Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In acute diarrhea of infancy we distinguish between infectious and noninfectious causes. In the latter we know some autosomal recessive disorders, e.g. the glucose-galactose-malabsorption, the lactase deficiency as well as the sucrase-isomaltase deficiency. In addition the most frequent acquired disorders like the cow's milk protein intolerance and celiac disease contribute also to the group of noninfectious causes of diarrhea. Here the most effective therapy consists of the elimination of the toxic agent from the diet. In infectious diarrhea we find most frequently rotavirus as the agent but also yersinia, campylobacter fetus, salmonella, shigella, E. coli, lamblia giardia and entameba hystolytica. Generally a conservative treatment with a dietetic regimen is preferred. Only in severe cases with yersinia and campylobacter infection the addition of antibiotic drugs is necessary. Giardia lamblia and amebiasis however have to be treated with metronidazol. As the absorption of glucose is coupled with that of sodium within the small intestine in acute gastroenteritis we find a combined disturbance between salt and carbohydrate absorption. A solution containing glucose and salt is recommended therefore for oral rehydration. The amount administered within the first 24 hours should be between 150-250 ml/kg per day. So called "antidiarrhoic drugs" are questionably effective.
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PMID:[Useful and superfluous measures in the treatment of infant diarrhea]. 717 37

Rotavirus infection is the most common cause of severe infantile gastroenteritis worldwide. These viruses infect mature enterocytes of the small intestine and cause structural and functional damage, including a reduction in disaccharidase activity. It was previously hypothesized that reduced disaccharidase activity resulted from the destruction of rotavirus-infected enterocytes at the villus tips. However, this pathophysiological model cannot explain situations in which low disaccharidase activity is observed when rotavirus-infected intestine exhibits few, if any, histopathologic changes. In a previous study, we demonstrated that the simian rotavirus strain RRV replicated in and was released from human enterocyte-like Caco-2 cells without cell destruction (N. Jourdan, M. Maurice, D. Delautier, A. M. Quero, A. L. Servin, and G. Trugnan, J. Virol. 71:8268-8278, 1997). In the present study, to reinvestigate disaccharidase expression during rotavirus infection, we studied sucrase-isomaltase (SI) in RRV-infected Caco-2 cells. We showed that SI activity and apical expression were specifically and selectively decreased by RRV infection without apparent cell destruction. Using pulse-chase experiments and cell surface biotinylation, we demonstrated that RRV infection did not affect SI biosynthesis, maturation, or stability but induced the blockade of SI transport to the brush border. Using confocal laser scanning microscopy, we showed that RRV infection induces important alterations of the cytoskeleton that correlate with decreased SI apical surface expression. These results lead us to propose an alternate model to explain the pathophysiology associated with rotavirus infection.
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PMID:Rotavirus infection reduces sucrase-isomaltase expression in human intestinal epithelial cells by perturbing protein targeting and organization of microvillar cytoskeleton. 969 17