Fellow, Department of Surgical Oncology, Princess Alexandra Hospital, Australia

Emma Igras, MBBS, FRACS is a member of the following medical societies: Royal Australasian College of Surgeons

Disclosure: Nothing to disclose.

Alex Jacocks, MD  Program Director, Professor, Department of Surgery, University of Oklahoma School of Medicine

Disclosure: Nothing to disclose.

Judith R Kelsen, MD  Clinical Instructor in Pediatrics, University of Pennsylvania School of Medicine; Attending Physician, Division of Gastroenterology, Hepatology and Nutrition, The Children's Hospital of Philadelphia

Judith R Kelsen, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Study of Liver Diseases, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

Disclosure: Nothing to disclose.

Tri H Le, MD  Assistant Professor of Medicine, Division of Gastroenterology and Hepatology, Penn State Milton S Hershey Medical Center

Tri H Le, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society of Gastrointestinal Endoscopy, and Crohns and Colitis Foundation of America

Disclosure: Nothing to disclose.

Luis M Lovato, MD  Associate Clinical Professor, University of California, Los Angeles, David Geffen School of Medicine; Director of Critical Care, Department of Emergency Medicine, Olive View-UCLA Medical Center

Luis M Lovato, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Petar Mamula, MD  Associate Professor, Department of Pediatrics, Division of Gastroenterology and Nutrition, The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine

Petar Mamula, MD, is a member of the following medical societies: American Academy of Pediatrics, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Brian J Miller, MBBS, LRCP, MRCS, FRCSC, FRACS  Associate Professor in General Surgery and Colorectal Surgery, Department of Surgery, University of Queensland, Princess Alexandra Hospital

Brian J Miller, MBBS, LRCP, MRCS, FRCSC, FRACS is a member of the following medical societies: Colorectal Surgical Society of Australia and New Zealand, Gastroenterological Society of Australia, Royal Australasian College of Surgeons, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

David A Piccoli, MD  Chief of Pediatric Gastroenterology, Hepatology and Nutrition, The Children's Hospital of Philadelphia; Professor, University of Pennsylvania School of Medicine

David A Piccoli, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Jorge H Vargas, MD  Professor of Pediatrics and Clinical Professor of Pediatric Gastroenterology, University of California, Los Angeles, David Geffen School of Medicine; Consulting Physician, Department of Pediatrics, University of California at Los Angeles Health System

Jorge H Vargas, MD is a member of the following medical societies: American Liver Foundation, American Society for Gastrointestinal Endoscopy, American Society for Parenteral and Enteral Nutrition, Latin American Society of Pediatric Gastroenterology, Hepatology & Nutrition, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Specialty Editor Board

Anil Minocha, MD, FACP, FACG  Professor of Medicine, Director of Digestive Diseases, Medical Director of Nutrition Support, Medical Director of Gastrointestinal Endoscopy, Internal Medicine Department, University of Mississippi Medical Center; Clinical Professor, University of Mississippi School of Pharmacy

Anil Minocha, MD, FACP, FACG is a member of the following medical societies: American Academy of Clinical Toxicology, American Association for the Study of Liver Diseases, American College of Forensic Examiners, American College of Gastroenterology, American College of Physicians, American Federation for Clinical Research, American Gastroenterological Association, and American Society of 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

Harsh Grewal, MD, FACS, FAAP  Professor of Surgery and Pediatrics, Temple University School of Medicine; Chief, Section of Pediatric Surgery, Temple University School of Medicine

Harsh Grewal, MD, FACS, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Surgeons, American Pediatric Surgical Association, Association for Surgical Education, Children's Oncology Group, Eastern Association for the Surgery of Trauma, International Pediatric Endosurgery Group, Society of American Gastrointestinal and Endoscopic Surgeons, Society of Laparoendoscopic Surgeons, and Southwestern Surgical Congress

Disclosure: Nothing to disclose.

Carmen Cuffari, MD  Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine

Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada

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.

References
  1. Heuschen UA, Hinz U, Allemeyer EH, Stern J, Lucas M, Autschbach F. Backwash ileitis is strongly associated with colorectal carcinoma in ulcerative colitis. Gastroenterology. Mar 2001;120(4):841-7. [Medline].

