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PubMed1996

A flow cytometric platelet immunofluorescence crossmatch for predicting successful HLA matched platelet transfusions.

Platelet crossmatching may provide a useful way of selecting donors for effective platelet transfusions in patients refractory to random donor platelet concentrates due to alloimmunization. We assessed the predictive value of a flow cytometric platelet immunofluorescence crossmatch test for the outcome of HLA matched platelet transfusions in a group of alloimmunized patients. Platelet immunofluorescence (PIFT) crossmatches were performed for 104 HLA-matched platelet transfusions administered to 30 patients. A negative PIFT crossmatch correctly predicted a successful platelet transfusion (1 h post-transfusion platelet recovery >20%) in 56/75 (75%) cases. We also considered non-immunological factors that, in combination with alloimmunization, might have contributed to an unsuccessful transfusion result, i.e. fever, septicaemia, splenomegaly, disseminated intravascular coagulation and bleeding. The predictive value of a negative PIFT crossmatch was better when these non-immunological factors were absent [48/59 (81%) correct predictions] than when these factors were present [8/16 (50%) correct predictions] (P=0.01; chi-square test). The effect of ABO incompatibility between donor and recipient on the predictive value of the PIFT crossmatch was also analysed. Positive PIFT crossmatches occurred more frequently in ABO incompatible donor-recipient combinations [in 18/28 (64%) cases] than in ABO-compatible donor-recipient combinations [in 11/76 cases (14%)] (P<0.001, chi-square test). Successful platelet transfusions were observed on 53/76 (70%) occasions in ABO compatible transfusions as compared to 16/28 (57%) in ABO incompatible transfusions. This difference was not statistically significant (P=0.23; chi-square test). Consequently, a negative PIFT crossmatch appeared to be non-predictive for the transfusion outcome in cases of ABO incompatibility between donor and recipient. We conclude that the PIFT crossmatch for platelet donor selection in addition to matching for HLA antigens, is predictive for the outcome of ABO compatible transfusions in alloimmunized recipients and prediction levels are increased when non-immunological causes for platelet refractoriness are absent.

ABO Blood-Group System↗
PubMed2002

Thrombocytopenia in patients with malaria: automated analysis of optical platelet counts and platelet clumps with the Cell Dyn CD4000 analyser.

Platelet counts and automated detection of platelet clumps were evaluated by optical analysis with the Abbott CD4000 analyser (Abbott Diagnostics, Santa Clara, CA, USA) in this South African study of 828 samples referred for malaria investigations. Based on microscopy (Micro) and rapid tests (RT) for HRP2 protein and parasite-associated LDH, malaria negative samples (n = 417) were defined as Micro-, RT-. Convalescent cases (n = 64) were Micro-, RT+ and had a recent record of positive microscopy. Malaria positive cases were subdivided into Micro+ (n = 315) and Micro-, RT+, PCR+ (polymerase chain reaction) (n = 32) subgroups. The mean platelet count for Micro+ cases (89.7 x 10(9)/l) was significantly lower than both the malaria negative (mean 212.6 x 10(9)/l) and convalescent malaria (mean 152.8 x 10(9)/l) groups; 89% of microscopy positive cases were thrombocytopenic (< 150 x 10(9)/l) and 30% had severe thrombocytopenia (< 50 x 10(9)/l). For comparison, 32% of the 417 malaria negative samples were thrombocytopenic and 6% of these were severe. Two thirds of samples with parasitaemia above 10% had platelet counts of < 50 x 10(9)/l while the counts were largely independent of parasite numbers when the parasitaemia was below 10%. Thirty percent of samples with microscopically detectable parasites had a PltClmp flag compared to 13% of the malaria negative group but, when the actual platelet count was taken into account, it became apparent that appearance of the flag was primarily associated with thrombocytopenia per se rather than malaria status. In most samples with a PltClmp flag, the CD4000 optical platelet clump 'signature' was indicative of small platelet aggregates and giant platelets. Morphological examination confirmed the presence of varying numbers of small platelet aggregates (3-12 individual platelets), often together with increased giant platelets, in many samples with a PltClmp flag. The observations suggest that while patients with malaria may be predisposed to the development of thrombocytopenia, a reduced platelet count in some patients may also be due in part to pseudo-thrombocytopenia.

Artifacts↗
PubMedDate not supplied

The production of platelet controls for assays quantitating platelet-associated IgG.

