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At least 19 recordsLinked to original sources
PubMed1992

Platelet immunology. ELISA for detection of platelet antibodies, platelet-specific antigens and platelet glycoproteins.

The development of an enzyme linked immuno-sorbent assay (ELISA) for detection of platelet antibodies and platelet specific-antigens has been described. In the assay, intact platelets fixed to the bottom of microplates have been used as targets. After incubation with serum, the attached antibody has been detected by antiglobulin serum labelled with enzyme followed by assay of the enzyme reaction with its substrate. The clinical significance of platelet antibodies in alloimmune neonatal thrombocytopenia (AINT), post-transfusion purpura (PTP), and refractoriness to platelet transfusion therapy has been described. The clinical significance of autoantibodies in autoimmune thrombocytopenic purpura (AITP) and the detection of platelet surface glycoproteins by a modification of the platelet ELISA has also been described. In addition, a survey of the present state of knowledge of human platelet immunology, especially platelet-specific alloantigens and alloantibodies has been given. The studies of AINT and PTP have revealed a human immune response gene located in the MHC region: The susceptibility to anti-Zwa alloimmunization is strongly associated with the HLA-B8 and even more DR3 and DRw52a tissue types. In the studies of PTP, the first example of PTP due to anti-Zwb (only detectable in the platelet ELISA) has been described, and an association of the presence of anti-Zw antibodies of IgG3 subclasses (defined in the platelet ELISA using monoclonal mouse antibodies) and destruction of autologous platelets has been described. In an investigation of Ig classes and IgG subclasses of platelet associated Ig (PAIg) in children suffering from autoimmune thrombocytopenic purpura, no correlation was found between the immunochemical properties of the PAIg and the clinical course of the disease. However, a correlation between increased amounts of PAIgG3 and very low platelet counts was observed. A modification of the platelet ELISA using monoclonal antibodies against glycoproteins (GP) has been described. Using antibodies against GPIb and GPIIb/IIIa, it has been possible to diagnose Glanzmann's thrombasthenia (GT) and Bernard-Soulier syndrome (BSS). Especially in the diagnosis of thrombocytopenic patients suspected for BSS where platelet aggregation studies has been impossible due to low platelet counts, the detection of decreased amounts of surface GPIb in ELISA has been of great value. In conclusion, the platelet ELISA has been found simple and sensitive, and suitable for routine investigations of AINT, PTP, AITP, and refractoriness to platelet transfusion.

Blood Platelets↗
PubMed1990

A survey of platelet serology in UK laboratories (1987): an assessment of the efficacy of using chloroquine-treated platelets to distinguish between platelet-specific and anti-HLA antibodies. The UK Platelet and Granulocyte Serology Working Group.

This survey was designed to determine the ability of participants to distinguish between platelet specific and anti-HLA antibodies. Four well characterized reference reagents and 10 unknown samples were sent to 29 laboratories affiliated to the UK Platelet and Granulocyte Serology Working Group and to three overseas reference laboratories. Results were obtained from 27 Working Group laboratories and from 2 reference laboratories. Overall, the results indicate that the use of chloroquine-treated platelets alone, without an independent test for anti-HLA antibodies, was insufficiently reliable to elucidate mixtures of platelet specific and anti-HLA antibodies. Laboratories using chloroquine-treated platelets were no more successful in elucidating the antibody composition of sera containing platelet-specific and anti-HLA antibodies than those laboratories which did not use this technique. The results may indicate a lack of experience with the chloroquine technique and suggest that further studies into the performance of the technique are required. The survey also provided insights into other areas of platelet serology: (1) There was a decrease in the incidence of false-positive results compared to earlier UK surveys. [2) All laboratories detected potent platelet-specific antibodies but weakly reactive antibodies were less readily detected. (3) Laboratories using fluorescent antiglobulin techniques recorded fewer errors than laboratories using ELISA techniques. (4) Laboratories using paraformaldehyde (PFA)-treated platelets in fluorescent antiglobulin techniques did not perform better than laboratories using untreated platelets.

Antibody Specificity↗
PubMed1991

Wheat germ agglutinin potentiates specific binding of platelet-activating factor to human platelet membranes and induces platelet-activating factor synthesis in intact platelets.