  2. Kaufman SS, Vanderhoof JA, Young R, Perry D, Raynor SC, Mack DR. Gastroenteric inflammation in children with ulcerative colitis. Am J Gastroenterol. Jul 1997;92(7):1209-12. [Medline].

  3. Himmel ME, Hardenberg G, Piccirillo CA, Steiner TS, Levings MK. The role of T-regulatory cells and Toll-like receptors in the pathogenesis of human inflammatory bowel disease. Immunology. Oct 2008;125(2):145-53. [Medline].

  4. Xavier RJ, Podolsky DK. Unravelling the pathogenesis of inflammatory bowel disease. Nature. Jul 26 2007;448(7152):427-34. [Medline].

  5. Lindberg E, Magnusson KE, Tysk C, Jarnerot G. Antibody (IgG, IgA, and IgM) to baker's yeast (Saccharomyces cerevisiae), yeast mannan, gliadin, ovalbumin and betalactoglobulin in monozygotic twins with inflammatory bowel disease. Gut. Jul 1992;33(7):909-13. [Medline]. [Full Text].

  6. Barrett JC, Lee JC, Lees CW, Prescott NJ, Anderson CA, Phillips A, et al. Genome-wide association study of ulcerative colitis identifies three new susceptibility loci, including the HNF4A region. Nat Genet. Dec 2009;41(12):1330-4. [Medline]. [Full Text].

  7. Vasiliauskas E. Serum immune markers in inflammatory bowel disease. Gastroenterology and Endoscopy News. Available at http://www.gastroendonews.com.

  8. Peeters M, Joossens S, Vermeire S, Vlietinck R, Bossuyt X, Rutgeerts P. Diagnostic value of anti-Saccharomyces cerevisiae and antineutrophil cytoplasmic autoantibodies in inflammatory bowel disease. Am J Gastroenterol. Mar 2001;96(3):730-4. [Medline].

  9. Dubinsky MC, Ofman JJ, Urman M, Targan SR, Seidman EG. Clinical utility of serodiagnostic testing in suspected pediatric inflammatory bowel disease. Am J Gastroenterol. Mar 2001;96(3):758-65. [Medline].

  10. Hoffenberg EJ, Fidanza S, Sauaia A. Serologic testing for inflammatory bowel disease. J Pediatr. Apr 1999;134(4):447-52. [Medline].

  11. Kaditis AG, Perrault J, Sandborn WJ, Landers CJ, Zinsmeister AR, Targan SR. Antineutrophil cytoplasmic antibody subtypes in children and adolescents after ileal pouch-anal anastomosis for ulcerative colitis. J Pediatr Gastroenterol Nutr. Apr 1998;26(4):386-92. [Medline].

  12. Duggan AE, Usmani I, Neal KR, Logan RF. Appendicectomy, childhood hygiene, Helicobacter pylori status, and risk of inflammatory bowel disease: a case control study. Gut. Oct 1998;43(4):494-8. [Medline]. [Full Text].

  13. Andersson RE, Olaison G, Tysk C, Ekbom A. Appendectomy and protection against ulcerative colitis. N Engl J Med. Mar 15 2001;344(11):808-14. [Medline].

  14. Levenstein S, Prantera C, Varvo V, Scribano ML, Andreoli A, Luzi C, et al. Stress and exacerbation in ulcerative colitis: a prospective study of patients enrolled in remission. Am J Gastroenterol. May 2000;95(5):1213-20. [Medline].

  15. Almeida MG, Kiss DR, Zilberstein B, Quintanilha AG, Teixeira MG, Habr-Gama A. Intestinal mucosa-associated microflora in ulcerative colitis patients before and after restorative proctocolectomy with an ileoanal pouch. Dis Colon Rectum. Jul 2008;51(7):1113-9. [Medline].

  16. Felder JB, Korelitz BI, Rajapakse R, Schwarz S, Horatagis AP, Gleim G. Effects of nonsteroidal antiinflammatory drugs on inflammatory bowel disease: a case-control study. Am J Gastroenterol. Aug 2000;95(8):1949-54. [Medline].