A variety of assays are available for measuring platelet-associated IgG (PAIgG) but the complexity of these assays increases the potential for technical errors. These errors are difficult to detect and, if possible, known positive and negative control platelets should be included with each run. However, patient platelets with elevated levels of IgG are seldom available. This report describes a method for producing positive control platelets that can be labeled with differing amounts of IgG. Normal serum IgG (Cohn fraction II) was incubated with washed 2 percent formalin-fixed platelets for 60 minutes at 37 degrees C. The amount of IgG on the platelets was proportional to the concentration of soluble IgG and the number of incubations. Normal platelet IgG levels were 1.2 +/- 0.1 fg per platelet (mean +/- SEM, n = 34) and positive control platelets had 4.6 +/- 0.2 (n = 12) or 8.4 +/- 0.4 (n = 7). There was no change in the level of PAIgG when stored at 4 degrees C for 1 week, although there was a 28 percent loss in recoverable platelets. When mixed 1:1 with 60 percent glycerol and stored at -70 degrees C, the level of PAIgG was stable for 3 months, with less than 12 percent platelet loss on recovery (n = 12). These positive control platelets have proved useful for monitoring assay performance.

Blood Platelets↗
PubMed2001

The release of prion protein from platelets during storage of apheresis platelets.

BACKGROUND: Recent studies using a time-resolved fluoroimmunoassay method (dissociation-enhanced lanthanide fluoroimmunoassay) showed that platelets and plasma are the main reservoir of the normal isoform of cell-associated prion protein (PrPc) in human blood. The aims of the present study were to monitor PrPc levels in various fractions of apheresis platelets during storage by using the DELFIA method and to assess the association of this release with alpha-granule protein ss-thrombo-globulin and cytoplasmic LDH. STUDY DESIGN AND METHODS: Units of apheresis platelets (n = 6) were obtained from volunteer donors by the use of a cell separator and stored up to 10 days. Samples (7-9 mL) were aseptically collected from each unit on storage Days 1, 2, 3, 4, 5, 8, and 10. Platelet-poor plasma and apheresis platelets were prepared and the former split into two fractions, one centrifuged at 40,000 x g for 2 hours at 4 degrees C to remove microparticles. The spun microparticles, apheresis platelets and platelet samples, platelet-poor plasma, and high-spun plasma fractions were stored in a frozen state until they were tested. RESULTS: The results showed that the mean overall levels of PrPc throughout storage remained within 15 percent of Day 1 levels. In contrast, the mean cellular levels in platelets significantly decreased to 46 percent of Day 1 levels by Day 10 of storage (p<0.01), while the corresponding levels in plasma significantly rose as much as 329 percent (p<0.01). Moreover, although microparticle-bound PrPc was released during storage, it was increasingly superseded by soluble protein. PrPc and ss-thrombo-globulin release exhibited very similar patterns (p<0.01). In contrast, LDH showed a significant increase in high-spun plasma only toward the end of the storage period (p<0.01). CONCLUSION: These results indicate that PrPc is released from platelets during the storage of apheresis platelets and that this release is probably due mainly to platelet activation and alpha-granule release in the first few days of storage. Moreover, the released PrPc is increasingly composed of soluble proteins, as the storage period exceeds 5 days.

Blood Platelets↗
PubMed2001

Platelet storage lesion of WBC-reduced, pooled, buffy coat-derived platelet concentrates prepared in three in-process filter/storage bag combinations.

