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PubMed1997

[Evaluation of platelet function and tissue plasminogen activator activity in ischemic heart disease depending on concurrence with hyperlipoproteinemia and aspirin therapy].

Platelet activation, impairment of fibrinolysis and dyslipidemia are important factors in the pathogenesis and progression of ischemic heart disease. Aspirin therapy will reduce platelet activation both by its negative effect on platelet aggregation (SPA) and by inhibition of granule release which liberates such mediators as platelet factor 4 (PF4) and plasminogen activator inhibitor 1 (PAI-1). The present study was performed in 57 patients with ischemic heart disease (IHD), divided into groups depending on coexistent hyperlipoproteinemia (HLP) and aspirin treatment. The control group included 21 healthy individuals, matched for age and sex. Parameters of hemostasis (SPA, PF4, PAI-1) and concentration of lipid fractions (TC, TG, LDL, HDL) were measured in plasma. Increased PF4 levels were found in all groups with IHD, irrespective of hyperlipoproteinemia or aspirin treatment. Enhanced SPA and higher PAI-1 were limited to group IHD-HLP without aspirin. Highest PAI-1 activities were observed after stimulation of platelets in vitro. In conclusion, patients with IHD and hyperlipoproteinemia presented most pronounced platelet activation and impairment of fibrinolysis. Aspirin had a beneficial effect on these changes. Lower activities of PAI-1, in patients treated with aspirin, can be ascribed to its reduced release from platelets. Aspirin did not satisfactorily reduce the level of PF4, although it strongly inhibited SPA.

Adult↗
PubMed1997

Characterization of the humoral immune response in heparin-induced thrombocytopenia.

Recent reports indicate that antibodies associated with heparin-induced thrombocytopenia and thrombosis (HITP) are specific for complexes formed between heparin and the heparin-binding, platelet alpha granule protein, platelet factor 4 (PF4). As with other disorders mediated by immune complexes (IC), the characteristics of the involved immunoglobulins could affect the ability of IC to cause symptoms. We therefore studied the class, subclass, and potency of antibodies specific for heparin:PF4 complexes formed by two groups of patients: one with severe thrombocytopenia, with or without thrombosis, and a positive serotonin release assay (SRA) (Group 1) and another with mild or absent thrombocytopenia, absence of thrombosis, and a negative SRA despite having formed antibodies reactive with heparin:PF4 complexes (Group 2). IgG antibodies were more common in the Group 1 patients (100%) than in Group 2 (46%), whereas IgM antibodies were more common in Group 2 (81%) than in Group 1 (42%) (P = 0.009). About half of each group formed IgA antibodies. In each group, the IgG antibodies were predominantly IgG1 (82%); 42% were IgG3. Only one IgG2 antibody was identified in a total of 52 antibody formers. Antibodies of the IgG class were consistently of higher titer in Group 1 patients than in Group 2 patients (P < 0.001). Recent reports suggest that the H131 form of the Fc gammaRII receptor, which binds preferentially to IgG2 Fc, is found with greater than expected frequency in patients with HITP. Identification of only one IgG2 antibody among 38 antibodies of the IgG class argues against a unique role for antibodies of this subclass in the pathogenesis of HITP. The finding that titers of antibodies in Group 1 patients were a significantly higher titer than in Group 2 patients suggests that development of the full-blown HITP syndrome may require the formation of antibodies of unusually high titer.

Aged↗
PubMed1983

beta-Thromboglobulin and platelet-factor 4 in patients with cancer: correlation with the stage of disease and the effect of chemotherapy.

Plasma level of beta-thromboglobulin (BTG) and platelet factor 4 (PF4), two platelet-specific proteins, were measured in 20 patients with cancer. None of the patients had evidence of thromboembolism or impaired renal function, and none was taking drugs known to interfere with platelet function. In ten patients who were in complete remission or whose disease was thought to be inactive, the levels of both proteins were essentially within normal limits. The other ten patients had active or progressive symptomatic disease. BTG level was elevated in all but one patient, and PF4 was raised in two patients. These results suggest that in patients with clinically active cancer, a state of ongoing in vivo platelet activation may be present, a phenomenon which may contribute to the known increased occurrence of thromboembolism in patients with malignancy. The intravenous administration of various cytotoxic drugs used in cancer chemotherapy produced no immediate measurable changes in BTG and PF4 level.

Adult↗
PubMed1984

Platelet factor 4 release during exercise in patients with coronary artery disease.

