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A Ordinas

Publications and source records attributed to A Ordinas.

At least 73 records · Page 4Linked to original sources

Analysis of the involvement of the von Willebrand factor-glycoprotein Ib interaction in platelet adhesion to a collagen-coated surface under flow conditions.

The requisite initial reaction for in vivo thrombus formation in flowing blood is platelet adhesion to the exposed surface of the extracellular matrix. The contribution of von Willebrand factor (vWF ) in plasma and glycoprotein (GP) Ib on the platelet membrane to platelet adhesion has been well-documented. We have recently developed a procedure (the "flow adhesion assay") for measuring platelet adhesion under flow conditions that allowed us to characterize platelet adhesion to a collagen-coated surface. Here, we apply our method to analyze platelet adhesion to a vWF-coated surface to determine how this might differ from adhesion to a collagen-coated surface. Platelet adhesion to the vWF-coated surface was monitored as the linear increase in the area occupied by adherent platelets. The fluorescence image showed that platelets adhering to the vWF surface were mainly single platelets, and if any were present, the platelet aggregates were small, this being the primary difference from the adhesion to a collagen surface, where adherent platelets were mostly in aggregates. The flow adhesion assay detected the movement of platelets on the vWF surface, suggesting the reversible binding of vWF with platelets. The velocity of the platelets increased at higher shear rates or at lower vWF densities on the surface. Treatment of the vWF-coated surface with the aggregating agent botrocetin before initiation of blood flow increased platelet adhesion while dramatically decreasing the velocity of platelet movement. The present observations on the adhesion of platelets to the vWF-pretreated collagen surface and measurements of the velocity of platelets moving on the collagen surface suggest that the first interaction on the collagen-coated surface is the binding of vWF molecules to the collagen surface. This small number of vWF molecules would serve to attract and slow platelets flowing near the surface. This would facilitate the actual adhesion to the collagen surface that is mainly generated by the interaction between platelet collagen receptors, including GP Ia/IIa and GP VI, with collagen.

Adsorption↗

Differential effect of a low-molecular-weight heparin (dalteparin) and unfractionated heparin on platelet interaction with the subendothelium under flow conditions.

Effects of heparins on platelet function are controversial, but perfusion studies, that simulate physiological conditions, might help to explain their clinical behaviour. We used a perfusion system to test the effect unfractionated heparin and a low-molecular-weight heparin (dalteparin, Fragmin) on platelet adhesion promoted by a damaged vascular surface. Normal blood samples containing increasing concentrations of unfractionated heparin and dalteparin were perfused through annular chambers containing enzymatically denuded rabbit aorta segments (5 min at 800 sec-1). Segments were evaluated morphometrically measuring the total surface covered by platelets and by large aggregates (thrombi). Unfractionated heparin inhibited platelet interaction with subendothelium in a lesser extent than dalteparin in both covered surface and thrombi (p < 0.01). At heparin doses that caused maximal inhibition covered surface was 10.0% +/- 3.1% with dalteparin and 18.3% +/- 4.2% with unfractionated heparin, and thrombi were 5.6% +/- 3.2% and 12.3% +/- 3.0%, respectively. These results may collaborate to explain some differences observed in the clinical results obtained with unfractionated heparin and with dalteparin.

Animals↗

[Thrombotic thrombocytopenic purpura and hemolytic uremic syndrome (TTP/HUS). Description of a series of 35 patients].

BACKGROUND: Delay in application of massive plasmapheresis is the main unfavorable prognostic factor in TTP/HUS, and it is mainly due to difficulties in diagnosing this rare illness. The aim of our study is to analyze the clinical presentations of TTP/HUS. METHODS: The clinical and laboratory data of 35 patients with TTP/HUS were analyzed, as well as the treatment used and the patients outcome. Time intervals between the beginning of symptoms, the diagnosis and the start of treatment were also recorded. RESULTS: The median age was 37 (range: 11-77) years old and there were 19 (54%) women. The more frequent antecedent was chemotherapy with mitomycin C and 5-fluorouracil (7 cases). The diagnosis of TTP/HUS was reached after a median of 5 (interval 0-293) days, and only 11 (31%) patients were correctly diagnosed in the first medical attendance. Hemolytic anemia and thrombocytopenia was the most frequent clinical presentation (80% of patients). Neurologic signs or symptoms were found initially in 14 patients, and oligoanuria in 4. No patient presented initially with the so called "clinical pentad" considered to be typical of TTP/HUS. Plasmapheresis was used in 33 cases. A complete remission was attained in 16, a partial remission in 6, and 13 patients died. CONCLUSION: Due the fickleness of some clinical manifestations considered to be typical of TTP/HUS, these disorders should be considered in patients presenting with acute-onset hemolytic anemia and thrombocytopenia.

