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PubMed2004

[Platelet retention test Homburg (RTH) and drug monitoring of platelet adhesive properties of von Willebrand factor].

Platelet plug formation is initiated by the process of platelet adhesion, mainly mediated by the von Wille-brand factor (VWF). Therefore, apart from established criteria the platelet adhesion property is a further criterion to determine VWF e. g. in diagnosis and treatment of von Willebrand disease (VWD). The new platelet retention test Homburg (RTH) is designed to close this gap. It is characterized by its non-thrombogenic filter with interconnecting pores, which retains platelets from blood when pressed through this filter due to the resulting shear stress. The RTH, in particular, proved to be highly sensitive in detecting the platelet adhesive property of VWF after its release from endogenous storage sites by desmopressin or infusion in VWD patients or its supplementation in vitro.

Drug Monitoring↗
PubMed2002

Prospective study of liver dysfunction in pregnancy in Southwest Wales.

BACKGROUND: Liver dysfunction in pregnancy has serious consequences. Its frequency and characteristics have not been systematically documented in Britain. We have prospectively determined incidence, causes, and outcome of liver dysfunction in pregnancy in an obstetric unit in Southwest Wales, UK. METHODS: A central laboratory identified all abnormal liver tests (bilirubin >25 micro mol/l, aspartate transaminase >40 U/l, or gamma glutamyl transpeptidase >35 U/l) from patients in antenatal clinics and wards of an obstetric unit serving a population of 250 000. Patients with abnormal liver tests were assessed and followed throughout and after pregnancy [corrected]. Medical advice was provided to obstetric teams. FINDINGS: There were 4377 deliveries during the 15 month study. A total of 142 patients had abnormal liver tests. There were 206 contributing diagnoses, the great majority being pregnancy specific. Among the most important were pre-eclampsia (68), HELLP (haemolysis, elevated liver enzymes, low platelets) syndrome (30), obstetric cholestasis (23), hyperemesis gravidarum (11), acute fatty liver of pregnancy (five), and hepatic infarct (one). Sepsis, postoperative factors, and placental pathology (51) were not uncommonly responsible but incidental or pre-existing hepatobiliary disease was infrequent (17). Sixty five patients were delivered early by induction or caesarean section because of liver dysfunction. Despite substantial liver related morbidity, there were no maternal deaths and only two intrauterine deaths. CONCLUSIONS: Liver dysfunction was seen in 3% of deliveries during a 15 month prospective study and was usually directly related to pregnancy with spontaneous recovery in the puerperium. Incidence of the most serious conditions, acute fatty liver of pregnancy and HELLP syndrome, was much greater than previously reported. Profound effects on maternal and infant health were observed but close medical and obstetric collaboration ensured low mortality.

Adult↗
PubMed1990

[Follow-up in HELLP syndrome].

The so-called HELLP-syndrome, a special form of severe preeclampsia, is characterized by (H-) hemolysis, (EL-) elevated liver enzymes and (LP-) low platelet count. The data of three HELLP-cases are shown, the development and outcome of the pathologic laboratory parameters are presented. After a several months control it was evident that after delivery the initial improvement of all laboratory findings proceeds and lasts. A special medical treatment is not necessary.

Adult↗
PubMed1984

Platelet and other tests followed sequentially for 14 days after operation.

Nineteen patients were studied twice before and sequentially from 1 h to 14 days after operations lasting about 1 h. Eighteen tests were carried out, ideally on all the nine occasions blood collections were planned. Only significant changes are summarized. Immediately after the operation the plasma PF4 and beta TG were raised in parallel suggesting some platelet 'release' had occurred. At this time platelet aggregation to ADP and collagen had decreased by 57% to 64% and the plasma cyclic AMP had doubled. Next day these abnormalities had returned towards normal. By day 2 the fibrinogen and the heparin neutralizing activity were maximal; they returned towards normal by day 14. On day 14, when presumably all platelets present at operation had been removed the new platelets were 53% more numerous and 9.5% smaller; they contained 23% less PF4 and 42% less serotonin and 5-HT uptake was decreased, but the total amount of 5-HT and PF4 in the circulation probably remained constant. In summary these operations transitorily upset platelet function for a few hours and the platelets formed postoperatively were abnormal.

Adult↗
PubMed1980

Prevention of venous thromboembolism after total knee replacement by high-dose aspirin or intermittent calf and thigh compression.

