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{{Tropical sprue}}
{{Tropical sprue}}
{{CMG}}; {{AE}}
{{CMG}}; {{AE}}  {{AKI}}
 
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==Overview==
==Overview==
TS causes mucosal abnormalities of the small intestine leading to intestinal malabsorption and multiple nutritional deficiencies. Although, the precise etiology of the disease is unknown, many studies have observed small intestinal bacterial overgrowth and prior episodes of infectious gastroenteritis in patients with TS, suggesting infection, as the possible etiology of TS.
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==
==Pathophysiology==
'''Infection'''
===Pathogenesis===
* Accompanied by Fever at the onset of the disease
[[Tropical sprue]] leads to villous atrophy which primarily affects the proximal and the distal gastrointestinal tract including the terminal [[ileum]] causing [[Vitamin B12 Deficiency|vitamin B12]] and [[Folate deficiency|folate]] deficiencies. The pathogenesis of [[tropical sprue]] is unclear and multiple theories have been proposed. The pathogenesis of [[tropical sprue]] includes:<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>
* Increase in the gram-negative bacterial toxins and bacterial colony counts
*Post infectious [[diarrhea]] theory is the most supported due to:
* Precipitated by a history of acute gastroenteritis.<ref name="pmid26115751">{{cite journal| author=McCarroll MG, Riddle MS, Gutierrez RL, Porter CK| title=Infectious Gastroenteritis as a Risk Factor for Tropical Sprue and Malabsorption: A Case-Control Study. | journal=Dig Dis Sci | year= 2015 | volume= 60 | issue= 11 | pages= 3379-85 | pmid=26115751 | doi=10.1007/s10620-015-3768-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26115751 }} </ref>
**The occurrence of the disease following an episode of acute [[gastroenteritis]].
* There is an increase in the inflammatory cells in the lamina propria with variable edema
**Occurrence of the disease in epidemics in rural areas with poor [[sanitation]].
* Good clinical response to Tetracycline with restoration of the normal histology.
**Susceptibility of visitors from developed countries to endemic regions in developing countries.
Small intestinal bacterial colonization.
**The frequency of [[small bowel bacterial overgrowth]] in patients with [[tropical sprue]].
Prolonged orocecal transit time. Clinical improvement following antibacterial treatment was known to normalize the OCTT.<ref name="GhoshalGhoshal2003">{{cite journal|last1=Ghoshal|first1=Uday C|last2=Ghoshal|first2=Ujjala|last3=Ayyagari|first3=Archana|last4=Ranjan|first4=Piyush|last5=Krishnani|first5=Narendra|last6=Misra|first6=Asha|last7=Aggarwal|first7=Rakesh|last8=Naik|first8=Sita|last9=Naik|first9=Subhash R|title=Tropical sprue is associated with contamination of small bowel with aerobic bacteria and reversible prolongation of orocecal transit time|journal=Journal of Gastroenterology and Hepatology|volume=18|issue=5|year=2003|pages=540–547|issn=08159319|doi=10.1046/j.1440-1746.2003.03006.x}}</ref>
***The [[small intestinal bacterial overgrowth]] affects the [[enterocyte]] brush border activity, duodenal morphology causing [[Villous folds|villous]] atrophy and [[lymphocytosis]] in the intestinal cells.
Bacterial overgrowth leading to toxin production.<ref name="Walker2003">{{cite journal|last1=Walker|first1=Marjorie M|title=What is tropical sprue?|journal=Journal of Gastroenterology and Hepatology|volume=18|issue=8|year=2003|pages=887–890|issn=0815-9319|doi=10.1046/j.1440-1746.2003.03127.x}}</ref>
*Other factors that can result in [[tropical sprue]] include the following:<ref name="BrownBettington2014">{{cite journal|last1=Brown|first1=Ian S.|last2=Bettington|first2=Andrew|last3=Bettington|first3=Mark|last4=Rosty|first4=Christophe|title=Tropical Sprue|journal=The American Journal of Surgical Pathology|volume=38|issue=5|year=2014|pages=666–672|issn=0147-5185|doi=10.1097/PAS.0000000000000153}}</ref>
{| class="wikitable"
**Impaired host [[immune]] response results in prolonged [[inflammation]] of the [[small bowel]] affecting the [[enterocyte]] function.
! colspan="2" |Differences in presentation between Indian and Caribbean TS
**Reduced gut defense mechanisms results in increased bacterial overgrowth which damages the [[enterocytes]] and crypt cells leading to intestinal [[Villous folds|villous]] atrophy and eventually chronic [[diarrhea]].
|-
**[[Bile acid]] deconjugation affects the [[Enterohepatic circulation|enterohepatic]] circulation and causes [[steatorrhea]].
|'''Indian'''
**[[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.
|'''Caribbean'''
**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.
|No association with small bowel colonization
* The [[bacteria]] after an episode of [[diarrhea]] damages the [[enterocytes]] resulting in small bowel stasis, bacterial over-growth, reduced gut [[motility]], [[malabsorption]] and loss of [[Folic Acid|folate]] with further damage to the [[enterocyte]]. All these factors contribute to the vicious cycle of events resulting in [[tropical sprue]].
|Associated with small bowel colonization
*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.
|-
 
