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Soluble plasma VE-cadherin concentrations are elevated in patients with STEC infection and haemolytic uraemic syndrome: a case–control study

OBJECTIVES: To investigate whether the adherens junction protein vascular endothelial cadherin (VE-cadherin) is released during Shiga toxin 2 producing Escherichia coli (STEC) infection with haemolytic uraemic syndrome (HUS) and thus could be used to assist diagnosis. DESIGN: Using data from the lar...

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Detalles Bibliográficos
Autores principales: Doulgere, Julia, Otto, Benjamin, Nassour, Maher, Wolters-Eisfeld, Gerrit, Rohde, Holger, Magnus, Tim, Wagener, Christoph, Streichert, Thomas
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BMJ Publishing Group 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4360836/
https://www.ncbi.nlm.nih.gov/pubmed/25757942
http://dx.doi.org/10.1136/bmjopen-2014-005659
Descripción
Sumario:OBJECTIVES: To investigate whether the adherens junction protein vascular endothelial cadherin (VE-cadherin) is released during Shiga toxin 2 producing Escherichia coli (STEC) infection with haemolytic uraemic syndrome (HUS) and thus could be used to assist diagnosis. DESIGN: Using data from the large 2011 STEC outbreak in northern Europe, we determined VE-cadherin plasma concentrations in 356 patients distributed over three patient cohorts: patients with STEC infection accompanied by HUS (STEC-HUS), STEC patients without HUS (STEC) and control patients with diarrhoea but without STEC infection. We then looked for associations between VE-cadherin concentrations and disease severity defined by changes in lactate dehydrogenase, haemoglobin, creatinine, platelet count, haptoglobin and neurological symptoms. SETTING: This study was conducted at the University Medical Center Hamburg-Eppendorf, Germany. PARTICIPANTS: 79 STEC-HUS patients, 77 STEC patients and 200 control patients were enrolled in the study. RESULTS: We analysed 864 specimens (207 STEC, 449 STEC-HUS and 208 controls) in total. At admission, VE-cadherin concentration tended to be lower in STEC-HUS patients compared to other patients. However, HUS patients later showed an increase in VE-cadherin concentrations with prolonged elevation beyond remission. This pattern clearly differs from that observed in non-HUS patients. CONCLUSIONS: VE-cadherin concentrations are elevated in STEC-HUS patients and might be a biomarker reflecting endothelial damage in patients with HUS.