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PubMed2004

Von Willebrand factor accelerates platelet adhesion and thrombus formation on a collagen surface in platelet-reduced blood under flow conditions.

Plasma von Willebrand factor (VWF) has been identified as an indispensable factor for platelet adhesion and thrombus formation on a collagen surface under flow conditions. VWF binds to collagen and then tethers platelets to the collagen surface through interaction with platelet glycoprotein Ib and also contributes to the thrombus formation on the collagen surface. In the present study, we demonstrated that the addition of VWF/factor VIII complex or purified VWF (> 2 ristocetin cofactor activity units/mL) increased platelet adhesion to the collagen surface in platelet-reduced blood ( approximately 5 x 10(4) platelets/microL) to the normal level. VWF had no stimulatory effect when it was allowed to bind to the collagen surface before blood flow was initiated. Addition of an excess of FITC (fluorescein-5-isothiocyanate)-labeled VWF to platelet-reduced blood under these flow conditions demonstrated that the VWF was mainly incorporated into the platelet aggregates. These results indicated that the supplemented VWF stimulates the platelet adhesion onto the collagen surface by enhancing platelet aggregation in the platelet-reduced condition. This also suggests a possibility that supplementation of VWF to individuals with thrombocytopenia might be effective for increasing their hemostatic potential.

Anticoagulants↗
PubMed1980

Platelet survival and platelet production in systemic lupus erythematosus (SLE).

Platelet survival studies were carried out on 36 patients suffering from SLE. Twelve of them received no therapy, 17 were on corticosteroids (CS), and the remaining 7 received CS and azathioprin (AT). Ten healthy hospital employees served as controls. Only 1 of our SLE patients had thrombocytopenia (platelet count 42 x 10(9)/l). All the remaining 35 patients had venous platelet counts greater than or equal to 120 x 10(9)l. In the control group the average platelet mean life-span (MLS) was 5.8 +/- 0.3 (range 4.0-6.8) days. In the group of untreated SLE patients 3 out of 12 subjects (25%) had a platelet MLS below the lower range for the controls. The mean platelet MLS in the control group did not differ statistically from any of the means of the three groups of SLE patients studied. The lowest mean for platelet MLS (5.2 +/- 0.6 days) was encountered in the group of patients who received no therapy. The means for platelet MLS in the two groups of SLE patients who received immunosuppressive therapy were higher (6.5 +/- 0.4 and 6.6 +/- 0.4 days, respectively) but did not differ statistically from the mean of untreated patients (0.10 > p > 0.05). The mean platelet production rate in the control group (23 +/- 10(10) platelets per day) did not differ from any of the three groups of SLE patients investigated. In the literature it has been proposed that a state of compensated thrombocytolysis is present in most cases of SLE. The results of the present study do not support this hypothesis, however.

Adrenal Cortex Hormones↗
PubMed2000

Platelet ultrastructural morphometry for diagnosis of partial delta-storage pool disease in patients with mild platelet dysfunction and/or thrombocytopenia of unknown origin. A study of 24 cases.

BACKGROUND AND OBJECTIVE: Exact diagnosis is sometimes difficult in patients presenting with a slight bleeding diathesis, prolonged bleeding times, non-specific aggregometric abnormalities, and/or mild thrombocytopenia. The objective of this study was to evaluate the use of platelet ultrastructural morphometry in detecting a partial d-storage pool disease in such patients. DESIGN AND METHODS: Platelets from 52 patients and 15 controls were fixed immediately in glutaraldehyde in White's saline without anticoagulant and processed for transmission electron microscopy. Using computer-assisted morphometry, the size and shape of the platelets were measured, as were the size and number per platelet of the dense- and a-granules. Ultrastructural morphology of the above and other intraplatelet structures was observed. RESULTS: Twenty-four cases were diagnosed as having a partial d-storage pool disease. Mean platelet area (2.28 microm(2)) and maximum diameter (2.58 microm) were significantly greater in patients than in control subjects (1.64 microm(2) and 2. 25 microm, respectively) but discoid shape was preserved. Mean dense-granule number was decreased, both per platelet and per microm(2) of platelet area (patients 0.22 and 0.09; controls 0.42 and 0.24). Seven patients also had a marked decrease in a-granules, resulting in a significantly lower mean number of granules per microm(2 )(patients 2.43; controls 3.15). Additionally, the patients' platelets had significant increases in both lipid droplets and surface-connected canalicular system. INTERPRETATION AND CONCLUSIONS: A partial dense-granule deficiency, sometimes associated with partial a-granule deficiency, should be borne in mind faced with patients who have a slight bleeding diathesis, non-specific platelet dysfunction tests and/or mild thrombocytopenia of unknown origin. Platelet ultrastructural morphometry is useful in diagnosing this condition.

