Aetiology and pathogenesis of postinfective tropical malabsorption (tropical sprue).
Postinfective tropical malabsorption (TM; tropical sprue) starts with an acute intestinal infection (bacterial, viral, or parasitic) which can affect predominantly the small or the large intestine. Miscellaneous invasive pathogens cause subsequent enterocyte damage affecting the entire small intestine and, to a lesser extent, the colon. Enteroglucagon, a tropic hormone, is then liberated and reaches a high plasma concentration. Small-intestinal stasis results. Further bacterial colonisation (in the lumen and also at the enterocyte surface) is encouraged. Continuing enterocyte damage is worsened by coexistent folate depletion, which is initiated at the onset of disease; body stores of folate reach a low concentration by 3 or 4 months. The cycle continues until the bacterial overgrowth is eliminated with an antibiotic (eg, tetracycline), or mucosal integrity recovers (hastened by oral folic-acid supplements), or both.
D002908:Chronic Disease; D003106:Colon / Q000382:microbiology / Q000503:physiopathology; D004756:Enterobacteriaceae Infections / Q000150:complications*; D005494:Folic Acid Deficiency / Q000150:complications; D005768:Gastrointestinal Hormones / Q000097:blood; D005769:Gastrointestinal Motility; D006801:Humans; D007413:Intestinal Mucosa / Q000382:microbiology; D007421:Intestine, Small / Q000382:microbiology; D008954:Models, Biological; D013182:Sprue, Tropical / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology
D005768:Gastrointestinal Hormones