Inflammatory bowel disease: Difference between revisions
imported>Howard C. Berkowitz (Link to ANCA artic le) |
mNo edit summary |
||
| Line 32: | Line 32: | ||
| publisher = Lange}}, pp. 602-608</ref> | | publisher = Lange}}, pp. 602-608</ref> | ||
==References== | ==References== | ||
<references/> | <references/>[[Category:Suggestion Bot Tag]] | ||
Latest revision as of 06:01, 1 September 2024
Inflammatory bowel disease is "chronic, non-specific inflammation of the gastrointestinal tract. Etiology may be genetic or environmental. This term includes Crohn disease and ulcerative colitis."[1]
Classification
Crohn's disease
Crohn's disease is a "chronic transmural inflammation that may involve any part of the digestive tract from mouth to anus, mostly found in the ileum, the cecum, and the colon. In Crohn disease, the inflammation, extending through the intestinal wall from the mucosa to the serosa, is characteristically asymmetric and segmental. Epithelioid granulomas may be seen in some patients.[2]
Ulcerative colitis
Ulcerative colitis is "inflammation of the colon that is predominantly confined to the mucosa. Its major symptoms include diarrhea, rectal bleeding, the passage of mucus, and abdominal pain."[3]
Etiology/cause
Genetics
Twin studies show that both Crohn's disease and ulcerative colitis are due to a combination of genetic and environmental factors. In Crohn's disease, 20% to 50% of monozygotic twins are concordant whereas less than 10% of dizygotic twins are concordant.[4] For ulcerative colitis, the concordance rate in monozygotic twins is about 16% and in dizygotic twins is about 4%.[4]
Environment
Microbes may contribute to expression of inflammatory bowel disease.[5]
Diagnosis
Stool tests
Fecal calprotectin levels have accuracy of:[6]
- Sensitivity 93%
- Specificity 96%
Blood antibodies
Perinuclear antineutrophil cytoplasmic autoantibodies (pANCA) and anti-Saccharomyces cerevisiae antibodies (ASCA) may be helpful.[7] ASCA+ with pANCA- suggests Crohn's disease.
Treatment
There is no curative treatment, but both syndromes are treatable with 5-aminosalicylic acid derivatives, cortiosteroids, and immunomodulators. In the first category are sulfasalazine, mesalamine, and azo drugs such as balsalazide and olsalazine. The main immunomodulators are the thiopurines mercaptopurine and azathioprine, as well as methotrexate. Recently, a monoclonal antibody against tumor necrosis factor-alpha, infliximab, has come into use either independently of the aforementioned immunomodulators or administered with them. Concomitant administration of methotrexate or thiopurines reduces the chance of formation of antibodies to infliximab (ATI).[8]
References
- ↑ Anonymous (2024), Inflammatory bowel disease (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Anonymous (2024), Crohn Disease (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Anonymous (2024), Colitis, Ulcerative (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ 4.0 4.1 Halme L, Paavola-Sakki P, Turunen U, Lappalainen M, Farkkila M, Kontula K (2006). "Family and twin studies in inflammatory bowel disease". World J. Gastroenterol. 12 (23): 3668–72. PMID 16773682. [e]
- ↑ Hecht GA (January 2008). "Inflammatory bowel disease--live transmission". N. Engl. J. Med. 358 (5): 528–30. DOI:10.1056/NEJMcibr0707718. PMID 18234759. Research Blogging.
- ↑ van Rheenen PF, Van de Vijver E, Fidler V (2010). "Faecal calprotectin for screening of patients with suspected inflammatory bowel disease: diagnostic meta-analysis.". BMJ 341: c3369. DOI:10.1136/bmj.c3369. PMID 20634346. PMC PMC2904879. Research Blogging.
- ↑ Reese GE, Constantinides VA, Simillis C, et al (2006). "Diagnostic precision of anti-Saccharomyces cerevisiae antibodies and perinuclear antineutrophil cytoplasmic antibodies in inflammatory bowel disease". Am. J. Gastroenterol. 101 (10): 2410–22. DOI:10.1111/j.1572-0241.2006.00840.x. PMID 16952282. Research Blogging.
- ↑ Kenneth R. McQuaid, Chapter 14: Inflammatory bowel disease, in Current Medical Diagnosis & Treatment, pp. 602-608