Medication Summary
Many inflammatory mediators have been identified in inflammatory bowel disease (IBD); antibodies against these mediators and methods to block the production or receptors for these mediators hold great promise as potential therapy for IBD.
Although mild inflammatory disease can be treated with aminosalicylates, moderate to severe disease should be aggressively treated early in the disease course to prevent inflammatory and structuring complications of the intestinal disease. Although the standard immune modulators mercaptopurine and azathioprine are very effective, the delay in onset of therapeutic effect is suboptimal. Early use of biologic agents can promote mucosal healing and maintain remission while preventing complications. Early use of biologic agents should be considered in any patient with severe IBD, although it may require aggressive dealing with pharmacy benefits managers to get coverage for these agents without having failed some of the less aggressive medications.
The stepwise approach for mild disease is as follows:
Aminosalicylates and symptomatic agents are early step; antibiotics are step IA drugs, given the limited situations in which they are used.
Corticosteroids are used in more symptomatic disease; they should be used if the earlier step drugs fail to adequately control the IBD. These agents can also be used in more severe disease to attempt to induce remission.
Immune-modifying agents are used if corticosteroids fail or are required for prolonged periods, but they have the disadvantage of delay before efficacy; infliximab, adalimumab, and vedolizumab are drugs that should be used early in moderate to severe inflammatory disease.
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.
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.
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.
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 bone 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, Uceris, Uceris Foam)
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.
Immunosuppressants
Class Summary
Immunosuppressant agents are useful as steroid-sparing agents, in healing fistulas, and in patients with serious contraindications to surgery. [109] 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 the 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.
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), enhances leukocyte migration, activates 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. [133] Infliximab is indicated for patients who have experienced inadequate response to conventional therapy. [109]
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.
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.
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.
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.
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. 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.
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.
Monoclonal Antibodies
Ustekinumab (Stelara)
Ustekinumab (Stelara) is an antibody that blocks IL-12 and IL-23. It interferes with the triggering of the body's inflammatory response through the suppression of cytokines (interleukins IL-12 and IL-23) which help activate certain T-cells. Ustekinumab binds to the p-40 subunit of both IL-12 and IL-23 so that they subsequently cannot bind to their receptors.
Corticosteroids, Rectal
Budesonide rectal (Uceris Rectal Foam)
Budesonide rectal foam is a glucocorticosteroid indicated for the induction of remission in patients with active mild to moderate distal ulcerative colitis extending up to 40 cm from the anal verge.
DMARDs, JAK Inhibitors
Tofacitinib (Xeljanz, Xeljanz XR)
Tofacitinib is an inhibitor of the enzyme janus kinase 1 (JAK1) and janus kinase 3 (JAK 3). It interferes with the JAK-STAT signaling pathway, which transmits extracellular information into the cell nucleus, influencing DNA transcription.
Bile Acid Sequestrants
Cholestyramine (Questran, Prevalite)
Cholestyramine may be used to treat diarrhea associated with excess bile acids. It binds bile acids, thus reducing the 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.
Colestipol (Colestid)
Colestipol forms a soluble complex after binding to bile acid, increasing fecal loss of bile acid-bound low-density lipoprotein cholesterol.
Colesevelam (WelChol)
Colesevelam forms complex with bile acids that is not absorbed through intestine; inhibits enterohepatic reuptake of intestinal bile salts. It can be used for symptomatic chronic diarrhea due to bile salt malabsorption (bile acid diarrhea) secondary to Crohn's disease.
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Inflammatory bowel disease. 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.
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Inflammatory bowel disease. 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.
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Inflammatory bowel disease. Enteroenteric fistula noted on a 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.
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Inflammatory bowel disease. The table distinguishes features of Crohn disease (CD) and ulcerative colitis (UC).
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Inflammatory bowel disease. Toxic megacolon. Courtesy of Dr. Pauline Chu.
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Inflammatory bowel disease. 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.
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Inflammatory bowel disease. Pyoderma gangrenosum. Courtesy of Dr. Gene Izuno.
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Inflammatory bowel disease. Severe advanced pyoderma gangrenosum of the medial aspect of the left ankle in a patient with inflammatory bowel disease.