  17. Bousvaros A, Zurakowski D, Duggan C, Law T, Rifai N, Goldberg NE, et al. Vitamins A and E serum levels in children and young adults with inflammatory bowel disease: effect of disease activity. J Pediatr Gastroenterol Nutr. Feb 1998;26(2):129-35. [Medline].

  18. Garland CF, Lilienfeld AM, Mendeloff AI, Markowitz JA, Terrell KB, Garland FC. Incidence rates of ulcerative colitis and Crohn's disease in fifteen areas of the United States. Gastroenterology. Dec 1981;81(6):1115-24. [Medline].

  19. Cotran RS, Collins T, Robbins SL, Kumar V. Pathologic Basis of Disease. Philadelphia, Pa: WB Saunders; 1998.

  20. Jang ES, Lee DH, Kim J, Yang HJ, Lee SH, Park YS. Age as a clinical predictor of relapse after induction therapy in ulcerative colitis. Hepatogastroenterology. Sep-Oct 2009;56(94-95):1304-9. [Medline].

  21. Gooding IR, Springall R, Talbot IC, Silk DB. Idiopathic small-intestinal inflammation after colectomy for ulcerative colitis. Clin Gastroenterol Hepatol. Jun 2008;6(6):707-9. [Medline].

  22. Slatter C, Girgis S, Huynh H, El-Matary W. Pre-pouch ileitis after colectomy in paediatric ulcerative colitis. Acta Paediatr. Mar 2008;97(3):381-3. [Medline].

  23. Falcone RA Jr, Lewis LG, Warner BW. Predicting the need for colectomy in pediatric patients with ulcerative colitis. J Gastrointest Surg. Mar-Apr 2000;4(2):201-6. [Medline].

  24. Lichtiger S, Present DH, Kornbluth A, Gelernt I, Bauer J, Galler G, et al. Cyclosporine in severe ulcerative colitis refractory to steroid therapy. N Engl J Med. Jun 30 1994;330(26):1841-5. [Medline].

  25. Rowe FA, Walker JH, Karp LC, Vasiliauskas EA, Plevy SE, Targan SR. Factors predictive of response to cyclosporin treatment for severe, steroid-resistant ulcerative colitis. Am J Gastroenterol. Aug 2000;95(8):2000-8. [Medline].

  26. Bernstein CN, Blanchard JF, Rawsthorne P, Yu N. The prevalence of extraintestinal diseases in inflammatory bowel disease: a population-based study. Am J Gastroenterol. Apr 2001;96(4):1116-22. [Medline].

  27. de Vlam K, Mielants H, Cuvelier C, De Keyser F, Veys EM, De Vos M. Spondyloarthropathy is underestimated in inflammatory bowel disease: prevalence and HLA association. J Rheumatol. Dec 2000;27(12):2860-5. [Medline].

  28. Cox KL, Cox KM. Oral vancomycin: treatment of primary sclerosing cholangitis in children with inflammatory bowel disease. J Pediatr Gastroenterol Nutr. Nov 1998;27(5):580-3. [Medline].

  29. Marchesa P, Lashner BA, Lavery IC, Milsom J, Hull TL, Strong SA. The risk of cancer and dysplasia among ulcerative colitis patients with primary sclerosing cholangitis. Am J Gastroenterol. Aug 1997;92(8):1285-8. [Medline].

  30. Murata I, Satoh K, Yoshikawa I, Masumoto A, Sasaki E, Otsuki M. Recurrent subcutaneous abscess of the sternal region in ulcerative colitis. Am J Gastroenterol. Mar 1999;94(3):844-5. [Medline].

  31. Kimura K, Hunter SF, Thollander MS, Loftus EV Jr, Melton LJ 3rd, O'Brien PC, et al. Concurrence of inflammatory bowel disease and multiple sclerosis. Mayo Clin Proc. Aug 2000;75(8):802-6. [Medline].

  32. Egan CA, Meadows KP, Zone JJ. Ulcerative colitis and immunobullous disease cured by colectomy. Arch Dermatol. Feb 1999;135(2):214-5. [Medline].

  33. Kim B, Barnett JL, Kleer CG, Appelman HD. Endoscopic and histological patchiness in treated ulcerative colitis. Am J Gastroenterol. Nov 1999;94(11):3258-62. [Medline].