Specific binding of tritium-labeled platelet-activating factor (PAF) and a nonmetabolizable bioactive analog of PAF, 1-O-alkyl-2-N-methylcarbamyl-sn-glyceryl-3-phosphorylcholine, to human platelet membranes was found to be potentiated by wheat germ agglutinin (WGA) and erythroagglutinin. As demonstrated in Scatchard plots, the potentiation effect is due to an increase in the maximal number of receptor sites, with no alteration in the equilibrium dissociation constant. The WGA-potentiated specific binding can be specifically inhibited by N-acetylglucosamine, shows identical affinity for PAF agonists and a receptor antagonist, L-659,989, and has an identical Na+ inhibition pattern to non-treated membranes in the absence of WGA. The WGA-induced potentiation is preferential in the plasma membrane-enriched fraction. The maximal number of receptor sites increases in membranes pretreated with neuraminidase and beta-N-acetylglucosaminidase. Therefore, WGA may bind to an endogenous PAF receptor modulator, which then either dissociates from or associates with the PAF receptor and regulates the receptor conformation. The membrane fraction enriched with intracellular membranes is also enriched with PAF receptors. WGA was also found to increase the maximal aggregation of rabbit and human platelets induced by PAF and to induce the synthesis of PAF, which preceded aggregation in human platelets. An intracellular PAF receptor may also exist, and it could modulate the function of PAF retained inside of the stimulated cells.

Acetylglucosaminidase↗
PubMed1990

The platelet extinction coefficient measured by aggregometry is dependent on platelet composition rather than size: implications for studies of platelet heterogeneity and abnormalities.

Extinction (E) or light transmission measurements of platelet suspensions have been widely used to evaluate platelet structure and aggregation for platelet populations of varying mean platelet size (V). However, useful comparisons of platelet suspensions from donors having abnormally-sized platelets with those from healthy controls require a knowledge of the dependence of E on V. We have analyzed the extinction per platelet (e) as a function of the geometric scattering cross-section of equivalent spheres, V2/3, related to the apparent mean platelet optical efficiency, k. Such an analysis using data previously reported by Holme et al., for healthy controls and a variety of platelet-associated disorders showed e/V2/3 or k to be constant over an eight-fold variation in V. The outstanding exception was platelet suspensions from myeloproliferative disorder patients (MPD) which showed approximately 25% reduction in k values. When we analyzed e/V2/3 data for different-sized platelet subpopulations which were isolated by elutriation from healthy donors, we found that k doubled with a doubling in V from small to large platelets. It appears that the use of aggregometry devices with wide light acceptance angles yields k values for platelets which are insensitive to variations in V, but rather are sensitive to the expected variations in refractive index associated with distinct platelet internal composition and organization expected for different-sized normal subpopulations and "diseased" platelets as found in MPD. We relate these observations to photometric studies of platelet heterogeneity and of aggregation of platelets with different V and k values.

Adult↗
PubMed1990

The association of platelet and red cell count with platelet impedance changes in whole blood and light-scattering changes in platelet rich plasma: evidence from the Caerphilly Collaborative Heart Disease Study.

This epidemiological study was undertaken to explore possible relationships among various haematological indices, prevalent ischaemic heart disease and platelet "function" as measured by two rather different methods. ADP-induced platelet impedance changes in whole blood were strongly associated with prevalent ischaemic heart disease in a general population of 49-66 year men at increased risk. Adenosine diphosphate (ADP) induced platelet aggregation in platelet rich plasma (PRP) at a constant platelet count and also the whole blood platelet count and red cell (RBC) count were strongly and independently related to ADP-induced platelet impedance changes. Both platelet count and platelet aggregation in PRP assessed by changes in optical density were directly related to increasing platelet "sensitivity" as measured by impedance changes in whole blood but RBC count was inversely related. Positive independent relationships between platelet impedance changes and plasma viscosity and fibrinogen were markedly attenuated when platelet count was taken into account, but this finding does not discount a role for these factors in platelet aggregation. No relationship was noted between white blood cell (WBC) count and platelet impedance changes; however, a significant inverse relationship was noted with platelet aggregation in PRP. These findings indicate that laboratory-based experimental findings can be observed in population based studies, and that these haematological factors may be important indicators of ischaemic disease in the population.

