eMedicine Specialties > Gastroenterology > Systemic Disease

Crohn Disease: Treatment & Medication

Author: George Y Wu, MD, PhD, Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine
Coauthor(s): Marcy L Coash, DO, Staff Physician, Department of Internal Medicine, University of Connecticut; Senthil Nachimuthu, MD, FACP, Fellow, Department of Internal Medicine, Heart and Vascular Institute, Tulane University School of Medicine
Contributor Information and Disclosures

Updated: Jan 20, 2009

Treatment

Medical Care

  • Diarrhea
    • Chronic diarrhea in Crohn disease responds well to antidiarrheal agents such as loperamide (2-4 mg), diphenoxylate with atropine (1 tab), and tincture of opium (8-15 gtt). Such agents may be administered up to 4 times daily, but they should not be given to patients with active colitis because of the risk of developing toxic megacolon.
    • Patients with terminal ileal disease may not absorb bile acids normally, which can lead to secretory diarrhea in the colon. These patients may benefit from bile acid sequestrants (eg, cholestyramine [2-4 g], colestipol [5 g] bid/tid ac). Those who have extensive ileal disease or resection of more than 100 cm of the ileum have defective bile salt absorption and develop steatorrhea. These patients benefit from a low-fat diet and medium-chain triglyceride preparations. Bile sequestrants exacerbate this type of diarrhea.
    • Diarrhea may also develop because of bacterial overgrowth, short-bowel syndrome, and lactase deficiency.
    • Abdominal cramps may be reduced with propantheline (0.125 mg), dicyclomine (10-20 mg), or hyoscyamine (0.125 mg). These drugs should not be used if there is the possibility of a bowel obstruction.2,13
  • For colon and small bowel inflammation, anti-inflammatory drugs or antibiotics are helpful.
    • Sulfasalazine is mainly useful in colonic disease, because the active compound, 5-aminosalicylic acid (5-ASA), is released in the large bowel by bacterial degradation of the parent compound. Sulfasalazine does not alleviate small bowel disease. Products such as mesalamine (Asacol) that release 5-ASA in the distal small bowel secondary to pH changes are more useful in patients with small intestinal Crohn disease. Long-term maintenance with mesalamine (800 mg tid) may delay clinical relapse. Sulfasalazine does not have an additive effect or a steroid-sparing effect when used in conjunction with corticosteroids. In contrast to its action in ulcerative colitis, sulfasalazine does not seem to maintain remission in Crohn disease.
    • A short course of steroid therapy is indicated in patients with severe systemic symptoms (eg, fever, nausea, weight loss) and in those whose condition does not respond to anti-inflammatory agents. Prednisone (40-60 mg/d) is generally helpful in acute inflammation. Once remission is achieved, the agent is slowly tapered (5-10 mg q1-2wk). It should be noted that steroids are not disease modifying and do not induce sustained mucosal healing.
    • In patients who relapse after the withdrawal of steroids, other treatment options are required. Steroids are not indicated for maintenance therapy because of serious complications, such as aseptic necrosis of the hip, osteoporosis, cataract, diabetes, and hypertension.
    • In patients with a tender, palpable mass, exclude the possibility of an underlying abscess before starting steroids. Adding antibiotics is always beneficial if coexisting infection is considered likely.
    • Consider immunosuppressants such as azathioprine (2 mg/kg/d) or its active metabolite, 6-mercaptopurine (6-MP), if steroid withdrawal proves difficult. Response is usually observed within 3-6 months. Careful supervision is needed because of the risk of bone marrow suppression.
    • If medical therapy fails, surgical resection of the inflamed bowel, with restoration of continuity, is indicated. Urgent surgery may be required in rare cases of sustained or recurrent hemorrhage and toxic megacolon. Partial small bowel obstruction may sometimes be treated conservatively with intravenous hydration, nasogastric suction, and parenteral nutrition if there is no evidence of adhesion or strangulation.2,13
  • Fistulae
    • Fistulae between bowel loops (eg, ileoileal, ileocecal, ileosigmoid) are usually benign and may not produce any major problems.
    • Enterovesicular, enterocutaneous, cologastric, and coloduodenal fistulae are more serious. Surgical intervention is rarely required, unless fistulae are complicated by progressive obstruction or abscess formation or a large segment of bowel is bypassed, leading to severe diarrhea and malabsorption. Otherwise, medical management is used to treat underlying infections and symptoms with oral metronidazole (1 g/d) for at least 1-2 months. Ciprofloxacin confers additional benefit if no improvement occurs. One study demonstrated that the combination of ciprofloxacin and metronidazole in 14 patients with perianal fistulae healed the fistulae in 3 patients and improved 85% of them.
