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Results for “Platelet Function Tests”

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At least 1,189 records · Page 66Linked to original sources
PubMed2001

Evaluation of women with clinically suspected thrombotic thrombocytopenic purpura-hemolytic uremic syndrome during pregnancy.

Thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS) is more common in women, and commonly occurs during pregnancy and the immediate postpartum period. An important clinical issue is the distinction of TTP-HUS from the more common obstetric complications, preeclampsia and HELLP syndrome (hemolysis, elevated liver function tests, low platelets). Clinical suspicion of TTP-HUS requires urgent intervention with plasma exchange treatment, a procedure with substantial risk, while preeclampsia and HELLP syndrome typically resolve spontaneously following delivery. Since clinical features of these syndromes can be similar, especially if preeclampsia becomes severe or if seizures (defining eclampsia) occur, the differential diagnosis may be arbitrary. This review addresses the evaluation and management of these syndromes and describes a clinical approach for determining when plasma exchange is appropriate.

Acute Kidney Injury↗
PubMed2006

Studies of chronic ITP in children and adolescents.

This paper presents an ongoing study of children with chronic ITP in Sweden that addresses four specific questions: is there a subgroup of children with chronic ITP that have impaired platelet function? Do children in this subgroup have antibodies directed against surface glycoproteins that are crucial for platelet function? Can desmopressin improve the impaired platelet function in this subgroup? Do children with chronic ITP show signs of cell-mediated cytotoxicity?

Adolescent↗
PubMed2000

Quantification of platelet activation status by analyzing P-selectin expression.

Platelet activation status (PAS) is used for characterizing quality and function of platelets in various experimental and clinical settings. In this study, we created a set of platelet populations differing in PAS, using stimulation of platelets with thrombin in a wide range of concentrations, and analyzed a number of flow cytometric parameters, which characterize PAS by measuring P-selectin (CD62) expression. We found that PAS of a platelet population depends significantly on the specific parameters used for detecting CD62 expression and can differ several fold. We revealed the parameters which are more sensitive for distinguishing the differences between populations with similar low and similar high PAS. Selection of valid and sensitive flow cytometric parameters for PAS evaluation and distinguishing the differences between platelet populations with similar PAS can serve for diagnosis of platelet-associated disorders and monitoring their course and therapeutic interventions.

Flow Cytometry↗
PubMedDate not supplied

Selective labeling of zebrafish thrombocytes: quantitation of thrombocyte function and detection during development.

Zebrafish thrombocytes, the nucleated equivalents of mammalian platelets, have been characterized morphologically, but knowledge about their developmental synthesis and biochemistry is limited. Given the increasing use of zebrafish as a genetic model to study hemostasis, it is important to isolate and study the function of zebrafish thrombocytes. Therefore, the objective of this study was to isolate thrombocytes, study their function in vitro, and identify the developmental stage at which they enter circulation. To achieve these goals, we developed a method for the selective labeling of thrombocytes and assayed these cells for activation by known mammalian platelet agonists. In both in vitro incubations of whole blood and blood labeled in vivo with the lipophilic dye DiI-C(18), we found labeling in only a single population of cells. These cells were identified as zebrafish thrombocytes by Wright-Giemsa staining. Using selective DiI-C(18) labeling, we showed the formation of thrombocyte aggregates, filopodia, and lipid rafts in response to platelet agonists. Additionally, we showed that aggregates are labeled by binding FITC-conjugated annexin V to exposed phosphatidylserine on the thrombocyte membrane. Using these fluorescent-labeling methods, we developed the first microquantitative assay for thrombocyte aggregation. With this assay, we provided evidence for the presence of an ADP receptor, P2Y(1), in the zebrafish thrombocytes. To study the developmental stage at which thrombocytes appear, we microinjected DiI-C(18) into the circulation of zebrafish embryos and identified the presence of DiI-C(18)-labeled thrombocytes at the 36 h postfertilization stage. These findings will prove helpful in dissecting the functions of thrombocytes in hemostasis and provide further insight into the role of platelets in thrombosis.

Animals↗
PubMed2001

Platelet inhibition by sertraline and N-desmethylsertraline: a possible missing link between depression, coronary events, and mortality benefits of selective serotonin reuptake inhibitors.

