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.

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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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