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Inflammatory Bowel Disease Medication

  • Author: William A Rowe, MD; Chief Editor: BS Anand, MD  more...
 
Updated: Jun 17, 2016
 

Medication Summary

Many inflammatory mediators have been identified in IBD; antibodies against these mediators and methods to block the production or receptors for these mediators hold great promise as potential therapy for IBD.

Therapy for Crohn disease is generally less effective than that for ulcerative colitis. In addition to the therapies outlined herein, IV cyclosporine or infliximab is helpful in refractory ulcerative colitis. A conventional stepwise approach may be taken. With this approach, the most benign (or temporary) drugs are used first. If they fail to provide relief, drugs from a higher step are used. However, more aggressive disease requires immunomodulator and biologic therapy earlier in the treatment program.

The stepwise approach is as follows:

  1. Aminosalicylates and symptomatic agents are step I drugs; antibiotics are step IA drugs, given the limited situations in which they are used
  2. Corticosteroids constitute the step II drugs, which are to be used if the step I drugs fail to adequately control the IBD
  3. Immune-modifying agents are step III drugs and are used if corticosteroids fail or are required for prolonged periods; infliximab and adalimumab are also step III drugs
  4. Step IV drugs are experimental agents, are used only after the previous steps fail, and are administered only by physicians familiar with their use

Note that drugs from all steps may be used additively; in general, the goal is to wean the patient off steroids as soon as possible to prevent long-term adverse effects from these agents. Opinions differ regarding the use of certain agents in this stepwise approach.

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5-Aminosalicylic Acid Derivatives

Class Summary

The 5-aminosalicylic acid (ASA) derivatives are effective in reducing inflammatory reactions. All of the aminosalicylates are useful for treating flares of mild to moderate ulcerative colitis and occasionally Crohn colitis and for maintaining remission.

Sulfasalazine (Azulfidine, Azulfidine EN-tabs, Sulfazine, Sulfazine EC)

 

Sulfasalazine is considered best for colonic disease, although it is also considered first-line therapy for Crohn disease. This agent is used for acute disease and for maintenance of remission.

Mesalamine (Asacol HD, Pentasa, Canasa, Rowasa, Lialda, Apriso, Delzicol)

 

Mesalamine is a 5-ASA that acts systemically and also has activity as a topical anti-inflammatory.

Balsalazide (Colazal, Giazo)

 

Balsalazide is a prodrug 5-ASA connected to a 4-aminobenzoyl-(beta)-alanine carrier by an azo bond; colonic bacteria break the azo bond, releasing the active 5-ASA. Metabolites of the drug may decrease inflammation by blocking the production of arachidonic acid metabolites in colonic mucosa.

Olsalazine (Dipentum)

 

Olsalazine is useful for active disease and maintenance of remission in ulcerative colitis. Dipentum is a 5-ASA connected to a 5-ASA by an azo bond; colonic bacteria break the azo bond, releasing the active 5-ASA. Note that an adverse event of high ileal secretion of chloride creates a different type of diarrhea, which lessens its acceptability.

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Antibiotics, Other

Class Summary

Metronidazole (Flagyl) and ciprofloxacin (Cipro) are the most commonly used antibiotics in persons with inflammatory bowel disease (IBD). Antibiotics are less effective in persons with ulcerative colitis, except in fulminant toxic megacolon or pouchitis. Rifaximin (Xifaxan) is an FDA-approved broad-spectrum antibiotic that may also help treat patients with IBD.

Metronidazole (Flagyl, Flagyl ER, Metro)

 

Metronidazole is a widely available, inexpensive antibiotic and antiprotozoal agent. This agent inhibits protein synthesis and causes cell death in susceptible organisms by diffusing into the organism and causing a loss of helical DNA structure and strand breakage. Metronidazole's adverse-event profile includes headache, dysgeusia, and neuropathy.

