Tropical sprue pathophysiology

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.

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]

• 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 in developing countries.
  • 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.
• 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 results in increased bacterial overgrowth which damages the enterocytes and crypt cells leading to intestinal villous atrophy and eventually 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 in 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.

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

There are no associated conditions with tropical sprue.

• 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

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