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PubMed1983

The effect of low-dose heparin on blood loss at abdominal hysterectomy.

In a double blind trial, the effect of prophylactic low-dose subcutaneous heparin or saline on peri-operative blood loss was studied in 100 women undergoing abdominal hysterectomy. Mean blood loss was 401 (SEM 75) ml and 246 (SEM 15) ml in the women who received heparin or saline, respectively. Coagulation studies were carried out during the pre- and post-operative phases in order to assess the contribution of any coagulation abnormalities to operative blood loss. In identifying patients at risk, platelet function tests were of some value.

Blood Coagulation Disorders↗
PubMed2006

Non-invasive diagnosis of large oesophageal varices with FibroTest in patients with cirrhosis: a preliminary retrospective study.

BACKGROUND AND AIMS: Primary prevention of variceal bleeding with beta-blockers improves survival in patients with large oesophageal varices (LOV). Therefore, cirrhotic patients frequently undergo screening endoscopy. As portal hypertension is related to liver fibrosis, this study aimed to assess the predictive value of FibroTest, a non-invasive marker of liver fibrosis, for the diagnosis of LOV in cirrhotic patients. METHODS: Ninety-nine cirrhotic patients had clinical examination, blood sample (liver function tests, platelet count, FibroTest) and upper endoscopy. Measurements of endoscopic and biochemical parameters were made blindly. Sensitivity, specificity, predictive values and area under the receiver operating characteristic curves were assessed for FibroTest, platelet count and Child-Pugh score. The main endpoint was the presence of LOV. RESULTS: Platelet count, prothrombin time, ascites, FibroTest and Child-Pugh class were significantly different among patients with or without LOV. FibroTest had the highest discriminative power with an area under receiver operating characteristics curves of 0.77 (SE=0.06), compared with 0.64 (0.08) and 0.68 (0.08) for platelet count and Child-Pugh score, respectively (P=0.08). A cut-off at 0.80 had a 86% negative predictive value for the diagnosis of LOV (Se=92%, Sp=21%). CONCLUSION: FibroTest could aid in the diagnosis of LOV and may therefore reduce the indication of endoscopic screening in cirrhotic patients.

Adult↗
PubMed1994

The PACE pilot study: 12-month results and implications for future primary prevention trials in the elderly. (Prevention with low-dose Aspirin of Cardiovascular disease in the Elderly)

OBJECTIVE: To document compliance with medication, drop-out and drop-in rates, and baseline cardiovascular event rates during the pilot phase of the PACE (Prevention with low-dose Aspirin of Cardiovascular disease in the Elderly) study. DESIGN: Randomized, double-blind, placebo-controlled trial of low-dose aspirin therapy. SETTING: Community-based, in general practices and residential retirement villages, in Victoria, Australia. SUBJECTS: Four hundred persons aged 70 years and older (53% females), ambulatory and living independently, who volunteered to participate. None had significant vascular disease, peptic ulceration, hemorrhagic symptoms, or were currently taking non-steroidal anti-inflammatory drugs. MAIN OUTCOME MEASURES: Compliance with medication (assessed by pill count and platelet function tests), self-reported drop-out and drop-in rates, and incidence of cardiovascular events reported by participants and their general practitioners during a 12-month period. RESULTS: Two fatal cardiovascular events, three non-fatal coronary events, and eight non-fatal cerebrovascular events were observed during the 12-month period. These incidence figures were approximately 15%, 15%, and 40%, respectively, of those in the general population of the same age and sex, based on morbidity data available from the Australian Bureau of Statistics. Compliance to medication was excellent (87%), and premature withdrawal (other than for a study end point) was limited to 14.5%. Secondary 'softer' endpoints, such as transient ischaemic attack and unstable angina, necessitated patient withdrawal from randomized therapy and possibly contributed to the small number of primary 'hard' end points observed. The projected power of the main study to detect a 20% treatment effect on overall cardiovascular mortality in 15,000 subjects over a 4-year period may, therefore, be substantially reduced. CONCLUSIONS: These results suggest that any future primary prevention study of cardiovascular disease in the elderly examining the effect of low-dose aspirin on overall cardiovascular mortality will likely need to use much larger numbers of patients or use a combined end point of fatal and non-fatal ischemic events.

