Liver and renal and platelet counts after delivery in patients with severe pre-eclampsia.
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Female↗
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Results for “Platelet Function Tests”
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Laboratory diagnosis of heparin-induced thrombocytopenia in Asian Indians as investigated with functional and immunologic methods.
Heparin-induced thrombocytopenia (HIT) was looked for in 33 Indian patients undergoing cardiovascular surgery who received unfractionated heparin (UFH). Platelet counts were performed before the initiation of UFH therapy and 5 to 16 days after administration of the therapy. A decrease in patients' platelet count > 35% of the baseline value or < 100,000/microL was considered to be suggestive of HIT syndrome. Heparin-induced platelet aggregation (HIPA) and enzyme-linked immunosorbent assay (ELISA) tests were performed in all the patients to detect antibodies against heparin/PF4 complex. Thrombocytopenia was found to be present in 10 (30%) patients. Of these, two patients were found to be positive as detected by HIPA and ELISA tests. These two patients were considered to have classic HIT syndrome. One of these had bleeding while the other was asymptomatic. Among the 23 non-thrombocytopenic patients and controls, HIT antibodies were not detectable by HIPA test in all but absent by ELISA in only 21 of them. Two of 23 non-thrombocytopenic patients had positive results on the ELISA test. Because the latter had negative test results on HIPA, they were considered to be false-positive results. Thus, HIT syndrome develops in approximately 6% of Indian patients treated with UFH.
Cardiac Surgical Procedures↗
The influence of nicardipine on platelet tests in patients with claudication.
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Aged↗
Evaluation of the xylum clot signature analyzer in normal subjects and patients with the Hermansky-Pudlak syndrome.
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Adolescent↗
High prevalence of abnormal preoperative coagulation tests in patients with adolescent idiopathic scoliosis.
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Adult↗
Modifications produced by indomethacin and L-NAME in the effect of ultralow-dose aspirin on platelet activity in portal hypertension.
In our previous study, we demonstrated the effect of ultralow-dose aspirin (ULDA) on platelet activity and bleeding in rats with portal hypertension (PHT) produced by portal vein ligation (PVL). This paper reports modifications in this effect caused by blocking NO production by nitro arginine methyl ester (NAME) and cyclooxygenase (COX) activity with indomethacin. PVL rats and sham-operated controls were treated with placebo, indomethacin or NAME and 30 min thereafter with placebo or ULDA treatment. Platelet activity was studied by a model of in vivo laser-induced thrombus production in the mesenteric circulation, induced hemorrhage time (IHT) and platelet aggregation ex vivo induced by adenosine diphosphate in an aggregometer. The PVL group receiving placebo showed a decreased platelet activity with prolonged IHT, an effect that was reversed by ULDA. Indomethacin induced a decreased platelet activity in the control rats and a prolonged IHT. In PHT with ULDA, in vivo platelet activity was enhanced but the normalization of IHT observed in rats without indomethacin was blunted. The addition of NAME normalized the diminished in vivo platelet aggregation and increased the IHT observed in PVL animals. These changes decreased the effect of ULDA in both sham-operated and PVL animals. The effect of indomethacin was more clearly modified by ULDA than the effect of NAME, thus suggesting that modifications in the COX pathway might alter the effect of ULDA. The simultaneous administration of indomethacin and ULDA could inhibit its beneficial effect on bleeding in rats with PHT.
Animals↗
[Defects in the prostaglandin system. VI. Acquired plasma factor defect].
A 44 year-old male was admitted to hospital in October 1984 presenting with enzymatic and electrocardiographic signs of posterior wall myocardial infarction. At this time 2 separate examinations revealed normal plasma factor activity. At the 1 year follow-up (November 1985) plasma factor activity was still present. However, in February 1987 for the first time, the patient's plasma failed to enhance PGI2 synthesis from vascular tissue in vitro. 3 further follow-up examinations within the next 6 weeks again revealed an acquired absence of plasma factor activity of unknown cause. No deterioration in clinical condition occurred. All relatives tested showed normal plasma factor activity.
Adult↗
Platelet function analysis with PFA-100 in patients medicated with acetylsalicylic acid strongly depends on concentration of sodium citrate used for anticoagulation of blood sample.
Our data from 214 patients after cessation of long-term therapy with 100 mg/d ASA demonstrate that the determination of platelet-related primary hemostasis in citrated whole blood with PFA-100 is a reliable and sensitive method for the detection of ASA-induced platelet dysfunction. However, the sensitivity of the method is strongly dependent on concentration of sodium citrate used as anticoagulant. The results of PFA-100 testing show a clearly enhanced sensitivity for ASA when blood samples were collected with 0.129 M rather than 0.106 M sodium citrate. According to sample stability, PFA-100 results can only be confirmed up to 1 hour postcollection when blood was anticoagulated with 0.129 M but not with 0.106 M sodium citrate. Therefore, we recommend that testing with PFA-100 in patients with suspected ASA-induced platelet dysfunction should be performed exclusively in blood collected in buffered 0.129 M sodium citrate.
