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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↗
PubMed1986

Relationship of platelet-associated immunoglobulin G and platelet protein to platelet size and density in normal individuals and patients with thrombocytopenia.

Total platelet-associated immunoglobulin G (PA-IgG) and platelet volume and protein content in normal individuals and in patients with idiopathic thrombocytopenic purpura (ITP) and other thrombocytopenias of presumed nonimmune origin have been measured on platelets separated into subpopulations on the basis of density on continuous polyvinylpyrrolidone (Percoll) gradients. In all subjects PA-IgG per platelet was primarily found in the lightest platelets at levels up to sevenfold greater than in the heavier platelets. PA-IgG level per platelet was raised in light platelets in 29% of patients with thrombocytopenia and in heavy platelets in 60%. In almost half of these instances the PA-IgG level fell to within the normal range when considered in relation to either platelet volume or protein content. PA-IgG levels of patients with untreated ITP did not differ significantly from those with treated ITP or thrombocytopenia of other causes. Mean platelet volume and protein content of the total platelet population of all subjects showed significant linear correlation (P less than 0.01). Thus PA-IgG of both controls and patients with thrombocytopenia of all causes is preferentially located in the lightest platelets, but increases in PA-IgG in immune thrombocytopenias occur more frequently in the heavier platelets. These findings suggest that part of the process of IgG accumulation by platelets is the same in normal individuals as in patients with thrombocytopenia.

Adolescent↗
PubMed1985

Platelet interaction with subendothelial extracellular matrix: platelet-fibrinogen interactions are essential for platelet aggregation but not for the matrix-induced release reaction.

Cultured endothelial cells produce an extracellular matrix (ECM) to which platelets adhere and spread, ultimately resulting in platelet aggregation, thromboxane B2 production, and serotonin release. We have investigated the role of fibrinogen binding to the platelet GPIIb/IIIa complex in these reactions by comparing normal platelet-rich plasma (PRP), PRP from patients with Glanzman's thrombasthenia (whose platelets lack the GPIIb/IIIa complex), PRP in the presence of a monoclonal antibody that blocks the binding of fibrinogen to the GPIIb/IIIa complex, platelets washed free of fibrinogen, and washed platelets to which fibrinogen was added. Although platelet aggregation was virtually completely inhibited in the samples in which the normal interaction between fibrinogen and GPIIb/IIIa was impaired, adhesion of platelets to the matrix, spreading, and release of [14C]-serotonin were not affected. All of the platelet preparations released significant amounts of T X B2 with time, but there was a decrease in the amount produced by both the thrombasthenic and antibody-treated platelets. We conclude that the interaction of fibrinogen with platelet GPIIb/IIIa is not required for platelet adhesion to ECM or for adhesion-induced shape change or serotonin release. On the other hand, the platelet-fibrinogen interaction may play some role in augmenting adhesion-induced T X B2 production, and it is absolutely required for adhesion-induced platelet aggregation.

Animals↗
PubMed1984

A platelet membrane protein expressed during platelet activation and secretion. Studies using a monoclonal antibody specific for thrombin-activated platelets.

To identify structures on the platelet surface which become expressed after platelet activation, we have prepared murine monoclonal antibodies specific for thrombin-activated platelets. Hybridomas were screened for clones producing antibodies which bound to thrombin-activated platelets but not to resting platelets. Clone KC4 was identified. The binding of purified I-labeled KC4 antibody, an IgG1k, to thrombin-activated platelets was saturable. Minimal binding was observed to resting platelets. The interaction of antibody with thrombin-activated platelets was characterized by a binding constant, KD, of 7.2 +/- 0.4 nM and revealed 13,400 +/- 3,000 binding sites per platelet. The presence of Ca2+ or EDTA, a pH ranging from 4 to 10, or high ionic strength had no influence on antigen-antibody interaction. The KC4 antigen was expressed on the platelet surface after activation with ADP, collagen, epinephrine, or thrombin. The extent of [14C] serotonin release during activation was directly proportional to the availability of antigen on the platelet surface regardless of agonist or platelet aggregation. The antibody is directed against a single protein which migrated between GPIIb and GPIIa after sodium dodecyl sulfate gel electrophoresis. This protein was purified from platelet membranes by immunoaffinity chromatography using KC4 antibody-agarose and demonstrated an apparent molecular weight of 140,000 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis under both nonreducing and reducing conditions. Of the cells examined, only platelets contained this protein. These results indicate that platelet secretion is associated with the expression of an Mr = 140,000 integral membrane protein composed of a single polypeptide chain. This protein may be component of the internal granule membrane which is fused with the plasma membrane during activation.