Aged↗
PubMed2007

Monitoring survival and function of transfused platelets in Bernard-Soulier syndrome by flow cytometry and a cone and plate(let) analyzer (Impact-R).

BACKGROUND: Bernard-Soulier syndrome (BSS) patients may repeatedly require transfusion of platelets (PLTs). The hemostatic competence of transfused PLTs requires monitoring. STUDY DESIGN AND METHODS: Flow cytometry and a cone and plate(let) analyzer (Impact-R, DiaMed) were used to monitor survival and function of transfused PLTs in a 7-year-old girl with BSS undergoing surgery. Flow cytometry was applied to differentiate autologous PLTs from transfused PLTs by staining for CD42b. The Impact, which measures PLT adhesion and aggregation in response to high shear stress, was used to evaluate PLT function. RESULTS: Transfused PLTs were detectable by flow cytometry for 1 week after transfusion. While the patient's PLTs did not respond to high shear stress before transfusion, a normal response was documented by the Impact on the day after transfusion and 1 week thereafter. CONCLUSION: Transfused PLTs were detectable by flow cytometry, and their functional activity was demonstrated by the Impact.

Bernard-Soulier Syndrome↗
PubMed2006

Defective platelet responsiveness to thrombin and protease-activated receptors agonists in a novel case of gray platelet syndrome: correlation between the platelet defect and the alpha-granule content in the patient and four relatives.

BACKGROUND: We report a novel case of gray platelet syndrome (GPS). A 14-year-old boy had bleeding diathesis, mild thrombocytopenia, giant platelets with severe defect of alpha-granule secretory proteins, myelofibrosis and splenomegaly. METHODS AND RESULTS: Platelet function studies showed a marked reduction of aggregation and Ca(2+) mobilization by thrombin, protease-activated receptor 1 (PAR1)-activating peptide (AP) and PAR4-AP, PAR1 expression at 55% of normal levels, and a more than two hundred fold reduction of in vitro whole-blood thromboxane B(2) (TXB(2)) production. Sequencing of coding regions of the PAR1 gene failed to show abnormalities. This patient was initially classified as a sporadic case of GPS, as electron microscopy failed to identify giant platelets and/or alpha-granule deficiency in his relatives. However, further studies on the father and three other relatives showed a relative lack of platelet alpha-granule proteins by immunofluorescence microscopy, a defective platelet response to PAR4-AP, and severely reduced in vitro whole-blood TXB(2) production. On this basis, we suggest that in this family, GPS was transmitted in a dominant fashion with highly variable penetrance. CONCLUSIONS: Our study suggests that current diagnostic criteria fail to identify some patients with a mild GPS phenotype and that such patients might be identified by the methods cited above. It also better characterizes the pathogenesis of defective platelet responses to thrombin, and raises interesting questions on the correlation between abnormal PAR function and the lack of alpha-granule content in GPS.

Adolescent↗
PubMed1982

Thrombocytopenia as presenting symptom of preleukaemia in 3 patients.

3 patients with preleukaemia (idiopathic acquired myelodysplasia) presenting with isolated peripheral thrombocytopenia and an increased number of megakaryocytes are described. The diagnosis of preleukaemia, however, was strongly suspected on bone marrow morphology, revealing an abnormal megakaryocytic series. Megakaryoblasts with characteristic nuclei and basophilic pseudopodes, and immature megakaryocytes were frequent. These last cells had 1 or 2 nuclei and a basophilic poorly granulated cytoplasm, often containing large vacuoles, corresponding to dilated interconnecting demarcation membranes in electron microscopy. Megakaryocytes were not considered able to produce a normal amount of platelets, explaining the peripheral thrombocytopenia; platelet survival (51Cr) was indeed too long for ITP. Cytogenetic analysis confirmed the diagnosis of an abnormal haematopoietic clone. Ferrokinetics, in vitro agar cultures, bone marrow biopsy and platelet function tests were helpful additional examinations for establishing the correct diagnosis. It is important to differentiate preleukaemia from ITP. Prognosis is totally different and the treatment is not only ineffective in the great majority of the preleukaemic patients, but may be hazardous.