    • Antimetabolites are beneficial in reducing drainage and closing fistulae in 30-40% of patients. Total parenteral nutrition (TPN) and bowel rest may promote fistulae healing during medical therapy.2,13
  • New medical therapies
    • Anti–TNF antibody
      • TNF, a key inflammatory cytokine and mediator of intestinal inflammation, is expressed prominently in IBD. Infliximab is a chimeric mouse-human monoclonal antibody against TNF and shows promise in Crohn disease; it blocks TNF in the serum and at the cell surface, leading to the lysis of TNF-producing macrophages and T cells.
      • In one study, nearly 65% of refractory cases of Crohn disease responded well to treatment with infliximab (5 mg/kg), and one third went into complete remission. Patients who relapsed after the initial response responded again to further infusions. Infliximab is also effective in patients who have refractory perianal and enterocutaneous fistulae. On average, the effect lasts for 12 weeks. Important adverse effects include the development of a lupus-like syndrome and an increased incidence of tuberculosis. Anti–double-stranded DNA is not always associated with clinical lupus. An added benefit of infliximab treatment is the ability to possibly taper steroids, which will decrease further adverse effects.14,15
      • Unfortunately, infliximab is immunogenic, and repeated administration may result in the development of antibodies to infliximab that lead to infusion reactions, loss of efficacy, and delayed hypersensitivity reactions.16
      • Two anti-TNF agents, adalimumab and certolizumab, may be less immunogenic than infliximab and have shown efficacy in the treatment of Crohn disease that is refractory to the standard medical treatment of corticosteroids and immunomodulatory agents.16
      • Adalimumab is a recombinant human immunoglobulin (Ig) G1 monoclonal antibody that binds with high affinity and specificity to human soluble TNF-alpha but not to lymphotoxin (TNF-beta). Results have shown that the immunogenicity of adalimumab is low compared with the chimeric mouse-human monoclonal antibody infliximab.16
      • Two placebo-controlled trials, CLASSIC I and CLASSIC II, showed that adalimumab was effective for both induction and maintenance of remission in patients who were previously naive to anti-TNF therapy. The CHARM trial demonstrated the same effect in a mixed population of patients who were either were naive to infliximab therapy or who had previously been on infliximab therapy. In patients who had lost response or become intolerant of infliximab, the GAIN trial results showed a benefit from adalimumab therapy induction with remission at 4 weeks. Furthermore, an open-label study conducted in France that assessed the long-term efficacy and safety of adalimumab maintenance therapy in this population showed that it was well tolerated and effective in maintaining clinical remission in patients who had Crohn disease with a lost response or intolerance to infliximab.9,17,18
      • Certolizumab pegol, a humanized Fab' antibody fragment conjugated to polyethylene glycol, has also demonstrated efficacy in maintaining remission in patients with moderately to severely active Crohn disease whose condition previously responded to induction therapy with the same agent (PRECISE trial). However, the data only covered a 6-month period.9
  • Immunosuppressive agents
    • Tacrolimus may be effective in treating Crohn disease.
    • Mycophenolate mofetil acts by inhibiting a de novo pathway of purine synthesis in lymphocytes, leading to intracellular depletion of guanosine monophosphate. This results in the suppression of cytotoxic T cells and the formation of antibodies by activated B cells. A dose of 500 mg twice a day in 2 divided doses is well tolerated by patients and can be used to reduce the steroid dose.2,13
    • Anti-inflammatory cytokines: The use of IL-10 ilodecakin resulted in a trend toward clinical improvement but not remission in chronic active Crohn disease, and IL-11 oprelvekin was found to be effective in inducing remission in a preliminary study in patients with mild to moderate Crohn disease. However, more trials are needed.2
    • Monoclonal antibody to IL-6 receptor tocilizumab has been suggested to have a beneficial clinical effect in Crohn disease as well as antibody to IL-12, which has been found to decrease the T helper-1 mediated inflammatory cytokines at the site of disease.2
    • Natalizumab is a monoclonal antibody against the alpha4 integrin subunit that inhibits leukocyte adhesion and migration to areas of inflammation. Pooled clinical data suggest that this drug may be effective for inducing clinical response and remission, although trials were suspended due to 3 reported cases of progressive multileukoencephalopathy (PML) in 2 patients with multiple sclerosis receiving this agent in combination with IFN beta-1A.2
    • Filgrastim or colony-stimulating factor (CSF) (granulocyte monocyte [GM]-CSF) has been shown to have a positive response to treatment in patients with fistulae.2
    • Fontolizumab is an antibody to IFN-gamma that has provided significantly better clinical response rates and remission than placebo.2

