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Browsing by Author "Pereira, J"

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C-reactive protein and atrial fibrillation: "Evidence for the presence of inflammation in the perpetuation of the arrhythmia"
(ELSEVIER IRELAND LTD, 2006) Acevedo, M; Corbalan, R; Braun, S; Pereira, J; Navarrete, C; Gonzalez, I
Background: Atrial fibrillation (AF) is associated to a high risk of systemic embolism. The mechanisms that contribute to thrombogenesis in these patients are still poorly understood. Systemic and/or local inflammation could be involved in the process of thrombogenesis and contribute to the perpetuation of the arrhythmia. The purpose of the study was to evaluate the role of inflammation and its relation to thrombogenesis and cardiac rhythm in AF.
Cardiovascular risk factors in vegetarians: Normalization of hyperhomocysteinemia with vitamin B-12 and reduction of platelet aggregation with n-3 fatty acids
(PERGAMON-ELSEVIER SCIENCE LTD, 2000) Mezzano, D; Kosiel, K; Martinez, C; Cuevas, A; Panes, O; Aranda, E; Strobel, P; Perez, DD; Pereira, J; Rozowski, J; Leighton, F
Hyperhomocysteinemia in association with vitamin B-12 deficiency, and increased platelet aggregation, probably due to dietary lack of n-3 fatty acids, constitute cardiovascular risk factors frequently observed in vegetarians. We tested if administration of vitamin B-12 normalizes the concentration of total plasma homocysteine, and if intake of eicosapentaenoic (20:5n-3) and docosahexaenoic (22:6n-3) fatty acids modulates platelet function in a population of lactoovovegetarians. One week after a single intramuscular injection of cyanocobalamin (10000 mug) in 18 individuals, serum vitamin B-12 increased from 149+/-63 pg/mL to 532+/-204 pg/mL (p<0.0001) and total tHcy dropped from 12.4+/-4.7 to 7.9+/-3.1 mol/L (p<0.0001). Ten of fourteen of these vegetarians completed an 8-week supplementation with 700 mg/day of each eicosapentaenoic and docosahexaenoic acids. Increased incorporation of these fatty acids into plasma lipids was observed in all of them, together with a significant reduction in maximum percentage or slope of platelet aggregation with all the agonists tested (ADP, epinephrin, collagen, arachidonic acid). No significant change in bleeding time was observed after n-3 fatty acid trial. Supplementation with vitamin B-12 and n-3 fatty acids corrects hyperhomocysteinemia and reduces platelet reactivity to agonists in vegetarians. Whether this supplementation improves the already reduced cardiovascular morbidity and mortality associated with vegetarian diet has yet to be demonstrated. (C) 2000 Elsevier Science Ltd. All rights reserved.
Circulating platelet-derived microparticles in systemic lupus erythematosus - Association with increased thrombin generation and procoagulant state
(GEORG THIEME VERLAG KG, 2006) Pereira, J; Alfaro, G; Goycoolea, M; Quiroga, T; Ocqueteau, M; Massardo, L; Perez, C; Saez, C; Panes, O; Matus, V; Mezzano, D
The risk for thrombosis is significantly increased in systemic lupus erythematosus (SLE), affecting both venous and arterial vessels. Activated platelets are known to participate in thrombus formation and growth. A general feature of activated cells is the shedding of microparticles (MP) which support coagulation by exposure of negatively charged phospholipids and possibly tissue factor (TF). In this work we characterized circulating MP in patients with SLE and their relationship with a procoagulant state. Thirty patients with SLE (aged 15-72 years, mean age 38 years) and 20 healthy controls (aged 22-54 years, mean age 34 years) were studied; patients fulfilled 4 revised criteria for SLE. The number and cellular source of circulating MP were determined by flow cytometry using double labeling with specific monoclonal antibodies and annexin V. Thrombin generation was measured as the endogenous thrombin potential (ETP) without the addition of exogenous phospholipids and TF; under these conditions the generation of thrombin depended directly on the number of MP present in plasma. Thrombin anti-thrombin (TAT) and plasmin-antiplasmin (PAP) complexes were measured by ELISA. Compared to the controls, circulating MP were significantly elevated in the patient group (1218 +/- 136 vs 653 +/- 74 x 10(3)/ml plasma, p: 0.0007). In both groups, most of these MP were of platelet origin (927 +/- 131 vs 517 +/- 72 x 10(3)/ml plasma, p:0.009). ETP was higher among patients as compared to the controls (804 +/- 64 vs 631 +/- 37 nM thrombin, p: 0.025). Plasma levels of TAT in patients and controls were 3.4 +/- 0.8 and 1.4 +/- 0.5 mu g/L, respectively (p:0.04), and of PAP complexes were 62.5 +/- 14 and 24.05 +/- 2.5 mu g/ml, respectively (p:0.014). The number of platelet-derived MP correlated significantly with thrombin generation (r: 0.42; p: 0.038) and TAT levels (r: 0.40; p: 0.035). We did not find an association of circulating MP with disease activity nor with the presence of antiphospholipid antibodies. The increased number of circulating platelet-derived microparticles and their association with high ETP and activation of the coagulation system suggest that these microparticles play an important role in the pathogenesis of the prothrombotic state in SLE patients.
Glycoprotein Ib/IX complex is the target in rifampicin-induced immune thrombocytopenia
(BLACKWELL SCIENCE LTD, 2000) Pereira, J; Hidalgo, P; Ocqueteau, M; Blacutt, M; Marchesse, M; Nien, Y; Letelier, L; Mezzano, D
Thrombocytopenia is a major adverse effect of several drug treatments. Rifampicin has been recognized as a cause of immune thrombocytopenia during intermittent high-dose therapy. We characterized the antibody of a patient who presented with purpura and thrombocytopenia during treatment of tuberculosis with rifampicin. Drug-dependent binding of the antibody to platelets was demonstrated by flow cytometry. In a glycoprotein-specific immunoassay, the binding epitope of the IgG antibody was found in the glycoprotein Ib/IX complex, using four different monoclonal antibodies (mAbs) against various epitopes on the GPIb/IX complex, as well as mAbs against GPIIb/IIIa, GPIa/IIa and GPIV. By immunoprecipitation of biotin-labelled platelets, reactivity of the antibody with GPIb/IX was found only in the presence of the drug. These findings clearly demonstrate that rifampicin induces the formation of drug-dependent antibodies capable of causing thrombocytopenia. The binding site of the rifampicin-dependent antibody, located in the GPIb/IX complex, seems to be a favoured target for antibodies induced by different drugs.
GUTI: a new antigen in the Cromer blood group system
(WILEY-BLACKWELL, 2003) Storry, JR; Sausais, L; Hue Roye, K; Mudiwa, F; Ferrer, Z; Blajchman, MA; Lublin, DM; Ma, BW; Miquel, JE; Nervi, F; Pereira, J; Reid, ME
BACKGROUND: The Cromer blood group system consists of seven high-incidence and three low-incidence antigens carried on decay-accelerating factor (DAF). This report describes the identification and characterization of a new Cromer high-incidence antigen, named GUTI.
Hemostatic disorder of uremia: The platelet defect, main determinant of the prolonged bleeding time, is correlated with indices of activation of coagulation and fibrinolysis
(GEORG THIEME VERLAG KG, 1996) Mezzano, D; Tagle, R; Panes, O; Perez, M; Downey, P; Munoz, B; Aranda, E; Barja, P; Thambo, S; Gonzalez, F; Mezzano, S; Pereira, J
Several parameters of primary hemostasis and markers of activation of coagulation and fibrinolysis were measured in 38 patients with severe (creatinine clearance <20 ml/min) chronic renal failure (CRF) without dialysis and diseases or drugs affecting hemostasis. Bleeding time (BT) was prolonged in 25/48 patients, and was correlated with age of patients, severity of renal failure, hematocrit, impairment in platelet aggregation-secretion and decrease in platelet ATP content. Defects in von Willebrand factor played no role in the prolongation of the BT. Multivariate analysis showed that only platelet dysfunction and severity of renal disease were independent predictors of the BT in uremia. The platelet functional disorder was significantly correlated with a reduction in platelet ATP and ADP.