Adult↗
PubMed1999

A quick simple method of determining platelet aggregability following glycoprotein IIb/IIIa receptor inhibitor administration.

Platelet aggregation assessment after therapeutic administration of a GP IIb/IIIa inhibitor has been difficult in routine practice due to the inherent nature of platelet preparation and aggregometry. Platelet microaggregation was performed via the utilisation of a Coulter counter. Citrate and heparin were evaluated as the anticoagulants, and ADP and adrenaline were evaluated as the stimulants. Aprotinin was also assessed. ReoPro was utilised in all assays as the GP IIb/IIIa inhibitor. Platelet microaggregation using the described methodology provides a quick, simple, reliable, and clinically valid method of assessing the percentage platelet inhibition due to the presence of a GP IIb/IIIa inhibitor.

Abciximab↗
PubMed1999

Acquired Bernard-Soulier syndrome: a case with necrotizing vasculitis and thrombosis.

We describe a patient with positive antinuclear antibodies, polyclonal gammopathy and high level of circulating immunocomplexes, resulting in vascular purpura. In addition, the patient had a slightly prolonged bleeding time and an isolated defect of ristocetin-induced platelet aggregation (RIPA) in platelet-rich plasma (PRP). The patient's plasma also inhibited RIPA in normal PRP and in normal platelet suspension. The activity and multimeric structure of plasmatic von Willebrand factor showed no alteration. We could demonstrate an autoantibody against platelet membrane glycoprotein (GP) Ib, using an ELISA-type assay. These data suggest an acquired Bernard-Soulier syndrome. We suggest that the patient had an immunocomplex-mediated leukocytoclastic vasculitis accompanied by production of antinuclear autoantibodies as well as the presence of an autoantibody against GPIb. The titer of the anti-GPIb antibody, however, was too low to induce significant platelet-type bleeding tendency, only laboratory alterations were found. Moreover, in a later stage of her disease, she developed a severe necrotizing vasculitis which was followed by a deep venous thrombosis.

Antibodies, Antinuclear↗
PubMedDate not supplied

Failure of platelet parameters and biomarkers to correlate platelet function to severity and etiology of heart failure in patients enrolled in the EPCOT trial. With special reference to the Hemodyne hemostatic analyzer. Whole Blood Impedance Aggregometry for the Assessment of Platelet Function in Patients with Congestive Heart Failure.

Data from small studies have suggested the presence of platelet abnormalities in patients with congestive heart failure (CHF). We sought to characterize the diagnostic utility of different platelet parameters and platelet-endothelial biomarkers in a random outpatient CHF population investigated in the EPCOT ('Whole Blood Impedance Aggregometry for the Assessment of Platelet Function in Patients with Congestive Heart Failure') Trial. Blood samples were obtained for measurement of platelet contractile force (PCF), whole blood aggregation, shear-induced closure time, expression of glycoprotein (GP) IIb/IIIa, and P-selectin in 100 consecutive patients with CHF. Substantial interindividual variability of platelet characteristics exists in patients with CHF. There were no statistically significant differences when patients were grouped according to incidence of vascular events, emergency revascularization needs, survival, or etiology of heart failure. Aspirin use did not affect instrument readings either. PCF correlates very poorly with whole blood aggregometry (r(2) = 0.023), closure time (r(2) = 0.028), platelet GP IIb/IIIa (r(2) = 0.0028), and P-selectin (r(2) = 0.002) expression. Furthermore, there was no correlation with brain natriuretic peptide concentrations, a marker of severity and prognosis in heart failure reflecting the neurohumoral status. Patients with heart failure enrolled in the EPCOT Trial exhibited a marginal, sometimes oppositely directed change in platelet function, challenging the diagnostic utility of these platelet parameters and biomarkers to serve as useful tools for the identification of platelet abnormalities, for predicting clinical outcomes, or for monitoring antiplatelet strategies in this population. The usefulness of these measurements for assessing platelets in the different clinical settings remains to be explored. Taken together, opposite to our expectations, major clinical characteristics of heart failure did not correlate well with the platelet characteristics investigated in this study.

