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)

Plasma VIII:von Willebrand factor antigen (VIII:vWF) levels were elevated approximately two- to eightfold in seven patients (three adults and four children) during acute episodes of thrombocytopenia, renal failure, and hemolytic anemia (the hemolytic-uremic syndrome, HUS). In all seven patients, there was an alteration in plasma VIII:vWF patterns during these acute HUS episodes, so that the largest VIII:vWF forms were relatively decreased. Plasma VIII:vWF multimer patterns returned to normal, or nearly to normal, as platelet counts returned to preexisting levels, even in the patients whose recovery of renal function was incomplete and whose plasma VIII:vWF antigen level remained above normal. The sister of one of the HUS patients had a similar clinical prodrome (gastroenteritis) that was not followed by thrombocytopenia or renal failure and was not accompanied by an elevated level or abnormal forms of plasma VIII:vWF. These results suggest that an alteration in VIII:vWF metabolism, distribution, or interaction with platelets is associated with acute HUS episodes. In contrast to patients with chronic relapsing thrombotic thrombocytopenic purpura, none of the HUS patients (either during or after the acute HUS episodes) had a defect in the conversion of unusually large VIII:vWF multimers derived from endothelial cells to the VIII:vWF forms found in normal plasma.
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PMID:Abnormal VIII: von Willebrand factor patterns in the plasma of patients with the hemolytic-uremic syndrome. 643 74

We examined the possibility of an association between the bacterial genotype of Escherichia coli O157:H7 and the likelihood of progression to neurological complications in childhood gastroenteritis-associated haemolytic uraemic syndrome (D+HUS). Bacterial stool isolates were available from 51 patients with HUS; 11 of these patients suffered a neurological complication. Bacteria were assessed for plasmid content, verotoxin (Shiga-like toxin) profile, verotoxin 2 subtype, and presence of the eaeA (effacement and attachment) marker. No association of bacterial genotype with central nervous system (CNS) manifestations was observed. Whilst the cause of CNS manifestations may be multifactorial, there is no evidence at present to implicate specific bacterial traits.
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PMID:Bacterial genotype and neurological complications of Escherichia coli O157:H7-associated haemolytic uraemic syndrome. 964 46

The objective of this study was to identify parameters indicating a risk for developing typical haemolytic uremic syndrome (D+HUS) during the prodromal phase of diarrhea caused by enterohaemorrhagic Escherichia coli (EHEC). Forty-eight children were studied prospectively with regard to inflammatory serum factors on admission to hospital. Ten patients developed D+HUS (group I), 15 suffered from viral-gastroenteritis (group IIa) and 23 from other types of bacterial gastroenteritis (group IIb). Mean levels of IL-8 tended to be elevated in group I compared to groups IIa and IIb. Neopterin and IL-10 levels particularly were significantly decreased in HUS in comparison to both gastroenteritis groups. Low IL-10 levels indicate a substantial disregulation of the immune response in HUS, as IL-10 downregulates the pro-inflammatory response and suppresses pro-coagulant activity in experimental endotoxemia. Our results suggest low neopterin, high IL-8 and especially low IL-10 levels are indicators of a high risk for developing HUS.
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PMID:Inflammatory and immunological parameters in children with haemolytic uremic syndrome (HUS) and gastroenteritis-pathophysiological and diagnostic clues. 1084 73

Every year in France, about 100 children, most of them less than 3 years old, have typical diarrhea-associated HUS (D + HUS). Evidence of exposure to verotoxin producing E. coli (VTEC), mostly the O157: H7 serotype, is demonstrated in about 85% of cases. A prodromal illness of acute gastroenteritis with diarrhea, often bloody, precedes the HUS by 1 to 15 days. HUS onset is sudden, with the typical association of hemolytic anemia with fragmented red blood cells, thrombocytopenia and acute renal insufficiency. Involvement of other organs than the kidneys may occur, such as severe hemorrhagic colitis with rectal prolapse, bowel wall necrosis or secondary stenosis, acute pancreatitis, central nervous system involvement which determines the vital outcome. Early accurate supportive treatment allows a current mortality rate below 5%, with most deaths due to central nervous system involvement. Five to 10% of children develop end stage renal disease, rarely directly, more often after having recovered some renal function with chronic renal insufficiency during a few years. After 15 or more years follow-up, at least one third of patients have some degree of proteinuria and/or hypertension, and eventually chronic or end stage renal failure. Predictive features of poor renal outcome at the acute phase are severe gastrointestinal involvement, severe CNS involvement, polyncleosis over 20,000/mm3, and duration of initial anuria longer than one week. The role of VTEC in D + HUS makes the disease a public health problem. Preventive measures are essential.
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PMID:[Post-diarrhea hemolytic-uremic syndrome: clinical aspects]. 1158 27

Verotoxin-producing Escherichia coli (VTEC) are nowadays among the most important emerging group of food-borne pathogens (VTEC strains cause gastroenteritis that can be complicated by the hemorrhagic colitis or hemolytic uremic syndrome, HUS). Escherichia coli 026 producing verotoxin 2 was isolated and its identity confirmed by examination of phenotype and genotype; the strain was first described in Slovakia in association with the development of HUS in a 4-year-old girl.
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PMID:Hemolytic uremic syndrome caused by verotoxin-producing Escherichia coli O26. Case report. 1611 Sep 10

Diarrhea in children is often caused by enteropathogen infections that might benefit from early empirical antibiotic therapy. However, when the definition of the pathogen requires sophisticated laboratory studies, the etiology of enteritis is not known early in illness. Empirical therapy may be dangerous if the child is infected with a Shiga toxin-producing Escherichia coli (STEC) strain because antimicrobials may increase Shiga toxin (Stx) release, resulting in increased risk of microangiopathic hemolytic anemia with acute renal failure (hemolytic-uremic syndrome [HUS]) and death. There is a need for antimicrobials that would be effective against multiple bacterial enteropathogens yet not induce Stx release or increase the risk of HUS. Rifaximin has been evaluated in adults for treatment of bacterial enteritis and has a good record for safety and efficacy, but it has not been evaluated extensively in children with gastroenteritis. We therefore evaluated rifaximin's potential for phage induction, drug-induced bacteriolysis, and toxin release in 57 STEC strains (26 O157 and 31 non-O157 strains). Growth in ciprofloxacin, a known Stx phage inducer, caused bacteriolysis and release of toxin in 25/26 (96%) O157 strains and 15/31 (48%) non-O157 strains. In contrast, rifaximin did not induce phage replication or lysis in any strain. Toxin release in the presence of rifaximin was not different from release in the absence of antibiotic. Rifaximin, unlike many antibiotics used to treat pediatric gastroenteritis, does not induce phage-mediated bacteriolysis and Stx release.
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PMID:Rifaximin does not induce toxin production or phage-mediated lysis of Shiga toxin-producing Escherichia coli. 1752 59