Antibodies, Monoclonal↗
PubMed1989

Platelet aggregability and in vivo platelet deposition in patients with ischemic cerebrovascular disease--evaluation by indium-111-platelet scintigraphy.

In ischemic cerebrovascular disease, it is not clear whether platelet function in vitro actually reflects the situation in vivo. Using indium-111 platelet scintigraphy as a method for detecting platelet activation in vivo, we tried to elucidate this problem. Twenty eight patients with chronic stage of ischemic cerebrovascular disease (CVD) and 17 control subjects were examined. Platelet scintigrams were positive in 9 of 28 patients in CVD, while all were negative in control. A comparison of the results obtained from qualitative platelet imaging and platelet aggregability was performed to evaluate whether threshold aggregation concentration (TAC) grade differed across the three groups (control, CVD patients without platelet deposition and CVD patients with platelet deposition). CVD patients with platelet deposition showed a higher TAC than those patients who did not show platelet deposition (P less than 0.05) or control subjects without platelet deposition (P less than 0.05). These results suggest that some patients in chronic stages of CVD may have active platelet deposition on carotid atheromatous lesions, and presence of platelet deposition in vivo could contribute to reduce platelet reactivity in peripheral blood.

Adult↗
PubMed1986

Platelet surface glycoproteins. Studies on resting and activated platelets and platelet membrane microparticles in normal subjects, and observations in patients during adult respiratory distress syndrome and cardiac surgery.

The accurate definition of surface glycoprotein abnormalities in circulating platelets may provide better understanding of bleeding and thrombotic disorders. Platelet surface glycoproteins were measured on intact platelets in whole blood and platelet membrane microparticles were assayed in cell-free plasma using 125I-monoclonal antibodies. The glycoproteins (GP) studied were: GP Ib and GP IIb-IIIa, two of the major intrinsic plasma membrane glycoproteins; GMP-140, an alpha-granule membrane glycoprotein that becomes exposed on the platelet surface following secretion; and thrombospondin (TSP), an alpha-granule secreted glycoprotein that rebinds to the platelet surface. Thrombin-induced secretion in normal platelets caused the appearance of GMP-140 and TSP on the platelet surface, increased exposure of GP IIb-IIIa, and decreased antibody binding to GP Ib. Patients with adult respiratory distress syndrome had an increased concentration of GMP-140 and TSP on the surface of their platelets, demonstrating in vivo platelet secretion, but had no increase of platelet microparticles in their plasma. In contrast, patients after cardiac surgery with cardiopulmonary bypass demonstrated changes consistent with membrane fragmentation without secretion: a decreased platelet surface concentration of GP Ib and GP IIb with no increase of GMP-140 and TSP, and an increased plasma concentration of platelet membrane microparticles. These methods will help to define acquired abnormalities of platelet surface glycoproteins.

Antibody Specificity↗
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↗
PubMed1985

Enhanced platelet release reaction, shortened platelet survival time and increased platelet aggregation and plasma thromboxane B2 in chronic obstructive arterial disease.

Plasma beta-thromboglobulin (beta TG) and thromboxane B2 (TXB2) level, platelet aggregation (PA) in platelet rich plasma, platelet survival time using 111Indium radiolabelled platelets and platelet sensitivity to prostacyclin (PGI2) were measured in chronic obstructive arterial disease (COAD) patients. Severity of the disease was assessed by the ankle pressure index using Doppler auscultation. Platelet survival time was shorter, plasma beta TG and TXB2 and the rate and extent of PA induced by ADP or 1-epinephrine (but not collagen) were greater in the patients than in controls. Beta TG was inversly correlated with the pressure index and positively with TXB2 indicating increased platelet TXA2 synthesis. Platelet sensitivity to PGI2 was similar in the patients and controls. These results indicate increased platelet consumption and enhanced in vivo platelet activation and PA in COAD. The enhanced activation correlates with the severity of the disease and the activated platelets presumably synthesize increased amounts of TXA2. It is therefore concluded that platelets might be involved in the pathogenesis of COAD. The normal platelet sensitivity to PGI2 suggests that the administration of the compound may improve the abnormal platelet function in COAD patients and may attenuate the progression of the disease.

Adenosine Diphosphate↗
PubMed1985

Platelet adhesion to subendothelium--effect of shear rate, hematocrit and platelet count on the dynamic equilibrium between platelets adhering to and detaching from the surface.