Ciprofloxacin (Cipro, Cipro XR)

 

Ciprofloxacin is a fluoroquinolone antibiotic commonly used for the treatment of urinary, skin, and respiratory tract infections. This agent inhibits bacterial DNA synthesis and, consequently, growth by inhibiting DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. Caution is advised with the use of ciprofloxacin regarding tendon rupture.

Rifaximin (Xifaxan)

 

Rifaximin is a nonabsorbed (< 0.4%), broad-spectrum antibiotic specific for enteric pathogens of the gastrointestinal tract (ie, gram-positive, gram-negative, aerobic, anaerobic). It is a rifampin structural analog and it binds to the beta-subunit of bacterial DNA-dependent RNA polymerase, thereby inhibiting RNA synthesis.

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Corticosteroids

Class Summary

Corticosteroid agents are the treatments of choice for an acute inflammatory bowel disease (IBD) attack; administer intravenously in severe disease. Administer increased or stress doses to patients already on steroids. Do not use steroids for maintaining IBD remission, because of their lack of efficacy and potential complications, including avascular necrosis, osteoporosis, cataracts, emotional lability, hypertension, diabetes mellitus, cushingoid features, acne, and facial hair. Cortenema, Cortifoam, and Anusol-HC suppositories are useful in treating distal disease (proctitis and proctosigmoiditis).

Hydrocortisone (Solu-Cortef, Cortef, A-Hydrocort )

 

Adrenocortical steroids act as potent inhibitors of inflammation. They may cause profound and varied metabolic effects, particularly in relation to salt, water, and glucose tolerance, in addition to their modification of the immune response of the body. Alternative adrenocortical steroids may be used in equivalent dosage.

Prednisone (Rayos)

 

Prednisone acts as a potent inhibitor of inflammation. It may cause profound and varied metabolic effects, particularly in relation to salt, water, and glucose tolerance, in addition to their modification of the immune response of the body. Alternative corticosteroids may be used in equivalent dosage.

Methylprednisolone (Medrol, Solu-Medrol, Depo-Medrol, A-Methapred)

 

Adrenocortical steroids act as potent inhibitors of inflammation and may cause profound and varied metabolic effects, particularly in relation to salt, water, and glucose tolerance, in addition to modification of the immune response. Alternative adrenocortical steroids may be used in equivalent dosage. Methylprednisolone has a greater salt- and water-retention side effect.

Prednisolone (Orapred, Pediapred, Millipred, Veripred 20, Flo-Pred)

 

Corticosteroids act as potent inhibitors of inflammation. They may cause profound and varied metabolic effects, particularly in relation to salt, water, and glucose tolerance, in addition to modification of the immune response. Alternative corticosteroids may be used in equivalent dosage.

Budesonide (Entocort EC)

 

Budesonide alters the level of inflammation in tissues by inhibiting multiple types of inflammatory cells and decreasing the production of cytokines and other mediators involved in inflammatory reactions. Only 10% is bioavailable because of first-pass metabolism.

Dexamethasone (Baycadron, DoubleDex)

 

Dexamethasone has many pharmacologic benefits, but there are also significant adverse effects. It stabilizes cell and lysosomal membranes, increases surfactant synthesis, increases serum vitamin A concentrations, and inhibits prostaglandin and proinflammatory cytokines.

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Immunosuppressants

Class Summary

Immunosuppresant agents are useful as steroid-sparing agents, in healing fistulas, and in patients with serious contraindications to surgery.[105] These drugs are used in patients who are refractory to or unable to tolerate steroids and in patients in whom remission is difficult to maintain with the aminosalicylates alone. Azathioprine and its metabolite, 6-mercaptopurine (MP), are useful in Crohn disease complicated by recurrent rectal fistulas or perianal disease; however, the clinical response can take up to 6 months. Methotrexate has also been tried.

Azathioprine (Imuran, Azasan)

 

Azathioprine inhibits mitosis and cellular metabolism by antagonizing purine metabolism and inhibiting synthesis of DNA, RNA, and proteins; these effects may decrease proliferation of immune cells and result in lower autoimmune activity.

