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Pathogenesis of Shiga toxin-associated hemolytic uremic syndrome

Proulx, Francois; Seidman, Ernest G and Karpman, Diana LU (2001) In Pediatric Research 50(2). p.163-171
Abstract
The aim of this review is to examine recent advances in experimental and clinical research relevant to the pathogenesis of diarrhea-associated hemolytic uremic syndrome with special reference to histopathologic findings, virulence factors of Shiga toxin-producing Escherichia coli, the host response, and the prothrombotic state. Despite significant advances during the past decade, the exact mechanism by which Shiga toxin-producing E. coli leads to hemolytic uremic syndrome remains unclear. Factors such as Shiga toxin, lipopolysaccharide, the adhesins intimin and E. coli-secreted proteins A, B, and D, the 60-MD plasmid, and enterohemolysin likely contribute to the pathogenesis. Data on the inflammatory response of the host, including... (More)
The aim of this review is to examine recent advances in experimental and clinical research relevant to the pathogenesis of diarrhea-associated hemolytic uremic syndrome with special reference to histopathologic findings, virulence factors of Shiga toxin-producing Escherichia coli, the host response, and the prothrombotic state. Despite significant advances during the past decade, the exact mechanism by which Shiga toxin-producing E. coli leads to hemolytic uremic syndrome remains unclear. Factors such as Shiga toxin, lipopolysaccharide, the adhesins intimin and E. coli-secreted proteins A, B, and D, the 60-MD plasmid, and enterohemolysin likely contribute to the pathogenesis. Data on the inflammatory response of the host, including leukocytes and inflammatory mediators, are updated. The pathogenesis of the prothrombotic state leading to thrombocytopenia secondary to endothelial cell damage and platelet activation is also discussed. A hypothetical sequence of events from ingestion of the bacteria to the development of full-blown hemolytic uremic syndrome is proposed. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Pediatric Research
volume
50
issue
2
pages
163 - 171
publisher
International Pediatric Foundation Inc.
external identifiers
  • pmid:11477199
  • scopus:0034924948
ISSN
1530-0447
language
English
LU publication?
yes
id
ade1de85-2e87-4cd9-aba1-3b38576952b6 (old id 1119894)
date added to LUP
2008-07-10 10:34:31
date last changed
2018-07-01 03:33:09
@article{ade1de85-2e87-4cd9-aba1-3b38576952b6,
  abstract     = {The aim of this review is to examine recent advances in experimental and clinical research relevant to the pathogenesis of diarrhea-associated hemolytic uremic syndrome with special reference to histopathologic findings, virulence factors of Shiga toxin-producing Escherichia coli, the host response, and the prothrombotic state. Despite significant advances during the past decade, the exact mechanism by which Shiga toxin-producing E. coli leads to hemolytic uremic syndrome remains unclear. Factors such as Shiga toxin, lipopolysaccharide, the adhesins intimin and E. coli-secreted proteins A, B, and D, the 60-MD plasmid, and enterohemolysin likely contribute to the pathogenesis. Data on the inflammatory response of the host, including leukocytes and inflammatory mediators, are updated. The pathogenesis of the prothrombotic state leading to thrombocytopenia secondary to endothelial cell damage and platelet activation is also discussed. A hypothetical sequence of events from ingestion of the bacteria to the development of full-blown hemolytic uremic syndrome is proposed.},
  author       = {Proulx, Francois and Seidman, Ernest G and Karpman, Diana},
  issn         = {1530-0447},
  language     = {eng},
  number       = {2},
  pages        = {163--171},
  publisher    = {International Pediatric Foundation Inc.},
  series       = {Pediatric Research},
  title        = {Pathogenesis of Shiga toxin-associated hemolytic uremic syndrome},
  volume       = {50},
  year         = {2001},
}