Adolescent↗
PubMed2000

Correlation of plasma and serum vascular endothelial growth factor levels with platelet count in colorectal cancer: clinical evidence of platelet scavenging?

Most studies measuring circulating vascular endothelial growth factor (VEGF) have sampled serum rather than plasma. There has been much debate whether the collection of sera (which causes the activation of platelets and VEGF release) is a true reflection of tumor angiogenic activity or whether platelets act as scavengers of VEGF. Addressing this issue, we measured serum and plasma VEGF, before and after colorectal resection, with reference to platelet counts. Serum and plasma samples were collected from 116 colorectal cancer (CRC) and 116 control patients. Ninety CRC and 32 benign resections were performed. Both plasma and serum VEGF were significantly higher in CRC patients (18.5 and 327 pg/ml, respectively) compared with controls (9.0 and 151.5 pg/ml, respectively; P < 0.0001). Paired serum and plasma VEGF measurements correlated in both CRC (r = 0.56) and control patients (r = 0.73; P < 0.0001). Serum and plasma VEGF levels correlated with platelet count in CRC patients (r = 0.58 and 0.44, respectively) but not in controls. Plasma and serum VEGF levels, and VEGF concentration per platelet, increased with advancing disease stage. The correlation of serum and plasma VEGF with platelet counts in CRC but not in benign disease may be attributable to the scavenging of VEGF from the tumor source by platelets, with plasma levels reflecting free circulating VEGF in equilibrium with platelet levels. VEGF levels in citrated plasma are low and lie close to the limits of ELISA sensitivity. We recommend that a standardized measurement of serum VEGF--normalized by the patient's platelet count to give a value of serum VEGF per platelet--be adopted.

Adult↗
PubMed2001

Role of platelet glycoprotein IIb/IIIa in ADP-activated platelet adhesion to aortic endothelial cells in vitro: observation with video-enhanced contrast microscopy.

Intravascular thrombus formation downstream of cerebral arterial occlusion may result in necrosis of ischemic tissue. To clarify the causative mechanisms, interaction between adenosine-5'-diphosphate (ADP)-activated platelets and cultured human aortic endothelial cells (HAEC) was examined by employing video enhanced contrast-differential interference contrast (VEC-DIC) microscopy. The numbers of (1) control/platelets, (2) ADP-activated platelets, (3) ADP-activated, anti-platelet GP Ibalpha antibody (GUR20-5)-treated platelets, and (4) ADP-activated, platelet GP IIb/IIa antagonist (TAK-029)-treated platelets, associated with HAEC after superfusion and wash-out were counted in visual fields of 30 x 30 microm2. Many ADP-activated platelets adhered to HAEC directly, while almost no platelets adhered to HAEC in the control. The adhesion was almost completely blocked by the GP IIb/IIIa antagonist, but not by GP Ibalpha antibody. We conclude that initial binding of ADP-activated platelets to HAEC is mediated by platelet GP IIb/IIIa in this in vitro system.

Adenosine Diphosphate↗
PubMed2002

Intracellular factor XIII crosslinks platelet cytoskeletal elements upon platelet activation.

