Hemolytic uremic syndrome in children: Platelet aggregation and membrane glycoproteins

Purpose: Several mechanisms have been proposed to explain the fibrin- platelet thrombosis at the microcirculation level in the different clinical conditions of hemolytic uremic syndrome (HUS). The relationships between platelet structure and function during the first 4 weeks of evolution of the dise...

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Autores principales:	Sassetti, Beatriz, Kordich, Lucía Clelia
Publicado:	1999
Materias:	Children Glycoproteins GPIIbIIIa HUS Platelets Uremic hemolytic syndrome fibrinogen receptor glycoprotein glycoprotein Ib glycoprotein IIb membrane protein very late activation antigen 2 article clinical article controlled study female hemolytic uremic syndrome human human cell human tissue infant male molecular dynamics pathophysiology preschool child priority journal protein expression structure activity relation thrombocyte aggregation thrombocyte count Bacterial Toxins Blood Coagulation Factors Blood Proteins Child, Preschool Diarrhea, Infantile Dysentery, Bacillary Endothelium, Vascular Escherichia coli Infections Female Hemolytic-Uremic Syndrome Humans Infant Male Microcirculation Platelet Aggregation Platelet Count Platelet Membrane Glycoproteins Shiga-Like Toxin I Spleen Thrombophilia Trihexosylceramides
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10774114_v21_n2_p123_Sassetti http://hdl.handle.net/20.500.12110/paper_10774114_v21_n2_p123_Sassetti
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