6-Mercaptopurine (Purinethol, Purixan)

 

6-Mercaptopurine is a purine analog that inhibits DNA and RNA synthesis, causing arrest of cell proliferation.

Methotrexate (Rheumatrex, Trexall, Otrexup, Rasuvo)

 

Methotrexate impairs DNA synthesis and induces the apoptosis and reduction in interleukin (IL)-1 production. It is indicated for moderate to severe disease and maintenance of remission. The onset of action is delayed.

Cyclosporine (Sandimmune, Neoral, Gengraf)

 

According to the American Gastroenterological Association (AGA) guidelines, intravenous cyclosporine is effective for avoiding surgery in patients with ulcerative colitis who have failed to respond to 7-10 days of high-dose oral or parenteral corticosteroids. Concomitant administration of IV corticosteroids is recommended in these cases.

Cyclosporine is a cyclic polypeptide that suppresses some humoral immunity and, to a greater extent, cell-mediated immune reactions, such as delayed hypersensitivity, allograft rejection, experimental allergic encephalomyelitis, and graft-versus-host disease.

For children and adults, dosing is based on ideal body weight.

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TNF Inhibitors

Class Summary

Monoclonal antibodies targeted against tumor necrosis factor alpha (TNFα) interrupt endogenous TNF. Increased TNFα levels have been observed in Crohn disease and ulcerative colitis and are thought to be part of the pathogenesis of IBD. TNFα induces proinflammatory cytokines (eg, interleukins), enhance leukocyte migration, activate neutrophils and eosinophils, and induces enzymatic degradation.

This class includes adalimumab, certolizumab, golimumab, and infliximab. Infliximab and adalimumab are FDA approved for both Crohn disease and ulcerative colitis, whereas certolizumab is FDA approved only for Crohn disease and golimumab only for ulcerative colitis.

Infliximab was the first of this class for use in inflammatory bowel disease.[70] Infliximab is more effective against Crohn disease than ulcerative colitis. This drug promotes mucosal healing; heals perianal and enterocutaneous fistulas; and has been shown to reduce signs and symptoms, achieve clinical remission and mucosal healing, and eliminate corticosteroid use.[124] Infliximab is indicated for patients who have experienced inadequate response to conventional therapy.[105]

Infliximab (Remicade)

 

Infliximab neutralizes cytokine TNF-alpha and inhibits its binding to the TNF-alpha receptor. It is mixed in 250 mL of normal saline and infused IV over 2 hours. It is indicated for both ulcerative colitis and Crohn disease.

Adalimumab (Humira)

 

Adalimumab is a TNF blocking agent that has been FDA approved for both Crohn disease and ulcerative colitis. It is administered by subcutaneous injection.

Adalimumab is recombinant human immunoglobulin (Ig) G1 monoclonal antibody specific for human TNF. It binds specifically to TNF-alpha and blocks the interaction with p55 and p75 cell-surface TNF receptors.

Certolizumab pegol (Cimzia)

 

Certolizumab is a TNF blocking agent that has been FDA approved for the treatment of Crohn disease but not for ulcerative colitis. It is administered by subcutaneous injection.

Certolizumab pegol is a pegylated antitumor necrosis factor (TNF)–alpha blocker, which results in disruption of the inflammatory process. It is indicated for moderate to severe Crohn disease in individuals whose condition has not responded to conventional therapies.

Golimumab (Simponi, Simponi Aria)

 

Human anti-TNF-alpha monoclonal antibody. Indicated for ulcerative colitis but not Crohn disease. It is administered by SC injection.

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Alpha 4 Integrin Inhibitors

Class Summary

Integrin inhibitors are emerging as options for moderate-to-severe IBD in patients who have had an inadequate response with, lost response to, or were intolerant to a TNF blocker or immunomodulator; or had an inadequate response with, were intolerant to, or demonstrated dependence on corticosteroids.