Aged↗
PubMed2003

Fatal thrombocytopenia and thrombocytopathia: an unusual onset of non-small cell lung cancer.

BACKGROUND: Although bone marrow is a common site of micrometastases for non-small cell lung cancer (NSCLC), thrombocytopathia and hemorrhagic diathesis are rare causes of death. CASE REPORT: A 57-year-old patient was admitted to the emergency room because of massive nosebleeding and hemoptysis. Routine blood analysis showed thrombocytopenia and prolonged bleeding time; results of functional platelet tests suggested concomitant thrombocytopathia. Routine chest X-ray revealed an 18 mm large spot in the right superior lobe. During the first hour of recovery the patient had another episode of nosebleeding. A bone marrow biopsy showed a wide infiltration with neoplastic cells. Histology was compatible with NSCLC. The clinical conditions and hematological parameters progressively deteriorated, and on the third day the patient died because of hypovolemic shock. CONCLUSION: This is a very rare clinical presentation of NSCLC characterized by massive bleeding due to thrombocytopenia and thrombocytopathia secondary to wide bone marrow infiltration.

Biopsy↗
PubMed1980

Essential thrombocythaemia.

The results of detailed studies of 3 patients with essential thrombocythaemia (ET) are presented. Qualitative tests of platelet function were abnormal, and autologous platelet survivals were diminished. Megakaryocyte ploidy distribution analysis showed an increased proporttion of cells with high ploidy, and buoyant density distribution analysis showed increased proportions of less dense platelets. Ultrastructural studies of the platelets showed proliferation of the dense tubular system with deficiency of the surface-connected canalicular system. Megakaryocyte electron microscopy showed abnormal distribution of demarcation membrane complex and granules. The precise functional abnormality of the platelets in ET has not yet been defined, but a release defect of variable severity with corresponding morphological abnormalities of dense tubular and surface-connected canalicular systems, seems the most likely explanation.

Adult↗
PubMedDate not supplied

Single-donor platelet concentrates: changes of surface glycoproteins during storage.

Storage of single-donor platelet concentrates is currently limited to 5 days. During this period, however, numerous morphologic and biochemical changes have been observed. These changes result in functional impairment of stored platelets. The present study describes increased binding of a monoclonal antibody against GMP 140 on the surface of stored single-donor platelets revealing an activation process. In contrast, binding of monoclonal antibodies directed against glycoprotein complex (GP) IIb-IIIa and ligand-induced binding site (LIBS1) is slightly diminished during storage. When platelets are stimulated with ADP GMP 140, GP IIb-IIIa, and LIBS1 are expressed to a higher extent than on the surface on nonstimulated platelets. The quantity exposed, however, depends upon the storage time. It is significantly reduced when platelets are stored for longer than 1-2 days. The present data indicate that storage of single-donor platelet concentrates affects fibrinogen binding, cell to cell cohesion, and release reaction. The results are in good agreement with conventional aggregation and in vitro bleeding time measurements.

Antigens, CD↗
PubMed2004

The effect of recombinant IgG antibodies against the leucine-33 form of the platelet beta3 integrin (HPA-1a) on platelet function.

Recombinant HPA-1a antibodies with Fc, mutated to remove destructive effector functions, have been developed as a potential therapy for fetomaternal alloimmune thrombocytopenia (FMAIT), via blockade of binding of human HPA-1a polyclonal antibodies to fetal HPA-1a1b platelets. We have assessed the effect of the IgG1 HPA-1a antibody B2G1 and two mutated derivatives in various functional assays in resting and agonist-stimulated platelets of the three HPA-1 genotypes. With HPA-1a1b platelets (fetal genotype), the antibodies did not activate signalling or CD62P expression in resting platelets, did not change in vitro bleeding time (IVBT), and did not inhibit platelet adhesion to collagen in flowing blood. Adhesion of HPA-1a1b platelets to fibrinogen was reduced by 20%, and aggregation induced by ADP by 50%, but collagen-related peptide (CRP-XL)-induced aggregation was normal. With HPA-1a1a platelets, aggregation to both ADP and CRP-XL was inhibited, with total blockade of adhesion to fibrinogen and of IVBT responses. Interestingly, a monovalent antibody fragment with identical specificity had no inhibitory effect on aggregation. In static adhesion assays using human alphaIIbbeta3 or alphaVbeta3 transfectants of HPA-1a (Leu(33)) phenotype, attachment to fibrinogen of the latter but not of the former was completely blocked by the HPA-1a antibodies. These observations are best explained by antibody-mediated blockade of the RGD binding site on beta3 by a mechanism of steric hindrance. As the effect on platelet function is modest with HPA-1a1b (fetal type) platelets, the mutated HPA-1a antibodies described here could be developed further for FMAIT therapy.