Adenosine Diphosphate↗
PubMed2026

Design of a modified platelet immunofluorescence test to assess platelet-reactive antibody burden and its association with platelet functional exhaustion and clinical features in chronic immune thrombocytopenia.

Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by platelet destruction and dysfunction associated with anti-platelet antibodies. This study evaluated the relationship between total anti-platelet antibody burden, measured using a modified platelet immunofluorescence test (PIFT), platelet functional responses and clinical features in chronic ITP. Thirty-one patients with chronic ITP and 20 healthy controls were included. Bleeding severity was assessed, and platelet function was analysed in peripheral blood by measuring P-selectin expression, PAC-1 binding (antibody against active conformation of GPIIb/IIIa)&#xa0;and reactive oxygen species (ROS) generation at baseline and following agonist stimulation. Relative platelet-reactive antibody burden was assessed using a ratio-based PIFT assay. ITP patients demonstrated significantly higher antibody burden compared with controls. Increased platelet-reactive immunoglobulin G (IgG) signals were associated with reduced platelet responsiveness to agonist stimulation. Antibody burden correlated with bleeding severity (p&#x2009;<&#x2009;0.01) but not with platelet count. Non-responders exhibited significantly higher antibody levels than responders. receiver operator characteristic (ROC) analysis demonstrated discrimination between responder groups at a PIFT cut-off &#x2265;3.85 (area under the curve [AUC] 0.877, sensitivity 80%; specificity 87%). Patients above this threshold showed attenuated platelet functional responses. Taken together, this study concluded that quantitative assessment of total antibody burden against platelets using modified PIFT is associated with platelet dysfunction, bleeding severity and treatment response status in chronic ITP.

Humans↗
PubMed1976

Platelet retention in glass bead columns: adhesion to glass and subsequent platelet-platelet interactions.

In normal heparinized blood, the retention of platelets in glass bead columns was low in the first 1 or 2 ml, increasing to more than 80% by the 4th or 5th ml. Prior flushing of the columns with platelet-poor plasma or saline lowered retention in all 5 ml. Additional studies were carried out with a two-stage procedure in which a sample of blood (A) was pumped through a column, immediately flushed out with saline or plasma, and followed by a second blood sample (B). When as little as 1 ml of blood A preceded the flushing solution, retention was very high in all 5 ml of the subsequent blood B. This enhancement of retention in B occurred, providing blood A contained platelets (other than thrombasthenic), fibrinogen, and adequate divalent cations. Enhancement did not require von Willebrand factor (vWF) in A, nor was ADP necessary, since enhancement occurred even when heparinized blood as A contained prostaglendin E1 (PGE1) or creatine phosphokinase with creatine phosphate (CPK-CP). However, the presence of PGE1 or CPK-CP in the plasma used to flush the columns prevented the enhancement of retention in the first milliliter of B. Retention in the first milliliter of B (following normal blood as A and saline or normal plasma for flushing) was high when B was afibrinogenemic, moderately high when B contained PGE1 or CPK-CP, and low in thrombasthenic, EDTA, or vWF-deficient blood. Retention declined in subsequent milliliters of PGE1 or CPK-CP blood and remained low in thrombasthenic, vWF-deficient, or EDTA blood. Our findings suggest that (1) the platelets in A adhere to glass; this adhesion requires fibrinogen but not vWF or ADP; (2) the adherent platelets release ADP and become sticky; (3) adhesion of platelets in the first milliliter of B to the sticky platelets from A requires vWF and divalent cations but not ADP; (4) retention is maintained thereafter by repetitive platelet-platelet interactions involving ADP release, alteration of adherent platelets by released ADP, and adhesion of further platelets to these ADP-altered platelets which requires vWF.

Adenosine Diphosphate↗
PubMed1990

Platelet activation during preparation of platelet concentrates: a comparison of the platelet-rich plasma and the buffy coat methods.