Human intraplatelet 5-hydroxytryptamine is correlated with mean platelet survival time
(PERGAMON-ELSEVIER SCIENCE LTD, 1996) Aranda, E; Pereira, J; Ajenjo, C; Prieto, C; Sepulveda, S; Mezzano, D
Inflammation, not hyperhomocysteinemia, is related to oxidative stress and hemostatic and endothelial dysfunction in uremia
(BLACKWELL SCIENCE INC, 2001) Mezzano, D; Pais, EO; Aranda, E; Panes, O; Downey, P; Ortiz, M; Tagle, R; Gonzalez, F; Quiroga, T; Caceres, MS; Leighton, F; Pereira, J
Background. Several cardiovascular risk factors are present in patients with chronic renal failure (CRF), among which are systemic inflammation and hyperhomocysteinemia. Increased oxidative stress, endothelial activation/dysfunction, and coagulation activation are considered integral components of the inflammatory response, but have also been proposed as mediators of plasma homocysteine (tHcy)-induced cell damage. Using correlation analysis, we assessed the relative contributions of inflammation and hyperhomocysteinemia in the abnormal oxidative stress, endothelial activation/dysfunction, and hemostasis activation in patients with CRF.
Platelet aging in vivo is associated with activation of apoptotic pathways: Studies in a model of suppressed thrombopoiesis in dogs
(SCHATTAUER GMBH-VERLAG MEDIZIN NATURWISSENSCHAFTEN, 2002) Pereira, J; Soto, M; Palomo, I; Ocqueteau, M; Coetzee, LM; Astudillo, S; Aranda, E; Mezzano, D
The mechanism(s) involved in the clearance of senescent platelets are largely unknown. We have recently demonstrated that platelet aging in vivo is associated with loss of membrane phospholipid asymmetry, a universal phenomenon in cells undergoing apoptosis. Thus, We postulated that senescent platelets may exhibit programmed cell death changes, which may trigger their removal from circulation. Since platelets contain the apoptosis machinery as well as mitochondria, a key organelle in the regulation of apoptosis, we studied the appearance of apoptotic-like changes during platelet aging in vivo. To investigate this, we assessed changes in mitochondrial membrane potential in circulating canine platelets during decline in platelet Count after suppression of thrombopoiesis by estradiol injection. a validated model to obtain circulating platelets of increasing mean ace. Phosphatidyl-serine (PS) exposure was determined by flow cytometry by binding of FITC-labeled annexin V. Mitochondrial Deltapsi was studied with the cationic lipophilic dye DIOC6 (3) and the J-aggregate-forming cation JC-1 and analysis by flow cytometry. The proportion of platelets with exposed PS rose significantly with age, from 2.88% before to 6.7%. 8 days after estradiol injection. By flow, cytometry it was demonstrated a significant decreased in DIOC6 (3) fluorescence (median fluorescence intensity 791 98 vs 567 1021 day 0 vs day 8 post injection of estradiol, respectively n:11; p<0.01), consistent with mitochondrial &UDelta;ψ collapse. JC-1 has the unique property of forming J-aggregates tinder high mitochondrial &UDelta;ψ (red fluorescence, FL2) whereas the monomeric form fluoresces in green (FL1). Aged platelets in vivo, loaded with JC-1, exhibited a significant increase in FL1/FL2 ratio (2.5&PLUSMN;1.7 vs 4.7&PLUSMN;1.6, day 0 vs day 8 post injection of estradiol, respectively n:13; p<0.05). confirming the mitochondrial Deltapsi alteration.
