Tropical sprue pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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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.
Pathophysiology
Infection
- Accompanied by Fever at the onset of the disease
- Increase in the gram-negative bacterial toxins and bacterial colony counts
- Precipitated by a history of acute gastroenteritis.[1]
- There is an increase in the inflammatory cells in the lamina propria with variable edema
- Good clinical response to Tetracycline with restoration of the normal histology.
Small intestinal bacterial colonization.
Prolonged orocecal transit time.
Clinical improvement following antibacterial treatment was known to normalize the OCTT.[2]
- Enterocyte damage: Small intestinal mucosal damage leads to decreased serum folate concentration, which inturn leads to a reduction in sodium-ATPase levels and number of enterocytes.
- Gut-Hormone concentrations: High plasma enteroglucagon concentration leads to delayed small intestinal transit.[3]
Bacterial overgrowth leading to toxin production.[4]
| Differences in presentation between Indian and Caribbean TS | |
|---|---|
| Indian | Caribbean |
| No association with small bowel colonization | Associated with small bowel colonization |
| Small bowel transit time is not prolonged | Prolonged small bowel transit time |
| Higher mortality | Lower mortality |
| Spontaneous remissions common | Spontaneous remissions rare |
| Fever present in 25% of cases | Fever- rare |
| 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).
| 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
- ↑ McCarroll MG, Riddle MS, Gutierrez RL, Porter CK (2015). "Infectious Gastroenteritis as a Risk Factor for Tropical Sprue and Malabsorption: A Case-Control Study". Dig Dis Sci. 60 (11): 3379–85. doi:10.1007/s10620-015-3768-8. PMID 26115751.
- ↑ Ghoshal, Uday C; Ghoshal, Ujjala; Ayyagari, Archana; Ranjan, Piyush; Krishnani, Narendra; Misra, Asha; Aggarwal, Rakesh; Naik, Sita; Naik, Subhash R (2003). "Tropical sprue is associated with contamination of small bowel with aerobic bacteria and reversible prolongation of orocecal transit time". Journal of Gastroenterology and Hepatology. 18 (5): 540–547. doi:10.1046/j.1440-1746.2003.03006.x. ISSN 0815-9319.
- ↑ Cook, G.C. (1984). "AETIOLOGY AND PATHOGENESIS OF POSTINFECTIVE TROPICAL MALABSORPTION (TROPICAL SPRUE)". The Lancet. 323 (8379): 721–723. doi:10.1016/S0140-6736(84)92231-1. ISSN 0140-6736.
- ↑ Walker, Marjorie M (2003). "What is tropical sprue?". Journal of Gastroenterology and Hepatology. 18 (8): 887–890. doi:10.1046/j.1440-1746.2003.03127.x. ISSN 0815-9319.