Tropical sprue pathophysiology: Difference between revisions

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===Pathogenesis===
===Pathogenesis===
Pathogenesis of tropical sprue is unclear and multiple theories are proposed.The factors involved in the pathogenesis of tropical sprue include:<ref name="pmid23481053">{{cite journal| author=Ghoshal UC, Kumar S, Misra A, Choudhuri G| title=Pathogenesis of tropical sprue: a pilot study of antroduodenal manometry, duodenocaecal transit time & fat-induced ileal brake. | journal=Indian J Med Res | year= 2013 | volume= 137 | issue= 1 | pages= 63-72 | pmid=23481053 | doi= | pmc=3657900 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23481053  }} </ref>
Pathogenesis of tropical sprue is unclear and multiple theories are proposed.The factors involved in the pathogenesis of tropical sprue include:<ref name="pmid23481053">{{cite journal| author=Ghoshal UC, Kumar S, Misra A, Choudhuri G| title=Pathogenesis of tropical sprue: a pilot study of antroduodenal manometry, duodenocaecal transit time & fat-induced ileal brake. | journal=Indian J Med Res | year= 2013 | volume= 137 | issue= 1 | pages= 63-72 | pmid=23481053 | doi= | pmc=3657900 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23481053  }} </ref>
* The most accepted theory is the small intestinal bacterial overgrowth affecting the enterocyte brush border activity, duodenal morphology causing villous atrophy and lymphocytosis in the intestinal cells.
*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 cause steatorrhea.
*Vitamin B12 deficiency can occur if the ileum is involved and the megaloblastic change in the intestinal mucuosal epithelium results in the formation of dysfunctional epithelial cells.
*Slow mouth to ceacum 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.
*Mucosal disaccharidase deficiency is also a potential cause as patients with tropical sprue have higher levels of urinary lactulose excretion suggesting a deficiency of lactase enzyme.
*Post infectious diarrhea theory is supported by 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.
*Post infectious diarrhea theory is supported by 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:
**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 mucuosal epithelium results in the formation of dysfunctional epithelial cells.
**Slow mouth to ceacum 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.
**Mucosal disaccharidase deficiency is also a potential cause as patients with tropical sprue have higher levels of urinary lactulose excretion suggesting a deficiency of lactase enzyme.


===Genetics===
===Genetics===

Revision as of 15:03, 13 April 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Pathophysiology

Pathogenesis

Pathogenesis of tropical sprue is unclear and multiple theories are proposed.The factors involved in the pathogenesis of tropical sprue include:[1]

  • Post infectious diarrhea theory is supported by 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:
    • 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 mucuosal epithelium results in the formation of dysfunctional epithelial cells.
    • Slow mouth to ceacum 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.
    • Mucosal disaccharidase deficiency is also a potential cause as patients with tropical sprue have higher levels of urinary lactulose excretion suggesting a deficiency of lactase enzyme.

Genetics

People with HLA haplotype with Aw-19 haplotype are at higher risk of developing tropical sprue.

Gross Pathology

Microscopic Pathology

  • Small bowel biospy reveals similar changes as gluten sensitive enteropathy.
  • The features demonstrated on a duodenal biopsy include :[2]
    • Incomplete villous blunting
    • Intra epithelial lymphocytosis
    • Eosinophilic infilteration of the mucosa

Associated Conditons

References

  1. 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.
  2. SWANSON VL, THOMASSEN RW (1965). "PATHOLOGY OF THE JEJUNAL MUCOSA IN TROPICAL SPRUE". Am J Pathol. 46: 511–51. PMC 1920377. PMID 14278662.

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