Recently, clinical depression has been identified as an independent risk factor for increased mortality in patients following acute coronary events. Although the underlying mechanisms of this link remain uncertain, increased platelet activity has been suggested but never proven as the mechanism responsible for this association. Sertraline hydrochloride is a selective serotonin reuptake inhibitor (SSRI), and is an effective antidepressant agent. Its major liver metabolite, N-desmethylsertraline (NDMS), is known to be neurologically inactive. We assessed the in vitro effects of escalating concentrations of sertraline and NDMS on human platelets by aggregometry in plasma and whole blood, by expression of major surface receptors with flow cytometry in washed cells and in the whole blood, and quantitatively by various platelet function analysers in healthy volunteers and patients with coronary artery disease. Pretreatment of blood samples with sertraline and NDMS resulted in a dose-dependent inhibition of platelet-rich plasma aggregation induced by 5 microM ADP (P =, 0.002), by 10 microM ADP (P = 0.0017), by collagen (P = 0.008), and by thrombin (P = 0.026). Whole blood platelet aggregability was also significantly reduced when induced by 20 microM ADP (P = 0.006), and by collagen (P = 0.01). Surface expression of CD9 (P = 0.004), GP Ib (P = 0.0001), GP IIb/IIIa (P = 0.007), VLA-2 (P = 0.01), P-selectin (P = 0.02), and PECAM-1 (P = 0.01), but not the vitronectin receptor, was also reduced in sertraline and NDMS pretreated washed platelets. Whole blood flow cytometry revealed significant inhibition of GP IIb/IIIa (P = 0.008), and P-selectin expression (P = 0.0001) in NDMS treated samples. Closure time was delayed for the collagen-ADP cartridge (P = 0.009), and for the collagen-epinephrin cartridge (P = 0.01), indicating platelet inhibition in whole blood under high shear conditions. Rapid platelet-function assay revealed a decreased (P = 0.002) ability of platelets to agglutinate fibrinogen-coated beads, suggesting GP IIb/IIIa inhibition. Both sertraline, and its neurologically inactive metabolite NDMS, exhibited significant dose-dependent inhibition of human platelets. The documented anti-platelet effects of sertraline and NDMS may be directly related to the mortality benefits of SSRIs after ischemic events including myocardial infarction and stroke.

Coronary Disease↗
PubMed1987

Bleeding time and PAF-acether-induced platelet aggregation in atopy.

In a double-blind cross-over study 20 mg of aspirin or placebo were administered to 18 patients with respiratory atopy without eczema and to 12 healthy controls. Mean bleeding time before administration of either aspirin or placebo was on average about 1 min. longer in atopics than in the controls, and this difference was significant (p 0.05). Atopics' platelets also aggregated less well in response to arachidonic acid in comparison to controls. On the contrary, no difference in platelet aggregability was detected in response to either PAF-acether alone or to combination of subthreshold, synergistic concentrations of PAF-acether and collagen. Aspirin at a dose used did not affect either bleeding time or platelet aggregability. Thus, in respiratory atopy there exists a moderate hemostatic imbalance, the reason of which remains to be established.

Adult↗
PubMed1993

Mechanism of thrombocytopenia in liver cirrhosis: kinetics of indium-111 tropolone labelled platelets.

Using indium-111 tropolone-labelled platelets, a study of platelet kinetics was performed on the basis of the relationship between platelet count, platelet survival time, platelet dynamics, platelet-associated immunoglobulin G (PA-IgG) and splenic volume in 31 patients with liver cirrhosis and a platelet count of less than 100 x 10(9)/l. The mean platelet count was 46.6 +/- 25.3 x 10(9)/l, and the mean platelet survival time was 6.50 +/- 1.33 days. The mean uptake into the spleen was 43.2% +/- 14.8% on the 1st day, and 53.7% +/- 14.3% on the 7th day. The mean PA-IgG level was 107.6 +/- 66.0 ng/10(7) platelets in five patients with chronic active hepatitis who were studied as controls, the mean platelet count was 197 +/- 30 x 10(9)/l, the mean platelet survival time 9.33 +/- 0.78 days, and the mean PA-IgG 21.2 +/- 2.9 ng/10(7) platelets. The former two parameters were significantly higher (P < 0.05), and the latter significantly lower (P < 0.05). In liver cirrhosis, the platelet count showed a positive correlation with the platelet survival time and a negative correlation with PA-IgG and the splenic volume. These results suggest that the increases in both the splenic platelet pool and platelet destruction in the spleen through immunological mechanisms may influence thrombocytopenia in liver cirrhosis.

Blood Platelets↗
PubMed1984

A comparative study of the effects of aspirin and paracetamol (acetaminophen) on platelet aggregation and bleeding time.

In a double blind, randomised trial, the effects of 1 g aspirin and 1 g paracetamol were compared on bleeding time and platelet aggregation in 40 volunteers (20 females). Also investigated was the relationship between plasma aspirin esterase activity and both bleeding time and platelet aggregation after aspirin. Following 1 g aspirin there was a significant increase in bleeding time at 24 h (p less than 0.01). A significant reduction (P less than 0.01) in platelet aggregation with collagen was observed at 1, 6 and 24 h after aspirin, but no significant reduction (P greater than 0.05) was observed with ADP. Paracetamol had no effect on bleeding time or platelet aggregation. Plasma aspirin esterase activity ranged from 0.26-0.6 mumol/ml/min. A significant negative correlation (R = -0.55, P less than 0.001) was observed between percentage increase in bleeding time (24 h) and plasma aspirin esterase activity. Further significant correlations were observed between plasma aspirin esterase activity and change in platelet aggregation with collagen at 1 h (R = 0.68, P less than 0.001), 6 h (R = -0.73, P less than 0.001) and 24 h (R = -0.67, P less than 0.001). These results suggest that it might be possible to predict an individual's haemostatic response to aspirin from knowledge of their plasma aspirin esterase activity.