The adherence of human 3H-adenine-labeled platelets to rat subendothelium was quantitated using a rotating probe device. Platelet adhesion increased in relation to the rotation time, reaching a plateau value in about 4-6 min without any further increase. A non-linear fitting analysis of experimental data allowed calculations of initial rate and plateau value of platelet adhesion. Increasing the shear rates (from 35 to 150 sec-1) or the hematocrit (from 10% to 40%), both the adhesion rate and the plateau value were increased. When different platelet concentrations were used the adhesion rate and the plateau calculated increased with platelet concentration. Different plateau values were obtained in the experimental conditions considered. This suggests that the plateau was not reached for the complete occupation of the subendothelial surface by the adherent platelets. Experiments using two different vessels rotated in the same platelet suspension or, viceversa, the same vessel rotated successively in two fresh platelet suspensions, showed that the plateau was not determined by reduced platelet reactivity. Rotating the same vessel first in radiolabeled platelets, until the plateau was reached, and secondly in non labeled platelets, or viceversa, showed that the plateau was indeed a dynamic condition where the number of platelets adhering and detaching reached equilibrium. These observations suggest that the platelet adhesion to subendothelium is the final equilibrium of two platelet fluxes, one adhering to the surface and another detaching from the surface.

Animals↗
PubMed1986

Morphological changes of platelets during the process of platelet aggregation in gray platelet syndrome.

Morphological changes of platelets during the process of platelet aggregation in gray platelet syndrome were observed by means of light microscopy, and scanning and transmission electronmicroscopy. Light microscopic examinations showed normal platelets and slightly enlarged, gray colored ones due to a deficiency in alpha-granules by May-Giemsa stain. At the time of maximum aggregation, normal platelets aggregated completely to form a mass by addition of ADP. On the other hand, patient's platelets only aggregated loosely and each platelet could be recognized separately, resembling primary aggregation of normal platelets. When collagen was added, almost no aggregation was noted in the patient's platelets. Scanning electronmicroscopic examinations revealed the same results as seen by light microscopy. Centralization of platelet organelles and almost complete aggregation and degranulation of platelets were noted immediately after 30 sec and 3-4 min after addition of ADP and collagen on the transmission electronmicrographs in normal platelets, whereas most patient's platelets remained to be unchanged. From these results, we concluded that these morphological changes were consistent with the changes of "release abnormalities" as shown in the functional examinations. Although some relationships between alpha-granule deficiency and functional abnormalities are considered, there is no definitive opinion.

Adenosine Diphosphate↗
PubMed1981

[Congenital anomalies of the human blood platelet, models for understanding mechanisms of platelet secretion: gray platelet disease].

The fundamental role of different platelet glycoproteins and proteins in platelet function is well known. Glycoproteins II b and III a, missing from platelets of patients with Glanzmann's thrombasthenia, appear to play a role in the mechanism of platelet cohesion. Platelet adhesion to sub-endothelium components depends on the binding of von Willebrand factor to the platelet membrane and this is defective in the Bernard Soulier syndrome which is characterised by the absence from the platelets of membrane glycoprotein Ib. The gray platelet syndrome is a new platelet disorder characterized by the absence of alpha granules and a reduced platelet aggregation response associated with an abnormal dense body section. Analysis of the protein and glycoprotein content of gray platelets has shown that they lack or have markedly reduced concentrations of the alpha granule proteins. It would appear that proteins secreted from the alpha granules may play a role during the later stages of platelet secretion leading to platelet aggregation.

Blood Platelet Disorders↗
PubMed1989

Assembly of the platelet prothrombinase complex is linked to vesiculation of the platelet plasma membrane. Studies in Scott syndrome: an isolated defect in platelet procoagulant activity.