BACKGROUND: With the implementation of universal WBC reduction in the United Kingdom, in-process WBC-reduction filters for pooled buffy coat (BC)-derived platelet concentrates (PCs) are used in routine production. The effects of three filter/storage bag combinations on platelet activation and microvesiculation and on the activation of coagulation were investigated. STUDY DESIGN AND METHODS: Using pooled BCs from the same donors, three filter/storage bag combinations (Autostop BC/CLX, Pall Biomedical; Sepacell PLX5/PL2410, Asahi Medical; and Imugard III-PL 4P/Teruflex, Terumo) were compared with unfiltered controls for their effects on microvesiculation and other storage-induced changes in platelets. Process efficiency was measured by platelet yield and residual WBC count. The storage changes were assessed: pH, activation of platelets measured by CD62P on the platelet surface and in supernatant plasma, quantitation of platelet-derived and RBC-derived microvesicles, cellular injury measured by annexin V in the supernatant plasma, and activation of the coagulation system measured by kallikrein-like and thrombin-like activities, prothrombin fragment 1+2, and thrombin-antithrombin complex. RESULTS: All three filters were comparable in terms of platelet recovery and WBC removal, and none induced immediate platelet activation or microvesiculation. With storage, platelet activation or microvesiculation increased in platelets prepared by all three filters and in unfiltered controls, but these effects were significantly less in the Imugard PCs than in controls. These findings were consistent with those for annexin V in the supernatant plasma, which were lower in Imugard PCs than in other products. Sepacell and Imugard filters reduced RBC-derived microvesicles to 50 percent of control levels, but the Autostop filter had no effect. On storage, levels of RBC-derived microvesicles in filtered products remained static, but levels in the unfiltered control doubled. Kallikrein- and thrombin-like activities were generated only by the Autostop filter without any further increment on storage. CONCLUSION: WBC-reduced pooled BC-PCs prepared by various filter/bag combinations were equivalent on Day 1 but differed during storage in terms of platelet activation or microvesiculation.

Annexin A5↗
PubMed2001

Problems with platelet counting in thrombocytopenia. A rapid manual method to measure low platelet counts.

Because most automated platelet counters cannot be relied on in thrombocytopenia, clinicians face a problem when decision making is based on platelet counts. Therefore we evaluated a visual platelet counting method from a blood smear with white blood cells (WBCs) as reference (PCW = platelet count based on WBC). Platelet counting for 74 thrombocytopenic (<120 x 10(9)/L) children was performed with PCW and with an automated counter (impedance principle); both methods were compared with evaluation by phase-contrast microscopy as the standard method. The PCW correlated well with the phase-contrast microscopy evaluation (y = -0.38 + 1.01x, r2 = 0.99). For platelet counts <20 x 10(9)/L the maximal deviation was 2 x 10(9)/L. The correlation between automated counts and the standard method was poor. The regression was y = 9.63 + 0.94x, r2 = 0.86. For platelet counts <20 x 10(9)/L the maximal deviation was 37 x 10(9)/L; on average, 7 x 10(9)/L platelets were counted in excess when compared with the standard method. PCW, in contrast to the automated impedance method, discriminated platelets from nonplatelet particles such as debris, fragments of red blood cells (hemolytic-uremic syndrome [HUS]) and of blast cells, and identified platelets of abnormal size. In addition, the appearance ofplatelets, WBCs, and RBCs gave clues to the etiology of thrombocytopenia, such as leukemia, infection, HUS, familial macrothrombocytopenia, and immune thrombocytopenia. PCW is a fast, reliable platelet counting method requiring less experience than the phase-contrast method. Visual evaluation from a stained smear clearly differentiates platelets and nonplatelet particles in contrast to most automated counters. In addition, the original smear can be preserved and reevaluated.

Blood Platelets↗
PubMed1979

Platelet receptors for human Factor VIII/von Willebrand protein: functional correlation of receptor occupancy and ristocetin-induced platelet aggregation.

Previous studies of von Willebrand disease indicate that a deficiency of blood clotting Factor VIII/von Willebrand factor (FVIII/vWF) activity is responsible for the failure of platelets to participate fully in the initial stages of hemostasis. We have recently identified specific FVIII/vWF binding sites on platelets, suggesting that the interaction of these sites with FVIII/vWF may be functionally important in the development of platelet clumps. We have now studied how different ristocetin concentrations, various known platelet aggregation inhibitors, and the exposure of platelets to proteases affect the ability of platelets to bind FVIII/vWF and to form aggregates. Our results demonstrate a highly significant linear correlation between the degree of FVIII/vWF receptor binding and the extent of ristocetin-induced platelet aggregation. Because neither FVIII/vWF binding nor platelet aggregation occurs after platelets are exposed to low concentrations of proteases, the FVIII/vWF receptors must be in the platelet membrane. We conclude that the interaction between FVIII/vWF protein and its receptors on the platelet membrane is an important mechanism by which platelet aggregation occurs during primary phase hemostasis.

Binding, Competitive↗
PubMed1998

Platelet agonists enhance the import of phosphatidylethanolamine into human platelets.

