scholarly journals Pseudothrombocytopenia: Manifestation of a New Type of Platelet Agglutinin

Blood ◽  
1973 ◽  
Vol 42 (4) ◽  
pp. 541-549 ◽  
Author(s):  
David P. Shreiner ◽  
William R. Bell
Keyword(s):  
Clinical Significance ◽  
Divalent Cation ◽  
Gamma Globulin ◽  
Platelet Rich Plasma ◽  
Platelet Counts ◽  
Normal Plasma ◽  
Blood Smears ◽  
New Type

Abstract Spuriously low electronic platelet counts were obtained on blood collected in EDTA from six patients. Platelet numbers on blood smears and electronic counts performed on blood collected in other anticoagulants were normal. Plasma or sera from these patients agglutinated homologous, as well as autologous platelets, in the presence of EDTA or DTPA, but agglutination did not occur in blood or platelet-rich plasma anticoagulated with heparin, oxalate, or citrate. Agglutination in the presence of EDTA was not inhibited by heparin, α-tocopherol, or N-ethylmaleimide, but was inhibitied by excess EDTA or divalent cation. The agglutinin was temperature independent in five of the six patients and had the physical and immunologic characteristics of a gamma globulin. The clinical significance and mechanism of EDTA-dependent agglutination of platelets is unknown.

Differing Susceptibilities of Platelets from Normal Individuals and Patients with von Willebrand’s Disease to Attack by Quinine- and Quinidine-Dependent Antiplatelet Antibodies

1989 ◽  
Vol 61 (01) ◽  
pp. 111-116
Author(s):  
Sharron L Pfueller ◽  
Robyn A Bilston ◽  
Dana Logan ◽  
Rosemary David ◽  
Ian G Sloan ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Serotonin Release ◽  
Von Willebrand's Disease ◽  
Von Willebrand’S Disease ◽  
Antiplatelet Antibodies ◽  
Normal Plasma ◽  
Igg Binding ◽  
Normal Individuals ◽  
Drug Dependent

SummaryReactivity of quinine- and quinidine-dependent antiplatelet antibodies has been compared in platelet-rich-plasma (PRP) from normal donors and from patients with von Willebrand’s disease (vWd). One quinine-dependent antibody (Q. Ab) caused platelet aggregation and [14C] serotonin release with only 7 of 12 normal donors, while another Q. Ab and a quinidine-dependent antibody (Qd. Ab) caused aggregation and release with all 12. Drug- dependent IgG binding and PF 3 availability induced by the antibodies were, however, comparable in all donors. Differences in responsiveness were associated with platelets and not plasma. vWd platelets showed normal drug-dependent IgG binding, but decreased aggregation and serotonin release to most drug- dependent antibodies. Responsiveness was not restored by purified vWf:Ag, but, in one case, was corrected by normal plasma or cryoprecipitate. Drug-dependent binding of the Q. Ab which caused variable responsiveness in normals was to the same platelet antigens (GPIb and GPIIIa) in both normal and vWd platelets and did not require plasma components. Reduced PF 3 availability was seen with some antibodies in some vWd patients. Plasma from two of these patients inhibited aggregation of normal platelets to Q. Ab and one of these inhibited aggregation to ADP. Antiplatelet antibodies were detected in these two plasmas by ELISA. Thus some Q. Ab produce different responses with platelets from different donors. In vWd, reduced responsiveness to Q.Ab and Qd. Ab may result from production of inhibitory antiplatelet antibodies.

Interactions of Staphylokinase with Human Platelets

1995 ◽  
Vol 73 (03) ◽  
pp. 472-477 ◽  
Author(s):  
H R Lijnen ◽  
B Van Hoef ◽  
D Collen
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Specific Binding ◽  
Platelet Rich Plasma ◽  
Human Platelets ◽  
Normal Plasma ◽  
Atp Secretion ◽  
Platelet Disaggregation ◽  
Activation Rate