Adolescent↗

[Hemopoietic progenitor cell transplantation: 20 years' experience at the Hematology School "Farreras-Valentí"/Clinical Hospital of Barcelona].

BACKGROUND: Hemopoietic progenitor cell transplantation (HPCT) is acquiring an increasing role in the therapy for a variety of disorders. In this study, main characteristics and results of HPCT along 20 years are analyzed from the experience of Postgraduate School of Hematology "Farreras-Valentí" at the Hospital Clínic in Barcelona. PATIENTS AND METHODS: Six-hundred ninety-five patients transplanted between June 1976 and January 1996 were analyzed. Median age (range) were 33 (4-63) years. The following aspects were considered: donor type, source or progenitor cells, type of disease and disease-stage at transplantation, transplant related mortality and survival. RESULTS: A total of 714 HPCT were performed (448 allogeneic, 13 isogeneic, 253 autogeneic). Allogeneic HPCT were from an HLA-identical sibling in 408 cases, from other familial donors in 10, and from non-familial donors in 30. Most HPCT from non-familial donors (93%) were performed during the last five years of the study (1991-1995). The source of hemopoietic progenitor cells was bone marrow in 625 instances (88%), peripheral blood in 88 (12%), and fetal liver in one. During more than 15 years, the only source of progenitors was the bone marrow; in contrast, in the last 3 years (1993-1995) transplants using peripheral blood were predominant. Main indications for HPCT were the following: acute leukemias (n = 387) (54%), chronic leukemias (n = 134) (19%), severe aplastic anemia (n = 58) (8%), lymphomas (n = 80) (11%), multiple myeloma (n = 39) (5%) and myelodysplastic syndromes (n = 14) (2%). In patients with hematological malignancies (n = 656), HPCT was performed in first complete remission or in first chronic phase in 321 instances (49%), in subsequent remissions in 144 (22%), and in more advanced stages in the remaining 191 (29%). In the more recent years, a progressive decrease in the number of HPCT for acute leukemia or aplastic anemia was observed, contrasting with an increase in transplants for lymphoma, multiple myeloma and myelodysplastic syndromes. Of note, a significant decrease in transplant related mortality was evident along the years, both after autogeneic HPCT (21% during 1985-1992 and 6% thereafter) (p = 0.001) and after allogeneic transplantation (54%, 44%, and 20% during the periods 1976-1984, 1985-1992 and 1993-1995, respectively) (p = 0.004). The fact translated into an increase in the actuarial probability of survival after allogeneic HPCT (25%, 33% and 58% in the three mentioned periods, respectively) (p = 0.0003), and after autogeneic HPCT (33% in the interim 1985-1992, and 55% in the period 1993-1995) (p = 0.001). CONCLUSIONS: During the last 20 years, HPCT has significantly evolved in aspects such as type of donor, source of progenitor cells and indications. Remarkably, a progressive decrease in transplant related mortality has been observed translating into a improvement in survival after the procedure.

Actuarial Analysis↗

Antibodies to thromboplastin in systemic lupus erythematosus: isotype distribution and clinical significance in a series of 92 patients.