It is unknown whether the endocytosis-independent transfer of phospholipids from lipoproteins to platelets is regulated by platelet agonists such as thrombin. The movements of the choline phospholipids phosphatidylcholine and sphingomyelin (labeled with either 14C or the fluorescent pyrenedecanoic acid) between low density lipoproteins and platelets were unaffected by thrombin (0.5 unit/ml). In contrast, thrombin accelerated the import of diacyl phosphatidylethanolamine (PE) and alkenylacyl phosphatidylethanolamine into platelets by about 4-fold. Similarly, thrombin receptor-activating peptide (15 microM), collagen (10 microgram/ml), and ADP (10 microM) enhanced PE uptake. High density lipoprotein particles and egg phosphatidylcholine vesicles were also donors for stimulation of platelet PE import. Part of the [14C]arachidonic acid-labeled PE transferred from low density lipoprotein to platelets activated by thrombin and collagen was metabolized to 14C-eicosanoids. Inhibitors of protein kinase C partially prevented thrombin-induced [14C]PE uptake, while direct activators of protein kinase C increased incorporation of [14C]PE into platelets. Proteinaceous factor(s) recovered in the extracellular medium from ADP- and thrombin-activated platelet suspensions were found to accelerate the transfer of pyrenedecanoic acid-labeled PE between donor and acceptor lipid vesicles. The stimulation of import of ethanolamine phospholipids led to a 2-fold enhancement of the prothrombinase activity of thrombin-activated platelets. Our study demonstrates that physiological platelet stimuli increase specifically the transfer of ethanolamine phospholipids from lipoproteins to platelets through a secretion-dependent mechanism. This might contribute to the increase of procoagulant activity of stimulated platelets.

Adenosine Diphosphate↗
PubMedDate not supplied

Platelet activity, sensitivity to agonist, and platelet--leukocyte conjugate formation after long-term exercise.

For rehabilitation training it is recommended that the intensity of exercise should be distinctly below the individual anaerobic threshold (IAT). We investigated platelet activity, reactivity and platelet-leukocyte conjugate formation following a stardardized treadmill (TR) ergometer test at 90% IAT for 60-120 min. Seventeen healthy male non-smokers underwent TR. Blood samples were taken after a 30-min rest, immediately after exercise, and 2 h after exercise completion. Platelets were detected flow cytometrically by CD41 in whole blood, activated platelets by CD62P. In addition, stimulation of platelets in vitro with 7.5 microM TRAP-6 was performed. For testing platelet-leukocyte conjugates, antibodies against CD45 and CD41 were used. After TR the percent of non-stimulated CD62P-positive platelets (%PC) remained unchanged (1.65 +/- 0.56 to 1.73 +/- 0.79%PC) (mean +/- SD). In contrast, an increase (P<0.05) from 31.9 +/- 13.5 to 37.4 +/- 15.0 %PC in CD62P, TRAP-6 stimulated and enhanced (P<0.01) platelet-leukocyte conjugates (11.7 +/- 3.7 to 16.1 +/- 6.9, CD41-%PC) after TR were observed. Both changes were independent of thrombin generation measured by F1+2 and TAT, and reversible after 2 h. Long-term exercise (90% IAT) on a treadmill ergometer only leads to a moderate increase of platelet reactivity and platelet-leukocyte conjugates. The determination of platelet-leukocyte conjugates may offer the possibility to detect an early activation stage of platelets in vivo.

Adult↗
PubMed1992

Platelet alpha 2 adrenoceptor characteristics during the morning increase in platelet aggregability.

The incidence of myocardial infarction and sudden cardiac death increases in the morning, as do platelet aggregability and sympathetic activity. We considered the possibility that increased platelet aggregability in the morning was due to an increase in platelet alpha 2 adrenergic receptor number or agonist binding affinity, or to a temporal disparity between the increase in sympathetic activity that accompanies arising and the anticipated decrease in platelet high affinity alpha 2 adrenoceptors. To evaluate these possibilities, we studied eight healthy male volunteers (20-35 years) before and 1-1.5 and 3-4 h after they arose at 08.00 h and performed routine morning activities. Platelet aggregability was determined in platelet-rich plasma; alpha 2 adrenoceptor density and agonist binding affinity were determined in intact platelets and in membrane preparations using the alpha 2 selective ligand [3H]-yohimbine. The threshold concentration of epinephrine required to produce biphasic aggregation decreased (i.e. platelet aggregability increased) from 3.6 +/- 1.2 to 0.9 +/- 0.3 microM (P less than 0.05) after arising. However, alpha 2 adrenoceptor density (380 +/- 71 to 365 +/- 51 sites per platelet) and agonist binding affinity assessed simultaneously did not change after arising, suggesting that the increase in platelet aggregability is due to factors extrinsic to the platelets or to an intra-platelet mechanism distal to the receptor level.

