[Glanzmann's thrombasthenia. Apropos of 22 cases].
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Adolescent↗
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Coagulation and fibrinolysis study in systemic lupus erythematosus: haematological, urinary and tissue parameters.
Haematochemical, urinary and tissue parameters were examined in the elaboration of the coagulation and fibrinolysis profile in 33 cases of systemic lupus erythematosus in different stages of the disease. Coagulation abnormalities varied from hypo- to hyper-coagulability, these being often associated in the same patient, either simultaneously or at different stages of the disease. Activation of coagulation, closely related to the immunological activity of the disease, was present in 80% cases in the acute stage, and 36% of those in the remission stage. The lupus-like anticoagulant was not much involved, and platelets were the prime figures in the haemostatic abnormalities of lupus, those being the preferred target of direct antibody activities, or possibly of immune complexes as well. Activation of the coagulatory cascade is not uncommonly accompanied by a thrombophilic tendency coupled with signs of consumption, this being the expression of a continuously stimulated haemostatic balance.
Autoantibodies↗
Xylum CSA: automated system for assessing hemostasis in simulated vascular flow.
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Adult↗
Laboratory tests for the diagnosis of heparin-induced thrombocytopenia.
Heparin-induced thrombocytopenia (HIT) is associated with high morbidity and mortality. Because the pathophysiology of this complex disorder has remained unclear, so has the development of supportive diagnostic laboratory assays. The currently available laboratory methods for HIT diagnosis include several platelet function assays: the platelet aggregation assay, platelet aggregation with simultaneous measurement of ATP release (lumi-aggregometry), the serotonin release assay, and flow cytometric assays. ELISA assays, which quantitate anti-heparin/platelet factor 4 antibody titers, have recently become available. Assay characteristics for these assays were studied using sera collected from clinically diagnosed HIT patients with and without thrombosis, normal individuals, various types of hospitalized patients without HIT, heparin or low molecular weight heparin-treated patients without HIT, and patients with platelet-immune disorders other than HIT. The results of our studies suggest that none of the assays can be considered a "gold standard" for the laboratory diagnosis of HIT as many false-negative and false-positive results were obtained. Furthermore, antibodies against the heparin/platelet factor 4 complex, as identified by the current ELISA tests, are not the sole cause of HIT since many patients lacking clinical symptoms associated with HIT exhibited high antibody titers following heparin treatment. An assay using flow cytometry, being developed for HIT testing, will be described. At this time, clinical impression remains important for the diagnosis of HIT.
Adult↗
Mechanisms underlying increased platelet reactivity in patients with peripheral arterial disease. Preliminary results.
BACKGROUND: In peripheral arterial disease (PAD) atherosclerosis is disseminated and thrombosis risk is high. We have not only shown the platelets of PAD patients to by hyperreactive and aspirin resistant, but have recently verified them to be hypersensitive to heparin as well. In the present study we have begun to clarify the mechanisms underlying these regularly observed clinical findings. METHODS: Platelet function was tested with conventional, ADP-primed aggregation and with stagnation point flow adhesio-aggregometry (SPAA). SPAA permits real time, quantitative assessment of platelet adhesion and aggregation under biologically relevant flow conditions. The platelets from a female patient with congenital afibrinogenemia, were analyzed before and after intravenous fibrinogen substitution. In 14 PAD patients and 14 controls, platelet reactivity was assessed before and after incubation with the two platelet membrane glycoprotein (GP)-IIb/IIIa inhibitors Ro 43-8857 and 7E3. Lastly, experiments were performed before and after addition of plasma aliquots stemming from 4 PAD patients to platelet rich plasma and to solutions of gel-filtered platelets (GFP) stemming from 4 healthy volunteers. Before fibrinogen substitution, the platelets of