Acetaminophen↗
PubMed1990

[Thrombocyte function and thrombocyte-associated immunoglobulins in patients with systemic lupus erythematosus and chronic polyarthritis].

The investigation of in vitro platelet functions from patients with SLE and rheumatoid arthritis (RA) revealed a distinctly reduced aggregation mass after both collagen und ADP induction. The platelet serotonin contents were significantly decreased in both groups. An "aspirin-like" platelet defect could be excluded by finding a normal malonyldialdehyde release of patients' platelets upon thrombin stimulation. Significantly increased platelet associated IgG was also detected, whereas platelet associated IgM remained within normal limits. These results are interpreted as indicating an ongoing platelet release reaction induced by IgG platelet antibodies, which induce the observed impairment of platelet functions and may also lead to the release of proinflammatory platelet mediators.

Arthritis, Rheumatoid↗
PubMed1992

Phosphodiesterase-inhibitors enoximone and piroximone in cardiac surgery: influence on platelet count and function.

OBJECTIVE: Some phosphodiesterase (PDE)-inhibitors are believed to alter platelet count and function due to changes in intracellular cAMP. Whether newly developed (specific) PDE-inhibitors negatively influence platelet function in cardiac surgery should be investigated in a randomized study. METHODS: Eighty patients undergoing aorto-coronary bypass grafting were divided into 4 groups and received either the new PDE-III-inhibitor piroximone (group 1), the PDE-III-inhibitor enoximone (group 2), epinephrine (group 3) or no inotropic support (control). PDE-III-inhibitors were given as a bolus followed by infusion until starting of cardiopulmonary bypass (CPB). In addition to platelet count and a thrombelastogram, platelet function was assessed by aggregometry (ADP, epinephrine, collagen). Measurements were done before, during and after CPB until the 1st postoperative day. RESULTS: Platelet count and postoperative blood loss did not differ between the groups within the entire investigation period. Maximum aggregation and maximum gradient of platelet aggregation to all stimuli were not changed by either PDE-inhibitor enoximone or piroximone. CPB resulted in a significant decrease of all aggregation variables which was without differences due to treatment. Platelet aggregation recovered in the post-bypass period and exceeded baseline values on the 1st postoperative day. CONCLUSION: It is concluded that enoximone and the new PDE-III-inhibitor piroximone do not affect platelet function and can be used before CPB without risking platelet-related bleeding in cardiosurgical patients in the perioperative period.

Adenosine Triphosphate↗
PubMed1993

Does platelet size correlate with function in patients undergoing cardiac surgery?

OBJECTIVE: Platelet dysfunction secondary to cardiopulmonary bypass (CPB) is one of the major reasons for nonsurgical post-operative bleeding in cardiac surgery. Whether platelet size is an indicator for platelet function was investigated in patients undergoing coronary artery bypass grafting. DESIGN: Prospective study. SETTING: Intra-operative, cardiac surgery operations. PATIENTS: 80 consecutive patients undergoing coronary artery bypass grafting. Excluding criteria were pre-operative coagulation disorders and medication with anticoagulants within the last 10 days before the operation day. MEASUREMENTS AND RESULTS: Platelet function was assessed by aggregometry using a turbidimetric method (inductors: ADP 2.0 mumol/l, collagen 4 micrograms/l, epinephrine 25 mumol/l). Mean platelet volume (MPV) was measured by an electrical conductivity method. Measurements were carried out before, during, and after CPB until the 1st post-operative day on intensive care unit (ICU). Platelet size decreased significantly during CPB (max. -25% after weaning from bypass) and returned to baseline values on the 1st post-operative day. Platelet count (ranging from 93 - 304 x 10(9)/l) did not correlate significantly with MPV or aggregation variables. Maximum aggregation and maximum gradient of aggregation induced by ADP and collagen were significantly decreased by CPB with the most pronounced reduction at the end of CPB (ranging from -25% to -45%). Analyses of co-variance revealed a significant correlation between changes in MPV and changes in aggregation variables (ADP, collagen). CONCLUSIONS: Platelet volume is easy to measure even in the operation room or in ICU and may indicate abnormalities in platelet function in the post-bypass period of cardiac surgery patients.

Adult↗
PubMed1988

[Prevalence of plasma factor deficiency in the Vienna population. Results of a screening study of 1,300 adults].

A screening investigation for the presence of risk factors for the development of atherosclerosis demonstrates a plasma factor deficiency in 0.8% in the Viennese population. These findings are in agreement with the data of a newborn screening performed earlier. All the persons were clinically healthy. In 4 of them at least 1 family member suffered from the same defect. The pathogenetic relevance of the plasma factor defect for thrombophilia at young age is discussed.

Adolescent↗