Jump to content

Inflammatory bowel disease: Difference between revisions

From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
m →‎Treatment in development: fix DOI to 10.1053/j.gastro.2005.05.026
Tag: repeating characters
Line 23: Line 23:
* [[Collagenous colitis]]
* [[Collagenous colitis]]
* [[Lymphocytic colitis]]
* [[Lymphocytic colitis]]
* [[Ischaemic colitis]]
* [[Ischaemic colitis]]hghghghghghghghghghghgh
* [[Diversion colitis]]
* [[Diversion colitis]]
* [[Behçet's disease]]
* [[Behçet's disease]]

Revision as of 17:35, 4 June 2011

This article is about bowel inflammation. For functional disorder, see Irritable bowel syndrome.
Inflammatory bowel disease
SpecialtyGastroenterology Edit this on Wikidata

In medicine, inflammatory bowel disease (IBD) is a group of inflammatory conditions of the colon and small intestine. The major types of IBD are Crohn's disease and ulcerative colitis.[1][2][3]

Forms

The main forms of IBD are Crohn's disease and ulcerative colitis (UC).

Accounting for far fewer cases are other forms of IBD, which are not always classified as typical IBD:

The main difference between Crohn's disease and UC is the location and nature of the inflammatory changes. Crohn's can affect any part of the gastrointestinal tract, from mouth to anus (skip lesions), although a majority of the cases start in the terminal ileum. Ulcerative colitis, in contrast, is restricted to the colon and the rectum.[4]

Pathophysiology
Crohn's disease Ulcerative colitis
Cytokine response Associated with Th17[5] Vaguely associated with Th2

Microscopically, ulcerative colitis is restricted to the mucosa (epithelial lining of the gut), while Crohn's disease affects the whole bowel wall ("transmural lesions").

Finally, Crohn's disease and ulcerative colitis present with extra-intestinal manifestations (such as liver problems, arthritis, skin manifestations and eye problems) in different proportions.

Rarely, a definitive diagnosis of neither Crohn's disease nor ulcerative colitis can be made because of idiosyncrasies in the presentation. In this case, a diagnosis of indeterminate colitis may be made. Although a recognised definition, not all centres refer to this.

Symptoms and diagnosis

Signs and symptoms
Crohn's disease Ulcerative colitis
Defecation Often porridge-like,[6]
sometimes steatorrhea		 Often mucus-like
and with blood[6]
Tenesmus Less common[6] More common[6]
Fever Common[6] Indicates severe disease[6]
Fistulae Common[7] Seldom
Weight loss Often More seldom
High magnification micrograph of intestinal crypt branching, an indicator of chronic inflammation and a histopathologic finding associated with inflammatory bowel disease. Colonic biopsy of the mucosa in an individual with Crohn's disease. H&E stain.

Although very different diseases, both may present with any of the following symptoms: abdominal pain, vomiting, diarrhea, rectal bleeding, severe internal cramps/muscle spasms in the region of the pelvis, weight loss and various associated complaints or diseases like arthritis, pyoderma gangrenosum, and primary sclerosing cholangitis. Diagnosis is generally by colonoscopy with biopsy of pathological lesions.

Diagnostic findings
Crohn's disease Ulcerative colitis
Terminal ileum involvement Commonly Seldom
Colon involvement Usually Always
Rectum involvement Seldom Usually (95%)[8]
Involvement around
the anus		 Common[9] Seldom
Bile duct involvement No increase in rate of primary sclerosing cholangitis Higher rate[10]
Distribution of disease Patchy areas of inflammation (skip lesions) Continuous area of inflammation[8]
Endoscopy Deep geographic and serpiginous (snake-like) ulcers Continuous ulcer
Depth of inflammation May be transmural, deep into tissues[9][2] Shallow, mucosal
Stenosis Common Seldom
Granulomas on biopsy May have non-necrotizing non-peri-intestinal crypt granulomas[9][11][12] Non-peri-intestinal crypt granulomas not seen[13]

Treatment

Management
Crohn's disease Ulcerative colitis
Mesalazine Less useful[14] More useful[14]
Antibiotics Effective in long-term[15] Generally not useful[16]
Surgery Often returns following
removal of affected part		 Usually cured by removal
of colon