id	paper:paper_10774114_v21_n2_p123_Sassetti
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spelling	paper:paper_10774114_v21_n2_p123_Sassetti2023-06-08T16:05:28Z Hemolytic uremic syndrome in children: Platelet aggregation and membrane glycoproteins Sassetti, Beatriz Kordich, Lucía Clelia Children Glycoproteins GPIIbIIIa HUS Platelets Uremic hemolytic syndrome fibrinogen receptor glycoprotein glycoprotein Ib glycoprotein IIb membrane protein very late activation antigen 2 article clinical article controlled study female hemolytic uremic syndrome human human cell human tissue infant male molecular dynamics pathophysiology preschool child priority journal protein expression structure activity relation thrombocyte aggregation thrombocyte count Bacterial Toxins Blood Coagulation Factors Blood Proteins Child, Preschool Diarrhea, Infantile Dysentery, Bacillary Endothelium, Vascular Escherichia coli Infections Female Hemolytic-Uremic Syndrome Humans Infant Male Microcirculation Platelet Aggregation Platelet Count Platelet Membrane Glycoproteins Shiga-Like Toxin I Spleen Thrombophilia Trihexosylceramides Purpose: Several mechanisms have been proposed to explain the fibrin- platelet thrombosis at the microcirculation level in the different clinical conditions of hemolytic uremic syndrome (HUS). The relationships between platelet structure and function during the first 4 weeks of evolution of the disease were studied to understand the mechanism of platelet alteration. Patients and Methods: Coagulation parameters, platelet counts, and aggregation were studied in 49 children, and membrane glycoproteins (GPs) in 20 of the 49 children (mean age, 17 months) with HUS (Group 2) were studied during the first 4 weeks of evolution of the disease. Results: No disseminated intravascular coagulation was found in patients with recurrent or persistent thrombocytopenia. Platelet aggregation was sequentially performed during the first weeks of evolution. All patients had a functional decrease in the acute period of HUS. Platelet GPs GPIb, GPIIbIIIa, GPIIb, and GPIIIa were evaluated. GPIIbIIIa complex presented low level and never reached normal values during the first 4 weeks of disease. Conclusions: Platelet alterations are probably caused by multiple mechanisms: 'exhausted' platelets, structural membrane alterations caused by arginine-glycine- aspartic peptide blockade, or diminished or nonfunctional membrane GPIb and GPIIbIIIa complexes. Fil:Sassetti, B. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Kordich, L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 1999 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10774114_v21_n2_p123_Sassetti http://hdl.handle.net/20.500.12110/paper_10774114_v21_n2_p123_Sassetti
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	Children Glycoproteins GPIIbIIIa HUS Platelets Uremic hemolytic syndrome fibrinogen receptor glycoprotein glycoprotein Ib glycoprotein IIb membrane protein very late activation antigen 2 article clinical article controlled study female hemolytic uremic syndrome human human cell human tissue infant male molecular dynamics pathophysiology preschool child priority journal protein expression structure activity relation thrombocyte aggregation thrombocyte count Bacterial Toxins Blood Coagulation Factors Blood Proteins Child, Preschool Diarrhea, Infantile Dysentery, Bacillary Endothelium, Vascular Escherichia coli Infections Female Hemolytic-Uremic Syndrome Humans Infant Male Microcirculation Platelet Aggregation Platelet Count Platelet Membrane Glycoproteins Shiga-Like Toxin I Spleen Thrombophilia Trihexosylceramides
spellingShingle	Children Glycoproteins GPIIbIIIa HUS Platelets Uremic hemolytic syndrome fibrinogen receptor glycoprotein glycoprotein Ib glycoprotein IIb membrane protein very late activation antigen 2 article clinical article controlled study female hemolytic uremic syndrome human human cell human tissue infant male molecular dynamics pathophysiology preschool child priority journal protein expression structure activity relation thrombocyte aggregation thrombocyte count Bacterial Toxins Blood Coagulation Factors Blood Proteins Child, Preschool Diarrhea, Infantile Dysentery, Bacillary Endothelium, Vascular Escherichia coli Infections Female Hemolytic-Uremic Syndrome Humans Infant Male Microcirculation Platelet Aggregation Platelet Count Platelet Membrane Glycoproteins Shiga-Like Toxin I Spleen Thrombophilia Trihexosylceramides Sassetti, Beatriz Kordich, Lucía Clelia Hemolytic uremic syndrome in children: Platelet aggregation and membrane glycoproteins
topic_facet	Children Glycoproteins GPIIbIIIa HUS Platelets Uremic hemolytic syndrome fibrinogen receptor glycoprotein glycoprotein Ib glycoprotein IIb membrane protein very late activation antigen 2 article clinical article controlled study female hemolytic uremic syndrome human human cell human tissue infant male molecular dynamics pathophysiology preschool child priority journal protein expression structure activity relation thrombocyte aggregation thrombocyte count Bacterial Toxins Blood Coagulation Factors Blood Proteins Child, Preschool Diarrhea, Infantile Dysentery, Bacillary Endothelium, Vascular Escherichia coli Infections Female Hemolytic-Uremic Syndrome Humans Infant Male Microcirculation Platelet Aggregation Platelet Count Platelet Membrane Glycoproteins Shiga-Like Toxin I Spleen Thrombophilia Trihexosylceramides
description	Purpose: Several mechanisms have been proposed to explain the fibrin- platelet thrombosis at the microcirculation level in the different clinical conditions of hemolytic uremic syndrome (HUS). The relationships between platelet structure and function during the first 4 weeks of evolution of the disease were studied to understand the mechanism of platelet alteration. Patients and Methods: Coagulation parameters, platelet counts, and aggregation were studied in 49 children, and membrane glycoproteins (GPs) in 20 of the 49 children (mean age, 17 months) with HUS (Group 2) were studied during the first 4 weeks of evolution of the disease. Results: No disseminated intravascular coagulation was found in patients with recurrent or persistent thrombocytopenia. Platelet aggregation was sequentially performed during the first weeks of evolution. All patients had a functional decrease in the acute period of HUS. Platelet GPs GPIb, GPIIbIIIa, GPIIb, and GPIIIa were evaluated. GPIIbIIIa complex presented low level and never reached normal values during the first 4 weeks of disease. Conclusions: Platelet alterations are probably caused by multiple mechanisms: 'exhausted' platelets, structural membrane alterations caused by arginine-glycine- aspartic peptide blockade, or diminished or nonfunctional membrane GPIb and GPIIbIIIa complexes.
author	Sassetti, Beatriz Kordich, Lucía Clelia
author_facet	Sassetti, Beatriz Kordich, Lucía Clelia
author_sort	Sassetti, Beatriz
title	Hemolytic uremic syndrome in children: Platelet aggregation and membrane glycoproteins
title_short	Hemolytic uremic syndrome in children: Platelet aggregation and membrane glycoproteins
title_full	Hemolytic uremic syndrome in children: Platelet aggregation and membrane glycoproteins
title_fullStr	Hemolytic uremic syndrome in children: Platelet aggregation and membrane glycoproteins
title_full_unstemmed	Hemolytic uremic syndrome in children: Platelet aggregation and membrane glycoproteins
title_sort	hemolytic uremic syndrome in children: platelet aggregation and membrane glycoproteins
publishDate	1999
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10774114_v21_n2_p123_Sassetti http://hdl.handle.net/20.500.12110/paper_10774114_v21_n2_p123_Sassetti
work_keys_str_mv	AT sassettibeatriz hemolyticuremicsyndromeinchildrenplateletaggregationandmembraneglycoproteins AT kordichluciaclelia hemolyticuremicsyndromeinchildrenplateletaggregationandmembraneglycoproteins
_version_	1768545239826432000

Hemolytic uremic syndrome in children: Platelet aggregation and membrane glycoproteins

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