The platelet cytoplasm contains approximately half of the factor XIII (FXIII) transglutaminase content circulating in blood, yet the function of cytoplasmic FXIII is poorly understood. This study investigated functions of platelet FXIII in internal platelet processes by studying the interactions of FXIII with platelet cytoskeletal proteins. FXIII was present in cytoskeletal fractions of platelet lysate separated by centrifugation. When cytoskeletal fractions were immobilized on nitrocellulose membranes, thrombin-activated rFXIII (rFXIIIa*) or calcium ion-treated rFXIII (rFXIIIa degree) bound to some of these proteins, whereas untreated rFXIII did not. Utilizing fluorescence microscopy, an actin polymerization-dependent transient translocation of FXIII from a diffuse homogeneous distribution throughout the cytoplasm to the platelet periphery was observed upon platelet activation, suggesting an association with cytoskeletal proteins. Transglutaminase activity increased in cytoskeletal fractions of activated versus non-activated platelets. Immunoblotting analysis of platelet cytoskeletal fractions identified filamin and vinculin as being crosslinked upon platelet activation.

Blood Platelets↗
PubMedDate not supplied

Counting of platelet derived growth factor and transforming growth factor-beta in platelet-rich-plasma used in jaw bone regeneration.

AIM: Growth factors (GFs) as platelet derived growth factor (PDGF) and transforming growth factor (TGF-beta), found in platelet beta-granules also present in platelet-rich-plasma (PRP), accelerate bone revascularization and regeneration and for this reason they have been employed successfully in dental and maxillofacial surgery. Platelet concentrate is commonly used for this purpose as long as platelet release reaction and the consequent GFs loss are avoided. To reduce this phenomenon we set up an easy and fast procedure for preparing a satisfying clotted PRP by adding CaCl2 only (no exogenous thrombin). METHODS: ELISA essay has been used to measure PDGF and TGF-beta in plasma, platelets and serum and platelet GMP-140, with the cytofluorometric technique in order to quantify the degranulation entity. RESULTS: In the 13 examined patients receiving clotted PRP to enhance bone regeneration in post-extractive alveolar sockets, PRP showed no sign of platelet activation (degranulation) and short recalcification times (8-12 min). The autologous clotted PRPs specimen have been evaluated in laboratory in terms of GFs percent: 76% of initial GFs content could be recovered in clotted PRP. This result confirms the absence of platelet degranulation in our procedure. CONCLUSIONS: Significant clinical results in alveolar bone regeneration are reached only with a high percentage of GFs inserted in bone matrix, avoiding early platelet degranulation.

Adult↗
PubMed2005

[The secretory activity of blood platelets--beta-thromboglobulin and platelet factor 4 in echinococcosis].

UNLABELLED: Parasitic infection can cause local or systemic inflammatory process. Antibody-dependent cellular cytotoxicity, with eosinophils as the effector cells, is the major mechanism of antiparasitic defence. The cytotoxic activity against antibody-coated parasites is also demonstrated by blood platelets. Platelets initiate and maintain inflammatory processes, become activated due to contact with immunocompetent cells or due to a direct contact with a parasite. THE OBJECTIVE: The aim of the examination was to evaluate the cytotoxic activity of platelets in patients infected with Echinococcus granulosus. MATERIAL AND METHODS: The study was conducted on a group of 24 patients (aged 26-69) infected with Echinococcus granulosus, 19 women and 5 men. The patients were treated with albendazole (Zentel) and did not give consent to surgical procedure. Blood for analysis was collected prior to treatment. Patients infected with E. granulosus were subjected to the examination of platelet activation through the assessment of beta-thromboglobulin and platelet factor 4 concentrations. The concentration of beta-thromboglobulin and platelet factor 4 were assayed using a set of ASSERACHROM (Boehringer Mannheim) according to the immunoenzymatic method with labelled antibodies. Platelet count and their morphological parameters were determined with haematologic analyser Technicon H-3 System. Although platelets do not get into a direct contact with the parasite, an increase is observed in the concentrations of beta-thromboglobulin (16.09 +/- 2.68 IU/ml) and platelet factor 4 (8.47 +/- 3.32 IU/ml), which may indicate the involvement of platelets in the parasitic disease.

Adult↗
PubMed2006

Immature platelet fraction as a predictor of platelet recovery following hematopoietic progenitor cell transplantation.