Artifacts↗
In vitro platelet function in infantile autism.
It has previously been demonstrated that patients with infantile autism demonstrate impaired in vivo platelet behaviour. Therefore, in 14 children (13 boys and 1 girl) with infantile autism (aged 2-14, mean 6 years) and 12 healthy control boys (aged 6-15, mean 11 years) we studied in vitro platelet reactivity using ADP- and collagen-induced platelet aggregation. In each child a total of 7 different final concentrations of ADP and 4 different concentrations of collagen were employed. At all concentrations of ADP and collagen used the autistic children consistently exhibited diminished platelet aggregability; the differences, however, did not reach statistical significance. Therefore a wider panel of in vitro tests is apparently required and a larger group of patients be studied to help elucidate the functional/metabolic platelet defect met in infantile autism.
Adolescent↗
Urinary excretion of thromboxane B2 in patients with venous thromboembolic disease.
Platelet activation occurs in the initial phase of venous thrombus formation. To determine if thromboxanes (Tx) are released during this process and if Tx measurements are useful in the diagnosis, urinary immunoreactive TxB2 was measured by a rapid, inexpensive assay in 100 consecutive patients with suspected thromboembolic disease. Urinary iTxB2 was not increased in patients who took aspirin, nor in patients studied several weeks after onset of symptoms. Of the remaining patients, iTxB2 was increased in 11 of 15 with confirmed deep vein thrombosis and in seven of ten with confirmed pulmonary emboli. Of the 54 patients in whom acute thrombosis was excluded, iTxB2 was increased in only four (7 percent). A second study evaluated 25 additional patients with nondiagnostic lung scans who required pulmonary angiography; iTxB2 was increased in seven of ten with positive angiograms and in 0 of 15 with negative angiograms. The three patients with negative iTxB2 and positive angiograms were receiving heparin when studied. These data suggest that, in the absence of aspirin, platelet Tx is released during thrombus formation. In combination with other noninvasive tests, urinary iTxB2 is a useful adjunct to diagnosing acute thromboembolic disease.
Angiography↗
Effects of increasing doses of activated recombinant factor VII on haemostatic parameters in swine.
This study examined dose-response relationships between activated recombinant factor VII (rFVIIa) and (1) in vivo haemostasis and (2) in vitro measures of coagulation and platelet function. Anesthetized swine were used. Ear bleeding time (BT) was measured and blood was sampled following increasing doses of rFVIIa (0, 90, 180, 360 and 720 microg/kg; n=6) or saline (n=6). BT was not altered by rFVIIa. Prothrombin time (PT) using standard or pig-specific methods was decreased by rFVIIa. Activated clotting time (ACT) was decreased by rFVIIa. Thromboelastography using collagen (COLL) or pig thromboplastin (p-ThP) as agonist demonstrated shorter reaction times, shortened time to reach maximum velocity of clot formation, and increased alpha-angle in the presence of rFVIIa. rFVIIa dosing increased maximum velocity of clot formation when p-ThP was used to initiate the reaction but not when COLL was used. rFVIIa at the highest concentration increased maximum amplitude when COLL was used to initiate the reaction. Platelet aggregation was not altered by rFVIIa. Following completion of the dose escalation phase, a severe liver injury was produced. rFVIIa altered neither blood loss nor survival time following injury but improved mean arterial pressure. A small increase in systemic thrombin-antithrombin III complex occurred after administration of rFVIIa at doses of 180 microg/kg and above. However, there was no histological evidence of intravascular coagulation after rFVIIa administration. In summary, rFVIIa activity was detectable in vitro but did not change haemostasis in normal swine.
Animals↗
The platelet adhesion immunofluorescence test: a modification of the platelet suspension immunofluorescence test.
Platelets can adhere to surfaces by forming pseudopods. This ability is made use of here to simplify conventional platelet suspension immunofluorescence tests, since steps like serum and FITC incubations, washing and microscopic evaluation are done on platelets adhered to glass surfaces. By eliminating time-consuming manipulations like washing in individual test tubes and mounting platelets to microscopic slides, large scale studies can now be performed (up to 480 tests per day and technician). Antibodies can be detected with fresh as well as with frozen platelets from a well defined cell panel. The PAIFT is 2 to 3 times more sensitive than the NIH-standard-micro-lymphocytotoxicity-test (NIH-LCT), thus allowing earlier recognition of alloimmunization of patients.
Female↗
In vitro comparison of the effects of contrast media on coagulation and platelet activation.
The aim of this study was to compare the in vitro effects of different classes of contrast media on both the blood coagulation system and on platelet function. Global tests (APTT, TT) and FpA and F1 + 2 generation measurements showed that ioxaglate (ionic dimer) presents the highest anticoagulant potential. The anticoagulant effects of nonionic agents were less marked, iodixanol (nonionic dimer) being significantly less anticoagulant than iohexol (nonionic monomer). Major platelet activation was observed with release of PF4, serotonin and PDGF-AB when iohexol was incubated for 1 min in whole blood. Iodixanol showed no effect over the same period, while moderate platelet activation was observed after 30 min. Under the same experimental conditions, ioxaglate had no effect on platelets even after incubation for 30 min, whereas activation was observed with 9 g/l saline control at this time. Prevention of thrombin formation and platelet activation is only achieved with ioxaglate, the ionic dimer. These findings may be clinically important in the thrombotic environment of radiological procedures and may explain the increased thrombotic risks observed with nonionic agents in interventional procedures.