Optimal treatment of inflammatory bowel disease depends on what form it consists of. For example, mesalazine is more useful in ulcerative colitis than in Crohn's disease.[14] Generally, depending on the level of severity, IBD may require immunosuppression to control the symptom, such as prednisone, TNF inhibition, azathioprine (Imuran), methotrexate, or 6-mercaptopurine. More commonly, treatment of IBD requires a form of mesalazine. Often, steroids are used to control disease flares and were once acceptable as a maintenance drug. In use for several years in Crohn's disease patients and recently in patients with ulcerative colitis, biologicals have been used such as TNF inhibitors. Severe cases may require surgery, such as bowel resection, strictureplasty or a temporary or permanent colostomy or ileostomy. Alternative medicine treatments for bowel disease exist in various forms, however such methods concentrate on controlling underlying pathology in order to avoid prolonged steroidal exposure or surgical excisement.[17]

Usually the treatment is started by administering drugs with high anti-inflammatory effects, such as prednisone. Once the inflammation is successfully controlled, the patient is usually switched to a lighter drug to keep the disease in remission, such as Asacol, a mesalamine. If unsuccessful, a combination of the aforementioned immunosuppression drugs with a mesalamine (which may also have an anti-inflammatory effect) may or may not be administered, depending on the patient.

Histoplasma produces toxins that cause intestinal disease called histoplasmosis that is a “serious consideration” in an immunocompromised patient with signs and symptoms of IBD. Antifungal drugs such as nystatin (a broad spectrum gut antifungal) and either itraconazole (Sporanox) or fluconazole (Diflucan) have been suggested as a treatment for IBD disorders such as Crohn’s disease and ulcerative colitis that all share the same symptoms such as diarrhea, weight loss, fever, and abdominal pain.[18]

Treatment in development

The following treatment strategies are not used routinely, but appear promising in most forms of inflammatory bowel disease.

Initial reports[19] suggest that "helminthic therapy" may not only prevent but even cure (or control) IBD: a drink with roughly 2,500 ova of the Trichuris suis helminth taken twice monthly decreased symptoms markedly in many patients. It is even speculated that an effective "immunization" procedure could be developed—by ingesting the cocktail at an early age.

Prebiotics and probiotics are showing increasing promise as treatments for IBD[20] and in some studies have proven to be as effective as prescription drugs.[21]

In 2005 New Scientist published a joint study by Bristol University and the University of Bath on the apparent healing power of cannabis on IBD. Reports that cannabis eased IBD symptoms indicated the possible existence of cannabinoid receptors in the intestinal lining, which respond to molecules in the plant-derived chemicals. CB1 cannabinoid receptors – which are known to be present in the brain – exist in the endothelial cells which line the gut, it is thought that they are involved in repairing the lining of the gut when damaged. The team deliberately damaged the cells to cause inflammation of the gut lining and then added synthetically produced cannabinoids; the result was that gut started to heal: the broken cells were repaired and brought back closer together to mend the tears. It is believed that in a healthy gut, natural endogenous cannabinoids are released from endothelial cells when they are injured, which then bind to the CB1 receptors. The process appears to set off a wound-healing reaction, and when people use cannabis, the cannabinoids bind to these receptors in the same way. Previous studies have shown that CB1 receptors located on the nerve cells in the gut respond to cannabinoids by slowing gut motility, therefore reducing the painful muscle contractions associated with diarrhoea. The team also discovered another cannabinoid receptor, CB2, in the guts of IBD sufferers, which was not present in healthy guts. These receptors, which also respond to chemicals in cannabis, appear to be associated with apoptosis – programmed cell death – and may have a role in suppressing the overactive immune system and reducing inflammation by mopping up excess cells.[22]

Prognosis

While IBD can limit quality of life because of pain, vomiting, diarrhea, and other socially unacceptable symptoms, it is rarely fatal on its own. Fatalities due to complications such as toxic megacolon, bowel perforation and surgical complications are also rare.

Complications
Crohn's
disease		 Ulcerative
colitis
Nutrient deficiency Higher risk
Colon cancer risk Slight Considerable
Prevalence of extraintestinal complications[23][24][25]
Iritis/uveitis Females 2.2% 3.2%
Males 1.3% 0.9%
Primary sclerosing
cholangitis		 Females 0.3% 1%
Males 0.4% 3%
Ankylosing
spondylitis		 Females 0.7% 0.8%
Males 2.7% 1.5%
Pyoderma
gangrenosum		 Females 1.2% 0.8%
Males 1.3% 0.7%
Erythema nodosum Females 1.9% 2%
Males 0.6% 0.7%

While patients of IBD do have an increased risk of colorectal cancer, this is usually caught much earlier than the general population in routine surveillance of the colon by colonoscopy, and therefore patients are much more likely to survive.