SummaryThe interactions of recombinant staphylokinase (SakSTAR) with human platelets were investigated in a buffer milieu, in a human plasma milieu in vitro, and in plasma from patients with acute myocardial infarction (AMI) treated with SakSTAR.In a buffer milieu, the activation rate of plasminogen by SakSTAR or streptokinase (SK) was not significantly altered by addition of platelets. Specific binding of SakSTAR or SK to either resting or thrombin- activated platelets was very low. ADP-induced or collagen-induced platelet aggregation in platelet-rich plasma (PRP) was 94 ± 2.7% or 101 ± 1.7% of control in the presence of 0.1 to 20 μM SakSTAR, with corresponding values of 95 ± 2.8% or 90 ± 4.6% of control in the presence of 0.1 to 4 μM SK. No effects were observed on platelet disaggregation. ATP secretion following collagen-induced platelet aggregation was 4.3 ± 0.26 μM for SakSTAR (at concentrations of 0.1 to 20 μM) and 4.4 ± 0.35 μM for SK (at concentrations of 0.1 to 4 μM), as compared to 3.4 ± 0.70 μM in the absence of plasminogen activator.Fifty % lysis in 2 h (C50) of 60 μl 125I-fibrin labeled platelet-poor plasma (PPP) clots prepared from normal plasma or from plasma of patients with Glanzmann thrombasthenia and immersed in 0.5 ml normal plasma, was obtained with 12 or 16 nM SakSTAR and with 49 or 40 nM SK, respectively. C50 values for lysis of 60 μl PRP clots prepared from normal or patient plasma were also comparable for SakSTAR (19 or 21 nM), whereas SK was 2-fold more potent toward PRP clots prepared from Glanzmann plasma as compared to normal plasma (C50 of 130 versus 270 nM).No significant effect of SakSTAR on platelet function was observed in plasma from patients with AMI treated with SakSTAR, as revealed by unaltered platelet count, platelet aggregation and ATP secretion.Thus, no effects of high SakSTAR concentrations were observed on human platelets in vitro, nor of therapeutic SakSTAR concentrations on platelet function in plasma.

The Influence of Serotonin on Clot Retraction and the Thrombelastogram

1958 ◽  
Vol 02 (01/02) ◽  
pp. 111-124 ◽  
Author(s):  
E Deutsch ◽  
K Martiny
Keyword(s):  
Human Plasma ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Specific Effect ◽  
High Dose ◽  
Clot Retraction ◽  
Platelet Counts ◽  
Essential Value ◽  
High Doses ◽  
Free Plasma

Summary1. Normal platelets are necessary for induction of normal clot retraction.2. Serotonin does not induce retraction in human platelet-free plasma-clots or enhance clot firmness as measured in the coagulogram.3. Serotonin does not improve clot retraction or firmness in plasma clots with sub-optimal platelet counts.4. Methylserotonin inhibits clot retraction of platelet-rich plasma to a certain extent in moderate doses, whereas, high doses are ineffective. BOL 148 has a similar, but less significant action. There is a possibility that these effects are specific antiserotonin-effects.5. LSD 25 was ineffective in all concentrations used.6. Largactil and reserpin inhibit retraction in high doses. There seems to be a non specific effect caused by the high dose.7. Reserpine does not release a retraction-inducing agent from the platelets, which could be detected in the centrifuged platelet-free plasma used for the incubation.8. Serotonin does not replace the retraction-cofactor of Hartert, or the dialyzable factor of Lüscher in synthetic clotting substrates.9. Serotonin is of no essential value in inducing normal retraction of human plasma clots.

scholarly journals Three Manual Noncommercial Methods to Prepare Equine Platelet-Rich Plasma

Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1478
Author(s):  
Lorenzo G. T. M. Segabinazzi ◽  
Giorgia Podico ◽  
Michael F. Rosser ◽  
Som G. Nanjappa ◽  
Marco A. Alvarenga ◽  
...  
Keyword(s):  
Blood Transfusion ◽  
Platelet Rich Plasma ◽  
Upright Position ◽  
Platelet Counts ◽  
Cell Counts ◽  
Blood Cell Counts ◽  
Platelet Concentration ◽  
Manual Methods ◽  
White Blood Cell Counts ◽  
Over Time

In light of PRP’s increasing popularity in veterinary practice, this study aimed to compare three manual methods to prepare and cool equine PRP. The blood of 18 clinically healthy mares was collected via venipuncture in a blood transfusion bag (method 1), blood tubes (method 2), and a syringe (method 3). In method 1, samples were double centrifuged; method 2 involved one centrifugation, and in method 3 the syringe was kept in an upright position to sediment for 4 h. After processing with three methods, PRP and platelet-poor plasma (PPP) were extracted and assessed for red (RBC) and white blood cell counts (WBC), platelet counts, and viability. In a subset of mares (n = 6), samples were processed with the three methods, and PRP was evaluated at 6 and 24 h postcooling at 5 °C. Method 1 resulted in the highest and method 3 in the lowest platelet concentration (p < 0.05), and the latter also had greater contamination with WBC than the others (p < 0.001). Platelet viability was similar across treatments (p > 0.05). Cooling for 24 h did not affect platelet counts in all methods (p > 0.05); however, platelet viability was reduced after cooling PRP produced by method 3 (p = 0.04), and agglutination increased over time in all methods (p < 0.001). The three methods increased (1.8–5.6-fold) platelet concentration in PRP compared to whole blood without compromising platelet viability. In conclusion, all three methods concentrated platelets and while cooling affected their viability. It remains unknown whether the different methods and cooling would affect PRP’s clinical efficacy.