Surgical Care

  • Surgery plays an integral role in the treatment of Crohn disease to control symptoms and treat complications. By the 20th year of onset of symptoms, approximately 75% of patients with Crohn disease will have had surgery. Due to the high rate of disease recurrence after segmental bowel resection, the guiding principle of surgery is preservation of intestinal length and function.1
  • The recommended guidelines for those requiring surgery include persistent symptoms despite high-dose corticosteroids, treatment-related complications including intra-abdominal abscesses, medically intractable fistulae, fibrotic strictures with obstructive symptoms, toxic megacolon, hemorrhage, and cancer.1
  • Fibrostenotic obstruction may require surgical correction; in some cases, endoscopic dilation is effective.1
  • Patients with perianal fistulae will usually have a good response to medical treatment (eg, metronidazole, 6-MP, cyclosporin [in refractory cases]). Surgical treatment is indicated if medical treatment fails or if an abscess is present.1
  • The postoperative recurrence rate remains high despite medical management in the postoperative period. The recurrence rate for patients undergoing total colectomy and ileostomy appears to be lower than for those undergoing segmental procedures.1

Diet

The diet should be balanced in patients with Crohn disease. Fiber supplementation is said to be beneficial for patients with colonic disease due to the fact that dietary fiber can be converted to short-chain fatty acids, which provide fuel for colonic mucosal healing, whereas a low-roughage diet is usually indicated for patients with obstructive symptoms.

  • Patients with Crohn disease of the small intestine often have lactose intolerance; therefore, avoidance of dairy products may be indicated. However supplementation with calcium may be required. Osteoporosis is a common nutritional complication of Crohn disease due to the above reason, as well as the release of cytokines from inflammatory cells, which stimulate osteoclast activity and lead to increased bone breakdown. Corticosteroid use is also another significant risk factor for the development of osteoporosis.19,20,21
  • Patients who undergo extensive resection of the terminal portion of the ileum may benefit from a low-fat diet with the addition of medium-chain triglyceride preparations.
  • Enteral therapy with an elemental diet has been suggested to induce remission in acute Crohn disease, consumption of at least 1200 kcal/day was associated with lower rates of disease relapse, but patients' conditions have frequently relapsed after initiation of a normal diet.19,20,21
  • Indications for TPN
    • Short-term use: Patients with active inflammation and severe malnutrition and those with fistulae (given preoperatively)
    • Long-term use: Patients who have had extensive intestinal resection, resulting in short bowel syndrome13

Medication

The goals of pharmacotherapy in patients with Crohn disease are to reduce morbidity, to prevent complications, and to maintain nutritional status.

Anti-inflammatory agents

Anti-inflammatory agents reduce inflammation by acting on host responses.