Natalizumab (Tysabri)

 

Natalizumab is a recombinant humanized IgG4-1C monoclonal antibody produced in murine myeloma cells. It binds to alpha-4 subunits of α4β1 and α4β7 integrins expressed on the leukocyte surface, which inhibit α4-mediated leukocyte adhesion to their receptors. In Crohn disease, the interaction of the α4β7 integrin with the endothelial receptor MAdCAM-1 has been implicated as an important contributor to the chronic inflammation that is a hallmark of the disease.

Vedolizumab (Entyvio)

 

Vedolizumab is a recombinant humanized monoclonal antibody that binds specifically to α4β7 integrin. It blocks the interaction of α4β7 integrin with a gut-associated addressin cell adhesion molecule-1 (MAdCAM-1) and inhibits the migration of memory T-lymphocytes across the endothelium into inflamed gastrointestinal parenchymal tissue. It is indicated for both ulcerative colitis and Crohn disease.

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Histamine H2 Antagonists

Class Summary

H2-receptor antagonists are reversible competitive blockers of histamines at the H2 receptors, particularly those in the gastric parietal cells, where they inhibit acid secretion. The H2 antagonists are highly selective, do not affect the H1 receptors, and are not anticholinergic agents.

Cimetidine (Tagamet)

 

Cimetidine inhibits histamine at H2 receptors of gastric parietal cells, which results in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.

Ranitidine (Zantac, Deprizine FusePaq)

 

Ranitidine inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which, in turn, reduces gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Famotidine (Pepcid)

 

Famotidine competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Nizatidine (Axid)

 

Nizatidine competitively inhibits histamine at the H2 receptor of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.

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Proton Pump Inhibitors

Class Summary

Proton pump inhibitors (PPIs) reduce gastric acid secretion by inhibition of the H+ -K+ -ATPase enzyme system in the gastric parietal cells. These agents are used in patients with severe esophagitis and in patients whose disease is not responsive to H2-antagonist therapy.

Omeprazole (Prilosec)

 

Omeprazole decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATPase pump.

Lansoprazole (Prevacid)

 

Lansoprazole suppresses gastric acid secretion by specific inhibition of the H+/K+-ATPase enzyme system (ie, proton pump) at the secretory surface of the gastric parietal cell. It blocks the final step of acid production. The effect is dose-related and inhibits both basal and stimulated gastric acid secretion, thus increasing the gastric pH.

Esomeprazole magnesium (Nexium)

 

Esomeprazole magnesium is an S-isomer of omeprazole. It inhibits gastric acid secretion by inhibiting the H+/K+-ATPase enzyme system at the secretory surface of gastric parietal cells. Esomeprazole is used in severe cases and in patients not responding to H2-antagonist therapy. This agent is used for up to 4 weeks to treat and relieve symptoms of active duodenal ulcers; however, it may be used for up to 8 weeks to treat all grades of erosive esophagitis.

Rabeprazole sodium (Aciphex)

 

Rabeprazole sodium decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATPase pump.

Pantoprazole (Protonix)

 

Pantoprazole suppresses gastric acid secretion by specifically inhibiting the H+/K+-ATPase enzyme system at the secretory surface of gastric parietal cells.

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Antidiarrheals

Class Summary

These agents provide symptomatic relief when patients report symptoms of diarrhea.

Diphenoxylate and atropine (Lomotil)

 

Diphenoxylate and atropine is a drug combination that acts as an antidiarrheal agent chemically related to the narcotic analgesic meperidine. This agent acts on intestinal muscles to inhibit peristalsis and slow intestinal motility, prolonging the movement of electrolytes and fluid through the bowel, and increasing the viscosity and loss of fluids and electrolytes. A subtherapeutic dose of anticholinergic atropine sulfate is added to discourage overdosage, in which case diphenoxylate may clinically mimic the effects of codeine.