Blood Coagulation↗
Sodium valproate, platelet dysfunction, and bleeding.
The antiepileptic drug sodium valproate (VPA) can provoke a thrombocytopenia or platelet dysfunction, with or without hemorrhages. These unwanted side effects are probably infrequent or, at least, have little clinical importance except in patients undergoing surgery. Thromboelastography appears to be a reliable screening test. As hematological abnormalities are often dose related, VPA dosages greater than 40 mg/kg/day are not advised.
Blood Platelet Disorders↗
Effect of sex difference on platelet aggregation using an optical method in healthy subjects.
There are many studies reporting conflicting results of sex differences on various platelet functions. The purpose of this study was to investigate whether sex differences could affect platelet aggregation results using an optical method in healthy subjects. A total of 42 subjects, 21 males and 21 females, were included in the study. Platelet aggregation was induced by adenosine diphosphate (ADP; 5 microm), collagen (2 microg/ml), and epinephrine (10 microm). Optical aggregation was performed using a turbidometric method. In all platelet aggregation tests ADP, collagen and epinephrine were studied; there was no significant difference between females and males in platelet aggregation amplitudes and slopes. As a result, sex difference does not affect platelet aggregation performed with this optical method in healthy subjects. This result supports that there is no need for sex differentiation while composing control groups in platelet aggregation studies using the optical method.
Adenosine Diphosphate↗
Platelet function in the dorsal skin fold chamber of the rat.
The majority of the preparations described for studying platelet functions in vivo require the administration of anesthetic agents and surgery. Some anesthetic which are frequently used in microvascular research (such as ketamine hydrochloride and pentobarbital) are reported to exert an effect on platelet properties themselves. Using a modified chamber preparation situated in the rat's dorsal skin fold, it is possible to study platelet function in the same rat with or without anesthesia. Thrombus formation is induced in arterioles and venules by argon-laser irradiation with a local capacity of 25mW and an exposure time of 1/30 s. Platelet function was studied for ten successive days in the same group of rats to examine the model's aptitude for long-term investigations. There was no significant alteration in platelet response during the experimental period. To evaluate the potential antithrombotic effects of the anesthetics, the animals were studied before and after the application of ketaminehydrochloride (130 mg/kg b.w., pentobarbital (25 mg/kg b.w.), or urethane (1,25 g/kg i.m.). The first two drugs caused significant increase in the number of laser injuries in arterioles and venules, although the effect of pentobarbital was weaker especially in venules. The influence of thrombus formation while using these anesthetics could influence the testing of antithrombotic drugs. Urethane had no effect on laser-induced thrombus formation. Furthermore, special attention was paid to spontaneous and laser-induced vasomotion with respect to thrombus formation.
Anesthetics↗
Effect of aspirin on prostaglandin synthesis by human platelets.
When platelet rich plasma is exposed to N-ethylmaleimide, a ten fold increase in measurable prostaglandin E synthesis occurs. This effect is almost completely abolished within 2 hours of ingestion of 600 mg of aspirin by human volunteers. Recovery of this platelet function is slow for the first two days, returning sharply to normal over the next six days and plateauing approximately 8 days following initial removal from aspirin. It is suggested from these studies that platelet prostaglandin E production following NEM may be a useful test of platelet function.
Aspirin↗
Effect of heparin on in vitro platelet reactivity in cardiac surgical patients--a comparative assessment by whole blood platelet aggregometry and haemostatometry.
The in vitro effect of heparin on platelet reactivity was assessed simultaneously by haemostatometry (response to shear stress) and whole blood platelet aggregometry response to collagen (WBPA). From each blood sample a ratio (HR for haemostatometry and MR and IR for WBPA) showing platelet reactivity in the presence or absence of heparin (5 U/ml) was calculated. A value less than 1 represented a proaggregatory effect and greater than 1 an inhibitory effect. Non-anticoagulated blood samples obtained from 290 cardiac surgical patients were tested by haemostatometry and citrated whole blood samples from 100 patients with aggregometry. Haemostatometry demonstrated a proaggregatory effect of heparin in 8.6% (25) and an inhibitory effect in 91.4% (265). Assessed by WBPA, heparin was proaggregatory in 41-46% and inhibitory in 54-59%. In the 100 patients tested by both methods there was a significant correlation between the findings with the two techniques (r = 0.46, p less than 0.0001). A wide individual variation in the platelet effect of heparin was demonstrated. This variation appeared greater and a higher proportion showed inhibition when blood was tested by haemostatometry.
Blood Platelets↗