Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Piglet cryptosporidiosis is characterized by intestinal villous damage and malabsorption, and by reduced NaCl absorption in response to prostaglandins (PGs), which act directly on the epithelium and indirectly through enteric nerves. We hypothesized that phagocyte-derived reactive oxygen metabolite (ROM) production contributed to PG synthesis and altered transport in inflamed ileum. Ileal mucosa from control and infected piglets was analyzed for villous height, PGE2, catalase (an endogenous antioxidant), and malondialdehyde (MDA, a by-product of lipid peroxidation) from d 2-8 after infection. The response of control ileal mucosa to exogenous ROM and infected mucosa to antioxidant treatment was also studied in tissues mounted in Ussing chambers. Increased levels of MDA on d 2 preceded increased PGE2 on d 3-4, which correlated with the acute diarrheal phase; however the most severe villous atrophy (d 8) correlated with the highest levels of catalase and MDA but low levels of PGE2. Control mucosa responded to H2O2 with indomethacin- and tetrodotoxin-sensitive transient increases in short circuit current (Isc), which were accompanied by increased tissue production of 6-keto-PGF1a, the stable metabolite of PGI2; however, no increased PGE2 production was detectable. A stable analog of PGI2, carbacyclin, mimicked the transient Isc response to H2O2; however, several antioxidants failed to alter the abnormal Isc of infected tissue. These results suggest that there is evidence of increased ROM production in cryptosporidial infection and that intestinal PG synthesis and inhibited NaCl absorption may be mediated partially by ROM in this model. Additional, cooperative factors, such as PGE2 production, however, are likely needed to induce the alterations in ion transport seen in this infection.
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PMID:Reactive oxygen metabolites in piglet cryptosporidiosis. 909 54

Increased concentrations of reactive oxygen species (ROS) and depleted antioxidant defences have been implicated in a cycle of infection, malabsorption and malnutrition, leading to persistent diarrhea. In order to determine whether in non-malnourished children oxidative stress predisposes to the development of persistent diarrhea, infants with acute diarrhea (< 7 days) (n = 39) were compared to infants with persistent diarrhea (> 14 days) (n = 38). Lipid peroxidation was assessed by the TBARs assay and expressed as malondialdehyde equivalent content (nmol MDA/ml plasma), and levels of plasma antioxidants vitamin A and vitamin E were determined. In infants with acute and persistent diarrhea nutritional status, as assessed by weight/height and height-for-age, hemoglobin levels, serum albumin and immunoglobulin levels, did not differ between groups. Serum vitamin A and vitamin E levels did not differ in infants with acute or persistent diarrhea. TBARs, expressed as nmol MDA/ml plasma did not differ between infants with acute or persistent diarrhea and furthermore did not differ from levels in a healthy, similar age, control group. Non-malnourished infants with persistent diarrhea do not exhibit plasma antioxidant depletion or enhanced lipid peroxidation. In these infants, oxidative stress, as reflected in plasma, does not play a role in the pathogenesis of persistent diarrhea.
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PMID:Oxidative stress is not enhanced in non-malnourished infants with persistent diarrhea. 1169 27