the afibrinogenemic patient were unable to adhere in the SPAA-system and maximal ADP-primed aggregability was below 10%. After substitution, normal platelet adhesion was measured and primed aggregation increased three-fold. Mean baseline adhesion in the patient collective was twice that compared to controls (p<0.001). SPAA-measured, spontaneous aggregation was observed in ten patients and in none of the controls (p<0.001). RESULTS: Both SPAA-measured and primed aggregation were abolished at the lowest substrate concentrations (0.1 microM Ro 43-8857, 1 microg/ml 7E3). At these concentrations adhesion was reduced by 65% and 40% (respectively) in patients, and by 55% and 25% in controls. Total abolition of adhesion in both groups was seen with 0.5 microM Ro 43-8857 and 10 microg/ml 7E3. Platelet response to inhibitory agent was similar in patients and controls, as were the differences in dose-response between aggregation and adhesion. Upon addition of patient plasma to volunteer PRP, the platelets of all 4 healthy individuals aggregated spontaneously and the mean adhesivity in the group rose three-fold. The overall ability of the GFP to adhere when re-added to their own plasma was decreased, whereas, in the presence of patient plasma, adhesion increased significantly. CONCLUSIONS: On the basis of these findings we conclude that: 1) SPAA measures and quantifies platelet interactions with both fluid-phase (aggregation) and immobilized (adhesion) fibrinogen, 2) these reactions are mediated by the GP, IIb/IIIa receptor complex 3) the binding affinity, metabolic pathways and signal transduction underlying platelet adhesion differ from those involved in aggregation (possibly reflecting their varying roles in hemostasis), 4) the functionally normal platelets of patients with PAD are primed in vivo by a circulating plasma constituent, which leads to enhanced recruitment of activated GP, IIb/IIIa onto the platelet surface and, thereby, to an overall increase in reactivity.
Acetates↗
A comparison of methods for the study of platelet hyperfunction in thromboembolic disorders.
To gain insight into the interrelationship of various methods for the study of platelet hyperfunction, we compared plasma beta-thromboglobulin (beta-TG), circulating platelet aggregates (CPA), and ADP-induced platelet aggregation in 119 patients with thromboembolic disorders and 28 control subjects. CPA correlated fairly well with beta-TG, suggesting that both methods measure similar in vivo platelet activation and aggregation. CPA had an excellent correlation with platelet survival half-time. In contrast, there was a poor correlation between in vitro platelet aggregation and CPA or beta-TG. These results confirm the notion that both CPA and beta-TG procedures are suitable for determination of in vivo platelet activation whereas platelet aggregation technique has serious limitations to test in vivo platelet activity. In order to have an accurate assessment of platelet hyperfunction, a battery of tests are needed.
Adenosine Diphosphate↗
Studies of the platelet filter test (shear dependent platelet aggregation) in patients with uncommon haemorrhagic disorders.
Platelets of anticoagulated whole blood forced at 40 mmHg through a fine filter are activated, aggregated and retained, so block the filter (platelet filter test, O'Brien JR, Salmon GP. Blood 1987; 1354-1361). Our clinical experiences with this simple and quick haemostasis test are summarized. Patients were investigated with different types of vWD (type-1 = 35, type-2A = 7, type-2B = 7, type-3 = 1), Glanzmann's thrombasthenia, congenital deficiency of cyclo-oxygenase, acquired Bernard-Soulier syndrome, FXII-, FXIII-deficiency and a control group. The cumulative drop count and the platelet retention were carefully measured during two phases of the filter test. Platelet count, bleeding time, vWF:Ag and vWF:Rcof activity were measured along with the platelet filter test. The filter was not blocked and the platelet retention was abnormally low in all patients with thrombasthenia, type-2a, type-2B, type-3 vWD. Treatment with 1-desamino-8-D-arginine-vasopressin (DDAVP) caused enhanced platelet retention in 16 patients with type-1 vWD. The test is simple, quick and cheap, has good reproducibility, and may be useful in clinical haemostasis laboratories for examination of high shear induced platelet functions.
Adolescent↗
[Does controlled hypotension with nitroprusside affect platelet function?].