We determined the prevalence and relationship with clinical manifestations of antibodies to thromboplastin (aTP) in 92 patients with systemic lupus erythematosus (SLE). Thirty-two (35%) patients had aTP: 13 (14%) were positive for IgG aTP, 13 (14%) for IgM aTP, and 6 (7%) for both. Patients with aTP had an increased incidence of thrombosis (p = 0.01), thrombocytopenia (p < 0.001), hemolytic anemia (p < 0.001), and fetal losses (p = 0.03). When the IgG and IgM aTP isotypes were analysed separately, the IgG aTP were found to be associated with thrombosis (p < 0.001), thrombocytopenia (p < 0.001), and fetal losses (p = 0.02). The IgM aTP were associated with hemolytic anemia (p < 0.001). A correlation was found between the titers of aTP and those of anticardiolipin antibodies, in both IgG (p < 0.01, r = 0.6) and IgM (p < 0.01, r = 0.64) isotypes, and between the titers of IgG aTP and the diluted Russell's viper venom time used to detect the lupus anticoagulant (p < 0.001, r = 0.42). This test is a reliable, reproducible and sensitive assay for the detection of antiphospholipid antibodies, specially in those patients under anticoagulant therapy.

Adolescent↗

Thrombomodulin and induced tissue factor expression on monocytes as markers of diabetic microangiopathy: a prospective study on hemostasis and lipoproteins in insulin-dependent diabetes mellitus.

Vascular complications are the main cause of morbidity in diabetes mellitus. To evaluate lipoprotein and hemostatic parameters and their relationship with clinically detectable microangiopathy, we studied 58 insulin-dependent diabetes mellitus patients and 60 controls matched for age, sex, and body mass index. Thirteen patients presented clinically detectable microangiopathy (8 retinopathy and 5 both retinopathy and microalbuminuria). A cross-sectional study of lipid profile, coagulation parameters, and a flow-cytometric evaluation of tissue factor expression in normal monocytes induced by patient plasma were performed. Patients were re-evaluated for microangiopathy in a 3-year median follow-up. Patients showed triglyceride enrichment in low (P = 0.00002) and high density lipoproteins (P = 0.004) and increased levels of D-dimer (P < 0.00001), prothrombin fragment 1 + 2 (P < 0.00001), and thrombin-antithrombin III complex (P = 0.0001). Patients with clinically detectable microangiopathy had increased type 1 plasminogen activator inhibitor (P = 0.00001), thrombomodulin (P = 0.02), and induced monocyte tissue factor expression (P < 0.00001). Nine patients developed clinically detectable microangiopathy in the follow-up and the only predictive variable was increased induced tissue factor expression. In conclusion, in these patients elevated thrombin and fibrin generation reflects a hypercoagulable state but clinically detectable microangiopathy seems related to endothelial cell injury markers and to increased induced tissue factor expression on monocytes.

Adolescent↗

Cocaine administration enhances platelet reactivity to subendothelial components: studies in a pig model.

Myocardial infarction in cocaine abusers may be related to a direct platelet-activating effect. We analysed this possibility in an experimental model. Studies were carried out in eight normal, anaesthetized pigs with a weight of 30.7 +/- 3.7 kg. Blood samples were withdrawn before and 20 min after i.v. administration of cocaine (10 mg kg-1; at 1 mg kg-1 every 2 min). Modifications in platelet responses to arachidonic acid (AA; 1.4 mmol L-1), ADP (1-4 microM), synthetic thromboxane endoperoxide analogue (U46619; 1 microM), collagen (2.5-5 micrograms mL-1), adrenaline (10 microM) and ristocetin (0.8-1 mg mL-1) were tested by conventional aggregometry. Changes in the capacity of platelets to form aggregates on damaged subendothelium were assessed by means of an ex vivo perfusion system in which blood was circulated for 10 min at 800 s-1, a shear rate similar to that found in normal coronary arteries. The interaction of platelets with perfused denuded arterial segments was morphometrically quantified and expressed as a percentage of damaged vessel surface covered by platelets (%CS). Cocaine administration did not influence platelet aggregation patterns in pigs. However, there was a significant increase in the interaction of pig platelets with subendothelial structures after cocaine infusion (%CS = 40 +/- 17% vs. 27 +/- 16% baseline; mean +/- SD; P < 0.01). Cocaine administration in this animal model increases the reactivity of platelets exposed to subendothelium. These results support the concept that the administration of cocaine to pigs has a prothrombotic effect by facilitating the interaction of platelets with damaged arteries.