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Inflammatory bowel disease. Crohn disease involving the terminal ileum. Note the "string sign" in the right lower quadrant (viewer's left).
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Inflammatory bowel disease. Increased postrectal space is a known feature of ulcerative colitis.
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Inflammatory bowel disease. 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.
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Inflammatory bowel disease. Double-contrast barium enema study shows pseudopolyposis of the descending colon in a patient with ulcerative colitis.
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Inflammatory bowel disease. 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.
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Inflammatory bowel disease. This 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.
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Inflammatory bowel disease. This 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.
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Inflammatory bowel disease. Inflamed colonic mucosa demonstrating pseudopolyps in a patient with ulcerative colitis.
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Inflammatory bowel disease. 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.
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Inflammatory bowel disease. High-power view of a crypt abscess in ulcerative colitis shows the crypt to be dilated and filled with neutrophils and debris.
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Inflammatory bowel disease. Chronic architectural changes in ulcerative colitis. Note the trifid crypt.
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Inflammatory bowel disease. Basal plasmacytosis in ulcerative colitis. Plasma cells separate the crypt bases from the muscularis mucosae.
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Inflammatory bowel disease. 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.
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Inflammatory bowel disease. 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.
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Inflammatory bowel disease. Another gross specimen illustrating ulcerative colitis.
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Inflammatory bowel disease. 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.
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Inflammatory bowel disease. 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.
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Inflammatory bowel disease. Histologic section from another location in the same patient as described in the previous image. This field shows glands that are suspicious for invasive carcinoma.
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Inflammatory bowel disease. Computed tomography scan depicting Crohn disease in the fundus of the stomach.
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Inflammatory bowel disease. Double-contrast barium enema study demonstrates marked ulceration, inflammatory changes, and narrowing of the right colon in a patient with Crohn colitis.
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Inflammatory bowel disease. 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.
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Inflammatory bowel disease. Crohn disease involving the terminal ileum. Note the "string sign" in the right lower quadrant (viewer's left).
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Inflammatory bowel disease. This computed tomography scan from a patient with terminal ileal Crohn disease shows an enteroenteral fistula (arrow) between loops of diseased small intestine.
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Inflammatory bowel disease. A teenage 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).
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Inflammatory bowel disease. Computed tomography scan depicting Crohn disease in the fundus of the stomach.
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Inflammatory bowel disease. This colonoscopic image of a large ulcer and inflammation of the descending colon in a 12-year-old boy with Crohn disease.
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Inflammatory bowel disease. This laparoscopic view depicts creeping fat along the mesentery of the terminal ileum in a patient with Crohn disease.
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Inflammatory bowel 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.
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Inflammatory bowel disease. 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.
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Inflammatory bowel disease. Colonic granuloma in a patient with Crohn disease (arrow). Hematoxylin-eosin staining. Courtesy of Dr E. Ruchelli.
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Inflammatory bowel disease. A deep knifelike, fissuring, transmural ulcer in Crohn disease is shown in this histologic image.
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Inflammatory bowel disease. Another example of a deep, fissuring ulcer in a patient with Crohn disease. Note the increase in submucosal inflammation and scattered lymphoid aggregates.
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Inflammatory bowel disease. 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.
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Inflammatory bowel disease. A crypt abscess demonstrating active, neutrophilic inflammation in Crohn disease.
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Inflammatory bowel disease. Granuloma in the mucosa in a Crohn disease patient.
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Inflammatory bowel disease. Double-contrast barium enema study shows changes of ulcerative colitis disease. Note the granular mucosa.
Tables
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. |
|
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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- Overview
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- Symptomatic Therapy/Supportive Care
- Overview of Therapy
- Aminosalicylates
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- Immunomodulators
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- British Society of Gastroenterology Guidelines (BSG) (2019)
- European Crohn's and Colitis Organisation Guidelines on Medical Treatment (ECCO) (2019)
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- American Gastroenterological Association Guidelines (AGA) (2020)
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- 5-Aminosalicylic Acid Derivatives
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- Proton Pump Inhibitors
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