The activation of platelets during the preparation of platelet concentrates (PCs) by two methods was compared. To eliminate interdonor differences, 2 units of whole blood were pooled and subsequently divided into two batches. From one batch, the platelets were harvested as pelleted platelets from platelet-rich plasma (PRP) and from the other as nonpelleted platelets from the buffy coat (BC). The activation of platelets in these PCs was studied immediately after preparation and during storage for up to 9 days at 22 degrees C with gentle agitation. The binding of monoclonal antibodies (MoAbs) against the GP IIb/IIIa complex and against activation-dependent antigens (GMP 140 from the alpha granules and a 53-kDa glycoprotein from the lysosomal granules) was measured. Beta-thromboglobulin (beta-TG) release was also determined. Disc-to-sphere transformation was quantitated by measuring on an aggregometer the difference in light transmission during stirring at different rates and also by light microscopy. Immediately after preparation, platelets derived from PRP had a more spheric morphology (p less than 0.01), had a higher beta-TG release (p less than 0.01), bound more MoAbs against GP IIb/IIIa (p less than 0.01), and expressed more GMP 140 and 53-kDa glycoprotein (p less than 0.01) than did BC-derived platelets. However, these differences had disappeared after 2 days of storage. It was concluded that, immediately after preparation, PRP-derived platelets are more activated than BC-derived platelets. This is most likely a result of the pelleting that follows the second high-speed centrifugation of the PRP.

Antibodies↗
PubMed1992

DDAVP-induced enhancement of platelet retention: its dependence on platelet-von Willebrand factor and the platelet receptor GP IIb/IIIa.

Although DDAVP has been shown to be haemostatically efficacious in patients with various congenital or acquired platelet disorders, no reasonable explanation has been found for this effect. We have previously shown DDAVP to increase platelet adhesiveness as measured with a platelet retention test. The aim of the present study was to investigate the mechanism of action responsible for the increased platelet retention in response to DDAVP. Patients with vWD type III and type Ia, severe haemophilia and severe thrombasthenia, as well as healthy controls, were included in the study. The effect of different concentrations of vWF in plasma and platelets was explored, as was the effect on platelet function of apyrase and monoclonal antibodies against GP IIb/IIIa and GP Ib. We found the effect of DDAVP on platelet retention to be unaffected by changes in the plasma concentration of vWF. The enhanced platelet retention after DDAVP is apparently dependent on the presence of platelet-vWF and on a normal function of the GP IIb/IIIa. The effect is not mediated via ADP or thrombin. The platelet-stimulating effect of DDAVP may be one explanation for the positive haemostatic effect in patients with certain platelet disorders.

Adolescent↗
PubMed1975

Platelet antiheparin activity. The isolation and characterisation of platelet factor 4 released from thrombin-aggregated washed human platelets and its dissociation into subunits and the isolation of membrane-bound antiheparin activity.

Platelet factor 4 was isolated by gel filtration from the soluble release products of thrombin-aggregated washed human platelets as a proteoglycan-platelet factor 4 complex of molecular weight 358 000, Stokes radius (r-s) of 14.0 nm, sedimentation coefficient (s) of 7.1 S and frictional ratio (f/f-o) of 3.04. The complex was dissociated at high ionic strength (I equals 0.75) and the proteoglycan separated from platelet factor 4 by gel filtration. Platelet factor 4 had a molecular weight of 27 100, r-s of 2.52 nm, s of 2.4 S and f/f-o of 1.26, was insoluble under physiological conditions but readily soluble at pH 3. Under these conditions platelet factor 4 dissociated into four subunits with a molecular weight of 6900, r-s of 1.92 nm, s of 0.8 S, and f/f-o of 1.52. Qualitative N-terminal amino acid analysis showed the presence of glutamic acid or glutamine as the major end group. Platelet factor 4 was compared with protamine sulphate, which has similar biological properties, by electrophoresis at pH 2.2, in which both migrated as single bands but with differing mobility, and by amino acid analysis which showed a more normal distribution of residues than occurred in protamine sulphate. Of the basic amino acids platelet factor 4 (molecular weight 27 100) contained 5.97% arginine, 3.18% histidine, and 12.31% lysine compared to protamine sulphate with 64.2% arginine, 0.6% lysine and no histidine. A partial specific volume (v) of 0.747 was calculated for platelet factor 4 from its amino acid analysis. A membrane fraction with antiheparin activity, an isopycnic density of 1.090-1.110 and r-s of 15-35 nm, was also isolated by sucrose density gradient centrifugation from the ultrasonicated insoluble platelet residue remaining after thrombin-induced aggregation of washed human platelets. Trypsin treatment of the membrane fraction neither solubilised nor destroyed the activity.