Loperamide (Imodium A-D, Diamode)

 

Loperamide acts on intestinal muscles to inhibit peristalsis and slow intestinal motility. It prolongs the movement of electrolytes and fluid through the bowel and increases viscosity and loss of fluids and electrolytes.

Cholestyramine (Questran, Prevalite)

 

Cholestyramine may be used to treat diarrhea associated with excess bile acids. It binds bile acids, thus reducing damage to the intestinal mucosa. Cholestyramine also reduces the induction of colonic fluid secretion and forms a nonabsorbable complex with bile acids in the intestine, which, in turn, inhibits enterohepatic reuptake of intestinal bile salts.

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Anticholinergic, Antispasmodic Agents

Class Summary

Anticholinergic antispasmodic agents are used to treat spastic disorders of the gastrointestinal tract.

Dicyclomine (Bentyl)

 

Dicyclomine is used to treat gastrointestinal motility disturbances. It blocks the action of acetylcholine at parasympathetic sites in secretory glands, smooth muscle, and the central nervous system (CNS).

Hyoscyamine (Levbid, Levsin, Levsin-SL, HyoMax SL, Symax-SL, Symax-SR, NuLev, Oscimin)

 

Hyoscyamine blocks the action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands, and the CNS, which, in turn, has antispasmodic effects. The sublingual (SL) tablets may be administered orally, sublingually, or chewed.

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Contributor Information and Disclosures
Author

William A Rowe, MD President, Gastroenterology Associates of Central Pennsylvania, PC; Manager, Endoscopy Center of Central Pennsylvania, LLC; Clinical Associate Professor of Surgery, Division of Colon and Rectal Surgery, Milton S Hershey Medical Center, Pennsylvania State University College of Medicine

William A Rowe, MD is a member of the following medical societies: American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Coauthor(s)

Gary R Lichtenstein, MD Professor of Medicine, Director, Center for Inflammatory Bowel Disease, Department of Medicine, Division of Gastroenterology, University of Pennsylvania School of Medicine

Gary R Lichtenstein, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

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, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Acknowledgements

Mounir Bashour, MD, CM, FRCS(C), PhD, FACS Assistant Professor of Ophthalmology, McGill University; Clinical Assistant Professor of Ophthalmology, Sherbrooke University; Medical Director, Cornea Laser and Lasik MD

Mounir Bashour, MD, CM, FRCS(C), PhD, FACS is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American College of International Physicians, American College of Surgeons, American Medical Association, American Society of Cataract and Refractive Surgery, American Society of Mechanical Engineers, American Society of Ophthalmic Plastic and Reconstructive Surgery, Biomedical Engineering Society, Canadian Medical Association,Canadian Ophthalmological Society, Contact Lens Association of Ophthalmologists, International College of Surgeons US Section, Ontario Medical Association, Quebec Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

William K Chiang, MD Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center

William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Andrew A Dahl, MD Director of Ophthalmology Teaching, Mid-Hudson Family Practice Institute, The Institute for Family Health; Assistant Professor of Surgery (Ophthalmology), New York College of Medicine

Andrew A Dahl, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American College of Surgeons, American Medical Association, American Society of Cataract and Refractive Surgery, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Steven C Dronen, MD, FAAEM Chair, Department of Emergency Medicine, LeConte Medical Center

Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Eugene Hardin, MD, FAAEM, FACEP Former Chair and Associate Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine, Martin Luther King Jr/Drew Medical Center

Disclosure: Nothing to disclose.

Sarvotham Kini, MD Assistant Professor of Emergency Medicine, Emory University School of Medicine, Atlanta, GA

Sarvotham Kini, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Surgeons, and South Carolina Medical Association

Disclosure: Nothing to disclose.