|Small bowel transit time is not prolonged
==Genetics==
|Prolonged small bowel transit time
People with Aw-19 [[HLA]] haplotype are at higher risk of developing [[tropical sprue]].
|-
 
|Higher mortality
==Associated Conditons==
|Lower mortality
There are no associated conditions with [[tropical sprue]].
|-
 
|Spontaneous remissions common
==Microscopic Pathology==
|Spontaneous remissions rare
*Small bowel biopsy reveals similar changes as [[Celiac Disease|gluten sensitive enteropathy]].
|-
*The features demonstrated on a [[Duodenum|duodenal]] [[biopsy]] include:<ref name="pmid14278662">{{cite journal| author=SWANSON VL, THOMASSEN RW| title=PATHOLOGY OF THE JEJUNAL MUCOSA IN TROPICAL SPRUE. | journal=Am J Pathol | year= 1965 | volume= 46 | issue= | pages= 511-51 | pmid=14278662 | doi= | pmc=1920377 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14278662  }} </ref>
|Fever present in 25% of cases
**Incomplete [[Villous folds|villous]] blunting
|Fever- rare
**Intra epithelial [[lymphocytosis]]
|-
**[[Eosinophilic]] infilteration of the mucosa
|Variable response to folic acid and antibiotics
|Good response to folic acid and antibiotics
|}


==Histology==
The histological changes of TS include: Flattening of the villi and small intestinal inflammation which are similar to an [[autoimmune disorder]] Coeliac disease (also known as ''[[coeliac sprue]]'').
{| class="wikitable"
!Diagnosis
!Villous morphology
!Findings in Lamina propria
!Involved portion of the GI tract
|-
|'''Tropical sprue'''
|Mild to moderate blunting of the villi with an increased number of Intraepithelial lymphocytes.
|Increased number of plasma cells and eosinophils.
|Ileum > Duodenum > Colon
|-
|'''Celiac sprue'''
|Variable, often there is a complete flattening of the villi. Always there is an increased number of Intraepithelial lymphocytes
|Plasma cells > Eosinophils > Neutrophils.
|Duodenum  > Ileum.
|}


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
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Latest revision as of 00:30, 30 July 2020

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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

Tropical sprue leads to villous atrophy which primarily affects the proximal and the distal gastrointestinal tract including the terminal ileum causing vitamin B12 and folate deficiencies. The pathogenesis of tropical sprue is unclear and multiple theories have been proposed. The pathogenesis of tropical sprue includes:[1]

Genetics

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

Associated Conditons

There are no associated conditions with tropical sprue.

Microscopic Pathology


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. 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.
  3. 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.
  4. 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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