Many recent studies provide evidence that increased platelet activation occurs in a significant number of patients with atherosclerotic coronary artery disease. The mechanisms responsible for this activation are unknown, although there have been studies suggesting a correlation with abnormal lipoproteinemia, acute myocardial infarction, unstable angina, and exercise-induced myocardial ischemia. We studied 84 patients undergoing standardized treadmill exercise using either a Bruce [N = 63] or symptom-limited Naughton protocol [N = 21]. In contrast to ten healthy volunteer subjects, the patient group demonstrated a significant increase in plasma concentrations of platelet factor 4 [PF4] between pre- and postexercise blood samples confirming earlier reports of exercise-induced platelet activation and secretion. As with previous studies, however, only a subset of patients demonstrated this response. When the entire group was analyzed for the presence or absence of electrocardiographic ischemic changes and the presence of documented versus suspected coronary artery occlusions, there were no differences noted between groups that explained the variable responses measured. However, there was a significant difference between patient groups when analyzed by whether or not they were being treated with beta-blocking agents. Patients who were being treated with propranolol or one of the longer-acting beta-blocking agents did not have a significant increase in plasma PF4 following exercise, in contrast to patients who were not beta-blocked. Plasma concentrations of epinephrine, norepinephrine, and lactic acid were measured in 49 patients and all normal subjects. There was no correlation between the changes in plasma PF4 concentrations and any of these three variables, suggesting that platelet activation was not occurring through direct platelet activation by circulating catecholamines. This study provides further evidence that there is a subset of CAD patients with platelet hyperactivity. This is the first time that beta-blockade has been demonstrated to modify this platelet response. The effectiveness of beta-blocking agents in CAD may be in part related to their antiplatelet effect.

Adrenergic beta-Antagonists↗
PubMed1994

Effects of interleukin-2 administration on platelet function in cancer patients.

Platelet function in 16 patients with metastatic renal cell carcinoma and melanoma was studied sequentially over the first 96 hr of treatment with moderate and high-dose interleukin-2 (IL-2). During the first 96 hr of therapy, an increased ex vivo platelet maximal aggregation (MA) response to ADP, epinephrine, and arachidonic acid was paralleled by a decrease in the peripheral platelet count. Plasma specimens from patients receiving the moderate dose schedule showed a significant IL-2 induced secretory response of the platelet alpha-granule components beta-thromboglobulin (BTG) and platelet factor 4 (PF4) and the eicosanoid thromboxane B2 (TBX2) as measured by RIA. The increase in TXB2 was highly correlated with MA when analyzed by bivariate regression analysis, whereas the addition of PF4 to TXB2 in a multiple regression analysis further increased their correlation to MA. The observed decrease in peripheral platelet count correlated significantly with MA and PF4 secretion. High-dose IL-2-treated patients showed a statistically significant increase in the percentage of large platelets exceeding 12 fl in diameter and platelet responsiveness to hypotonic shock. These observations suggest that IL-2 therapy results in a reduced peripheral platelet pool, with an increased proportion of the remaining pool of platelets larger, more viable, and activated.

Adult↗
PubMed2003

Exposure of fibrinogen-adherent platelets to plasma proteins: a new method for studying protein interactions with platelets.

To understand the effects of mediators in coagulating blood at biomaterial surfaces, it is important to use methods that resemble the normal sequence of events in wound healing around implants. The initial adhesion of platelets from whole blood onto material surfaces is mediated by the fibrinogen receptor glycoprotein IIb/IIIa, as shown in a previous study (Broberg et al., J Lab Clin Med 2002; 139:163-172). In this study, isolated platelets were adhered to fibrinogen and exposed to IgG, von Willebrand factor, or thrombin. The response was detected as the number of adherent platelets, the spreading of platelets, the exposure of CD62P (P-selectin), and the release of platelet factor 4 (PF4), ADP, and ATP. These results were compared to the response of platelets adhering to surfaces coated with the same proteins. Fibrinogen-adherent platelets exposed to thrombin generated the significantly highest exposure of CD62P and release of PF4, ADP, and ATP. When platelets were adhered to different protein coatings, von Willebrand factor generated the most CD62P exposure, IgG generated the most PF4 release, and thrombin generated the highest concentration of ADP. These results indicate that protein interactions with platelets may generate different results, depending on the mode of protein exposure.

