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DOI: 10.1055/s-0029-1241873
© Georg Thieme Verlag KG Stuttgart · New York
Colonic Stricture and Fistula Following Haemolytic Uraemic Syndrome with Toxic Megacolon
Publikationsverlauf
Publikationsdatum:
06. November 2009 (online)

Introduction
Haemolytic uraemic syndrome (HUS) was first described by Gasser et al. in 1955, as the occurrence of haemolytic anaemia, thrombocytopaenia and acute renal failure [1]. It is the most common cause of acute renal failure in children in the UK [2]. Although the causes of HUS are diverse, the most frequent cause remains infection with verotoxin (also known as shiga-like toxin)-producing Escherichia coli, primarily E. coli 0157:H7. Shiga-like toxins (SLT) are thought to be internalised by eukaryotic cells via interaction with a glycoprotein surface receptor, galactotriosylceramide (Gb3), expressed optimally during the early S-phase of the cell cycle. The most rapidly dividing cells, such as intestinal epithelium and glomeruli, have the highest expressed concentration of Gb3 and are therefore worst affected by infection with SLT-producing E. coli.
It is estimated that around 50% of people infected with E. coli 0157:H7 develop bloody diarrhoea, whilst only 6–9% develop HUS [3]. Children who develop HUS secondary to E. coli 0157:H7 infection classically present with a prodrome of bloody diarrhoea, sometimes associated with nausea, vomiting and abdominal pain. It is during this early acute phase of HUS, where significant gastrointestinal (GI) problems may occur, that surgical involvement is most often required in the paediatric population.
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Correspondence
Charles KeysMBChB
Royal Hospital for Sick Children, Glasgow
Paediatric Surgery
G3 8SJ Dalnair Street
Glasgow
United Kingdom
Telefon: 0141/201/00 00
Fax: 0141/201/00 00
eMail: charleskeys@doctors.org.uk