The immature platelet fraction (IPF) as determined by the Sysmex XE-2100 is a rapid automated measure of the least mature component of the platelet population and is thought to correlate with thrombopoietic activity of the marrow. We investigated the ability of IPF to predict platelet recovery following hematopoietic progenitor cell (HPC) transplantation. IPF was compared to standard parameters of hematopoietic recovery, including the immature reticulocyte fraction (IRF), an early predictor of recovery. Fifty patients undergoing peripheral blood HPC transplantation (38 autologous and 12 allogeneic) were followed daily for 11 to 28 days after transplantation with measurement of IPF, IRF, absolute neutrophil counts (ANC) and platelet counts. Mean days to recovery for IPF was 3.1 days less than for platelet count (P <.0001), 3.8 days less than for ANC (P <.0001), and 0.6 days less than for IRF (P = .0477). IPF recovered at least 1 day prior to platelet count in 79% (38 of 48) of patients, and was followed by platelet count recovery within 1 to 12 days (mean, 4.1 days). When autologous and allogeneic patient groups were analyzed separately, IPF recovered significantly earlier than platelet count and ANC in both groups (P <.0001). Thrombopoietin (TPO) levels in 5 patients receiving transplants correlated with IPF; however, this appeared to be secondary to an inverse correlation of both TPO and IPF with platelet count. IPF is comparable to IRF as one of the earliest predictors of hematopoietic recovery following peripheral blood HPC transplantation. IPF could potentially be useful as a predictor of platelet recovery in other bone marrow failure syndromes.

Adolescent↗
PubMed1990

Glomerular localization of platelet cationic proteins after immune complex-induced platelet activation.

Synthetic polycations bind to glomerular polyanions (GPA) and increase permeability to macromolecules and immune complexes. Platelet factor 4 and other platelet cationic proteins also bind to GPA and may play a role in immune complex deposition. Here we examine the potential of locally released cationic proteins to bind to GPA after immune complex-induced platelet activation within the renal microvasculature. Rabbits were immunized against bovine serum albumin (BSA), and BSA (2 or 4 mg/ml in buffered saline) was infused into the left renal artery to deliver 8 or 16 mg of BSA over 20 minutes. Thirty minutes later, kidneys were removed and tissue processed for light, immunofluorescence, and electron microscopy for the assessment of glomerular alterations and the localization of immune complexes (IgG and BSA), platelet factor 4, and platelet cationic proteins. GPA was measured by quantitative ultrastructural assessment of polyethyleneimine binding sites. Glomerular capillaries contained large intraluminal immune complexes and platelet aggregates. Also, numerous deposits were observed within subendothelial and subepithelial aspects of the glomerular basement membrane (GBM). Immunofluorescence and immunocytochemistry revealed prominent localization of platelet factor 4, platelet cationic proteins, IgG and BSA within peripheral capillary walls of glomeruli concomitant with a reduction in GPA. Glomeruli of controls or contralateral kidneys did not show GBM localization of immune complexes or platelet proteins. Thus, nascent formation of immune complexes in capillaries was associated with platelet activation and deposition of endogenous cationic proteins in the GBM. This mechanism may be involved in neutralization of GPA and mediation of increased permeability, which leads to GBM deposition of immune complexes.

Animals↗
PubMed1990

Different effects of human neutrophil elastase on platelet glycoproteins IIb and IIIa of resting and stimulated platelets.

The effect of human neutrophil elastase (HNE) on the structure and receptor activity of platelet glycoprotein IIb/IIIa complex was studied. Resting platelets, which bound only traces of 125I-fibrinogen in the absence of ADP, were found to be barely susceptible to HNE. As shown by immunoblotting experiments, treatment of such platelets with HNE (14 micrograms/ml) did not provoke a detectable cleavage of GPIIb but resulted in a partial digestion of GPIIIa and appearance of 110 kDa fragment. Such proteolytic modification of the GPIIb/IIIa complex was accompanied by a slight increase in the binding of fibrinogen to blood platelets in the absence of ADP. Treatment of partially activated platelets (spontaneous activation during washing procedure) with HNE caused a progressive loss of GPIIb and degradation of GPIIIa to 110 kDa and 60 kDa fragments. These spontaneously stimulated platelets had initially a high number of fibrinogen binding sites exposed, corresponding to approximately 50% of receptor capacity observed in platelets activated by the optimal concentration of ADP. Digestion of GPIIb/IIIa by HNE of such platelets markedly increased the exposure of fibrinogen receptors. Thus, the stimulation of platelets increases significantly the susceptibility of the GPIIb/IIIa complex to proteolysis by HNE. However, such modification of the GPIIb/IIIa does not destroy its function as a receptor for fibrinogen either on the resting or activated platelets.