Animals↗

Prolonged holding of whole blood at 22 degrees C does not increase activation in platelet concentrates.

OBJECTIVES: Platelets prepared after holding of whole blood overnight at 22 degrees C have a well-preserved metabolism. However, the possibility that such prolonged incubation with active granulocytes may increase platelet activation has not been fully tested. METHODS: We investigated this possibility by flow cytometric analysis of membrane glycoproteins (GPs) Ib and IIb/IIIa and the activation markers CD62P and CD63 in platelet concentrates (PCs) prepared from whole blood that was held for either 6 h without cooling plates (n = 20) or for 24 h on cooling plates of 1,4-butanediol (n = 20). PCs were prepared by the platelet-rich plasma method and analyzed on the second storage day. RESULTS: Platelet yield and aggregation response to ristocetin, collagen and epinephrine + ADP were similar in both types of PCs, as was the mean fluorescence intensity for GPs Ib and IIb/IIIa. PCs prepared by the overnight-hold method did not differ from those obtained 6 h after collection in the percentage of platelets expressing CD62P (12.3 +/- 6.2% vs. 14.1 +/- 4.0%; p > 0.1) or CD63 (9.8 +/- 6.4% vs. 8.8 +/- 3.6%; p > 0.1). CONCLUSION: Prolonged holding of whole blood at 22 degrees C prior to component preparation does not increase the level of platelet activation.

Adenosine Diphosphate↗

In vitro evaluation of the hemostatic effectiveness of non viable platelet preparations: studies with frozen-thawed, sonicated or lyophilized platelets.

OBJECTIVES: Because of the limited life span of platelets in regular storage systems, we were interested in investigating the effects on hemostasis of nonliving platelet derivatives. METHODS: We evaluated the effects of different platelet preparations on primary hemostasis in a well-established perfusion model. Studies were carried out with blood anticoagulated with low molecular weight heparin. Similar amounts of frozen-thawed, sonicated or lyophilized platelets were added to normal blood or to blood which had been experimentally depleted of platelets. Platelet interaction with the subendothelium and fibrin deposition were morphometrically evaluated. RESULTS: Addition of nonviable platelet preparations to thrombocytopenic blood always promoted a statistically significant increase in the deposition of fibrin on the subendothelium, but only lyophilized platelets retained some ability to interact with the subendothelium. Flow cytometry studies demonstrated the presence of GPIb, GPIIIa and P-selectin on lyophilized platelets. CONCLUSIONS: Preparations containing nonviable platelets may still retain some hemostatic properties.

Animals↗

Growth of bacteria in platelet concentrates obtained from whole blood stored for 16 hours at 22 degrees C before component preparation.

BACKGROUND: Previous studies have shown that cooling whole blood to 22 degrees C immediately after collection allows it to be held for up to 16 hours before component preparation (overnight-hold method) without a significant decrease in the quality of components obtained. A study was designated to evaluate the effect of the overnight-hold method on the growth of bacteria in experimentally contaminated blood units. STUDY DESIGN AND METHODS: Twenty whole-blood units were inoculated with Staphylococcus epidermidis (300 colony-forming units [CFU]/mL; n = 10) or Escherichia coli (50 CFU/mL; n = 10) immediately after collection. Half the units of each group were fractionated 6 hours after collection and the other half after storage for 16 hours at 22 degrees C. Twenty additional whole-blood units were divided in two equal parts, one of which was white cell reduced before inoculation. These 40 half-units were inoculated with S. epidermidis or E. coli and processed by the overnight-hold method. The growth of bacteria was assessed in platelet concentrates on the second and fifth days of storage, in packed red cells on Day 35, and in fresh-frozen plasma after 60 days. RESULTS: No bacteria growth was detected in plasma or red cell units. On the second day of storage, both bacteria strains grew more slowly in platelet concentrates obtained from blood processed by the overnight-hold method. This difference disappeared for S. epidermidis on the fifth day. When white cell-reduced and non-white cell-reduced whole-blood units were compared, platelet concentrates from the latter showed a delayed growth of both bacterial strains on the second and fifty days of storage. CONCLUSION: Prolonged storage of whole-blood units at 22 degrees C before component preparation delays bacteria growth. This effect seems to be mediated by white cells.