Platelet aging in vivo is associated with loss of membrane phospholipid asymmetry
(F K SCHATTAUER VERLAG GMBH, 1999) Pereira, J; Palomo, I; Ocqueteau, M; Soto, M; Aranda, E; Mezzano, D
The mechanism(s) involved in the clearance of senescent platelets are largely unknown. The loss of membrane phospholipid (PL) asymmetry, with phosphatidylserine (PS) exposure appears to be an important signal for the ingestion by macrophages of apoptotic nucleated cells and it has also been suggested as a signal for the removal of aged erythrocytes. Accordingly, it seems possible that the clearance of normal aged platelets from circulation might be triggered by PS exposure. To investigate this, we determined PS exposure in human aging platelets taking advantage of the relationship between platelet density and platelet age and in dog platelets in a model of platelet aging in vivo. PS exposure was determined in two experimental conditions: 1) human platelet density subpopulations obtained by centrifugation in arabinogalactan gradients; 2) circulating canine platelets during decline in platelet count after suppression of thrombopoiesis following estradiol injection. PS exposure was determined by flow cytometry after labeling the cells with FITC-conjugated annexin V. The proportion of human platelets with exposed PS was significantly higher in high density (HD) platelets compared to low density (LD) platelets (11.3 +/- 8.0% vs 5.2 +/- 3.7%; p < 0.05, respectively). In dogs, the proportion of cells with exposed PS rises dramatically with age, from 3.1 +/- 0.4% before to 17.7 +/- 12.3% ten days after estradiol injection. These findings suggest that platelet aging is associated with loss of phospholipid asymmetry and PS exposure on the outer leaflet of cell membrane, which may play an important role in the recognition and subsequent removal of senescent platelets.
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.
Prevalence of antiphospholipid and antiplatelet antibodies in human immunodeficiency virus (HIV)-infected Chilean patients
(WILEY, 2003) Palomo, I; Alarcon, M; Sepulveda, C; Pereira, J; Espinola, R; Pierangeli, S
Antiphospholipid (aPL) and antiplatelet (aPlt) antibodies, found in patients with autoimmune diseases, are also detected in infectious diseases. The purpose of this study was to examine the prevalence of these antibodies in HIV patients and to evaluate an association of these antibodies with thrombocytopenia and/or thrombosis. Sixty-three HIV-seropositive patients and 52 normal controls were studied. Anticardiolipin (aCL), anti-beta(2) glycoprotein I (anti-beta(2)GPI), and antiprothrombin (aPT) antibodies were determined and the lupus anticoagulant (LA) test was performed. Antiplatelet antibodies (aPlt) were also determined. Seven out of 63 (12.7%) HIV patients were positive for aCL, four of 63 (6.3%) for anti-beta(2)GPI, and five of 63 (7.9%) for aPT. No patients studied were LA positive. Six out of 63 (9.5%) patients were positive for aPlt. One of them showed weak reactivity for GPIb-IX. The platelet count of patients (202 +/- 63 x 10(3) platelets/muL) was significantly lower than in the controls (343+/-6 x 10(3) platelets/muL) (P<0.001). There was no correlation between the presence of aPL and/or aPlt and thrombocytopenia. Of the HIV-infected patients, 22.2% presented aPL and 9.4% aPlt antibodies. In this study, the presence of aPL and aPlt antibodies was not associated with the development of thrombosis and/or thrombocytopenia. (C) 2003 Wiley-Liss, Inc.