Blood Platelets↗
PubMed1989

Simvastatin reduces platelet thromboxane formation and restores normal platelet sensitivity against prostacyclin in type IIa hypercholesterolemia.

The effect of lowering total serum cholesterol and low-density lipoprotein (LDL) cholesterol on platelet function, thromboxane formation and platelet sensitivity against PGI2 was studied in platelet-rich plasma ex vivo. Additionally, PGI2 receptors were determined in membrane preparations of these platelets. Twelve patients suffering from familial hyperlipoproteinemia type IIa (FH) were treated for 8 months with simvastatin (20-40 mg/day) and compared with 10 untreated FH patients and 10 untreated normocholesterolemic subjects. Compared with those of healthy controls, platelets of untreated FH patients were hyperreactive, as shown by an enhanced aggregation response and release of ATP and thromboxane after stimulation by collagen (0.3-5 micrograms/ml) and ADP (0.3-10 micrograms/ml). Simvastatin reduced the total and LDL serum cholesterol towards control levels while HDL cholesterol remained unchanged. This was accompanied by a significant decrease of platelet aggregation, thromboxane formation and ATP secretion being no more different from normocholesterolemic controls. In addition, the reduced platelet sensitivity against prostacyclin (aggregation, stimulation of cAMP formation) in untreated FH patients was improved to normal values by simvastatin. This was associated with a significant elevation of the reduced prostacyclin binding sites and might be explained by an improved access of prostacyclin to its receptors at platelet membranes. These data demonstrate that the reduction of total and LDL serum cholesterol by simvastatin results in a normalization of platelet function by (i) reduction of platelet hyperreactivity and (ii) improvement of the sensitivity against prostacyclin towards normal via enhanced PGI2-binding sites.

Adenosine Triphosphate↗
PubMed1988

Role of tumor cytoskeleton and membrane glycoprotein IRGpIIb/IIIa in platelet adhesion to tumor cell membrane and tumor cell-induced platelet aggregation.

Components of the tumor cell cytoskeleton (i.e., microtubules, microfilaments, and intermediate filaments) have been reported to affect metastatic ability, since disruption of these components leads to a decrease in metastasis. One mechanism of metastasis which has not been previously considered is the decreased interaction of tumor cells with platelets. We present evidence that disruption of the tumor cell cytoskeleton decreases the ability of tumor cells to aggregate homologous platelets. This effect is dependent upon the disruption of microfilaments/intermediate filaments but not disruption of microtubules. In addition, tumor cell platelet interactions require the lateral mobility of specific receptors (i.e., clustering) on the tumor cell plasma membrane. A membrane glycoprotein immunologically related to the platelet glycoprotein IIb/IIIa complex was identified on Walker 256 carcinosarcoma cells using specific polyclonal and monoclonal antibodies and Northern blot analysis using complementary DNA probes for IIb and IIIa. Mobility of this receptor is dependent upon tumor cell microfilaments/intermediate filaments, but not microtubules. Furthermore, treatment of tumor cells with specific antibodies to the platelet glycoprotein IIb/IIIa complex inhibits tumor cell-platelet interaction at the macroscopic level (i.e., aggregation) and at the ultrastructural level (i.e., platelet adhesion to the tumor cell surface). These results suggest that this immunologically related glycoprotein IIb/IIIa is a receptor for platelet binding to the tumor cell surface, an event which precedes overt platelet aggregation and is dependent upon an intact tumor cell microfilament and intermediate filament network. Therefore, the decreased metastasis observed by others following disruption of the tumor cell cytoskeleton may be due, in part, to a decreased tumor cell-platelet interaction.