  34. Calabrese C, Fabbri A, Gionchetti P, Rizzello F, Morselli C, Liguori G, et al. Controlled study using wireless capsule endoscopy for the evaluation of the small intestine in chronic refractory pouchitis. Aliment Pharmacol Ther. Jun 1 2007;25(11):1311-6. [Medline].

  35. Carucci LR, Levine MS. Radiographic imaging of inflammatory bowel disease. Gastroenterol Clin North Am. Mar 2002;31(1):93-117, ix. [Medline].

  36. Eisenberg RL. Gastrointestinal Radiology: A Pattern Approach. Philadelphia, Pa: Lippincott-Raven; 1998:602-8.

  37. Wiesner W, Steinbrich W. [Imaging diagnosis of inflammatory bowel disease]. Ther Umsch. Mar 2003;60(3):137-44. [Medline].

  38. van den Broek FJ, Fockens P, Dekker E. Review article: New developments in colonic imaging. Aliment Pharmacol Ther. Dec 2007;26 Suppl 2:91-9. [Medline].

  39. Deutsch DE, Olson AD. Colonoscopy or sigmoidoscopy as the initial evaluation of pediatric patients with colitis: a survey of physician behavior and a cost analysis. J Pediatr Gastroenterol Nutr. Jul 1997;25(1):26-31. [Medline].

  40. Matsumoto T, Nakamura S, Jin-No Y, Sawa Y, Hara J, Oshitani N, et al. Role of granuloma in the immunopathogenesis of Crohn's disease. Digestion. 2001;63 Suppl 1:43-7. [Medline].

  41. [Guideline] Leighton JA, Shen B, Baron TH, Adler DG, Davila R, Egan JV, et al. ASGE guideline: endoscopy in the diagnosis and treatment of inflammatory bowel disease. Gastrointest Endosc. Apr 2006;63(4):558-65. [Medline].

  42. Esteve M, Gisbert JP. Severe ulcerative colitis: at what point should we define resistance to steroids?. World J Gastroenterol. Sep 28 2008;14(36):5504-7. [Medline]. [Full Text].

  43. Shen B. Crohn's disease of the ileal pouch: reality, diagnosis, and management. Inflamm Bowel Dis. Feb 2009;15(2):284-94. [Medline].

  44. Van Assche G, Vermeire S, Rutgeerts P. Treatment of severe steroid refractory ulcerative colitis. World J Gastroenterol. Sep 28 2008;14(36):5508-11. [Medline]. [Full Text].

  45. Ford AC, Achkar JP, Khan KJ, Kane SV, Talley NJ, Marshall JK, et al. Efficacy of 5-aminosalicylates in ulcerative colitis: systematic review and meta-analysis. Am J Gastroenterol. Apr 2011;106(4):601-16. [Medline].

  46. Ford AC, Khan KJ, Sandborn WJ, Kane SV, Moayyedi P. Once-Daily Dosing vs. Conventional Dosing Schedule of Mesalamine and Relapse of Quiescent Ulcerative Colitis: Systematic Review and Meta-Analysis. Am J Gastroenterol. Dec 2011;106(12):2070-7. [Medline].

  47. Ford AC, Bernstein CN, Khan KJ, Abreu MT, Marshall JK, Talley NJ, et al. Glucocorticosteroid therapy in inflammatory bowel disease: systematic review and meta-analysis. Am J Gastroenterol. Apr 2011;106(4):590-9. [Medline].

  48. Ford AC, Sandborn WJ, Khan KJ, et al. Efficacy of biological therapies in inflammatory bowel disease: systematic review and meta-analysis. Am J Gastroenterol. Apr 2011;106(4):644-59, quiz 660. [Medline].

  49. [Best Evidence] Sandborn WJ, Rutgeerts P, Feagan BG, Reinisch W, Olson A, Johanns J, et al. Colectomy rate comparison after treatment of ulcerative colitis with placebo or infliximab. Gastroenterology. Oct 2009;137(4):1250-60; quiz 1520. [Medline].

  50. Leblanc S, Allez M, Seksik P, Flourié B, Peeters H, Dupas JL, et al. Successive treatment with cyclosporine and infliximab in steroid-refractory ulcerative colitis. Am J Gastroenterol. Apr 2011;106(4):771-7. [Medline].