Alex J Mechaber, MD, FACP Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

William Shapiro, MD Consulting Staff, Department of Urgent Care and Emergency Medicine, Scripps Clinic and Research Foundation

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

Rajeev Vasudeva, MD, FACG Clinical Professor of Medicine, Consultants in Gastroenterology, University of South Carolina School of Medicine

Rajeev Vasudeva, MD, FACG is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, Columbia Medical Society, South Carolina Gastroenterology Association, and South Carolina Medical Association

Disclosure: Pricara Honoraria Speaking and teaching; UCB Consulting fee Consulting

R Christopher Walton, MD Professor, Director of Uveitis and Ocular Inflammatory Disease Service, Department of Ophthalmology, Assistant Dean for Graduate Medical Education, University of Tennessee College of Medicine; Consulting Staff, Regional Medical Center, Memphis Veterans Affairs Medical Center, St Jude Children's Research Hospital

R Christopher Walton, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Healthcare Executives, American Uveitis Society, Association for Research in Vision and Ophthalmology, and Retina Society

Disclosure: Nothing to disclose.

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Severe colitis noted during colonoscopy in a patient with inflammatory bowel disease. The mucosa is grossly denuded, with active bleeding noted. The patient had her colon resected very shortly after this view was obtained.
Stricture in the terminal ileum noted during colonoscopy in a patient with inflammatory bowel disease. This image depicts a narrowed segment visible upon intubation of the terminal ileum with the colonoscope. Relatively little active inflammation is present, indicating that this is a cicatrix stricture
Enteroenteric fistula noted on small bowel series of x-ray films in a patient with inflammatory bowel disease. The narrow-appearing segments filled out relatively normally on subsequent films. Note that barium is just starting to enter the cecum in the right lower quadrant (viewer's left), but the barium has also started to enter the sigmoid colon toward the bottom of the picture, thus indicating the presence of a fistula from the small bowel to the sigmoid colon.
Distinguishing features of Crohn disease (CD) and ulcerative colitis (UC). IBD = inflammatory bowel disease; vs. = versus.
Toxic megacolon. Courtesy of Dr. Pauline Chu.
Early pyoderma gangrenosum, before skin breakdown. Medial aspect of the right ankle in a patient with inflammatory bowel disease. Same day and same patient as in the next image.
Pyoderma gangrenosum. Courtesy of Dr. Gene Izuno.
Severe advanced pyoderma gangrenosum of the medial aspect of the left ankle in a patient with inflammatory bowel disease.
Crohn disease involving the terminal ileum. Note the "string sign" in the right lower quadrant (viewer's left).
Increased postrectal space is a known feature of ulcerative colitis.
Plain abdominal radiograph of a patient with known ulcerative colitis who presented with an acute exacerbation of his symptoms. This image shows thumbprinting in the region of the splenic flexure of the colon.
Double-contrast barium enema study shows pseudopolyposis of the descending colon in a patient with ulcerative colitis.
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 (<i>arrow</i>). 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 oriented.
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.
Inflamed colonic mucosa demonstrating pseudopolyps in a patient with ulcerative colitis.
Chronic architectural changes in ulcerative colitis. Note the crypt branching and irregularity of size and shape, with an increase in chronic inflammatory cells in the lamina propria.
High-power view of a crypt abscess in ulcerative colitis shows the crypt to be dilated and filled with neutrophils and debris.
Chronic architectural changes in ulcerative colitis. Note the trifid crypt.
Basal plasmacytosis in ulcerative colitis. Plasma cells separate the crypt bases from the muscularis mucosae.
Low-power image of a colon biopsy specimen in a patient with ulcerative colitis illustrates changes limited to the mucosa. These changes include chronic alterations of the crypt architecture and an increase in chronic inflammatory cells in the lamina propria.
