Tropical sprue pathophysiology: Difference between revisions
Jump to navigation
Jump to search
| Line 16: | Line 16: | ||
**Reduced gut defense mechanisms resulting in increased bacterial over growth damages the [[enterocytes]] and crypt cells to cause intestinal [[Villous folds|villous]] atrophy. This causes chronic [[diarrhea]]. | **Reduced gut defense mechanisms resulting in increased bacterial over growth damages the [[enterocytes]] and crypt cells to cause intestinal [[Villous folds|villous]] atrophy. This causes chronic [[diarrhea]]. | ||
**[[Bile acid]] deconjugation affects the [[Enterohepatic circulation|enterohepatic]] circulation and causes [[steatorrhea]]. | **[[Bile acid]] deconjugation affects the [[Enterohepatic circulation|enterohepatic]] circulation and causes [[steatorrhea]]. | ||
**Vitamin B12 deficiency can occur if the ileum is involved and the megaloblastic change in the intestinal | **[[Vitamin B12 deficiency]] can occur if the [[ileum]] is involved and the [[Megaloblastic Anemias|megaloblastic]] change in the intestinal musocal [[epithelium]] results in the formation of dysfunctional [[epithelial]] cells. | ||
**Slow mouth to [[cecum]] transit due to intestinal stasis promotes small intestinal bacterial over growth and patients with [[tropical sprue]] have higher levels of [[enteroglucagon]], [[peptide YY]], and [[neurotensin]] which decrease the [[motility]] of [[intestine]] all these can predispose to the development of [[tropical sprue]].<ref name="pmid12702046">{{cite journal| author=Ghoshal UC, Ghoshal U, Ayyagari A, Ranjan P, Krishnani N, Misra A et al.| title=Tropical sprue is associated with contamination of small bowel with aerobic bacteria and reversible prolongation of orocecal transit time. | journal=J Gastroenterol Hepatol | year= 2003 | volume= 18 | issue= 5 | pages= 540-7 | pmid=12702046 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12702046 }} </ref> | **Slow mouth to [[cecum]] transit due to intestinal stasis promotes small intestinal bacterial over growth and patients with [[tropical sprue]] have higher levels of [[enteroglucagon]], [[peptide YY]], and [[neurotensin]] which decrease the [[motility]] of [[intestine]] all these can predispose to the development of [[tropical sprue]].<ref name="pmid12702046">{{cite journal| author=Ghoshal UC, Ghoshal U, Ayyagari A, Ranjan P, Krishnani N, Misra A et al.| title=Tropical sprue is associated with contamination of small bowel with aerobic bacteria and reversible prolongation of orocecal transit time. | journal=J Gastroenterol Hepatol | year= 2003 | volume= 18 | issue= 5 | pages= 540-7 | pmid=12702046 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12702046 }} </ref> | ||
**Mucosal [[disaccharidase]] deficiency is also a potential cause as patients with [[tropical sprue]] have higher levels of urinary lactuose excretion suggesting a deficiency of [[lactase]] enzyme. | **Mucosal [[disaccharidase]] deficiency is also a potential cause as patients with [[tropical sprue]] have higher levels of urinary lactuose excretion suggesting a deficiency of [[lactase]] enzyme. | ||
Revision as of 15:35, 14 April 2017
|
Tropical sprue Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Tropical sprue pathophysiology On the Web |
|
American Roentgen Ray Society Images of Tropical sprue pathophysiology |
|
Risk calculators and risk factors for Tropical sprue pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2]
Overview
The exact pathophysiology of tropical sprue is unclear but is thought to be related to intestinal inflammation following an episode of diarrhea. The inflammation damages the intestinal villi and also result in lymphocytosis in the intestinal wall. Deficiency of lactase enzyme in results in malabsorption of carbohydrates and the dysfunctional enterocytes cause steatorrhea.