Antibodies↗
PubMed2005

Defective collagen-induced platelet activation in two patients with malignant haemopathies is related to a defect in the GPVI-coupled signalling pathway.

The occurrence of a thrombocytopathy concomitantly to the development of a malignant haemopathy has been reported for some time, but little is known about the mechanism(s) involved in the platelet dysfunction. Platelet glycoprotein VI (GPVI) has now been identified as a principal platelet receptor for collagen. In this paper, we report the cases of two patients with a myelodysplasia and a B lymphopathy, respectively, who presented with thrombocytopathy in relation to a defective GPVI-mediated platelet reactivity to collagen. Thus, with regard to the different steps of adhesion, activation secretion or aggregation, patients' platelet responses to collagen and to the GPVI specific agonists, collagen related peptide (CRP) or convulxin were null or dramatically impaired. Platelet responses to other agonists ADP, TRAP, Arachidonic acid were normal or showed only a moderate decrease. GPVI content was repeatedly normal, and binding of specific ligands, such as convulxin, satisfactory. Nevertheless, specific activating monoclonal antibodies and convulxin failed to induce platelet secretion; collagen, CRP or convulxin were unable to provoke calcium mobilisation. Furthermore, using a perfusion chamber model, we showed that ex vivo collagen-induced thrombi formation was very impaired. Taken together, these data provide evidence, for the first time, of an acquired defect in GPVI-mediated platelet reactivity to collagen, which reflects data observed in constitutional GPVI deficiencies, in two patients with malignant haemopathies.

Aged↗
PubMed2006

Polymorphisms of COX-1 and GPVI associate with the antiplatelet effect of aspirin in coronary artery disease patients.

The antiplatelet effect of aspirin varies individually. This study evaluated whether the antiplatelet effect of aspirin associates with polymorphisms in the genes coding for cyclo-oxygenase-1 (COX-1) and several platelet glycoprotein (GP) receptors in patients with stable coronary artery disease (CAD). Blood samples were collected from 101 aspirin-treated (mean 100 mg/d) patients. Compliance to treatment was assessed by plasma salicylate measurement. Platelet functions were assessed by two methods: 1) Response to arachidonic acid (AA, 1.5 mmol/L in aggregometry, and 2) PFA-100, evaluating platelet activation under high shear stress in the presence of collagen and epinephrine (CEPI). Aspirin non-response was defined as: 1) slope steeper than 12%/min in AA-aggregations, and 2) by closure time shorter than 170 s in PFA-100. The methods used detected different individuals as being aspirin non-responders. Five and 21 patients, respectively, were non-responders according to AA-induced aggregation and PFA-100. Increased plasma thromboxane B2 levels correlated with poor aspirin-response measured with both AA-induced aggregations and PFA-100 (P = 0.02 and P = 0.003, respectively). Of the non-responders detected by AA, 3 of 5 (60%) carried the rare G allele for the -A842G polymorphism of COX-1 in contrast to 16 of 96 (17%) responders (P = 0.016). Diabetes was associated with poor response. Aspirin non-response detected by PFA-100 associated with C13254T polymorphism of GP VI and female gender (P = 0.012 and P = 0.019, respectively). Although two patients were possibly non-compliant, this did not effect present conclusions. Evaluation of aspirin efficacy by AA-induced aggregation and PFA-100 detected different individuals, with different genotypic profiles, as being aspirin non-responders.

Adult↗