Platelet Counts Estimated from Platelet Rich Plasma

1962 ◽  
Vol 28 (2) ◽  
pp. 113-118 ◽  
Author(s):  
E. Davidson ◽  
S. Tomlin
Keyword(s):  
Platelet Rich Plasma ◽  
Platelet Counts

scholarly journals The Influence of Fibrinogen and Fibrin on Thrombin Generation - Evidence for Feedback Activation of the Clotting System by Clot Bound Thrombin

1994 ◽  
Vol 72 (05) ◽  
pp. 713-721 ◽  
Author(s):  
Rachana Kumar ◽  
Suzette Béguin ◽  
H Coenraad Hemker
Keyword(s):  
Snake Venom ◽  
Thrombin Generation ◽  
Platelet Rich Plasma ◽  
Lag Time ◽  
Factor Vii ◽  
Factor V ◽  
Clotting System ◽  
Platelet Poor Plasma ◽  
Normal Plasma ◽  
System Factor

SummaryIn plasma the bulk of thrombin generation takes place after a clot has formed. We therefore investigated in what way the clot influences thrombin generation in plasma. The forming clot withdraws thrombin from free solution. Consequently less thrombin activity is found and less thrombin-inhibitor complexes are formed. The thrombin that is adsorbed to the clot reduces the lag time before thrombin generation in intrinsically or extrinsically triggered platelet poor plasma as well as in platelet rich plasma. We investigated the mechanism of this activation.Clots were obtained by recalcification of plasma or by the addition of thrombin-like enzymes (Reptilase, Agihal) from snake venoms. They were thoroughly washed until the washing fluid was devoid of any detectable clotting enzyme activity. In platelet poor plasma (PPP), thrombin-induced clots shorten the factor Va-dependent lag-time of thrombin generation in the extrinsic system as well as the factor VUIa-dependent thrombin generation in the intrinsic system. Factor V or factor VII preparations that in itself hardly influence thrombin generation patterns aquire the capacity to shorten these lag-times when incubated with clot. The last washing fluid of the clot is inactive. Snake venom induced clots are not active either. Clots that are incubated in heparinised plasma for 1 h or more are as active as clots from normal plasma are. A role of factor Xa can not be excluded but must be minor because a clot made by addition of thrombin to plasma from which the factors II, VII, IX and X have been removed is as active as a clot from normal plasma is.When added to recalcified platelet rich plasma (PRP), in which the lag-time of thrombin formation is dependent upon activation of platelet procoagulant phospholipid activity, any type of clot shortens the lagtime before the burst of thrombin generation. Clots that are obtained by snake venom enzymes are also active in this system. This indicates that fibrin alone is capable to induce the procoagulant phospholipid activity in platelets.We conclude that three known thrombin-dependent feedback activations in the clotting system (factor V, factor VIII and platelets) are efficiently supported by thrombin bound to the fibrin clot and that there is an additional activating effect of fibrin on the procoagulant action of platelets.

The Role of Factor XI in a Dilute Thromboplastin Assay of Extrinsic Coagulation Pathway

2001 ◽  
Vol 85 (06) ◽  
pp. 1055-1059 ◽  
Author(s):  
Shilong Xiong ◽  
Xiaofan He ◽  
Fayi Liu ◽  
Jianzhong Han ◽  
Juncheng Li ◽  
...  
Keyword(s):  
Blood Coagulation ◽  
Platelet Rich Plasma ◽  
Critical Role ◽  
Extrinsic Pathway ◽  
Thrombin Inhibition ◽  
Normal Plasma ◽  
Low Concentrations ◽  
Plasma Depletion ◽  
Coagulation Pathway

SummaryBlood coagulation has been thought to be composed of both intrinsic and extrinsic pathways. Recent evidence strongly supports the critical role of the extrinsic pathway in the initiation of blood coagulation. This investigation established an assay that examines the role of FXI in the thromboplastin-initiated (extrinsic) coagulation based on this new concept. Plasma clotting times were measured at different concentrations of thromboplastin with activated FXII inhibited (FXIIa-inhibited Diluted Thromboplastin Time, FXIIaiDTT). Only at low concentrations of thromboplastin was FXIIaiDTT of FXI-deficient plasma significantly prolonged than that of normal plasma. Depletion of FXI from normal plasma prolonged its FXIIaiDTT and replenishment of FXI shortened it. FXIIaiDTTs of both FVIII-deficient and FIX-deficient plasma were remarkably prolonged, and addition of normal plasma dose-dependently shortened it. Furthermore, earlier α-thrombin inhibition was directly correlated with decreasing FXa generation. The amount of FXa production was: platelet-rich plasma > platelet-poor plasma > FXI-deficient plasma. Therefore, our findings from the FXIIaiDTT assays not only support the critical role of extrinsic pathway in blood coagulation initiation, but also demonstrate the importance of FXI as an amplifier of thrombin generation in thromboplastin-initiated coagulation.