Mesalamine (Asacol, Rowasa, Canasa)

Exerts anti-inflammatory effects. The mechanism of action is unknown, but it appears to act topically by modulating chemical mediators of inflammatory response. Available as PO or PR products.

Adult

PO: 800-mg DR tab tid for 6 wk; alternatively, 1-g DR cap qid for up to 8 wk
PR: 500-mg PR supp bid for 3-6 wk or until remission (retain at least 1-3 h); alternatively, 4-g enema qhs for 3-6 wk or until remission (retain at least 8 h)

Pediatric

Not established

Decreases the effect of iron, digoxin, and folic acid; increases the effect of oral anticoagulants, methotrexate, and oral hypoglycemic agents

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Elderly persons may have difficulty in retaining rectal suppositories; caution in patients with renal or hepatic impairment


Sulfasalazine (Azulfidine)

Useful in the management of Crohn disease. Acts locally in the colon by decreasing the inflammatory response and systemically by inhibiting prostaglandin synthesis.

Adult

3-5 g/d PO divided bid/tid

Pediatric

Not established

Decreases the effects of iron, digoxin, and folic acid; conversely, increases the effect of oral anticoagulants, oral hypoglycemic agents, and methotrexate

Documented hypersensitivity; sulfa drugs or any component; diagnosed GI obstruction

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in patients with renal or hepatic impairment, blood dyscrasias, or urinary obstruction

Immunosuppressants

Immunosuppressants interfere with the development of immunologic responses.


Infliximab (Remicade)

Chimeric IgG1k monoclonal antibody that neutralizes cytokine TNF-alpha and inhibits its binding to TNF-alpha receptors. Reduces infiltration of inflammatory cells and TNF-alpha production in inflamed areas.

Adult

5 mg/kg IV as single infusion over 2 h
For fistulating Crohn disease, an induction and maintenance regimen may be required: 5 mg/kg IV infusion at 0, 2, and 6 wk as induction regimen, then 5 mg/kg q6wk for maintenance
IV infusion must be administered over at least 2 h; must use an infusion set with in-line, sterile, nonpyrogenic, low-protein-binding filter (pore size <1.2 micrometers)

Pediatric

Induction: 5 mg/kg IV infusion; repeat for total of 3 doses at 2 and 6 wk
Maintenance: 5 mg/kg IV infusion q6wk

Documented hypersensitivity to murine proteins or components of formulation; serious clinical infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May adversely affect normal immune responses and allow development of superinfections; rare cases of lupuslike syndrome, demyelinating disorders, sepsis, tuberculosis, and fatal infections have been reported; discontinue treatment if sepsis or lupuslike syndrome develops


Adalimumab (Humira)

Recombinant human IgG1 monoclonal antibody specific for human TNF. Binds specifically to TNF-alpha and blocks interaction with p55 and p75 cell-surface TNF receptors. This interferes with cytokine driven inflammatory processes. It also lyses surface TNF-expressing cells in vitro in the presence of complement, but it does not bind to TNF-beta (lymphotoxin).

Adult

Induction dose: 160 mg SC once (administer by either dividing dose into 4 injections on day 1 or over 2 days), then follow with 80 mg SC once at week 2
Maintenance: 40 mg SC q2wk beginning at week 4

Pediatric

Not established

May interfere with the immune response to live virus vaccine (eg, MMR) and reduce efficacy; methotrexate (MTX) decreases clearance (available data do not support adjusting dose of either adalimumab or MTX); coadministration with anakinra (an IL-1 antagonist that also blocks TNF) may cause additive adverse effects, particularly the development of serious infections; use with echinacea may decrease its effect

Documented hypersensitivity; active infection

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Causes immunosuppression; may be associated with serious infections (some fatal), including reactivation of tuberculosis, sepsis, or opportunistic infections; increases the risk for lymphoma development; associated with CNS demyelination (rare); may cause optic neuritis; discontinue if serious infection develops; autoantibody development may occur, causing lupuslike syndrome; may cause hypersensitivity reactions, including anaphylaxis and hematologic adverse effects (ie, pancytopenia, aplastic anemia); exacerbation of CHF or new onset CHF has been observed with TNF-blocking agents


Certolizumab pegol (Cimzia)

Pegylated anti–TNF-alpha blocker, which results in disruption of the inflammatory process. Indicated for moderate to severe Crohn disease in individuals whose condition has not responded to conventional therapies.