Adenosine Diphosphate↗
PubMed2002

Increased plasma thrombospondin-1 (TSP-1) levels are associated with the TNF alpha-308A allele in children with juvenile dermatomyositis.

Vascular occlusion is more frequent in children with juvenile dermatomyositis (JDM) who have the TNF alpha-308A allele. One of the potent anti-angiogenic factors is thrombospondin-1 (TSP-1). This study investigated the association of the TNF alpha-308A allele with circulating levels of angiogenic mediators, TSP-1, and platelet factor 4 (PF4) using fresh, platelet-poor plasma (PPP). The TNF alpha-308A allele was characterized by PCR amplification and NcoI digestion. Concentrations of TSP-1 and PF4 in PPP from 31 JDM patients and 25 matched pediatric controls were determined by ELISA. The majority of the JDM children with the TNF alpha-308A allele (7/12) produced more TSP-1 than their TNF alpha-308G counterparts (P < 0.05), and their TSP-1 values were inversely related to those for PF4 (P < 0.0006). We conclude that the increased circulating concentrations of TSP-1 associated with the TNF alpha-308A allele suggest that this anti-angiogenic regulator may play a significant role in the augmented vascular occlusion observed in JDM children with this genetic marker.

Alleles↗
PubMed1989

Platelet specific proteins (beta-thromboglobulin and platelet factor 4) in normal pregnancy and in pregnancy complicated by preeclampsia.

Pregnancy is accompanied by significant alterations of platelet function. Platelet activity can be determined by measurement of plasma levels of secreted platelet proteins. In this study we determined plasma levels of beta-Thromboglobulin (beta-TG) and Platelet Factor 4 (PF4) simultaneously in 35 women with uncomplicated pregnancy and in 15 patients with preeclampsia in third trimester of gestation. Additionally, PF4 plasma levels were measured using a commercially available Radio Immunoassay (RIA) and an Enzyme Immunoassay (EIA) simultaneously and values obtained were compared. Platelet count and creatinine were in the normal range in both groups; however, significantly higher levels of beta-TG (P less than 0.0005) and PF4 (P less than 0.0001) were found in case of preeclampsia. High levels of platelet proteins emphasize the active role of the platelets in the alterations of hemostasis in cases of preeclampsia.

Female↗
PubMed1992

Markers for endothelial injury, clotting and platelet activation in preeclampsia.

The etiology of disseminated intravascular coagulation (DIC) in preeclampsia is not well understood. We measured plasma levels of fibronectin (FN), which may reflect endothelial cell injury, fibrinopeptide A (FPA), a specific marker of clotting, platelet counts (PLC) and mean platelet volumes (MPV), as well as beta-thromboglobulin (beta TG) and platelet factor 4 (Pf4), products of irreversible platelet activation in 24 preeclamptic patients and 24 controls matched for age, gestational age, labor status, and parity. In preeclampsia, FN and FPA were significantly elevated while PLC were significantly decreased (P less than 0.0001, less than 0.05 and less than 0.01, respectively). beta TG, Pf4, and MPV values did not show significant differences. These findings support the hypothesis that endothelial injury, clotting activation and platelet consumption are increased in preeclampsia. However, the much closer association of preeclampsia with FN levels as compared to FPA, beta TG, Pf4, suggests that endothelial injury is a more basic mechanism of preeclampsia than clotting or platelet activation.

Adolescent↗
PubMed2003

Platelet activity measured by plasma levels of beta-thromboglobulin and platelet factor 4 in seasonal allergic rhinitis during natural pollen exposure.

BACKGROUND: Upon activation, platelets release mediators with potent inflammatory properties in IgE-mediated immune responses. Moreover, the atopic state leads towards functional abnormalities of these cells. OBJECTIVE: The aim of our study was to examine the degree of activation of circulating platelets in patients with seasonal allergic rhinitis (SAR) during the symptomatic period, to improve the understanding of platelet function in atopy. SUBJECTS AND METHOD: Plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) - specific markers of platelet activation were measured by enzyme-linked immunoassay in 20 patients suffering from SAR and in 15 healthy, nonatopic subjects. RESULTS: There were no significant differences in peripheral blood platelet numbers and plasma levels of beta-TG and PF4 in SAR patients when compared with control subjects. CONCLUSION: It seems that increased in vivo platelet activity, assessed by measuring plasma beta-TG and PF4, may not occur during allergic inflammation that is associated with SAR.

