Platelet function disorders

Abstract

Platelet function defects comprise a large and heterogeneous group of bleeding disorders that range in severity from mild to severe. Patients may be asymptomatic; however, the majority who are diagnosed present with easy bruising and mucocutaneous bleeding, or with excessive haemorrhage following injury or surgery. As the complex internal biochemical and signal transduction pathways are further understood, and as structural analysis of platelets advances, more of the mechanisms leading to platelet function defects will be uncovered. Despite advances in the understanding of the etiology of these defects in function, treatment remains fairly rudimentary. For platelet function disorders associated with a defect in a plasma coagulation factor, such as vWD and afibrinogenemia, treatment consists of replacement of the deficient coagulation factor. Adjunctive therapies (such as antifibrinolytics, microfibular collagen, fibrin glue, etc.), DDAVP/Stimate, and platelet transfusions remain the mainstay of therapy available at this time. Corticosteroids may play a role in the management of some of these disorders and may lead to a shortening of bleeding time, especially in storage pool defects or release defects failing to respond to DDAVP/Stimate.

Anthocyanins from red cabbage extract — evidence of protective effects on blood platelets

“…Therefore, the purpose of our present study was to isolate, characterize and investigate, in vitro, the action and effects of ATH from red cabbage (Brassica oleracea) on blood platelet activation, and investigate the effects of exposing platelet proteins and lipids to the strong biological oxidative agents: peroxynitrite (ONOO -) and hydrogen peroxide (H 2 O 2 ). Excessive activation of blood platelets plays a crucial role in pathological development of CVDs [5], therefore the origin of anti-platelet properties found in dietary compounds of plants, fruits and vegetables are still explored in order to discover new supplements inhibiting platelet hyperactivity without any side effects. The participation of reactive oxygen species (ROS) in pathogenesis of CVDs is well known [6], and numerous studies support the concept that nutritional antioxidant status is inversely related to the occurrence of ROSmediated diseases [7].…”

Avaliação da relação entre produção plaquetária e expressão de proteínas do sistema apoptótico plaquetário em diferentes graus de plaquetopenia da Trombocitopenia Imune (PTI)

“…O período médio de permanência na circulação é em torno de 10 dias, quando então são removidas por células retículo endoteliais do baço e do fígado (Shapiro, 2000;Parise et al, 2001;Calverley;Maness et al, 2004;Grozovsky;Hoffmeister;Falet, 2010;Cine;Cuker;Semple, 2014 Yu;Cantor, 2012;Machlus;Thon;Italiano Jr, 2014).…”

“…Em condições de reduzidas força de cisalhamento a ligação inicial ao colágeno pode ser realizada por GPIa-IIa e GPVI (Shapiro, 2000;Jurk;Kehrel, 2005;Patel et al, 2005;Hartwig, 2006;Smyth, 2009;Scharf, 2012;Chang, 2012;Cimmino;Golino, 2013).…”

“…As plaquetas não ativadas possuem esta integrina na forma não ativa, portanto incapaz de se ligar a fibrinogênio, FvW, trombospondina, fibronectina e vitronectina. A ligação entre FvW e GPIb-IX-V no momento da adesão plaquetária, em condições de alta força de cisalhamento, promove uma alteração conformacional na molécula de GPIIbIIIa, que adquiri uma forma ativa, capaz de se ligar aos seus ligantes (Shapiro, 2000;Jurk;Kehrel, 2005;Patel et al, 2005;Hartwig, 2006;Smyth, 2009;Scharf, 2012;Chang, 2012).…”

“…Esses eventos ocorrem sem alteração da bioquímica celular que possa sugerir dano plaquetário (Shapiro, 2000;Baker;Brassar, 2011;Mattheij;Cosemans, 2012 A membrana plaquetária é fosfolipoprotéica, sendo que os fosfolipídios são importantes em várias funções da plaqueta, principalmente por servir de substrato para produção de tromboxano A 2 , um importante produto na ativação plaquetária e potente agonista plaquetário (Shapiro, 2000;Kamath et al, 2001).…”