Induced hypotension is an accepted technique to reduce intraoperative blood loss and thereby ensures satisfactory operating conditions, especially in microscopic interventions. Sodium nitroprusside (NP), which is often used for induced hypotension, was reported to inhibit platelet aggregation in vitro. Impairment of platelet function implies a higher bleeding risk, which would make the use of NP for induced hypotension questionable. METHODS. With the approval of the local ethics committee, 30 patients scheduled for nasal septum operations were included in this randomised study. For induction of anaesthesia 2 mg vecuronium, 0.1 mg fentanyl, 0.2 mg/kg etomidate, and 1 mg/kg succinylcholine were used. After tracheal intubation the patients inhaled 1.0-1.5 vol.% isoflurane in a gas mixture containing 66% nitrous oxide in oxygen. Fifteen patients received an i.v. infusion of NP for 60 min. The concentrations chosen produced a decrease of mean arterial blood pressure to 50 mm Hg. Blood samples were taken before induction of anaesthesia; after induction of anaesthesia but before beginning of the operation; and 60 min after the beginning of the operation. This time-point coincided with the end of NP administration in the study group. The last blood sample was drawn the morning after the operation. Platelet function was determined in platelet-rich plasma by a turbidometric method after adding 22 mumol/l epinephrine to induce aggregation. The spontaneous aggregation was measured in whole blood using impedance aggregometry. Data within one group were analysed using analysis of variance. Student's t-test for unpaired values served to compare data between the two groups. RESULTS. Biometric data in the two groups were comparable. The blood loss in the control group [265 (190-410) ml] significantly exceeded (P < 0.05) that in the hypotensive group [125 (75-210) ml]. No significant changes in platelet function were found throughout the study period in the patients treated with NP. In the control patients the epinephrine-induced aggregation increased significantly from 53.1 +/- 5.3% before anaesthesia to 72.1 +/- 3.3% the morning after the intervention. The spontaneous aggregation showed a significant increase from 0.718 +/- 0.338 Ohm/h before anaesthesia to 2.164 +/- 0.442 Ohm/h 60 min after the beginning of the operation. The value on the 1st postoperative day (2.266 +/- 0.448 Ohm/h) was also significantly higher than the basal value. CONCLUSIONS. In contradiction to in vitro studies using high concentrations of NP, we could not find a decrease in platelet aggregation due to hypotensive anaesthesia with this drug in vivo. In the control group a significant increase in platelet aggregation was observed, which was probably counteracted in the hypotensive patients by the interaction of NP with cyclic guanosine monophosphate (c-GMP). NP augments the intracellular concentration of c-GMP, which is known to decrease platelet aggregation.
Adolescent↗
Platelet function defects associated with hemorrhage or thrombosis.
Platelet dysfunction, especially acquired forms, is a common cause of hemorrhage, especially when associated with trauma or surgery. Although the hereditary platelet function defects are generally quite rare, hereditary storage pool disease is common enough to be suspected in an individual, usually a child, with characteristic historical and clinical findings. The acquired platelet function defects, especially those resulting from drugs, are common and should promptly be suspected in patients developing easy and spontaneous bruising, mild-to-moderate mucosal membrane hemorrhage, or unexplained bleeding associated with trauma or surgery. The template bleeding time is generally useful as a screening test of platelet function, but a normal template bleeding time, in the face of a suggestive history, suggestive clinical findings, or in a patient frankly bleeding, is not reliable, and platelet aggregation or lumiaggregation should be done in appropriate clinical situations. Also, prolongation of the template bleeding time is an unreliable predictor of clinical bleeding propensity. The mainstay of therapy for almost all these defects, if bleeding is significant, is the liberal infusion of appropriate numbers of platelet concentrates. The acquired platelet function defects should also be managed by attempts to treat or control the underlying disease, if possible, and offending drugs or potentially offending drugs should immediately be stopped.
Blood Platelet Disorders↗
Platelet function defects: a clinical review.