Adolescent↗
PubMed2002

Elevated plasma levels of beta-thromboglobulin and platelet factor 4 in patients with rheumatic disorders and cutaneous vasculitis.

The efficacy of plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) as markers of the presence and activity of vasculiditic processes in rheumatic diseases were evaluated, first by serial measurement of their levels in a patient with rheumatoid arthritis and a chronic leg ulcer in the course of treatment, and second in 11 patients with rheumatoid arthritis without cutaneous vasculitis, and in nine patients with a variety of rheumatic diseases with cutaneous vasculitis. In the former, plasma levels of beta-TG and PF4 were elevated and slowly reduced in parallel with healing, raised again after relapse, and normalized after disappearance of the leg ulcer. In the latter, both plasma levels were elevated in all of the nine patients with cutaneous vascular lesions and in one of the 11 patients rheumatoid arthritis without skin lesions. Levels of beta-TG and PF4 may be useful to estimate the presence of vascular lesions in rheumatic disorders.

Adolescent↗
PubMed1981

Enhanced in vivo platelet release reaction and malondialdehyde formation in patients with hyperlipidemia.

Plasma level of beta-thromboglobulin (beta TG), a useful marker of in vivo platelet "release reaction,"was determined by radioimmunoassay in 69 patients, with three types of primary hyperlipidemia (IIa, IIb, IV) and compared with the findings in age- and sex-matched healthy controls and 57 patients with established atherosclerosis and peripheral vascular disease. Malondialdehyde (MDA) formation, used for assessment of prostaglandin synthesis, was determined in 51 and plasma platelet factor 4 (PF4), measured by radioimmunoassay, in 48 of the patients with hyperlipidemia. Results were correlated to five serum lipids and lipoprotein levels in the patients with hyperlipidemia. beta TG was significantly increased in the patients with hyperlipidemia and peripheral vascular disease, compared to those in the controls (p < 0.001); it was significantly higher in the patients with hyperlipidemia than in those with peripheral vascular disease. PF4 and MDA formation were also increased in the patients with hyperlipidemia, and significantly higher levels of MDA were obtained in patients with type IIb and type IV hyperlipidemia than in those with type IIa hyperlipidemia (p < 0.02). beta TG and MDA correlated weakly with total serum cholesterol triglycerides and very low density lipoprotein-triglyceride. There was also a significant correlation between beta TG and PF4, and MDA production. These results indicate that in vivo platelet "release reaction" and MDA formation are increased in hyperlipidemic patients. The release reaction is more enhanced in those with hyperlipidemia than in the patients with peripheral vascular disease. They suggest that the abnormal platelet function is related to the elevated levels of serum lipids and lipoproteins in the hyperlipidemic patients and not only to the atherosclerotic changes associated with hyperlipidemia.

Aged↗
PubMed1995

Quarternary structure amplification of protein folding differences observed in 'native' platelet factor-4.

Platelet factor 4 (PF4), a protein of 70 residues, exists in solution as a distribution of monomer, dimer and tetramer (M-D-T) states in slow exchange on a 600 MHz 1H-NMR chemical shift time scale. Well-resolved Y60 ring proton resonances in each aggregate state allow derivation of M-D-T populations. Under the same set of solution conditions, M-D-T aggregate state distributions vary from prep to prep or with repeated freeze-drying or raising/lowering the solution pH. These variations are not the result of chemical modifications and reflect differences in the strength of subunit associations and therefore folding. Variations are greatest at pH values at or below the pKas of carboxylate groups, supporting the idea that electrostatic interactions modulate PF4 subunit interactions. Treating these distributions as true equilibria results in free energy differences of about 0.5 kcal/mol subunit. Quarternary structure amplifies free energy differences among various folded states of monomer PF4.

Humans↗
PubMed1983

Evidence for serotonin binding in vitro by platelet factor 4 and beta-thromboglobulin.

Evidence is presented for in vitro high affinity binding of serotonin (5-HT) by beta-thromboglobulin (beta TG) and platelet factor 4 (PF4) from human blood. Results include: 1) identification by radioimmunoassay of PF4 in specifically bound material obtained by 5-HT affinity chromatography of human platelet extracts; 2) binding of 72% and 6% of radiolabelled PF4 on 5-HT and control affinity columns, respectively; and 3) binding of approximately 8 moles of 5-HT per mole of purified beta TG in the presence of ferrous ion and heparin in ultrafiltration studies, with Scatchard analysis indicating a dissociation constant of about 4 X 10(-8) M.