Activation of human platelets by complement proteins C5b-9 is accompanied by the release of small plasma membrane vesicles (microparticles) that are highly enriched in binding sites for coagulation factor Va and exhibit prothrombinase activity. We have now examined whether assembly of the prothrombinase enzyme complex (factors VaXa) is directly linked to the process of microparticle formation. Gel-filtered platelets were incubated without stirring with various agonists at 37 degrees C, and the functional expression of cell surface receptors on platelets and on shed microparticles was analyzed using specific monoclonal antibodies and fluorescence-gated flow cytometry. In addition to the C5b-9 proteins, thrombin, collagen, and the calcium ionophore A23187 were each found to induce formation of platelet microparticles that incorporated plasma membrane glycoproteins GP Ib, IIb, and IIIa. These microparticles were enriched in binding sites for factor Va, and their formation paralleled the expression of catalytic surface for the prothrombinase enzyme complex. Little or no microparticle release or prothrombinase activity were observed when platelets were stimulated with epinephrine and ADP, despite exposure of platelet fibrinogen receptors by these agonists. When platelets were exposed to thrombin plus collagen, the shed microparticles contained activated GP IIb-IIIa complexes that bound fibrinogen. By contrast, GP IIb-IIIa incorporated into C5b-9 induced microparticles did not express fibrinogen receptor function. Platelets from a patient with an isolated defect in inducible procoagulant activity (Scott syndrome) were found to be markedly impaired in their capacity to generate microparticles in response to all platelet activators, and this was accompanied by a comparable decrease in the number and function of inducible factor Va receptors. Taken together, these data indicate that the exposure of the platelet factor Va receptor is directly coupled to plasma membrane vesiculation and that this event can be dissociated from other activation-dependent platelet responses. Since a catalytic membrane surface is required for optimal thrombin generation, platelet microparticle formation may play a role in the normal hemostatic response to vascular injury.

Antibodies, Monoclonal↗
PubMed1988

Platelet-associated immunoglobulins G, A and M are secreted during platelet activation: normal levels but defective secretion in grey platelet syndrome.

Platelet-associated (PA) IgG is known to be released from normal human platelets when they are stimulated by aggregating agents. We have studied whether PA-IgA and PA-IgM are also secreted during platelet activation or during blood collection and processing and whether their levels are related to those in serum. Processing of platelets from normal donors in the presence of secretion inhibitors prostaglandin E1 (PGE1) and theophylline increased levels of both surface and total PA-immunoglobulins (Ig) in intact and lysed platelets respectively, with increases being significant for surface PA-IgA and PA-IgM and total PA-IgM. About 50% of total PA-IgM, 40% PA-IgA and 20% PA-IgG was detectable on intact platelets. All three PA-Ig and PA-albumin were secreted in response to thrombin and this release was inhibited by PGE1. The platelet:serum ratio of each Ig and albumin were similar. In grey platelets deficient in alpha-granules, PA-Ig and PA-albumin levels were raised per platelet but when increased platelet size was taken into account PA-Ig were normal and PA-albumin just below normal. Although thrombin caused release of most of the small amounts of beta-thromboglobulin present, PA-Ig and PA-albumin were not released. This suggests that PA-Ig and albumin from plasma may enter a pool of secretory proteins in normal platelets, but in grey platelets they remain in some other site.

Alprostadil↗
PubMed1989

The relationship of human platelet density to platelet age: platelet population labeling by monoamine oxidase inhibition.

The relationship between platelet density and platelet age appears to vary between species with relatively few labeling studies in humans reported. In this study, irreversible monoamine oxidase (MAO) inhibitors were used to biochemically label the circulating platelet population in 15 humans. Platelet samples were then isolated during the 15 days after drug ingestion. The platelets were separated by density on continuous linear Percoll gradients and the density distributions were divided into five fractions containing approximately equal numbers of platelets. Baseline MAO activity was strongly correlated with platelet density. Twenty-four hours after a single dose of tranylcypromine, platelet MAO activities in the density subpopulations were reduced to 14% to 17% of the baseline values. During the first five days after inhibition, the rates of recovery of MAO activity (percentage per day) were inversely proportional to platelet density. The recovery rates in the two most dense fractions were initially slow but increased after five days. Percentage recovery of MAO activity in the least dense fraction was significantly greater than the percentage recovery in the most dense fraction on days 2, 3, 5, and 8 (P less than .01, sign test). These results support the hypothesis that normal human platelets show a small increase in density with age, but they do not exclude the additional possibility that human platelet lifespan is positively correlated with platelet density.