Pathophysiology
Pathogenesis
Pathogenesis of tropical sprue is unclear and multiple theories are proposed.The pathogenesis of tropical sprue includes:[1]
- Post infectious diarrhea theory is the most supported, due to the occurrence of the disease following an episode of acute gastroenteritis, occurrence of the disease in epidemics in rural areas with poor sanitation, susceptibility of visitors from developed countries to endemic regions and the frequency of small bowel bacterial overgrowth in patients with tropical sprue.
- The small intestinal bacterial overgrowth affects the enterocyte brush border activity, duodenal morphology causing villous atrophy and lymphocytosis in the intestinal cells.
- Tropical sprue affects the proximal and the distal gastrointestinal tract including the terminal ileum causing vitamin B12 and folate deficiencies.
- Other factors that can result in tropical sprue include the following:[2]
- Impaired host immune response results in prolonged inflammation of the small bowel affecting the enterocyte function.
- Reduced gut defense mechanisms resulting in increased bacterial over growth damages the enterocytes and crypt cells to cause intestinal villous atrophy. This causes chronic diarrhea.
- Bile acid deconjugation affects the enterohepatic circulation and causes steatorrhea.
- Vitamin B12 deficiency can occur if the ileum is involved and the megaloblastic change in the intestinal musocal epithelium results in the formation of dysfunctional epithelial cells.
- Slow mouth to cecum transit due to intestinal stasis promotes small intestinal bacterial over growth and patients with tropical sprue have higher levels of enteroglucagon, peptide YY, and neurotensin which decrease the motility of intestine all these can predispose to the development of tropical sprue.[3]
- Mucosal disaccharidase deficiency is also a potential cause as patients with tropical sprue have higher levels of urinary lactuose excretion suggesting a deficiency of lactase enzyme.
- The bacteria after an episode of diarrhea damages the enterocytes: resulting small bowel stasis, bacterial over-growth, reduced gut motility, malabsorption and loss of folate with further damage to the enterocyte. All these factors contribute to the vicious cycle of events resulting in tropical sprue.
- Treatment with tetracyclines eliminates the bacterial overgrowth and supplementation of folate helps in regeneration of the intestinal epithelium. The diagnosis of tropical sprue is confirmed only if the patient responds to treatment with tetracyclines and folate supplementation.
Genetics
People with Aw-19 HLA haplotype are at higher risk of developing tropical sprue.
Microscopic Pathology
- Small bowel biopsy reveals similar changes as gluten sensitive enteropathy.
- The features demonstrated on a duodenal biopsy include :[4]
- Incomplete villous blunting
- Intra epithelial lymphocytosis
- Eosinophilic infilteration of the mucosa
Associated Conditons
There are no associated conditions with tropical sprue.
References
- ↑ Ghoshal UC, Kumar S, Misra A, Choudhuri G (2013). "Pathogenesis of tropical sprue: a pilot study of antroduodenal manometry, duodenocaecal transit time & fat-induced ileal brake". Indian J Med Res. 137 (1): 63–72. PMC 3657900. PMID 23481053.
- ↑ Brown, Ian S.; Bettington, Andrew; Bettington, Mark; Rosty, Christophe (2014). "Tropical Sprue". The American Journal of Surgical Pathology. 38 (5): 666–672. doi:10.1097/PAS.0000000000000153. ISSN 0147-5185.
- ↑ Ghoshal UC, Ghoshal U, Ayyagari A, Ranjan P, Krishnani N, Misra A; et al. (2003). "Tropical sprue is associated with contamination of small bowel with aerobic bacteria and reversible prolongation of orocecal transit time". J Gastroenterol Hepatol. 18 (5): 540–7. PMID 12702046.
- ↑ SWANSON VL, THOMASSEN RW (1965). "PATHOLOGY OF THE JEJUNAL MUCOSA IN TROPICAL SPRUE". Am J Pathol. 46: 511–51. PMC 1920377. PMID 14278662.