Bowel-wall thickening and foreshortening are apparent in this specimen from a colectomy for ulcerative colitis. In addition, the mucosa is hyperemic, with focal nodularity and ulceration.
Another gross specimen illustrating ulcerative colitis.
This is an example of low-grade glandular dysplasia in a patient with longstanding ulcerative colitis. Note the loss of mucin, nuclear hyperchromasia, and nuclear pseudostratification. See the next image.
High-grade dysplasia in the same patient as the previous image. There is significant cytologic atypia, with rounding of the nuclei and a greater degree of pseudostratification.
Histologic section from another location in the same patient as the previous image. This field shows glands that are suspicious for invasive carcinoma.
Computed tomography scan depicting Crohn disease in the fundus of the stomach.
Double-contrast barium enema study demonstrates marked ulceration, inflammatory changes, and narrowing of the right colon in a patient with Crohn colitis.
Cobblestoning in Crohn disease. Spot views 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 involving the terminal ileum. Note the "string sign" in the right lower quadrant (viewer's left).
This computed tomography scan from a patient with terminal ileal Crohn disease shows an enteroenteral fistula (arrow) between loops of diseased small intestine.
A teenaged patient with Crohn disease underwent a contrast-enhanced upper gastrointestinal computed tomography study with small-bowel follow-through. Several loops of small bowel are in the pelvis. Note there is a loop of distal bowel with a thickened wall (solid arrow), which is contrasted with a less involved loop of bowel in which the intestinal wall is not thickened at all (dotted arrow).
Computed tomography scan depicting Crohn disease in the fundus of the stomach
Colonoscopic image of a large ulcer and inflammation of the descending colon in a 12-year-old boy with Crohn disease.
Laparoscopic view depicts creeping fat along the mesentery of the terminal ileum in a patient with Crohn disease
Cobblestone change of the mucosa of the terminal ileum in a patient with Crohn disease. Communicating fissures and crevices in the mucosa separate islands of more intact, edematous epithelium.
Fat wrapping on the serosal surface of the terminal ileum in Crohn disease. Fat wrapping often correlates directly with underlying strictures, stenosis, or areas of previous transmural inflammation.
Colonic granuloma in a patient with Crohn disease. Hematoxylin-eosin staining. Courtesy of Dr E. Ruchelli.
Deep knifelike, fissuring, transmural ulcer in Crohn disease.
Deep, fissuring ulcer in a patient with Crohn disease. Note the increase in submucosal inflammation and scattered lymphoid aggregates.
Prominent lymphoid aggregates and granuloma in the muscularis propria and pericolic fat of patient with Crohn disease. The inflammation extends through the full thickness of the bowel wall.
A crypt abscess demonstrating active, neutrophilic inflammation in Crohn disease
Granuloma in the mucosa in a Crohn disease patient.
Double-contrast barium enema study shows changes of early ulcerative colitis disease. Note the granular mucosa.
Table 1. Common Extraintestinal Complications of IBD in US and Europe [55]
Complication Prevalence
Scleritis 18%
Anterior uveitis 17%
Gall stones (particularly in Crohn disease) 13-34%
Inflammatory arthritis 10-35%
Anemia 9-74%
Aphthous stomatitis 4-20%
Osteoporosis 2-20%
Erythema nodosum 2-20%
Source:  Larson S, Bendtzen K, Nielsen OH. Extraintestinal manifestations of inflammatory bowel disease: epidemiology, diagnosis and management. Ann Med. 2010;42:97-114.
Table 2. Extraintestinal Complications of IBD in Swiss Patients [56]
Complication Crohn Disease Ulcerative Colitis
Arthritis 33% 4%
Aphthous stomatitis 10% 4%
Uveitis 6% 3%
Erythema nodosum 6% 3%
Ankylosing spondylitis 6% 2%
Psoriasis 2% 1%
Pyoderma gangrenosum 2% 2%
Primary sclerosing cholangitis 1% 4%
Source:  Vavricka SR, Brun L, Ballabeni P, et al. Frequency and risk factors for extraintestinal manifestations in the Swiss inflammatory bowel disease cohort. Am J Gastroenterol. 2011;106:110-9.
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