Platelet dysfunction, especially acquired forms, are common causes of hemorrhage, especially in association with trauma and surgery. Although the hereditary platelet function defects are generally quite rare, hereditary storage pool disease is common enough to be suspected in an individual, usually a child, with characteristic historical and clinical findings. The acquired platelet function defects, especially those resulting from drugs, are very common and should promptly be suspected in patients developing easy and spontaneous bruising, mild to moderate mucosal membrane hemorrhage, or unexplained bleeding associated with trauma or surgery. The template bleeding time is generally useful as a screening test of platelet function, but a normal template bleeding time, in the presence of a suggestive history, suggestive clinical findings, or in the patient frankly bleeding, is not reliable and platelet aggregation or lumi-aggregation should be done in appropriate clinical situations. The mainstay of therapy for essentially all these defects, if bleeding is significant, is the liberal infusion of appropriate numbers of platelet concentrates. The acquired platelet function defects, of course, should also be managed by attempts to treat or control the underlying disease, if possible, and offending drugs or potentially offending drugs should promptly be discontinued.
Blood Platelets↗
Acquired platelet function defects.
Platelet dysfunctions, especially acquired forms, are common causes of hemorrhage, especially when associated with trauma or surgery. Although the hereditary platelet function defects are generally quite rare, hereditary storage-pool disease is common enough to be suspected in an individual, usually a child, with characteristic historical and clinical findings. The acquired platelet function defects, especially those resulting from drugs, are very common and should promptly be suspected in patients developing easy and spontaneous bruising, mild to moderate mucosal membrane hemorrhage, or unexplained bleeding associated with trauma or surgery. The template bleeding time is generally useful as a screening test of platelet function, but a normal template bleeding time, in the face of a suggestive history, suggestive clinical findings, or in the patient frankly bleeding, is not reliable, and platelet aggregation or lumi-aggregation should be done in appropriate clinical situations. Also, prolongation of the template bleeding time is an unreliable predictor of clinical bleeding propensity. The mainstay of therapy for essentially all these defects, if bleeding is significant, is the liberal infusion of appropriate numbers of platelet concentrates. The acquired platelet function defects should also be managed by attempts to treat or control the underlying disease, if possible, and offending drugs or potentially offending drugs should immediately be stopped.
Blood Platelet Disorders↗
[The incidence of platelet hyperaggregability induced by cigarette smoke in a healthy population].
The effect of cigarette smoking on platelet function was investigated by means of whole blood aggregometry, a method suitable to reproduce in vitro the in vivo conditions. Platelet aggregation was evaluated before and after smoking two cigarettes. The coagulation tests performed in 26 volunteers, aged between 24-35 years, did not show any remarkable change. On the other hand, platelet aggregation was significantly increased in the majority of the volunteers (17 out of 26). No correlation was found between platelet aggregation and the coagulation parameters here considered.
Adenosine Diphosphate↗
[The hemolysate aggregation test].
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Blood Platelet Disorders↗
Pharmacodynamics of two different dosing regimens of tirofiban in citrate or PPACK anticoagulated blood.
The primary objective of this study was to compare the inhibitory activity of tirofiban measured with the rapid platelet function assay (RPFA) and with light transmission aggregometry using two different anticoagulants (citrate versus PPACK). Twenty patients treated with tirofiban for percutaneous coronary intervention were studied at six time points during tirofiban treatment. Tirofiban was given with a bolus dose of 10 microg/kg and an infusion of 0.10 microg/kg per min (10 patients) or with a bolus dose of 15 microg/kg and an infusion of 0.15 microg/kg per min (10 patients). Inhibition of platelet function appeared highest using citrated blood and the RPFA-device and lowest when assessed by aggregometry in PPACK-anticoagulated blood. Only the higher dose of tirofiban achieved an inhibition of platelet aggregation of at least 80% in all test systems.
Aged↗
Biocompatibility of poly(ether)urethane-gold nanocomposites.
We have prepared the nanocomposites of a polyether-type waterborne polyurethane (PU) incorporated with different amounts (17.4-174 ppm) of gold (Au) nanoparticles ( approximately 5 nm). The nanocomposite containing a certain amount (43.5 ppm) of gold was previously demonstrated to possess the optimal thermal and mechanical properties, as well as much reduced foreign body reactions in subcutaneous rats. In this study, the surface morphology, biocompatibility, oxidative degradation, and free radical scavenging ability of the nanocomposites were characterized in vitro. The nanocomposite at 43.5 ppm of gold ("PU-Au 43.5 ppm") exhibited different surface morphology confirmed by the atomic force microscope. PU-Au 43.5 ppm also showed enhanced cellular proliferation, reduced platelet and monocyte activation, and much less bacterial adhesion, relative to PU alone or nanocomposites at the other Au contents, in general. This better biocompatibility was associated with the surface morphological change in the presence of Au. The oxidative degradation in PU-Au 43.5 ppm was also inhibited. The increased oxidative stability corresponded to the greater free radical scavenging ability of the nanocomposites.