Adenosine Diphosphate↗
PubMed2003

Platelet storage solution improves the in vitro function of preserved platelet concentrate.

BACKGROUND AND OBJECTIVES: Stored platelets develop biochemical lesions, manifest as depressed haemostatic function, clot retraction and wound healing. ViaCyte trade mark, a proprietary experimental preservative solution (comprising D-ribose, D-glucose, Hanks solution, Hepes solution, bovine serum albumin, tic anticoagulant peptide and sterile water), was tested in comparison with the presently accepted storage solution, citrate-dextrose-phosphate-plasma (CDP-P), to evaluate its ability to preserve platelet function during storage. MATERIALS AND METHODS: Platelets stored in ViaCyte and platelets suspended in CDP-P were transferred to polypropylene tubes with PL732 covers and analysed for adenine nucleotide levels (ATP molecules), in vitro agonist-mediated P-selectin expression and aggregation. RESULTS: After 5 days of storage at room temperature, 12.2% of platelets stored in ViaCyte exhibited P-selectin expression at rest, and 64.2% exhibited P-selectin expression upon activation with thrombin challenge, an increase of 52%. Platelets stored in CDP-P exhibited 44.4% P-selectin expression at rest, suggesting significant activation during storage, and thrombin stimulation resulted in P-selectin expression of 47.9%, an increase of only 2.5% (P< or =0.002, untreated vs. treated). ViaCyte also maintained ATP levels throughout the storage period, while these levels became depressed in platelets stored in CDP-P (P< or =0.02, untreated vs. treated). Storing platelets in the experimental preservative solution maintained their ability to aggregate, while control platelets lost their ability to aggregate in response to agonist. CONCLUSIONS: ViaCyte appears to protect platelets during storage, reflected by a low level of induced lesions. Platelets stored in ViaCyte maintain energy levels at their resting state, which preserves their ability to aggregate and secrete granule contents, and ensures the availability of additional platelets for activation upon in vitro challenge.

Adenosine Triphosphate↗
PubMed1975

Dissociation of clot retraction from platelet granule fusion and degranulation: an ultrastructural study of Reptilase-human platelet-rich plasma clots.

Human platelet-rich plasma clots, formed with Reptilase, do not retract. Electron microscopy of such a clot reveals platelets of normal shape and ultrastructural features surrounded by fibrin. When ADP is added before Reptilase, the clot strongly retracts. A sequential ultrastructural study of this process shows that, before visible fibrin formation, the platelets form small clusters and show shape change, granule centralization and pseudopod formation. Upon immobilization of the platelets by fibrin, the pseudopods develop into large cytoplasmatic protrusions, which allow cell contact. During the retraction process, the platelet granules remain intact; some granule fusion only becomes apparent in fully retracted clots. When Thrombofax is added to platelet-rich plasma before Reptilase, the clots formed also retract. With this aggregation inducer, granule fusion occurs earlier and in more platelets. Platelet pseudopod enlargement and fibrin concentration around the platelet mass are similar to that in ADP-treated samples. Inhibitors of granule fusion and secretion (suprofen, indomethacin) do not modify ADP-Reptilase nor Thrombofax-Reptilase clot retraction but reduce the incidence of granule fusion in Thrombofax-Reptilase clots. Retraction of Thrombofax-Reptilase clots is unaffected by concentrations of apyrase which completely block ADP-Reptilase clot retraction. Prostaglandin E1, papaverine and amitryptiline inhibit both ADP-and Thrombofax-Reptilase clot retraction, platelet pseudopod formation and cell-to-cell adhesion. These findings suggest that interaction of fibrin with the mass of fused granules (granulomere) or platelet secretion are not responsible for clot retraction. Rather, contraction around adhesion sites formed by cytoplasmic protrusions from adjacent platelets would seem to be involved.

Adenosine Diphosphate↗
PubMed1982

Immunohistological comparison of platelet factor 4 (PF4), fibronectin (Fn) and factor VIII related antigen (VIIIR:Ag) in human platelet granules.