Animals↗
PubMed1986

Comparison of the inhibitory effects of aspirin and ticlopidine on platelet aggregation and Ca2+ mobilization in rat platelets.

To study the cause of the sex difference in the inhibitory effects of aspirin on platelet functions, we compared the effects of aspirin and ticlopidine in rat platelets. Aspirin showed the sex difference in the effects on the collagen-induced platelet aggregation and the malondialdehyde (MDA) production, but ticlopidine showed no sex difference in the effects on those. The C-AMP level in male rat platelets was the same as that in female rat platelets. Ticlopidine increased the C-AMP level in rat platelets, but aspirin did not. Aspirin suppressed the intracellular Ca2+ mobilization in male rat platelets more strongly than in female rat platelets. Ticlopidine suppressed the Ca2+ mobilization in both sexes equivalently. The above results suggest that the sex difference in the inhibitory effects of aspirin on rat platelet functions comes from the sex difference in the thromboxane (TX) production in rat platelets.

Animals↗
PubMed1988

Adenylate cyclase activation determines the effect of thromboxane synthase inhibitors on platelet aggregation in vitro. Comparison of platelets from responders and nonresponders.

The effect of five thromboxane-synthase inhibitors (UK-37248, UK-38485, UK-34787, CGS-13080 and OKY-1581) on arachidonic acid-induced platelet aggregation has been studied in vitro on platelets from 30 different healthy volunteers. The sensitivity of their platelets to adenylate cyclase stimulators or to dibutyryl cyclic AMP has been evaluated contemporarily. In 4 of the 30 volunteers tested no inhibition of platelet aggregation was obtained with any of the five thromboxane synthase inhibitors: these subjects were defined nonresponders; in 13 volunteers inhibition was observed with all the five drugs (responders). Significantly higher amounts of prostaglandin (PG)D2, prostacyclin and adenosine were required to suppress arachidonic acid-induced aggregation of platelets from nonresponders in vitro. No differences were instead observed between responders and nonresponders concerning platelet sensitivity to forskolin or dibutyryl cyclic AMP. The cyclic AMP rise obtained with exogenous prostacyclin was lower in platelets from nonresponders than in those from responders. PGE2 added in vitro to platelets from nonresponders exerted always a proaggregatory effect whereas this PG was antiaggregatory in most of the nonresponders. PGE2 blunted the antiaggregatory activity of PGD2 and limited the cyclic AMP increase induced by PGD2 in all the subjects tested. These data indicate that the unequal functional response of platelets from different subjects to thromboxane synthase inhibition depends essentially on adenylate cyclase function: a relative insensitivity of this enzyme to activating stimuli and the accumulation of substances (PGE2, PG endoperoxides, etc.) reducing the activity of adenylate cyclase may lead to continued platelet activation in some subjects despite the suppression of the synthesis of thromboxane A2.

Adenylyl Cyclases↗
PubMed1988

Ca2+ mobilization primes protein kinase C in human platelets. Ca2+ and phorbol esters stimulate platelet aggregation and secretion synergistically through protein kinase C.

Low concentrations of Ca2+-mobilizing agonists such as vasopressin, platelet-activating factor, ADP, the endoperoxide analogue U44069 and the Ca2+ ionophore A23187 enhance the binding of [3H]phorbol 12,13-dibutyrate (PdBu) to intact human platelets. This effect is prevented by preincubation of platelets with prostacyclin (except for A23187). Adrenaline, which does not increase Ca2+ in the platelet cytosol, does not enhance the binding of [3H]PdBu to platelets. In addition, all platelet agonists except adrenaline potentiate the phosphorylation of the substrate of protein kinase C (40 kDa protein) induced by PdBu. Potentiation of protein kinase C activation is associated with increased platelet aggregation and secretion. Stimulus-induced myosin light-chain phosphorylation and shape change are not significantly affected, but formation of phosphatidic acid is decreased in the presence of PdBu. The results may indicate that low concentrations of agonists induce in intact platelets the translocation of protein kinase C to the plasma membrane by eliciting mobilization of Ca2+, and thereby place the enzyme in a strategic position for activation by phorbol ester. Such activation enhances platelet aggregation and secretion, but at the same time suppresses activation of phospholipase C. Therefore, at least part of the synergism evoked by Ca2+ and phorbol ester is mediated through a single pathway which involves protein kinase C. It is likely that the priming of protein kinase C by prior Ca2+ mobilization occurs physiologically in activated platelets.