Adult

400 mg SC initially; repeat at weeks 2 and 4; if favorable response occurs, initiate maintenance dose of 400 mg SC q4wk
Administer as 2 separate 200-mg SC injections at 2 separate sites in abdomen or thigh

Pediatric

Not established

May interfere with the immune response to live virus vaccines (eg, MMR) and reduce efficacy; coadministration with anakinra (an IL-1 antagonist that also blocks TNF) may cause additive adverse effects, particularly the development of serious infections; may interfere with activated partial thromboplastin time (aPTT/aPPT) tests

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Common adverse effects include headache, upper respiratory tract infections, abdominal pain, injection site reactions, and nausea; increases the risk of serious infections, including infections that may result in hospitalization or death; may increase the risk of opportunistic infections (eg, tuberculosis [TB], invasive fungal), so test for latent TB, and, if positive, initiate TB treatment before starting certolizumab; if infection occurs, patients should contact their physician immediately; may cause reactivation of hepatitis B virus; may increase the risk of lymphoma and other malignancies because of immune suppression; anaphylaxis or serious allergic reactions, demyelinating disease, cytopenias, pancytopenia, heart failure, and lupuslike syndrome have been reported with TNF blockers


Azathioprine (Imuran)

Interferes with purine metabolism and inhibits synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells, which results in lower autoimmune activity.

Adult

1.5-2 mg/kg/d PO/IV

Pediatric

<3 years: Not established
>3 years: 2 mg/kg/d PO/IV

Toxicity increases with allopurinol; concurrent use with ACE inhibitors may induce severe leukopenia; may increase the levels of methotrexate metabolites and decrease the effects of anticoagulants, neuromuscular blockers, and cyclosporine

Documented hypersensitivity; low levels of serum thiopurine methyl transferase (TPMT)

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Increases the risk of neoplasia; caution in patients with liver disease and renal impairment; hematologic toxicities may occur; check TPMT level before therapy, and monitor liver, renal, and hematologic function; pancreatitis is rarely associated


Methotrexate (Rheumatrex, Trexall)

Structural analogue to folic acid that inhibits binding of dihydrofolic acid to the enzyme dihydrofolate reductase.

Adult

25 mg IM with concomitant lowering of prednisone dose; once response is achieved, may switch to PO therapy; folic acid at dose of 1 mg/d should be given during treatment

Pediatric

Not established

Oral aminoglycosides may decrease the absorption and blood levels of concurrent oral methotrexate (MTX); charcoal lowers MTX levels; coadministration with etretinate may increase the hepatotoxicity of MTX; folic acid or its derivatives that are contained in some vitamins may decrease the response to MTX; probenecid, NSAIDs, salicylates, procarbazine, and sulfonamides, including TMP-SMZ, can increase MTX plasma levels; may decrease phenytoin plasma levels; may increase plasma levels of thiopurines

Documented hypersensitivity; alcoholism; hepatic insufficiency; documented immunodeficiency syndromes; preexisting blood dyscrasias (eg, bone marrow hypoplasia, leukopenia, thrombocytopenia, significant anemia); renal insufficiency

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Monitor CBCs monthly, and liver and renal function q1-3mo during therapy (monitor more frequently during the initial dosing, dose adjustments, or when the risk of elevated MTX levels is present [eg, dehydration]); MTX has toxic effects on the hematologic, renal, GI, pulmonary, and neurologic systems; discontinue if a significant drop in blood counts occurs; fatal reactions have been reported when administered concurrently with NSAIDs

Corticosteroids

Corticosteroids exert both anti-inflammatory and immunosuppressant effects.


Prednisone (Deltasone, Orasone, Meticorten)

Immunosuppressant for treatment of immune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte (PMN) activity. Stabilizes lysosomal membranes and suppresses lymphocytes and antibody production.