New evidence suggests that patients with IBD may have an elevated risk of endothelial dysfunction and coronary artery disease[26]

The goal of treatment is toward achieving remission, after which the patient is usually switched to a lighter drug with fewer potential side effects. Every so often, an acute resurgence of the original symptoms may appear; this is known as a "flare-up". Depending on the circumstances, it may go away on its own or require medication. The time between flare-ups may be anywhere from weeks to years, and varies wildly between patients - a few have never experienced a flare-up.

References

  1. ^ Baumgart DC, Carding SR (2007). "Inflammatory bowel disease: cause and immunobiology". The Lancet. 369 (9573): 1627–40. doi:10.1016/S0140-6736(07)60750-8. PMID 17499605.
  2. ^ a b Baumgart DC, Sandborn WJ (2007). "Inflammatory bowel disease: clinical aspects and established and evolving therapies". The Lancet. 369 (9573): 1641–57. doi:10.1016/S0140-6736(07)60751-X. PMID 17499606. Cite error: The named reference "Baumgart" was defined multiple times with different content (see the help page).
  3. ^ Xavier RJ, Podolsky DK (2007). "Unravelling the pathogenesis of inflammatory bowel disease". Nature. 448 (7152): 427–34. doi:10.1038/nature06005. PMID 17653185.
  4. ^ "Crohn's & Colitis Foundation of America".
  5. ^ Elson CO, Cong Y, Weaver CT, Schoeb TR, McClanahan TK, Fick RB, Kastelein RA (2007). "Monoclonal anti-interleukin 23 reverses active colitis in a T cell-mediated model in mice". Gastroenterology. 132 (7): 2359–70. doi:10.1053/j.gastro.2007.03.104. PMID 17570211.
  6. ^ a b c d e f internetmedicin.se > Inflammatorisk tarmsjukdom, kronisk, IBD By Robert Löfberg. Retrieved Oct 2010 Translate.
  7. ^ Hanauer SB, Sandborn W (March 2001). "Management of Crohn's disease in adults". The American Journal of Gastroenterology. 96 (3): 635–43. doi:10.1111/j.1572-0241.2001.3671_c.x (inactive 31 January 2024). PMID 11280528. S2CID 31219115.{{cite journal}}: CS1 maint: DOI inactive as of January 2024 (link)
  8. ^ a b Rubin DT, Ananthakrishnan AN, Siegel CA, Sauer BG, Long MD (March 2019). "ACG Clinical Guideline: Ulcerative Colitis in Adults". The American Journal of Gastroenterology. 114 (3): 384–413. doi:10.14309/ajg.0000000000000152. PMID 30840605. S2CID 73473272.
  9. ^ a b c Hanauer SB, Sandborn W (March 2001). "Management of Crohn's disease in adults". The American Journal of Gastroenterology. 96 (3): 635–43. doi:10.1111/j.1572-0241.2001.3671_c.x (inactive 31 January 2024). PMID 11280528. S2CID 31219115.{{cite journal}}: CS1 maint: DOI inactive as of January 2024 (link)
  10. ^ Broomé U, Bergquist A (February 2006). "Primary sclerosing cholangitis, inflammatory bowel disease, and colon cancer". Seminars in Liver Disease. 26 (1): 31–41. doi:10.1055/s-2006-933561. PMID 16496231. S2CID 260320940.
  11. ^ Shepherd NA (August 2002). "Granulomas in the diagnosis of intestinal Crohn's disease: a myth exploded?". Histopathology. 41 (2): 166–8. doi:10.1046/j.1365-2559.2002.01441.x. PMID 12147095. S2CID 36907992.
  12. ^ Mahadeva U, Martin JP, Patel NK, Price AB (July 2002). "Granulomatous ulcerative colitis: a re-appraisal of the mucosal granuloma in the distinction of Crohn's disease from ulcerative colitis". Histopathology. 41 (1): 50–5. doi:10.1046/j.1365-2559.2002.01416.x. PMID 12121237. S2CID 29476514.
  13. ^ DeRoche TC, Xiao SY, Liu X (August 2014). "Histological evaluation in ulcerative colitis". Gastroenterology Report. 2 (3): 178–92. doi:10.1093/gastro/gou031. PMC 4124271. PMID 24942757.
  14. ^ a b c Agabegi, Elizabeth D; Agabegi, Steven S. (2008). "Inflammatory bowel disease (IBD)". Step-Up to Medicine (Step-Up Series). Hagerstwon, MD: Lippincott Williams & Wilkins. pp. 152–156. ISBN 0-7817-7153-6. Cite error: The named reference "agabegi2nd" was defined multiple times with different content (see the help page).
