Browsing by Author "Morales, M"

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    Platelet membrane glycoprotein polymorphisms do not influence the clinical expressivity of von Willebrand disease type I
    (SCHATTAUER GMBH-VERLAG MEDIZIN NATURWISSENSCHAFTEN, 2003) Pereira, J; Quiroga, T; Pereira, ME; Morales, M; Goycoolea, M; Hidalgo, P; Prieto, C; Mezzano, D
    Von Willebrand disease (VWD) is characterized by a significant variation in bleeding symptoms among patients with similar laboratory profiles and equivalent plasma levels of von Willebrand factor (VWF) activities. Considering the recent suggestion that platelet membrane glycoprotein polymorphisms (PltGPs) may play a role as modulators of thromboembolic or haemorrhagic diseases, we investigated the role of different PltGPs and GPVI content in the clinical expression of patients with VWD type 1. The diagnosis of VWD (n = 76) was based on laboratory findings (VWF:Ag, VWF:RCo, VWF:CB, FVIII:C, and multimer analysis), family and personal history of bleeding. All patients were interviewed using a standardized questionnaire, and classified into two categories: bleeders (unequivocal bleeding tendency, n = 53) and non bleeders (absence of bleeding symptoms, n = 23). PltGPs, HPA-1, 2 and 5 and C807T of GPla were determined by fluorophore-labelled hybridization probes on a LightCycler(TM). GPVI content was measured by western blotting.
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    Template bleeding time and PFA-100® have low sensitivity to screen patients with hereditary mucocutaneous hemorrhages
    (2004) Quiroga, T; Goycoolea, M; Muñoz, B; Morales, M; Aranda, E; Panes, O; Pereira, J; Mezzano, D
    Objectives and patients: We compared the template bleeding time (BT) and closure time (CT) in the PFA-100(R) as screening tests in 148 consecutive patients With unequivocal mucocutaneous bleeding and positive family history. Exclusion criteria: drug intake, concomitant diseases including minor infections, low platelet Count, diseases of secondary hemostasis. Results: Type I von Willebrand disease (VWD-1) was diagnosed in 26 patients, primary platelet secretion defect (PSD) in 33, VWD-1 + PSD in nine, whereas 80 patients did not comply with the criteria for known hemostatic disorders (UD, unknown diagnosis). BT and CT were prolonged in 35.8% and 29.7% of all the patients, respectively (P = 0.23). Sensitivity increased to 48% if an abnormality of BT and/or CT was considered. Same comparisons for BT and CT in each diagnostic category were. respectively: 42 vs. 61.5% in VWD-1 (P = 0.18), 42 vs. 24% in platelet secretion defects (P = 0.11), 67 vs. 89% in VWD-1 + PSD (P = 0.50), and 27.5 vs. 15% in UD (P = 0.06). Conclusion: Both tests were relatively insensitive and not significantly different in detecting incoming patients with mucocutancous hemorrhages. In patients with VWD-1 the PFA-100(R) performed slightly better, whereas the opposite occurred in those patients with platelet secretion defects. In the UD group, both tests lost sensitivity, but the BT detected 1.8 times more patients than the PFA-100(R). Given the large proportion of undiagnosed bleeders and the overall low sensitivity of these tests, clinical decisions still rely on the medical history and etiological diagnosis of the bleeding disorder.
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    Thrombin generation in platelet-poor plasma is normal in patients with hereditary mucoputaneous haemorrhages
    (2003) Quiroga, T; Goycoolea, M; Giesen, PLA; Morales, M; Muñoz, B; Aranda, E; Rodríguez, S; Panes, O; Martínez, C; Pereira, J; Mezzano, D
    Mild hereditary bleeding disorders presenting with mucocutaneous haemorrhages are usually difficult to diagnose. We measured thrombin generation in platelet-poor plasma (TG-PPP) in 206 patients with a clinically unequivocal bleeding tendency: 45 with von Willebrand disease (vWD), 49 with platelet aggregation/secretion defects (PASD), 10 with a combination of both and 102 who did not fit the diagnostic criteria for any known haemostatic disorder. TG-PPP was not significantly different from controls in all patient groups, indicating that an abnormality in the plasmatic clotting system is unlikely to contribute to the bleeding in patients with type 1 vWD and PASD. In patients with undiagnosed mild hereditary bleeding disorders, there must be other mechanisms which explain the abnormal haemorrhagic tendency, most likely as yet unrecognized defects in platelet-vessel wall interaction. As a next step we plan to investigate thrombin generation in PRP. Copyright (C) 2003 S. Karger AG, Basel.