Adult

40-60 mg/d PO divided bid/qid; once in remission, slowly taper by 5-10 mg q1-2wk

Pediatric

Not established

Coadministration with estrogens may decrease clearance; concurrent use with digoxin may increase the risk of digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase the metabolism of glucocorticoids (consider increasing the maintenance dose); monitor for hypokalemia when coadministered with diuretics

Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal skin infections or tuberculosis

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteoporosis, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, euphoria, psychosis, myasthenia gravis, growth suppression, and infections


Budesonide (Entocort EC)

Alters the level of inflammation in tissue by inhibiting multiple types of inflammatory cells and decreasing the production of cytokines and other mediators involved in inflammatory reactions.

Adult

9 mg (3 X 3-mg cap) qd for 8 wk

Pediatric

Not established

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Safety of treatment beyond 8 wk has not been established.

Antibiotics

Antibiotics are used in the treatment of bacterial infections that may be associated with the underlying disease processes.


Metronidazole (Flagyl)

Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Sometimes used in combination with other antimicrobial agents (except for Clostridium difficile enterocolitis). Also possesses immunosuppressive and anti-inflammatory properties.

Adult

1 g/d PO divided bid/qid for 30-60 d

Pediatric

Not established

May increase the toxicity of anticoagulants, lithium, and phenytoin; cimetidine may increase toxicity; disulfiram reaction may occur with orally ingested ethanol

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust the dose in patients with hepatic disease; monitor for seizures and the development of peripheral neuropathy.


Ciprofloxacin (Cipro)

Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, Staphylococcus epidermidis, and most gram-negative organisms, but it has no activity against anaerobes. Inhibits bacterial DNA synthesis, and, consequently, growth.

Adult

500 mg PO bid

Pediatric

Not established

Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in presence of renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy

More on Crohn Disease

Overview: Crohn Disease
Differential Diagnoses & Workup: Crohn Disease
Treatment & Medication: Crohn Disease
Follow-up: Crohn Disease
References
Further Reading

References

  1. Kornbluth A, Sachar DB, Salomon P. Crohn's disease. In: Feldman M, Scharschmidt BF, Sleisenger MH, eds. Sleisenger & Fordtran's Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, and Management. Vol 2. 6th ed. Philadelphia, Pa: WB Saunders Co; 1998:1708-34.

  2. Panes J, Gomollon F, Taxonera C, et al. Crohn's disease: a review of current treatment with a focus on biologics. Drugs. 2007;67(17):2511-37. [Medline].

  3. Tierney LM. Crohn's disease. In: Tierney LM, McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis and Treatment. 40th ed. New York, NY: McGraw-Hill Professional Publishing; 2001:638-42.

  4. Thoreson R, Cullen JJ. Pathophysiology of inflammatory bowel disease: an overview. Surg Clin North Am. Jun 2007;87(3):575-85. [Medline].

  5. Danese S, Semeraro S, Papa A, et al. Extraintestinal manifestations in inflammatory bowel disease. World J Gastroenterol. Dec 14 2005;11(46):7227-36. [Medline][Full Text].

  6. Nikolaus S, Schreiber S. Diagnostics of inflammatory bowel disease. Gastroenterology. Nov 2007;133(5):1670-89. [Medline][Full Text].

  7. Fiocchi C. Inflammatory bowel disease: etiology and pathogenesis. Gastroenterology. Jul 1998;115(1):182-205. [Medline].

  8. Friedman S, Blumberg RS. Inflammatory bowel disease. In: Braunwald E, Fauci AS, Kasper DS, et al, eds. Harrison's Principles of Internal Medicine. Vol 2. 15th ed. New York, NY: McGraw-Hill Professional Publishing; 2001:1679-91.

  9. Sandborn WJ, Hanauer SB, Rutgeerts P, et al. Adalimumab for maintenance treatment of Crohn's disease: results of the CLASSIC II trial. Gut. Sep 2007;56(9):1232-9. [Medline][Full Text].