Blood↗

Hemostasis in patients with severe von Willebrand disease improves after normal platelet transfusion and normalizes with further correction of the plasma defect.

BACKGROUND: A defective hemostatic effect of plasma concentrate infusion in patients with severe von Willebrand disease (vWD) has been ascribed to the absence of platelet von Willebrand factor (vWF) STUDY DESIGN AND METHODS: The role of platelet vWF in hemostasis of severe vWD was investigated. A plateletpheresis unit (4-5 x 10(11) platelets) from a normal compatible donor was transfused before any cryoprecipitate infusion to three type 3 vWD patients and to one patient with severe type 1 vWD with low levels of platelet vWF who required replacement therapy for bleeding episodes. Autologous platelets were transfused to one of the patients with type 3 vWD. RESULTS: Partial corrections of bleeding times (14-17 min vs. baseline >30 min) were observed in all patients after the transfusion of normal platelets. During cryoprecipitate infusion, bleeding times were normalized (<6 min), and bleeding episodes stopped when plasma levels of vWF activity ranged from 14 to 18 U per dL. Platelet interactions with the subendothelium increased in parallel with the correction of bleeding times. These results indicate that if approximately 20 percent of the total number of platelets have normal vWF antigen and if plasma vWF levels are at least 14 U per dL, then bleeding times will normalize and mucosal hemorrhages will stop. Transfusion of autologous platelets in one patient with type 3 vWD did not modify bleeding times or platelet adhesion on the subendothelium. CONCLUSION: The hemostatic effect of normal platelets in type 3 vWD seems to be related to the platelet vWF in the transfused platelets.

Bleeding Time↗

Hepatitis G virus infection in a haemodialysis unit: prevalence and clinical implications.

BACKGROUND: Hepatitis viruses have become one of the main infectious problems in patients on long-term haemodialysis. A new RNA virus, designated hepatitis G virus (HGV) has been recently identified. The pathogenic relevance of this virus is currently under investigation. The aim of this study was to analyse the prevalence and clinical implications of hepatitis G virus infection in patients on haemodialysis. METHODS: The presence of HGV-RNA was investigated in 96 patients on maintenance haemodialysis. Hepatitis viral markers (HBsAg, anti-HCV, HGV-RNA) and liver tests were assessed in all these patients, as well as the risk factors for hepatitis viruses acquisition. As a control group, 200 blood donors were tested for the presence of HGV-RNA. RESULTS: HGV-RNA was detected in 25 of 96 patients on haemodialysis (26%) and in six of 200 blood donors (3%) (P < 0.001). Thirteen of 25 HGV infected patients (52%) were coinfected with other hepatitis viruses (HBV and/or HCV). Evidences of chronic liver disease were more frequent in patients infected by HBV and/or HCV (61%) than in patients infected by HGV alone (17%) (P = 0.01). Although 80% of HGV infected patients had received blood products, the transfusion rate was not different from non HGV-infected patients. Time on haemodialysis was significantly shorter in patients infected with HGV alone (3.1 +/- 3.5 years) compared to patients infected with HBV and/or HCV (7.6 +/- 5.8 years) (P = 0.04). CONCLUSIONS: Patients on maintenance haemodialysis are at increased risk for HGV infection. HGV infection itself does not seem to be a frequent cause of chronic liver disease in these patients. Since the prevalence of HGV infection in blood donors is high, blood transfusion could be one of the main factors implicated in HGV transmission in patients on haemodialysis.

Adolescent↗

Anti-beta 2-glycoprotein I antibodies: a useful marker for the antiphospholipid syndrome.