Beta-Globulins↗
PubMed1987

Platelet factor 4 enhances fibrin fiber polymerization.

In order to further examine the role of platelet secretory products on fibrin assembly, we have examined the effects of purified platelet factor 4 (PF4) on fibrin formation in vitro. The kinetics of fibrin formation and the structural properties of the resulting fibrin gel are strongly affected by PF4. In the presence of 7.6 ng/mL PF4, the fibrin fiber mass-length ratio increases from 3.5 X 10(12) daltons/cm. These results emphasize the importance of the local microenvironment in clot structure and its subsequent fate at the site of vascular injury.

Fibrin↗
PubMed1989

The serial hemostasis-related changes in patients with cerebral infarction: comparison between progressing and non-progressing stroke.

Serial determinations of beta-thromboglobulin (BTG), platelet factor 4 (PF4), fibrinopeptide A (FPA), antithrombin III (ATIII), protein C (PC), fibrin (ogen) degradation product (FDP), FDP D-dimer, activated partial thromboplastin time (APTT), prothrombin time (PT), and euglobulin lysis time (ELT) were performed in 18 patients with non-progressing stroke and 14 patients with progressing stroke in order to predict the development of progressing stroke. Increasing levels of BTG, PF4 and FDP with frequent fluctuation were noted in both kinds of stroke. Fluctuation of FPA levels was also noted but was less pronounced. PC levels were found to be slightly decreased with fluctuation but the mean was still in the lower normal limit. BTG, PF4 and PC all elevated at the time of deterioration of physical condition in patients with progressing stroke, whereas FPA had no definite change at that time. From our study, we conclude that both platelet activation and coagulation process do occur in both kinds of stroke. But the latter plays a minor role in the formation of thrombosis. The hemostasis change, especially concerning the thrombosis formation, probably plays a role in the development of progressing stroke, but we cannot predict their development even by the detections of the newly known molecular substances appearing in various steps of the hemostatic mechanism. Development of new tests for understanding the whole dynamic change of the thrombosis process is necessary for accurate prediction of the progressing stroke in the future.

Aged↗
PubMed1994

Platelet activation in diabetic patients with asymptomatic atherosclerosis.

We studied 27 non-insulin-dependent diabetics without apparent atherosclerosis (AS) to investigate whether abnormal platelet function is related to asymptomatic atherosclerosis in diabetes mellitus. The degree of AS was quantitatively evaluated by determining the intimal plus medial thickness (IMT) of the carotid artery wall with ultrasound high-resolution B-mode imaging. Based on our previous finding that the upper threshold of the IMT was 1.1 mm in healthy subjects, the patients were divided into the AS-positive group with the IMT > 1.1 mm, (n = 17) and the AS-negative group with the IMT < 1.1 mm (n = 10). Among five variables measured as the factors concerned with thrombogenesis, only plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) were significantly higher in the AS-positive group than in the AS-negative group. Chronic administration of pentoxifylline (300 mg/day) significantly reduced the abnormally high plasma levels of beta-TG and PF4 in 7 patients of the AS-positive group to normal levels, without lowering the normal plasma beta-TG and PF4 levels in the remaining 10 patients. Pentoxifylline treatment did not affect the plasma levels of the 3 other variables, von Willebrand factor, 6-keto prostaglandin F1 alpha and thromboxane B2. This study suggests that the progress of atherosclerosis in diabetes mellitus is associated with in vivo platelet activation and platelet activation does not occur in diabetics without carotid atherosclerosis. Pentoxifylline may impede the vicious cycle in which atherosclerosis is accelerated by platelet activation.

Aged↗
PubMed1988

Food intake suppression by growth factors and platelet peptides by direct action in the central nervous system.

Intracerebroventricular (i.c.v.) microinfusion of epidermal growth factor (EGF), basic fibroblast growth factor (bFGF) and platelet factor 4 (PF4) suppressed 2 h and nighttime food intake in rats. The following daytime food intake did not change or increased. I.c.v. infusion of platelet-derived growth factor (PDGF) suppressed only 2 h food intake. I.c.v. infusion of bovine serum albumin (BSA), nerve growth factor (NGF), or inactivated EGF, bFGF and PF4 had no effect. Intraperitoneal (i.p.) administration of EGF, bFGF, PF4 and PDGF in doses equivalent to or higher than those administered centrally had no effect. The results suggest a central action of growth factors and platelet peptides on feeding regulation.

Animals↗