dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorSilveira, Margarida Maria
dc.creatorDa Fonseca, Luiz Marcos
dc.date2014-05-27T11:20:35Z
dc.date2016-10-25T18:18:18Z
dc.date2014-05-27T11:20:35Z
dc.date2016-10-25T18:18:18Z
dc.date2002-12-01
dc.date.accessioned2017-04-06T01:04:30Z
dc.date.available2017-04-06T01:04:30Z
dc.identifierRevista de Ciencias Farmaceuticas, v. 23, n. 1, p. 25-46, 2002.
dc.identifier0101-3793
dc.identifierhttp://hdl.handle.net/11449/67137
dc.identifierhttp://acervodigital.unesp.br/handle/11449/67137
dc.identifier2-s2.0-0037598641
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/888622
dc.descriptionHemolytic anemia and vasoocclusion are the cardinal clinical features of sickle cell anemia. Vasoocclusion is a complex process involving not only the polymerization of deoxygenated sickle hemoglobin tetramers, but also interactions between sickle erythrocytes, vascular endothelium, platelets, leukocytes, and plasma proteins. The increased adherence of sickle erythrocytes to endothelium has been implicated as an early step in vasoocclusion. Other researchers have focused on leukocytes and platelets which might also contribute to disturbed blood flow. Microvascular occlusion results in acute painful crises, whereas macrovascular occlusion seems to be the cause of organ failure. The anemia results from the markedly shortened circulatory survival of sickle erythrocytes, together with a limited erythropoietic response. The erythropoiesis increases intensively, but it is not enough to balance the increased rate of erythrocytes destruction to maintain normal levels of total erythrocytes and hemoglobin concentrations; mainly by the low oxygen affinity of hemoglobin S and increased 2,3-Diphosphoglycerate. It is very difficult to separate processes leading to anemia or to vasoocclusion. Understanding the involvement of multiple blood componentes in vasoocclusion may elucidate the clinical manifestations and complications of sickle cell anemia, and may give new insights into the preventive and curative therapy.
dc.languagepor
dc.relationRevista de Ciencias Farmaceuticas
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectLeukocytes
dc.subjectPlatelets
dc.subjectSickle cell anemia
dc.subjectVasoocclusion
dc.subject2,3 diphosphoglyceric acid
dc.subjecthemoglobin S
dc.subjecttetramer
dc.subjectblood component therapy
dc.subjectblood flow velocity
dc.subjectblood oxygenation
dc.subjectblood vessel occlusion
dc.subjectcell adhesion
dc.subjectcell damage
dc.subjectcell interaction
dc.subjectcell survival
dc.subjectcirculation time
dc.subjectclinical feature
dc.subjectconcentration response
dc.subjectendothelium cell
dc.subjecterythrocyte
dc.subjecterythrocyte adhesiveness
dc.subjecterythrocyte disorder
dc.subjecterythrocyte lifespan
dc.subjecterythropoiesis
dc.subjecthemoglobin analysis
dc.subjecthemolytic anemia
dc.subjecthuman
dc.subjectleukocyte
dc.subjectmultiple organ failure
dc.subjectoxygen affinity
dc.subjectpain
dc.subjectpathophysiology
dc.subjectpolymerization
dc.subjectprocess monitoring
dc.subjectprotein blood level
dc.subjectprotein structure
dc.subjectreview
dc.subjectsickle cell
dc.subjectsickle cell anemia
dc.subjectthrombocyte
dc.subjectvascular endothelium
dc.subjectvein occlusion
dc.titleA complexa fisiopatologia dos episódios vasooclusivos na anemia falciforme
dc.typeOtro


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