We studied anti-beta 2-glycoprotein I antibodies (a beta 2GPI) in autoimmune disease patients to evaluate their relationship to clinical findings. Seventy-nine systemic lupus erythematosus (SLE) patients [44 with antiphospholipid antibodies (aPL)], 21 with primary antiphospholipid syndrome (APS), eight asymptomatic individuals with aPL and 60 controls were studied. Sixteen SLE patients (14 with aPL and two without aPL) and six with primary APS had a beta 2GPI. A significant relationship was found between a beta 2GPI and aPL (P < 0.01). In SLE, a significant correlation was found between previous thrombosis or thrombocytopenia and a beta 2GPI or a beta 2GPI + aPL, but not between fetal losses and a beta 2GPI. These data suggest that a beta 2GPI may be useful in the study of APS.

Adult↗

In vivo evaluation of platelet activation by different cellulosic membranes.

This study was undertaken to evaluate platelet activation in vivo induced by different cellulosic membranes by measuring the expression of P-selectin on the platelet surface during hemodialysis in 9 uremic patients. Hollow fiber dialyzers of similar surface with different cellulosic membranes (Cuprophan, cellulose acetate, cellulose triacetate, and Hemophan) were evaluated and compared to a synthetic membrane (polysulfone). Blood samples were obtained before hemodialysis and from the efferent and afferent limbs 5 min after the beginning of dialysis. P-selectin exposure was evaluated by flow cytometry (FACScan) using a monoclonal antibody (RUU 2.17). The percentage of platelets expressing P-selectin before hemodialysis and the percentage from the arterial line during hemodialysis were similar. All membranes evaluated induced platelet activation (estimated as the increase in percentage of platelets expressing P-selectin in samples obtained from the venous line with respect to the arterial line). Cuprophan induced more platelet activation than any other membrane (p < 0.05). The activation induced by cellulose acetate and cellulose triacetate membranes was also higher than that observed with Hemophan (p < 0.05). Hemophan-induced platelet activation was similar to that of polysulfone. These results indicate that all cellulosic membranes induce platelet activation during hemodialysis although there are quantitative differences among them. While Cuprophan induced the highest degree of platelet activation, Hemophan was the only cellulosic membrane that showed a degree of platelet activation similar to the biocompatible membrane polysulfone.

Adult↗

Anti-endothelial cell antibodies in systemic autoimmune diseases: prevalence and clinical significance.

OBJECTIVE: To investigate the prevalence and characteristics of anti-endothelial cell antibodies (AECA) in a large cohort of patients with several well defined systemic autoimmune diseases, in order to determine their relationship with the clinical and laboratory features of these diseases. METHODS: Clinical and laboratory features of 216 consecutive Caucasian patients were prospectively studied. One hundred and seven patients had been diagnosed as having a primary systemic vasculitis-specifically, 39 had temporal arteritis (TA), 25 polyarteritis nodosa (PAN), 9 Wegener's granulomatosis (WG), and 34 Behcet's disease (BD)-, 90 patients had systemic lupus erythematosus (SLE), and 19 had a primary Sjogren's syndrome (SS). The AECA were determined by ELISA. RESULTS: One hundred and four (48%) patients with systemic autoimmune diseases were found to have a positive titre of AECA. Specifically, AECA were detected in 41 (38%) patients with a primary systemic vasculitis (13 (33%) with TA, 14 (56%) with PAN, 5 (56%) with WG and 9 (26%) with BD), in 58 (63%) patients with SLE, and in 5 (26%) patients with a primary SS. In patients with a primary systemic vasculitis, those with AECA were found to have an increased prevalence of disease activity (P < 0.05). In SLE patients, those with AECA were found to have an increased prevalence of vascular lesions (P < 0.05), lupus nephropathy (P < 0.05), and anticardiolipin antibodies (aCL) (P < 0.001). CONCLUSIONS: Patients with systemic autoimmune diseases have a high prevalence of AECA and they are associated with the presence of vascular lesions, nephropathy, and aCL in SLE, as well as with disease activity in several primary systemic vasculitis (TA, PAN, WG and BD).

Adult↗

Desmopressin (DDAVP) enhances platelet adhesion to the extracellular matrix of cultured human endothelial cells through increased expression of tissue factor.