scholarly journals Platelet Decrease and Efficacy of Platelet-Rich Plasma Return for Peripheral Blood Stem Cell Apheresis

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 29-30
Author(s):  
Takahiro Shima ◽  
Teppei Sakoda ◽  
Tomoko Henzan ◽  
Yuya Kunisaki ◽  
Takahiro Maeda ◽  
...  
Keyword(s):  
Multivariate Analysis ◽  
Stem Cell ◽  
Platelet Count ◽  
Peripheral Blood ◽  
Peripheral Blood Stem Cell ◽  
Platelet Rich Plasma ◽  
Blood Stem Cell ◽  
Platelet Recovery ◽  
Platelet Counts ◽  
Cd34 Cells

Peripheral blood stem cell (PBSC) transplantation is a key treatment option for hematological diseases and widely performed in clinical practice. Platelet loss is the major complication of PBSC apheresis, and platelet-rich plasma (PRP) return is recommended in case of severe platelet decrease following apheresis; however, little is known about the frequency and severity of platelet loss nor the efficacy of PRP return post-apheresis. To address these questions, we assessed changes in platelet counts following PBSC-related apheresis in 270 allogeneic (allo)- and 105 autologous (auto)-PBSC settings. We also evaluated efficacy of PRP transfusion on platelet recovery post-apheresis. Platelet counts reduced up to 70% post-apheresis in both allo- and auto-PBSC settings, while severe platelet count decrease (&lt; 50 x 109/L) was only observed in auto-PBSC patients (Figure 1). We next analyzed the relationship between severe platelet (&lt; 50 x 109/L) after apheresis and several clinical factors by using univariate and multivariate analysis for auto-PBSC patients. As shown in Table 1, in univariate analysis, severe platelet counts following auto-PBSC apheresis was found more frequently in patients with lower platelet count, lower percentage of CD34+ cells in PB at pre-apheresis, repeated round of apheresis, and smaller number of collected CD34+ cells. On the other hand, in multivariate analysis, the white blood cell (WBC) counts pre-apheresis was the only significant risk factor of severe platelet count following apheresis (p = 0.038). We finally analyzed the transitions of platelet counts in the setting of apheresis. The median platelet counts at pre-apheresis, post-apheresis, and post-PRP return were 187.0 x 109/L, 132.0 x 109/L, and 154.0 x 109/L for allo-PBSC apheresis, and 147.0 x 109/L, 111.0 x 109/L, and 127.0 x 109/L for auto-PBSC apheresis (p &lt; 0.0001 for all, allo-PBSC donors and auto-PBSC patients, respectively) (Figure 2), indicating that PRP return post-apheresis facilitated a rapid platelet recovery in both allo- and auto-settings. Collectively, our data suggest that WBC counts pre-apheresis is a useful predictor for severe platelet decrease following auto-PBSC apheresis and that PRP return is an effective mean to facilitate platelet recovery post-apheresis. Disclosures No relevant conflicts of interest to declare.

scholarly journals Platelets and Massive Transfusion

1977 ◽  
Author(s):  
J.J. McNamara ◽  
H. Leinberger ◽  
G. Suehiro
Keyword(s):  
Blood Coagulation ◽  
Half Life ◽  
Massive Transfusion ◽  
Platelet Rich Plasma ◽  
Unknown Origin ◽  
Clotting Factors ◽  
Survival Curves ◽  
Platelet Counts ◽  
Sufficient Magnitude ◽  
Stored Blood

Diffuse oozing is a common problem after massive transfusion of stored blood. Coagulation studies usually show depression of all clotting factors, presumably is rarely of sufficient magnitude to cause bleeding. Similarly, platelet counts, which are frequently between 60,000 and 100,000 are still in a range not associated with clinical bleeding. Recent studies have suggested that coagulopathy post transfusion is due primarily to a qualitative defect in platelet function of unknown origin. Five baboons had blood drawn and stored by usual blood banking techniques for 10 days. Platelet rich plasma (PRP) was then prepared and platelets tagged with Cr51. Another five animals had fresh PRP prepared and platelets tagged with Cr51. Survival curves for tagged platelets demonstrated a half life of 13 ± 3 hours for 10-day old platelets and 47 ± 9 hours for fresh platelets. Platelet counts in stored blood averaged 100,000/cmm. Although nearly all 10-day old platelets were cleared by 24 hours, 50% were still present at 13 hours. It is evident then that platelet counts immediately after massive transfusion may be composed in large part of old stored, non-functional platelets.

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