Prevalence of heparin-induced antibodies in patients with chronic renal failure undergoing hemodialysis
(WILEY, 2005) Palomo, I; Pereira, J; Alarcon, M; Diaz, G; Hidalgo, P; Pizarro, I; Jara, E; Rojas, P; Quiroga, G; Moore Carrasco, R
Heparin-induced thrombocytopenia (HIT) type II is a serious complication of heparin therapy. It presents initially as thrombocytopenia, and is associated with thrombosis in 20-50% of the cases. HIT is related to the presence of heparin-induced antibodies (HIA), which show specificity for the PF4-heparin (PF4-H) complex. The Fc gamma RIIa receptor has been suggested to participate in the pathogenic mechanism of HIA. Since patients undergoing chronic hemodialysis (HD) are exposed repeatedly to heparin, we studied the prevalence of HIA and their eventual relationship with thrombocytopenia and/or thrombosis, and the possible participation of the Fc gamma RIIa polymorphism. We studied 207 patients with chronic renal failure (CRF) undergoing HID. As a control we included 130 blood donors and 28 patients with CRF without HID. The HIA patients were studied with the use of a PF4-H ELISA. Additionally, in some positive cases for the previous test, a C-14- serotonin release assay (C-14-SRA) was performed. The polymorphism Fc gamma RIIa H/R131 was studied by polymerase chain reaction (PCR) with allele-specific primers. Thirty-seven patients (17.9%) undergoing HD presented with HIA. The majority of these antibodies were IgG, IgM, and IgA. The HIA investigated presented specificity against the PF4-H complex, but not against PF4 alone (P < 0.001). Twelve out of 22 (54.5%) PF4-H antibodies were positive when tested with the C-14-SRA. The distribution of the Fc gamma RIIa polymorphism in patients and healthy controls was 42.6% and 41.6% for H/H131, 41% and 48.9% for the H/R131 isoform, and 16.4% and 9.5% for the R/R131 isoform, respectively. No statistically significant difference in the Fc gamma RIIa isoform distribution was found. Twenty-nine out of 156 patients (18.5%) presented thrombocytopenia, and 21/207 (12.4%) had thrombosis of the native vein arterio-venous fistula (AVF). We did not find any statistically significant between HIA and thrombocytopenia or thrombosis. An important proportion of patients with CRF undergoing HD developed HIA, but these cases were not associated with thrombocytopenia or thrombosis of AVF. The frequency of the Fc gamma RIIa polymorphism did not statistically differ between HIT type II and normal controls.
Tranexamic acid inhibits fibrinolysis, shortens the bleeding time and improves platelet function in patients with chronic renal failure
(F K SCHATTAUER VERLAG GMBH, 1999) Mezzano, D; Panes, O; Munoz, B; Pais, E; Tagle, R; Gonzalez, F; Mezzano, S; Barriga, F; Pereira, J
Background: A defect in platelet function is the main determinant of the prolonged bleeding time in chronic renal failure (CRF). We previously reported a significant correlation between platelet abnormalities and elevated plasma markers of plasmin and thrombin generation. Our aim was to explore thr effect of inhibiting both plasmin action with tranexamic acid (TA) and thrombin production with low molecular weight heparin (LMWH), on the bleeding time (BT) and platelet function in patients with CRF. Methods: 37 patients with CRF (mean creatinine 8.6 +/- 4.4 mg/dl) under conservative treatment, with prolonged BT, entered this study and received TA during 6 days, with (n = 24) and without LMWH (n = 13). BT, platelet aggregation/secretion, platelet granule contents, von Willebrand factor and parameters of coagulation and fibrinolysis were recorded before and at the end of treatment. Results: The BT was shortened in 26/37 (67%) patients. This effect was associated with significant improvement of platelet aggregation and secretion, with decrease to a normal range of fibrin/fibrinogen degradation products, mild increase in plasmin-antiplasmin complexes and pronounced reduction of circulating plasminogen. No differences were seen among patients with or without LMWH. No serious side effects or complications were observed. Interpretation: These findings indicate that the activation of fibrinolysis plays a significant role in the defect of primary hemostasis in patients with CRF. inhibition of plasmin activity with TA shortens the BT and improves platelet function in the majority of patients with severe disease.

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