The effect of desmopressin (DDAVP) on thrombogenicity, expression of tissue factor and procoagulant activity (PCA) of extracellular matrix (ECM) generated by human umbilical vein endothelial cells cultures (HUVEC), was studied under different experimental conditions. HUVEC were incubated with DDAVP (1, 5 and 30 ng/ml) and then detached from their ECM. The reactivity towards platelets of this ECM was tested in a perfusion system. Coverslips covered with DDAVP-treated ECMS were inserted in a parallel-plate chamber and exposed to normal blood anticoagulated with low molecular weight heparin (Fragmin, 20 U/ml). Perfusions with run for 5 min at a shear rate of 800 s-1. Deposition of platelets on ECMs was significantly increased with respect to control ECMs when DDAVP was used at 5 and 30 ng/ml (p < 0.05 and p. < 0.01 respectively). The increase in platelet deposition was prevented by incubation of ECMs with an antibody against human tissue factor prior to perfusion. Immunofluorescence studies positively detected tissue factor antigen on DDAVP derived ECMs. A chromogenic assay performed under standardized conditions revealed a statistically significant increase in the procoagulant activity of the ECMs produced by ECs incubated with 30 ng/ml DDAVP (p < 0.01 vs. control samples). Northern blot analysis revealed increased levels of tissue factor mRNA in extracts from ECs exposed to DDAVP. Our data indicate that DDAVP in vitro enhances platelet adhesion to the ECMs through increased expression of tissue factor. A similar increase in the expression of tissue factor might contribute to the in vivo hemostatic effect of DDAVP.

Anticoagulants↗

[Comparative efficiency of 1 direct and 2 indirect methods for the detection of differences in erythrocyte aggregation, in normal blood and in blood with echinocytosis].

BACKGROUND: There are many different methods for assessing red cell aggregation, but they have been evaluated in isolated form. The aim of this work was to compare the efficacy and reliability of three different methods for evaluating red cell aggregation. MATERIAL AND METHODS: Blood was drawn on trisodium citrate, and after removal of platelet-rich plasma, the red cell were washed with sodium chloride, and blood was reconstituted until a haematocrit of 40% was achieved. Aspirin or dipyridamole were added, the latter for inducing echinocyte formation. Three methods of assessment of red cell aggregation were used; two of them, indirect, were based upon blood viscosimetry under shear rates indices, and sedimentation rate of centrifuged blood. The third, direct method was based on microscope observation of aggregation and digital analysis of its images for statistical evaluation. Both descriptive methods and analysis of variance were used. RESULTS: The addition of aspirin and dipyridamole increased blood viscosity with respect to the control (p < 0.001 and p < 0.005, respectively), thus showing increased red cell aggregation. Sedimentation rate was also increased, with, statistical significance in the case of dipyridamole (p < 0.05). Digital analysis of images showed significant increase of red cell aggregation with aspirin (37.48 +/- 2.16 vs 27.99 +/- 1.55 in controls, p < 0.05). The presence of dipyridamole-induced echinocytes impeded an adequate evaluation of red cell aggregation indices. CONCLUSION: It was included from these studies that blood viscosimetry proved to be as efficient as digital analysis of images for assessing the differences in red cell aggregation. Nevertheless, microscope examination was necessary for a correct evaluation of this phenomenon, and the presence of echinocytes invalidated any attempt to compare red cell aggregation with respect to normal blood.

Aspirin↗

[Staphylococcal sepsis associated with platelet transfusion: report of a new case and review of the literature].

Bacterial contamination of blood components is an infrequent although potentially fatal event. Bacterial contamination rate of platelet concentrates (PC) varies between 1/900 to 1/2,000 random donor units. However the risk of symptomatic bacteriemias is lower (between 1/2,000 to 1/12,000 random donor units). The organisms most commonly implicated in contaminated PC are gram-positive bacteria such as coagulase negative Staphylococci, Bacillus cereus or Propionibacterium acnes, although gram-negative organisms are also found that generally are associated to a higher mortality. Here, a fatal case of sepsis due to Staphylococcus carnosus associated to transfusion of a contaminated random donor platelet unit is reported.

Bacteremia↗