  15. ^ Feller M, Huwiler K, Schoepfer A, Shang A, Furrer H, Egger M (February 2010). "Long-term antibiotic treatment for Crohn's disease: systematic review and meta-analysis of placebo-controlled trials". Clinical Infectious Diseases. 50 (4): 473–80. doi:10.1086/649923. PMID 20067425.
  16. ^ Prantera C, Scribano ML (July 2009). "Antibiotics and probiotics in inflammatory bowel disease: why, when, and how". Current Opinion in Gastroenterology. 25 (4): 329–33. doi:10.1097/MOG.0b013e32832b20bf. PMID 19444096.
  17. ^ A Phytotherapeutic Approach to Lower Bowel Disease Gaia Garden
  18. ^ Holland D. The Fungal Etiology of Inflammatory Bowel Disease .
  19. ^ Summers RW, Elliott DE, Qadir K, Urban JF, Thompson R, Weinstock JV (2003). "Trichuris suis seems to be safe and possibly effective in the treatment of inflammatory bowel disease". Am. J. Gastroenterol. 98 (9): 2034–41. doi:10.1111/j.1572-0241.2003.07660.x. PMID 14499784.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  20. ^ Furrie E, Macfarlane S, Kennedy A; et al. (2005). "Synbiotic therapy ([[Bifidobacterium longum]]/Synergy 1) initiates resolution of inflammation in patients with active ulcerative colitis: a randomised controlled pilot trial". Gut. 54 (2): 242–9. doi:10.1136/gut.2004.044834. PMC 1774839. PMID 15647189. {{cite journal}}: Explicit use of et al. in: |author= (help); URL–wikilink conflict (help)CS1 maint: multiple names: authors list (link)
  21. ^ Kruis W, Fric P, Pokrotnieks J; et al. (2004). "Maintaining remission of ulcerative colitis with the probiotic Escherichia coli Nissle 1917 is as effective as with standard mesalazine". Gut. 53 (11): 1617–23. doi:10.1136/gut.2003.037747. PMC 1774300. PMID 15479682. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  22. ^ Wright K, Rooney N, Feeney M; et al. (2005). "Differential expression of cannabinoid receptors in the human colon: cannabinoids promote epithelial wound healing". Gastroenterology. 129 (2): 437–53. doi:10.1053/j.gastro.2005.05.026. PMID 16083701. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  23. ^ Greenstein AJ, Janowitz HD, Sachar DB (September 1976). "The extra-intestinal complications of Crohn's disease and ulcerative colitis: a study of 700 patients". Medicine. 55 (5): 401–412. doi:10.1097/00005792-197609000-00004. PMID 957999.
  24. ^ Bernstein CN, Blanchard JF, Rawsthorne P, Yu N (April 2001). "The prevalence of extraintestinal diseases in inflammatory bowel disease: a population-based study". The American Journal of Gastroenterology. 96 (4): 1116–1122. doi:10.1111/j.1572-0241.2001.03756.x. PMID 11316157.
  25. ^ Harbord M, Annese V, Vavricka SR, Allez M, Barreiro-de Acosta M, Boberg KM, Burisch J, De Vos M, De Vries AM, Dick AD, Juillerat P, Karlsen TH, Koutroubakis I, Lakatos PL, Orchard T, Papay P, Raine T, Reinshagen M, Thaci D, Tilg H, Carbonnel F (March 2016). "The First European Evidence-based Consensus on Extra-intestinal Manifestations in Inflammatory Bowel Disease". Journal of Crohn's & Colitis. 10 (3): 239–254. doi:10.1093/ecco-jcc/jjv213. PMID 26614685.
  26. ^ Roifman I, Sun YC, Fedwick JP, Panaccione R, Buret AG, Liu H, Rostom A, Anderson TJ, Beck PL (2009). [linkinghub.elsevier.com/retrieve/pii/S1542-3565(08)01109-9 "Evidence of endothelial dysfunction in patients with inflammatory bowel disease"]. Clin. Gastroenterol. Hepatol. 7 (2): 175–82. doi:10.1016/j.cgh.2008.10.021. PMID 19121648. Retrieved 2009-11-04. {{cite journal}}: Check |url= value (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

External links

Retrieved from "https://en.wikipedia.org/w/index.php?title=Inflammatory_bowel_disease&oldid=432547812"