Adult↗
PubMed1988

Occurrence of platelet basic protein, a precursor of low affinity platelet factor 4 and beta-thromboglobulin, in human platelets and megakaryocytes.

beta-thromboglobulin antigen, a platelet-specific secreted protein, occurs in three forms: platelet basic protein, low affinity platelet factor 4, and beta-thromboglobulin. The combined level of beta-thromboglobulin antigen in megakaryocytes, measured by radioimmunoassay, was 13 +/- 7 micrograms/10(6) cells (SD, n = 6). The relative proportions of the three forms of beta-thromboglobulin antigen present within platelets and megakaryocytes were determined in cells lysed with trichloroacetic acid to minimize artifactual proteolysis. Samples were analyzed by isoelectric focusing in polyacrylamide gel with quantitative immunological detection on a nitrocellulose transfer of the gel. In platelets, the major species found was low affinity platelet factor 4 with precursor platelet basic protein as only 25% +/- 11% (SD, n = 16) of total beta-thromboglobulin antigen. In megakaryocytes partially purified both from normal bone marrow aspirates and from whole marrow specimens obtained after surgery, platelet basic protein was a higher proportion of beta-thromboglobulin antigen (49% +/- 13% SD, n = 11) than was the case in platelets. beta-thromboglobulin itself was never detected under the conditions of cell lysis used. Our results suggest that platelet basic protein is synthesized in megakaryocytes and that its cleavage is associated with an earlier stage of cell development than simply maturation to platelets. Further support for the precursor status of platelet basic protein was found in the expression of predominantly this antigenic form in a human erythroleukemia cell line.

Antigens, Human Platelet↗
PubMed1985

Studies on the effect of platelet inhibitors on platelet adhesion to collagen and collagen-induced human platelet activation.

The effect of pyridoxal 5'-phosphate (PALP) and trifluoperazine (TFPZ), the calmodulin antagonist, on in vitro platelet adhesion to collagen and collagen-induced platelet activation was studied using platelet-rich-plasma (PRP) or washed platelets (WPL). Platelet aggregation and [14C]-5HT release induced by "threshold" or low concentrations of collagen (0.6 micrograms/ml) in PRP were completely abolished by PALP (24 mM), TFPZ (250 microM) as well as indomethacin (10 microM). At higher concentrations of collagen (10-15 micrograms/ml) in PRP and WPL, the use of stirred and unstirred platelets treated with collagen enabled a distinction to be made between aggregation and adhesion-mediated release reaction. Platelet aggregation and the aggregation-mediated release reaction induced by these concentrations of collagen in stirred platelets were completely abolished by PALP, TFPZ and indomethacin although neither adhesion to collagen nor the adhesion-mediated release reaction of unstirred platelets was significantly affected by these inhibitors. Interestingly, both adhesion and the adhesion-mediated release reaction were abolished by concentrations of PALP 10-40 fold higher than those required to abolish aggregation. Collagen-induced platelet aggregation, but not platelet adhesion, was inhibited in resuspended platelets pretreated with PALP and NaBH4 indicating a separation in the membrane sites involved in aggregation and adhesion. The results further emphasize the distinction between adhesion and aggregation-mediated events with regards to collagen with the latter being more susceptible to inhibition by antiplatelet agents such as PALP and TFPZ.

Collagen↗
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↗
PubMed1989

A new congenital platelet abnormality characterized by spontaneous platelet aggregation, enhanced von Willebrand factor platelet interaction, and the presence of all von Willebrand factor multimers in plasma.

A case is reported of a 49-year-old woman with a mild bleeding tendency. Her bleeding time, platelet count and size, plasma ristocetin cofactor activity, von Willebrand factor (vWF) antigen, and vWF multimeric pattern are all within normal limits. Spontaneous platelet aggregation is observed when citrated platelet-rich plasma (PRP) is stirred in an aggregometer cuvette. This aggregation is completely is only slightly diminished by an antiglycoprotein (GP) IIb/IIIa or by an anti GPIb monoclonal antibody. The patient's PRP shows increased sensitivity to ristocetin. The distinct feature of this patient, also present in two family members studied, is that platelet aggregation is initiated by purified vWF in the absence of any other agonist. The vWF-induced platelet aggregation is abolished by anti-GPIb and anti-GPIIb/IIIa monoclonal antibodies and by EDTA (5 mmol/L). Apyrase inhibits the second wave of aggregation. Patient's platelets in PRP are four to six times more reactive to asialo vWF-induced platelet aggregation than normal platelets. The amount of radiolabeled vWF bound to platelets in the presence of either low concentration of ristocetin or asialo vWF was increased 30% compared with normal. The patient's platelet GPIb was analyzed by SDS page and immunoblotting and by binding studies with anti-GPIb monoclonal antibodies showed one band with slightly increased migration pattern and a normal number of GPIb molecules. Unlike the previously reported patients with pseudo or platelet-type von Willebrand disease, this patient has normal vWF parameters.

Antibodies, Monoclonal↗