  51. Khan KJ, Ullman TA, Ford AC, et al. Antibiotic therapy in inflammatory bowel disease: a systematic review and meta-analysis. Am J Gastroenterol. Apr 2011;106(4):661-73. [Medline].

  52. Sakuraba A, Sato T, Naganuma M, Morohoshi Y, Matsuoka K, Inoue N, et al. A pilot open-labeled prospective randomized study between weekly and intensive treatment of granulocyte and monocyte adsorption apheresis for active ulcerative colitis. J Gastroenterol. 2008;43(1):51-6. [Medline].

  53. Miki C, Okita Y, Yoshiyama S, Araki T, Uchida K, Kusunoki M. Early postoperative application of extracorporeal leukocyte apheresis in ulcerative colitis patients: results of a pilot trial to prevent postoperative septic complications. J Gastroenterol. Jun 2007;42(6):508-9. [Medline].

  54. Emmrich J, Petermann S, Nowak D, Beutner I, Brock P, Klingel R, et al. Leukocytapheresis (LCAP) in the management of chronic active ulcerative colitis--results of a randomized pilot trial. Dig Dis Sci. Sep 2007;52(9):2044-53. [Medline].

  55. Ruuska T, Lahdeaho ML, Sutas Y, Ashorn M, Grönlund J. Leucocyte apheresis in the treatment of paediatric ulcerative colitis. Scand J Gastroenterol. Nov 2007;42(11):1390-1. [Medline].

  56. Rembacken BJ, Snelling AM, Hawkey PM, Chalmers DM, Axon AT. Non-pathogenic Escherichia coli versus mesalazine for the treatment of ulcerative colitis: a randomised trial. Lancet. Aug 21 1999;354(9179):635-9. [Medline].

  57. Tsuda Y, Yoshimatsu Y, Aoki H, Nakamura K, Irie M, Fukuda K. Clinical effectiveness of probiotics therapy (BIO-THREE) in patients with ulcerative colitis refractory to conventional therapy. Scand J Gastroenterol. Nov 2007;42(11):1306-11. [Medline].

  58. Simchuk EJ, Thirlby RC. Risk factors and true incidence of pouchitis in patients after ileal pouch-anal anastomoses. World J Surg. Jul 2000;24(7):851-6. [Medline].

  59. Farouk R, Dozois RR, Pemberton JH, Larson D. Incidence and subsequent impact of pelvic abscess after ileal pouch-anal anastomosis for chronic ulcerative colitis. Dis Colon Rectum. Oct 1998;41(10):1239-43. [Medline].

  60. Shamberger RC, Hergrueter CA, Lillehei CW. Use of a gracilis muscle flap to facilitate delayed ileal pouch-anal anastomosis. Dis Colon Rectum. Nov 2000;43(11):1628-31. [Medline].

  61. Karlbom U, Raab Y, Ejerblad S, Graf W, Thörn M, Pâhlman L. Factors influencing the functional outcome of restorative proctocolectomy in ulcerative colitis. Br J Surg. Oct 2000;87(10):1401-8. [Medline].

  62. Meagher AP, Farouk R, Dozois RR, Kelly KA, Pemberton JH. J ileal pouch-anal anastomosis for chronic ulcerative colitis: complications and long-term outcome in 1310 patients. Br J Surg. Jun 1998;85(6):800-3. [Medline].

  63. Ogilvie JW Jr, Goetz L, Baxter NN, Park J, Minami S, Madoff RD. Female sexual dysfunction after ileal pouch-anal anastomosis. Br J Surg. Jul 2008;95(7):887-92. [Medline].

  64. Cornish JA, Tan E, Teare J, Teoh TG, Rai R, Darzi AW. The effect of restorative proctocolectomy on sexual function, urinary function, fertility, pregnancy and delivery: a systematic review. Dis Colon Rectum. Aug 2007;50(8):1128-38. [Medline].

  65. Shen BO, Jiang ZD, Fazio VW, Remzi FH, Rodriguez L, Bennett AE. Clostridium difficile infection in patients with ileal pouch-anal anastomosis. Clin Gastroenterol Hepatol. Jul 2008;6(7):782-8. [Medline].