Adenosine Diphosphate↗
PubMed1987

Flow cytometric analysis of platelet surface glycoproteins: phenotypically distinct subpopulations of platelets in children with chronic myeloid leukemia.

To determine whether distinct subpopulations of platelets exist in individual patients, platelets were incubated with monoclonal antibodies to glycoprotein Ib and the glycoprotein IIb-IIIa complex, and analyzed by flow cytometry. Normal donors (n = 15) had single glycoprotein Ib-positive and glycoprotein IIb-IIIa complex-positive populations of platelets, with no subpopulations. In normal donors there was a direct relationship between platelet size and the number of surface glycoprotein Ib and glycoprotein IIb-IIIa complex antigens per platelet. In patients with Bernard-Soulier syndrome and Glanzmann's thrombasthenia, all platelets were equally negative with regard to the glycoprotein Ib and glycoprotein IIb-IIIa complex phenotype, respectively. In contrast, each of six children with chronic myeloid leukemia (four of whom were Philadelphia chromosome negative and two of whom were Philadelphia chromosome positive) had two phenotypically distinct subpopulations of platelets: one glycoprotein Ib negative, the other glycoprotein Ib positive. In each of these six children with chronic myeloid leukemia, phenotypically distinct subpopulations of glycoprotein IIb-IIia complex-negative and glycoprotein IIb-IIIa complex-positive platelets were also detected. Polyclonal antiplatelet antibody bound to both the glycoprotein Ib-negative and glycoprotein IIb-IIIa complex-negative subpopulations. Age-matched controls (n = 3) and adults with Philadelphia chromosome-positive chronic myeloid leukemia (n = 3) showed single glycoprotein Ib-positive and glycoprotein IIb-IIIa complex-positive populations. In conclusion, flow cytometry detected distinct subpopulations of platelets in children with chronic myeloid leukemia. Flow cytometry is an important new method of identification and investigation of subpopulations of platelets in individual patients.

Adult↗
PubMed1986

Increased platelet malondialdehyde, but normal platelet sensitivity to adenosine-5-diphosphate and prostacyclin in well-controlled type 1 diabetics without vascular complications.

Normal platelet sensitivity to in vitro ADP-induced aggregation (median 46, range 32-62% dT) and a normal antiaggregatory effect of prostacyclin (PGI2; ID50:0.65, range 0.18-2 ng PGI2/ml PRP) were found in a carefully selected group of 30 fairly well-controlled (average HbA1c 7.0%) Type 1 diabetic patients (14m/16f; median age 27.5, range 15-45 yr; duration of disease 7, range 1-24 yr) without macroangiopathy in comparison to 19 (9m/10f; age 26, range 17-40 yr) closely matched healthy controls (42, range 34-63% dT; 0.55, range 0.35-1 ng PGI2/ml PRP). By contrast, platelet malondialdehyde (MDA) release was significantly (p less than 0.001; Mann-Whitney, two-tailed, non-parametric test) increased in diabetics (6.55, range 0.91-18.94 nmol/10(9) platelets) in comparison to controls (3.9 range 2.6-6.9 nmol/10(9) platelets). Since MDA has been used as an indicator of platelet thromboxane formation (a potent stimulator of platelet aggregation), elevated platelet MDA in diabetics has been attributed to platelet activation. In the present study, for the first time increased platelet MDA release in diabetics has been shown to occur independently from enhanced platelet aggregation, even in well-controlled patients without evidence of either macroangiopathy or microangiopathy. This could be of clinical importance, since MDA is known to act on low density lipoprotein-uptake of human macrophages.

Adenosine Diphosphate↗