Haemolytic uraemic syndrome: prognostic factors

Green, D. A.; Murphy, William G.; Uttley, W. S.

doi:10.1046/j.1365-2257.2000.00272.x

Cited by 16 publications

(13 citation statements)

References 17 publications

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Section: Discussionmentioning

confidence: 99%

“…Taylor et al [5] and other studies [7][8][9][10] generated a hypothesis that expression of specific blood group antigens, such as ABO-B and P1, are protective against HUS. However, several more-recent analyses [7][8][9][10] have suggested that there is no association between P1 expression and infection outcome. The present study provides stronger data against a protective effect of P1, because it represents an analysis of children infected by a diversity of E. coli O157:H7 strains and not of children infected by a single strain, as in outbreaks [7,9].…”

Section: Discussionmentioning

confidence: 99%

“…The theory that erythrocytes could express toxin-binding glycolipids is also supported by the observation that the erythrocytes of children with HUS have lower Gb3 levels than do erythrocytes of children with diarrhea secondary to Shiga toxinproducing E. coli (STEC) who do not develop HUS [6]. However, several subsequent epidemiological studies, mostly of children infected during outbreaks, have failed to associate the expression of the P1 blood group antigen with diminished risk for the development of HUS after infection with E. coli O157:H7 [7][8][9][10].…”

mentioning

confidence: 92%

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ABO and P1 Blood Group Antigen Expression andstxGenotype and Outcome of ChildhoodEscherichia coliO157:H7 Infections

et al. 2002

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P1 and ABO antigens and bacterial stx genotypes might influence the risk of developing hemolytic uremic syndrome (HUS) after Escherichia coli O157:H7 infections. We determined ABO status and P1 antigen expression in 130 infected and 17 uninfected children, and we determined the stx genotype of the infecting isolate. P1 expression was weakly and directly related to HUS risk (P=.04), but this risk did not extend to the group with the greatest P1 expression. P1 expression remained constant as HUS evolved. The ABO frequency was similar in all groups. These associations were not affected by the stx genotype. stx1(-)/stx2(+) E. coli O157:H7 strains were more commonly associated with HUS than were stx1(+)/stx2(+) strains (P=.21), and 1 child with HUS was infected with a rare stx1(+)/stx2(-) isolate. In the present study, ABO antigens and stx genotypes were not major determinants of the outcome of E. coli O157:H7 infections, and P1 expression did not protect against the development of HUS.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 92%

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ABO and P1 Blood Group Antigen Expression andstxGenotype and Outcome of ChildhoodEscherichia coliO157:H7 Infections

et al. 2002

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“…Furthermore, our fluid dynamic modeling reveals that the flow conditions in our system are comparable to those in the in vivo microvasculature. Finally, recent work characterizing blood flow in square and rectangular microchannels has shown that those geometries are suitable for blood rheology experiments (51).…”

Section: Discussionmentioning

confidence: 99%

In vitro modeling of the microvascular occlusion and thrombosis that occur in hematologic diseases using microfluidic technology

Tsai

Kita²,

Leach³

et al. 2012

J. Clin. Invest.

253

264

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In hematologic diseases, such as sickle cell disease (SCD) and hemolytic uremic syndrome (HUS), pathological biophysical interactions among blood cells, endothelial cells, and soluble factors lead to microvascular occlusion and thrombosis. Here, we report an in vitro "endothelialized" microfluidic microvasculature model that recapitulates and integrates this ensemble of pathophysiological processes. Under controlled flow conditions, the model enabled quantitative investigation of how biophysical alterations in hematologic disease collectively lead to microvascular occlusion and thrombosis. Using blood samples from patients with SCD, we investigated how the drug hydroxyurea quantitatively affects microvascular obstruction in SCD, an unresolved issue pivotal to understanding its clinical efficacy in such patients. In addition, we demonstrated that our microsystem can function as an in vitro model of HUS and showed that shear stress influences microvascular thrombosis/obstruction and the efficacy of the drug eptifibatide, which decreases platelet aggregation, in the context of HUS. These experiments establish the versatility and clinical relevance of our microvasculature-on-a-chip model as a biophysical assay of hematologic pathophysiology as well as a drug discovery platform.

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“…Furthermore, our fluid dynamic modeling reveal that the flow conditions in our system are comparable to that in the in vivo microvasculature. Finally, recent work characterizing blood flow in square and rectangular microchannels has shown that those geometries are suitable for blood rheology experiments 15 .…”

Section: Figurementioning

confidence: 99%

Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases

Myers

Sakurai

Tran

et al. 2012

JoVE

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Advances in microfabrication techniques have enabled the production of inexpensive and reproducible microfluidic systems for conducting biological and biochemical experiments at the micro-and nanoscales 1,2 . In addition, microfluidics have also been specifically used to quantitatively analyze hematologic and microvascular processes, because of their ability to easily control the dynamic fluidic environment and biological conditions [3][4][5][6] . As such, researchers have more recently used microfluidic systems to study blood cell deformability, blood cell aggregation, microvascular blood flow, and blood cell-endothelial cell interactions 6-13 .However, these microfluidic systems either did not include cultured endothelial cells or were larger than the sizescale relevant to microvascular pathologic processes. A microfluidic platform with cultured endothelial cells that accurately recapitulates the cellular, physical, and hemodynamic environment of the microcirculation is needed to further our understanding of the underlying biophysical pathophysiology of hematologic diseases that involve the microvasculature.Here, we report a method to create an "endothelialized" in vitro model of the microvasculature, using a simple, single mask microfabrication process in conjunction with standard endothelial cell culture techniques, to study pathologic biophysical microvascular interactions that occur in hematologic disease. This "microvasculature-on-a-chip" provides the researcher with a robust assay that tightly controls biological as well as biophysical conditions and is operated using a standard syringe pump and brightfield/fluorescence microscopy. Parameters such as microcirculatory hemodynamic conditions, endothelial cell type, blood cell type(s) and concentration(s), drug/inhibitory concentration etc., can all be easily controlled. As such, our microsystem provides a method to quantitatively investigate disease processes in which microvascular flow is impaired due to alterations in cell adhesion, aggregation, and deformability, a capability unavailable with existing assays.

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Haemolytic uraemic syndrome: prognostic factors

Cited by 16 publications

References 17 publications

ABO and P1 Blood Group Antigen Expression andstxGenotype and Outcome of ChildhoodEscherichia coliO157:H7 Infections

ABO and P1 Blood Group Antigen Expression andstxGenotype and Outcome of ChildhoodEscherichia coliO157:H7 Infections

In vitro modeling of the microvascular occlusion and thrombosis that occur in hematologic diseases using microfluidic technology

Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases

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