  66. Falk A, Olsson C, Ahrné S, Molin G, Adawi D, Jeppsson B. Ileal pelvic pouch microbiota from two former ulcerative colitis patients, analysed by DNA-based methods, were unstable over time and showed the presence of Clostridium perfringens. Scand J Gastroenterol. Aug 2007;42(8):973-85. [Medline].

  67. Chia CS, Chew MH, Chau YP, Eu KW, Ho KS. Adenocarcinoma of the anal transitional zone after double stapled ileal pouch-anal anastomosis for ulcerative colitis. Colorectal Dis. Jul 2008;10(6):621-3. [Medline].

  68. Kornbluth A, Sachar DB. Ulcerative colitis practice guidelines in adults: American College Of Gastroenterology, Practice Parameters Committee. Am J Gastroenterol. Mar 2010;105(3):501-23; quiz 524. [Medline].

  69. Sarigol S, Wyllie R, Gramlich T, Alexander F, Fazio V, Kay M, et al. Incidence of dysplasia in pelvic pouches in pediatric patients after ileal pouch-anal anastomosis for ulcerative colitis. J Pediatr Gastroenterol Nutr. Apr 1999;28(4):429-34. [Medline].

  70. Pekow JR, Hetzel JT, Rothe JA, Hanauer SB, Turner JR, Hart J. Outcome after surveillance of low-grade and indefinite dysplasia in patients with ulcerative colitis. Inflamm Bowel Dis. Aug 2010;16(8):1352-6. [Medline].

  71. Parente F, Molteni M, Marino B, Colli A, Ardizzone S, Greco S, et al. Are colonoscopy and bowel ultrasound useful for assessing response to short-term therapy and predicting disease outcome of moderate-to-severe forms of ulcerative colitis?: a prospective study. Am J Gastroenterol. May 2010;105(5):1150-7. [Medline].

  72. Andersson T, Lunde OC, Johnson E, Moum T, Nesbakken A. Long-term functional outcome and quality of life after restorative proctocolectomy with ileo-anal anastomosis for colitis. Colorectal Dis. Dec 14 2009;[Medline].

  73. Bernstein CN, Fried M, Krabshuis JH, et al. World Gastroenterology Organization Practice Guidelines for the diagnosis and management of IBD in 2010. Inflamm Bowel Dis. Jan 2010;16(1):112-24. [Medline].

  74. Charron M, del Rosario JF, Kocoshis S. Use of technetium-tagged white blood cells in patients with Crohn's disease and ulcerative colitis: is differential diagnosis possible?. Pediatr Radiol. Nov 1998;28(11):871-7. [Medline].

  75. Choi JS, Potenti F, Wexner SD, Nam YS, Hwang YH, Nogueras JJ, et al. Functional outcomes in patients with mucosal ulcerative colitis after ileal pouch-anal anastomosis by the double stapling technique: is there a relation to tissue type?. Dis Colon Rectum. Oct 2000;43(10):1398-404. [Medline].

  76. Cottliar A, Fundia A, Boerr L, Sambuelli A, Negreira S, Gil A, et al. High frequencies of telomeric associations, chromosome aberrations, and sister chromatid exchanges in ulcerative colitis. Am J Gastroenterol. Sep 2000;95(9):2301-7. [Medline].

  77. Cucchiara S, Celentano L, de Magistris TM, Montisci A, Iula VD, Fecarotta S. Colonoscopy and technetium-99m white cell scan in children with suspected inflammatory bowel disease. J Pediatr. Dec 1999;135(6):727-32. [Medline].

  78. da Luz Moreira A, Kiran RP, Lavery I. Clinical outcomes of ileorectal anastomosis for ulcerative colitis. Br J Surg. Jan 2010;97(1):65-9. [Medline].

  79. Durno C, Sherman P, Harris K, Smith C, Dupuis A, Shandling B, et al. Outcome after ileoanal anastomosis in pediatric patients with ulcerative colitis. J Pediatr Gastroenterol Nutr. Nov 1998;27(5):501-7. [Medline].

  80. Ekbom A, Helmick C, Zack M, Adami HO. Ulcerative colitis and colorectal cancer. A population-based study. N Engl J Med. Nov 1 1990;323(18):1228-33. [Medline].