Amino Acid Sequence↗
PubMed1992

Defective platelet aggregation in response to platelet-activating factor in uremia associated with low platelet thromboxane A2 generation.

The bleeding tendency associated with uremia is likely due to a qualitative platelet dysfunction. So far the data available on platelet aggregation are conflicting. Since platelet-activating factor (PAF) plays a role in primary hemostasis, we studied platelet aggregation in response to PAF in 40 patients with chronic uremia on regular hemodialysis and 12 control subjects. Our results showed that in 28 of 40 uremics, platelet aggregation response to PAF was normal, whereas in the remaining 12 it was defective in that no second wave of aggregation was elicited even if the PAF concentrations were increased by a factor of 10,000. This abnormal response was peculiar to PAF and only partially related to factor(s) of plasma origin. The number of platelet PAF receptors and their affinity for the agonist were comparable in controls and "PAF-unresponsive" patients. The defective platelet aggregation in response to PAF was associated with a statistically significant reduction (P less than 0.01) in thromboxane A2 (TxA2) generation in platelet-rich plasma (PRP) challenged with PAF (10 and 100 nmol/L). When PRPs from PAF-unresponsive patients were preincubated with a stable analogue of prostaglandin endoperoxides/TxA2 U-46619, an irreversible platelet aggregation in response to PAF was obtained. Thus in a subpopulation of uremics, platelet aggregation in response to PAF is selectively abnormal as a consequence of a reduced TxA2 generation.

Adult↗
PubMed1978

Impairment of platelet thromboxane A2 generation and of the platelet release reaction in two patients with congenital deficiency of platelet cyclo-oxygenase.

Two cases of thrombocytopathia with congenital deficiency of platelet cyclo-oxygenase were investigated. The platelet release reaction was impaired. There was a marked decrease of aggregation with collagen and with adrenalin and a total absence of aggregation with sodium arachidonate. The platelet response to labile aggregation stimulating substance (LASS, mostly thromboxane A2) was normal. There was no biosynthesis of prostaglandin cyclic endoperoxides or of thromboxane A2 from arachidonic acid. Basal levels of platelet PGE1 were lowered although plasma levels were normal. Thrombin decreased the cyclic AMP content of patients' platelets and also that of control platelets pretreated with aspirin. The patients platelets showed no ultrastructural difference when compared with control platelets, except for a slight decrease of granule volume, but, in contrast to control platelets, thrombin (0.02 U/ml) did not provoke contraction of the patients' platelets.

Adult↗
PubMed1991

Leukocyte removal filtration of platelet concentrates. A study of platelet loss using 111In-labelled platelets and dynamic gamma camera scintigraphy.

111In labelled platelets and gamma camera scintigraphy were used for the study of the platelet loss during leukocyte removal filtration of stored platelets. Two different filters were examined, Imugard IG500 and Pall PL100, and platelet pools containing varying number of platelet concentrates were filtered. It was found that a sizeable amount of the platelets was trapped within the filter. Some of the trapped platelets could be recovered by rinsing the filters with normal saline. The most appropriate rinsing volume to recover lost platelets seemed to match with the "dead space" volume within the filter. It is concluded that radiolabelled platelets and gamma camera scintigraphy appears to be an excellent method to investigate the dynamic events of platelet loss during leukocyte removal filtration. This technique should be well applicable for the study of technological advances in filter construction.

Blood Platelets↗
PubMed1975

Detection of platelet isoantibodies by (3H)serotonin platelet release and its clinical application to the problem of platelet matching.

The detection of platelet isoantibodies by the release of (3H)serotonin from platelets has been evaluated. The conditions for optimal release of (3H)serotonin with platelet isoantibodies using a microtechnique have been defined. A group of cardiac surgery patients were followed pre- and post-transfusions, with 48percent developing a positive serotonin release assay. Of these patients, 16percent also had a platelet complement-fixing and/or lymphocytotoxic isoantibody. There was variation in the degree of correlation between (3H)serotonin release and lymphocytotoxicity using individual National Institutes of Health typing serum. The matching obtained between family members by both techniques showed a close correlation when each technique was evaluated separately using the same NIH typing serum. The detection of iso-antibodies in patients with hematological malignancies correlated with the unresponsiveness to unmatched platelet transfusions in 15 out of 17 cases. The use of the patient's isoantibody to matched platelets of family members by (3H)serotonin release correlated well with the clinical response to transfusion with these platelets. The data suggest that (a) platelet isoantibodies can be detected with increased frequency by (3H)serotonin release; (b) (3H)serotonin release is a specific reaction depending on the surface antigen of the platelet; and (c) the method can be used to match compatible family members for platelet transfusions.