  10. Mackalski BA, Bernstein CN. New diagnostic imaging tools for inflammatory bowel disease. Gut. May 2006;55(5):733-41. [Medline].

  11. Saibeni S, Rondonotti E, Iozzelli A, et al. Imaging of the small bowel in Crohn's disease: a review of old and new techniques. World J Gastroenterol. Jun 28 2007;13(24):3279-87. [Medline][Full Text].

  12. Schreyer AG, Seitz J, Feuerbach S, Rogler G, Herfarth H. Modern imaging using computer tomography and magnetic resonance imaging for inflammatory bowel disease (IBD) AU1. Inflamm Bowel Dis. Jan 2004;10(1):45-54. [Medline].

  13. Robinson M. Optimizing therapy for inflammatory bowel disease. Am J Gastroenterol. Dec 1997;92(12 suppl):12S-17S. [Medline].

  14. Present DH, Rutgeerts P, Targan S, et al. Infliximab for the treatment of fistulas in patients with Crohn's disease. N Engl J Med. May 6 1999;340(18):1398-405. [Medline][Full Text].

  15. Targan SR, Hanauer SB, van Deventer SJ, et al. A short-term study of chimeric monoclonal antibody cA2 to tumor necrosis factor alpha for Crohn's disease. Crohn's Disease cA2 Study Group. N Engl J Med. Oct 9 1997;337(15):1029-35. [Medline][Full Text].

  16. Peyrin-Biroulet L, Laclotte C, Bigard MA. Adalimumab maintenance therapy for Crohn's disease with intolerance or lost response to infliximab: an open-label study. Aliment Pharmacol Ther. Mar 15 2007;25(6):675-80. [Medline][Full Text].

  17. Sandborn WJ, Rutgeerts P, Enns R, et al. Adalimumab induction therapy for Crohn disease previously treated with infliximab: a randomized trial. Ann Intern Med. Jun 19 2007;146(12):829-38. [Medline][Full Text].

  18. Peppercorn MA. Clinical manifestations, diagnosis, and prognosis of ulcerative colitis in adults. UpToDate. Updated September 15, 2008. Available at http://www.uptodate.com/patients/content/topic.do?topicKey=~ufJTaZYEAmn5Gd. Accessed January 9, 2009.

  19. Harpavat M, Keljo DJ, Regueiro MD. Metabolic bone disease in inflammatory bowel disease. J Clin Gastroenterol. Mar 2004;38(3):218-24. [Medline].

  20. Heuschkel R. Enteral nutrition in Crohn disease: more than just calories. J Pediatr Gastroenterol Nutr. Mar 2004;38(3):239-41. [Medline].

  21. Razack R, Seidner DL. Nutrition in inflammatory bowel disease. Curr Opin Gastroenterol. Jul 2007;23(4):400-5. [Medline].

Further Reading

Related eMedicine topics

Keywords

Crohn disease, Crohn's disease, regional enteritis, granulomatous enteritis, regional ileitis, terminal ileitis, inflammatory bowel disease, IBD, ulcerative colitis, UC, ileitis, colitis, ileocolitis

Contributor Information and Disclosures

Author

George Y Wu, MD, PhD, Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine
George Y Wu, MD, PhD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, American Medical Association, American Society for Clinical Investigation, and Association of American Physicians
Disclosure: Humana Press Consulting fee Consulting; Novartis Consulting fee Review panel membership

Coauthor(s)

Marcy L Coash, DO, Staff Physician, Department of Internal Medicine, University of Connecticut
Marcy L Coash, DO is a member of the following medical societies: American Medical Student Association/Foundation and American Osteopathic Association
Disclosure: Nothing to disclose.

Senthil Nachimuthu, MD, FACP, Fellow, Department of Internal Medicine, Heart and Vascular Institute, Tulane University School of Medicine
Senthil Nachimuthu, MD, FACP is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Medical Editor

Waqar A Qureshi, MD, Associate Professor of Medicine, Chief of Endoscopy, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine and Veterans Affairs Medical Center
Waqar A Qureshi, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing 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, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, 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.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
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 and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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