Immunofluorescence microscopy was used to study the localization of platelet factor 4 (PF4), fibronectin (Fn) and factor VIII related antigen in washed normal platelets and those from patients with severe von Willebrand's disease (vWd). Platelets were prepared by an improved multi-unit modification of the Sayk chamber. This facilitated the preparation of samples with minimum disruption of platelets and readily permitted the demonstration of intact platelet granules by the immunological techniques used. The antigens were demonstrated by treating the same preparations sequentially with appropriate heterologous antisera and species specific fluorescein or rhodamine conjugated antisera. Comparison of the different antigens in identical platelets indicated that Fn and VIIIR:Ag were localized to the same granules as PF4 and the results were thus consistent with their presence in alpha granules. Fn and PF4, but not VIIIR:Ag, were present in platelet granules of patients with severe vWd. The antigens were always detected in the same granules, and major sub-populations of differently stained granules were not observed. The methods were applied to investigate normal platelets aggregated with collagen. Fn and VIIIR:Ag were detected in platelet granules after aggregation although the granules themselves were possibly differently distributed in these samples compared with the non-aggregated platelets. The localization of PF4 could not be reliably assessed in aggregated platelets by these methods. The techniques may be useful in localizing platelet antigens and studying release during aggregation.

Antigens↗
PubMed1994

Abnormal cAMP-induced phosphorylation of rap 1 protein in grey platelet syndrome platelets.

We previously demonstrated abnormal Ca2+ transport by microsomes in platelets from a grey platelet syndrome patient. Here, we investigated the platelet Ca2+ ATPases that mediate this transport, as well as its possible regulation by rap 1 protein. We showed that grey platelet syndrome platelets expressed the same two distinct Ca2+ ATPases as those recently described in normal platelets; the 100 kD SERCA2-b isoform (Sarco/Endoplasmic Reticulum Ca2+ATPase) and a new 97 kD SERCA isoform. The two Ca2+ATPases formed similar amounts of transient phosphorylated intermediates. The expression of these two Ca2+ATPases was compared by Western blotting using specific antibodies, which again emerged in similar amounts in normal and grey platelet syndrome platelets. As regards the protein phosphorylated by cAMP, it was found to be identical to rap 1 protein when it was immunoprecipitated with an antibody raised against a synthetic peptide specific for rap 1 protein. Although the expression of rap 1 protein was similar in membranes isolated from grey platelet syndrome and normal platelets, its exogenous phosphorylation by cAMP was abnormal, with a concentration (10 micrograms/ml) of the catalytic subunits of the cAMP-dependent protein kinase (C.Sub.), as it decreased to half the control level. It is concluded that the abnormal Ca2+ transport found in grey platelet syndrome platelets is not due to the abnormal expression of the Ca2+ATPases, but is associated with an abnormality of rap 1 protein phosphorylation by cAMP.

Adult↗
PubMed2005

Accuracy of platelet counting haematology analysers in severe thrombocytopenia and potential impact on platelet transfusion.

Although haematology analysers provide reliable full blood counts, they are known to be inaccurate at enumerating platelets in severe thrombocytopenia. If the thresholds for platelet transfusion, currently set at 10 x 10(9)/l, are to be further reduced, it is vital that the limitations of current analysers are fully understood. The aim of this large multicentre study was to determine the accuracy of haematology analysers in current routine practice for platelet counts below 20 x 10(9)/l. Platelet counts estimated by analysers using optical, impedance and immunological methods were compared with the International Reference Method for platelet counting. The results demonstrated variation in platelet counting between different analysers and even the same type of analyser at different sites. Optical methods for platelet counting on the XE 2100, Advia 120, Cell-Dyn 4000 and H3* were not superior to impedance methods on the XE 2100, LH750 and Pentra analysers. All analysers except one overestimated the platelet count, which would result in under transfusion of platelets. This study highlights the inaccuracies of haematology analysers in platelet counting in severe thrombocytopenia. It re-emphasizes the need for external quality control to improve analyser calibration for samples with low platelet counts, and suggests that the optimal thresholds for prophylactic platelet transfusions should be re-evaluated.

Humans↗
PubMed2005

Increased platelet count and leucocyte-platelet complex formation in acute symptomatic compared with asymptomatic severe carotid stenosis.