  81. Fonkalsrud EW, Bustorff-Silva J. Reconstruction for chronic dysfunction of ileoanal pouches. Ann Surg. Feb 1999;229(2):197-204. [Medline]. [Full Text].

  82. Fonkalsrud EW, Thakur A, Roof L. Comparison of loop versus end ileostomy for fecal diversion after restorative proctocolectomy for ulcerative colitis. J Am Coll Surg. Apr 2000;190(4):418-22. [Medline].

  83. Gorfine SR, Bauer JJ, Harris MT, Kreel I. Dysplasia complicating chronic ulcerative colitis: is immediate colectomy warranted?. Dis Colon Rectum. Nov 2000;43(11):1575-81. [Medline].

  84. Hunt LE, Eichenberger MR, Petras R, Galandiuk S. Use of a microsatellite marker in predicting dysplasia in ulcerative colitis. Arch Surg. May 2000;135(5):582-5. [Medline].

  85. Metcalf DR, Nivatvongs S, Sullivan TM, Suwanthanma W. A technique of extending small-bowel mesentery for ileal pouch-anal anastomosis: report of a case. Dis Colon Rectum. Mar 2008;51(3):363-4. [Medline].

  86. Rutter MD, Saunders BP, Wilkinson KH, Rumbles S, Schofield G, Kamm MA. Thirty-year analysis of a colonoscopic surveillance program for neoplasia in ulcerative colitis. Gastroenterology. Apr 2006;130(4):1030-8. [Medline].

  87. Shamberger RC, Masek BJ, Leichtner AM, Winter HS, Lillehei CW. Quality-of-life assessment after ileoanal pull-through for ulcerative colitis and familial adenomatous polyposis. J Pediatr Surg. Jan 1999;34(1):163-6. [Medline].

  88. Treem WR, Cohen J, Davis PM, Justinich CJ, Hyams JS. Cyclosporine for the treatment of fulminant ulcerative colitis in children. Immediate response, long-term results, and impact on surgery. Dis Colon Rectum. May 1995;38(5):474-9. [Medline].

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Increased postrectal space is a known feature of ulcerative colitis.
Plain abdominal radiograph on a patient with known ulcerative colitis who presented with an acute exacerbation of his symptoms. Image shows thumbprinting in the region of the splenic flexure of the colon.
Double-contrast barium enema study shows pseudopolyposis of the descending colon.
Single-contrast enema study in a patient with known ulcerative colitis in remission shows a benign stricture of the sigmoid colon.
Plain abdominal radiograph in a 26-year-old with a 10-year history of ulcerative colitis shows a long stricture/spasm of the ascending colon/cecum. Note the pseudopolyposis in the descending colon.
Single-contrast enema study in a patient with total colitis shows mucosal ulcers with a variety of shapes, including collar-button ulcers, in which undermining of the ulcers occurs, and double-tracking ulcers, in which the ulcers are longitudinally orientated.
Double-contrast barium enema study shows total colitis. Note the granular mucosa in the cecum/ascending colon and multiple strictures in the transverse and descending colon in a patient with a more than a 20-year history of ulcerative colitis.
Single-contrast barium enema study shows burnt-out ulcerative colitis.
Intravenous urogram in the same patient as in Image 11 shows features of ankylosing spondylitis.
Lateral radiograph of the lumbar spine in the same patient as in Images 10-11 shows a bamboo spine.
Single-contrast barium enema study in a patient with Shigella colitis.
Postevacuation image obtained after a single-contrast barium enema study shows extensive mucosal ulceration resulting from Shigella colitis.
Double-contrast barium enema studies show granular mucosa associated with Campylobacter colitis.
Ulcerative colitis as visualized with a colonoscope.
Inflamed colonic mucosa demonstrating pseudopolyps.
Table 1. Distinguishing Ulcerative Colitis from Crohn Disease
Ulcerative ColitisCrohn Disease
Only colon involvedPanintestinal
Continuous inflammation extending proximally from rectumSkip-lesions with intervening normal mucosa
Inflammation in mucosa and submucosa onlyTransmural inflammation
No granulomasNoncaseating granulomas
Perinuclear ANCA (pANCA) positiveASCA positive
Bleeding (common)Bleeding (uncommon)
Fistulae (rare)Fistulae (common)
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