Biocompatible Materials↗
Anti-thrombotic effect of proanthocyanidin, a purified ingredient of grape seed.
INTRODUCTION: Moderate and regular consumption of wine reduces the risk of acute coronary thrombotic events. The mechanism of the anti-thrombotic effect of wine is not clear. Extract or purified ingredients of grapes have not yet been studied for anti-thrombotic effect. MATERIALS AND METHODS: Anti-thrombotic effect of proanthocyanidin, a highly purified ingredient of grape seed, was assessed by a shear-induced thrombosis test in vitro and by a laser-induced thrombosis test in the mouse carotid artery, in vivo. RESULTS AND CONCLUSIONS: Intravenously (20 mg/kg body weight, BW) or orally (2 x 200 mg/kg BW) administered proanthocyanidin significantly inhibited the laser-irradiation induced thrombus formation in the carotid artery (both P=0.01). Subsequent to oral administration of proanthocyanidin, in vitro platelet reactivity to shear stress has been inhibited. The latter suggests that the in vivo anti-thrombotic effect of proanthocyanidin may be due to a direct inhibitory effect on platelets.
Animals↗
Platelet activation during exercise-induced myocardial ischemia.
Because platelet activation may be important in the worsening of coronary atherosclerosis, we used a radioimmunoassay for platelet factor 4 to study platelet behavior in patients with coronary-artery disease. Forty patients had paired blood samples withdrawn for measurement of the plasma level of platelet factor 4 before and after a standardized exercise-tolerance test. Twenty patients had positive tests, and 19 of those 20 had clinical or angiographic evidence of coronary-artery disease. Eleven of the 20 had a greater than 50 per cent increase in platelet factor 4 after exercise. The remaining nine had positive exercise tests without rises in platelet factor 4. Elevated levels returned to normal within 15 minutes of exercise. Eighteen of 20 patients with negative exercise tests had no rise in platelet factor 4 after exercise. We conclude that a subset of patients with coronary-artery disease and exercise-induced myocardial ischemia had evidence of platelet activation and secretion. (N Engl J Med 302:193-197, 1980).
Adolescent↗
Gorog Thrombosis Test: analysis of factors influencing occlusive thrombus formation.
We used the Gorog Thrombosis Test to analyze the factors influencing the occlusion time, which represents platelet activation and subsequent occlusive thrombus formation, in 132 healthy Japanese volunteers (116 men, 16 women; mean age, 45.0 +/- 12.0 years). The Gorog Thrombosis Test was designed to evaluate platelet aggregation and thrombolytic activity under a high shear stress condition (175 dynes/cm) in a native blood sample in vitro. The mean +/- SD occlusion time was 154.8 +/- 64.7 s (men, 153.4 +/- 64.2 s and women, 165.4 +/- 56.5 s). The occlusion time was inversely correlated with von Willebrand factor ristocetin cofactor activity (VWF:Rco) (r = -0.242, P = 0.0055) and von Willebrand factor antigen (r = -0.230, P = 0.0080). The mean occlusion time in the group with VWF:Rco of at least 170% (137 s) was significantly shorter than that in the group with VWF:Rco less than 170% (156 s, P < 0.05). Platelet counts, other coagulation markers and smoking showed no significant correlations with occlusion time. Red blood cells (r = -0.177, P = 0.0365), hemoglobin (r = -0.191, P = 0.0245) and hematocrit (r = -0.182, P = 0.0329) also showed inverse correlations with the occlusion time. This report is the first to clearly demonstrate the role of von Willebrand factor in the formation of occlusive thrombi in the Gorog Thrombosis Test.
Adult↗