OBJECTIVE: The risk of stroke in patients with recently symptomatic carotid stenosis is considerably higher than in patients with asymptomatic stenosis. In the present study it was hypothesised that excessive platelet activation might partly contribute to this difference. METHODS: A full blood count was done and whole blood flow cytometry used to measure platelet surface expression of CD62P, CD63, and PAC1 binding and the percentage of leucocyte-platelet complexes in patients with acute (0-21 days, n = 19) and convalescent (79-365 days) symptomatic (n = 16) and asymptomatic (n = 16) severe (> or =70%) carotid stenosis. Most patients were treated with aspirin (37.5-300 mg daily) although alternative antithrombotic regimens were more commonly used in the symptomatic group. RESULTS: The mean platelet count was higher in patients with acute and convalescent symptomatic compared with asymptomatic carotid stenosis. There were no significant differences in the median percentage expression of CD62P and CD63, or PAC1 binding between the acute or convalescent symptomatic and asymptomatic patients. The median percentages of neutrophil-platelet (p = 0.004), monocyte-platelet (p = 0.046), and lymphocyte-platelet complexes (p = 0.02) were higher in acute symptomatic than in asymptomatic patients. In patients on aspirin monotherapy, the percentages of neutrophil-platelet and monocyte-platelet complexes (p = 0.03) were higher in acute symptomatic (n = 11) than asymptomatic patients (n = 14). In the convalescent phase, the median percentages of all leucocyte-platelet complexes in the symptomatic group dropped to levels similar to those found in the asymptomatic group. CONCLUSION: Increased platelet count and leucocyte-platelet complex formation may contribute to the early excess risk of stroke in patients with recently symptomatic carotid stenosis.

Acute Disease↗
PubMed1987

Direct platelet-fibrin interaction that does not require platelet activation.

Interactions between platelets and fibrin are important in hemostasis but often confused with platelet-fibrinogen interactions. Fibrin solubilized in NaBr-acetic acid formed polymers in neutral pH buffers. A stirred mixture of solubilized fibrin and washed human platelets at neutral pH range showed drastic reduction in turbidity and concomitant platelet adhesion onto newly formed fibrin strands. Optimally, more than 99% of platelets could be associated with fibrin, whereas only 3% of erythrocytes were trapped in the fibrin network under similar conditions. This platelet-fibrin interaction was fibrin concentration dependent and polymerization stage dependent. It preceded any detectable platelet release of serotonin. Gly-Pro-Arg-Pro (250 times in excess) retarded the kinetics of fibrin polymerization as well as that of platelet-fibrin interaction. However, factors affecting platelet activation showed little effect on platelet-fibrin interaction. Our results support the existence of a platelet-fibrin interaction that does not require platelet activation.

Adenosine Diphosphate↗
PubMed2004

Platelet morphology, soluble P selectin and platelet P-selectin in acute ischaemic stroke. The West Birmingham Stroke Project.

The pathophysiology of ischaemic stroke involves the platelet. In this study, we hypothesised that abnormalities in platelet morphology, as well as soluble (sPsel) and total platelet P-selectin (pPsel) levels would be present in patients presenting with an acute ischaemic stroke, and that these changes would improve at > or = 3 months' follow-up. We studied 59 hypertensive patients (34 male; mean age 68 +/- 12 years) who presented with an acute ischaemic stroke (ictus < 24 hours), and compared them with 2 groups: (i) age-, sex- and ethnic- origin matched normotensive healthy controls; and (ii) uncomplicated 'high risk' hypertensive patients as 'risk factor control' subjects. Platelet morphology (volume and mass) was quantified, and sPsel (plasma marker of platelet activation) was measured (ELISA) in citrated plasma. The mass of P-selectin in each platelet (pPsel) was determined by lysing a fixed number of platelets and then determining the levels of P-selectin in the lysate. Results show that patients who presented with a stroke had significantly higher levels of sPsel and pPsel (both p < 0.001), compared to the normal controls and the hypertensive patients. Patients with an acute stroke had lower mean platelet mass (MPM) and mean platelet volume (MPV) as compared to the uncomplicated hypertensive patients, who had significantly higher mean MPM and MPV values, as compared to normal controls. On follow-up, the levels of both sPsel (p = 0.011), pPsel (< 0.001) and MPV (p = 0.03) were significantly lower. Mean MPM levels remained unchanged. We conclude that patients presenting with an acute ischaemic stroke have activated platelets, as evident by the increased levels of soluble and platelet P-selectin. Further study of platelet activation and the role of P-selectin is warranted.

Aged↗