Blood Donors↗
PubMed1992

[Efficacy of leukocyte-depleted platelet concentrates for prevention of HLA-alloimmunization in patients with frequent platelet transfusions: a prospective multi-institutional study using a polyester platelet filter].

A prospective multi-institutional study was conducted to assess the efficacy of leukocyte-depleted platelet concentrates, prepared by a method using a newly developed polyester filter, in the prevention of HLA-alloimmunization in patients with hematological disorders. Patients who were expected frequent platelet transfusions, were assigned into two groups, receiving either standard platelet concentrates (control group) or leukocyte-depleted platelet concentrates prepared through a polyester platelet filter, Sepacell-PL (filtered group). All patients received leukocyte-depleted red cell products. Of III patients enrolled, 72 were evaluable, 23 in the control and 49 in the filtered group. Both groups were comparable according to age, sex ratio, underlying disorders, previous exposure to alloantigens by transfusion and/or pregnancy. There was no statistically significant difference in the number and duration of transfusion in the two groups. There were significant differences in HLA-alloimmunization rate (9 cases out of 23, 39% in the control group versus 4 cases out of 49, 8% in the filtered group; p less than 0.01) and refractoriness to platelet transfusion from random donors (6 cases out of 23, 26% in the control group versus 2 cases out of 49, 4% in the filtered group; p less than 0.05). These results indicated that leukocyte-depleted platelet concentrates prepared through the polyester platelet filter are beneficial to reduce HLA-alloimmunization in patients with frequent platelet transfusions.

Adolescent↗
PubMed1992

Circulating aggregated platelets, number of platelets per aggregate, and platelet size during acute myocardial infarction.

Circulating aggregated platelets (total, reversibly and irreversibly aggregated), the number of platelets per aggregate and "big" platelets were measured by a modification of the Wu and Hoak method in 42 patients on the first, second and fifth day of acute myocardial infarction (AMI). Among them, 30 had an uncomplicated course and 12 patients had complications that occurred between the 5th and 10th day of hospitalization (7 patients had reinfarction and 5 died). In all patients the measured parameters were elevated compared with those of control subjects. There was a significant increase, especially after the first observation day, in the values of total aggregated platelets (37 +/- 11% vs 26 +/- 12%, p < 0.001), reversibly aggregated platelets (27 +/- 9% vs 17 +/- 8%, p < 0.001) and the average platelets per aggregate (8.6 +/- 0.3 vs. 2.3 +/- 0.4) in patients with versus without complications. In considering the role of platelets in the development of AMI, these findings may add information to the role of platelets in determining the course of AMI.

Blood Platelets↗
PubMed1991

Superoxide dismutase cooperates with prostacyclin to inhibit platelet aggregation: a comparative study in washed platelets and platelet rich plasma.

The role of superoxide anions (O2-) in human platelet aggregation in Krebs' buffer or plasma was investigated. In indomethacin (10 microM)-treated washed platelets superoxide dismutase (SOD; 60 U/ml) or ferricytochrome c (FCC; 70 microM) inhibited platelet aggregation by thrombin but not that by collagen or ADP. In addition, in indomethacin (10 microM)-treated washed platelets, SOD significantly potentiated the anti-aggregatory activity of prostacyclin (PGI2) or iloprost when thrombin but not collagen was used as the aggregating agent. In platelet rich plasma, SOD (60 U/ml) did not inhibit platelet aggregation nor did it potentiate the anti-aggregatory activity of iloprost when ADP, collagen or thrombin were used as aggregating agents. Thus, O2- participate in the aggregatory activity of thrombin but not collagen or ADP and PGI2 or iloprost, by reducing the sensitivity of platelets to thrombin, co-operate with SOD to inhibit thrombin-induced platelet aggregation. The interpretation of the use of SOD in experiments involving endothelium-derived relaxing factor (NO) is discussed.

Adenosine Diphosphate↗