A prospective study of patients undergoing total knee replacement was carried out by using a combination of 125I-fibrinogen scanning and phlebography, and showed a high incidence of venous thromboembolic disease (TE). Ventilation-perfusion lung scanning was performed to detect pulmonary emboli in most patients. High doses of aspirin and an intermittent low-pressure pneumatic compression device (IPCD) were effective, even in women, in preventing TE. Low doses of aspirin and placebo were equally ineffective in preventing TE. Lung-scan abnormalities compatible with pulmonary emboli were found in six out of 10 patients with isolated calf-vein thrombi. Conventional tests of platelet function did not predict the development of TE. No significant differences were found between the patients receiving low and high doses of aspirin with respect to the mean template bleeding time or platelet aggregation in response to adenosine diphosphate, collagen, and epinephrine, although these variables were significantly abnormal in the two groups receiving aspirin compared with those treated with placebo and the IPCD. Thus high doses of aspirin and a new low-pressure IPCD were effective in preventing venous TE in patients (predominantly women) undergoing total knee replacement.

Adult↗
PubMed2004

In vivo effect of losartan on platelet aggregation in patients with hypertension.

The angiotensin II receptor, losartan, has been found to inhibit platelet aggregability to some extent in in vitro experiments. There have been conflicting results about the in vivo effects of losartan. We sought to clarify the in vivo effect of losartan on platelet aggregation. Forty patients with grade I essential hypertension were treated with losartan for 3 weeks. Platelet aggregation tests with adenosine diphosphate (ADP) and ristocetin were analyzed and compared before and at the end of the study. Losartan effectively decreased systolic (SBP) and diastolic (DBP) blood pressure. Mean SBP before and after treatment was 159.6 +/- 12.8 and 149.2 +/- 17.3 mmHg, respectively. Mean DBP decreased from 93.7 +/- 8.2 to 87.7 +/- 10.3 mmHg after treatment. The results of the platelet aggregation tests with ADP and ristocetin were not significantly different when both rate and amplitude of maximal aggregation were included. Peak platelet aggregation with ADP regarding the lowest light transmission in the aggregometer was 59.8% +/- 24.3% before and 58.3% +/- 18.1% after the treatment. The same variables with ristocetin were 66.8% +/- 21.6% and 60.8% +/- 23.3%, respectively. In vivo effects of losartan on platelet aggregation with ADP and ristocetin were insignificant.

Adenosine Diphosphate↗
PubMed1983

[Thrombocyte migration test--method, value and reproducibility].

A method for platelet migration testing is presented. The results are comparable using sodium citrate and acid citrate dextrose as anticoagulants, whereas other anticoagulants lead to lower absolute migration. The day-to-day variability of the method is higher than the intra-day variability. The variability between the patients is higher than that between measurements carried out on the same patient. There is no correlation to ADP-induced platelet aggregation.

Adult↗
PubMed1987

Beneficial effects of U-63,557A, a thromboxane synthetase inhibitor, in an ovine model of pregnancy-induced hypertension.

Pregnancy-induced hypertension was induced in five ewes (gestational day 135; term 150 days) by 72 hours of food deprivation. Maternal arterial pressure, uterine blood flow, platelet function, renal function, and plasma levels of 6-ketoprostaglandin F1 alpha and thromboxane B2 were measured before and during hypertension and after three intravenous injections of U-63,557A; sodium 5-(3'-pyridinylmethyl) benzofuran-2-carboxylate, monohydrate (30 mg/kg every 8 hours). Blood pressure increased (p less than 0.03), and returned to normal after U-63,557A. Left uterine artery blood flow increased after U-63,557A (p less than 0.03). Creatinine clearance decreased during hypertension (p less than 0.03) and increased after U-63,557A. Urine protein increased during hypertension (p less than 0.03) and decreased after treatment. Platelet count dropped during hypertension (p less than 0.03) and was elevated after treatment. Collagen lag phase decreased during hypertension (p less than 0.03) and increased after treatment. After U-63,557A, 6-ketoprostaglandin F1 alpha levels were higher (p less than 0.04) than baseline or hypertensive values. Administration of a thromboxane synthetase inhibitor caused resolution of hemodynamic, renal, and coagulation dysfunctions that occurred in ovine pregnancy-induced hypertension.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Is primary haemostasis controlled by a 'platelet delay time'? Formulation of a new hypothesis.

A simple physical model is able to adequately describe platelet thrombus formation during primary haemostasis ex vivo, under the assumption of a 'platelet delay time' (Pdel), which is defined as the difference between the moment of platelet adhesion (to collagen or to another adherent platelet) and the time when the newly adherent platelet allows another platelet to adhere. Pdel was estimated with an ex vivo model of primary haemostasis (modified PFA-100, Dade Behring, Marburg). ADP and epinephrine test cartridges were perfused with human anticoagulated blood of control persons using a pressure/flow clamp technique (Kretschmer V, et al. Platelets 2001; 12: 462-9). Platelets gradually occluded the aperture in the test system. Pressure (p) across and flow (Q) through the aperture were measured versus time. The change of the aperture radius versus time (dr/dt) was calculated from p and Q using the Law of Hagen-Poiseuille. The surprising result was a constant decay of dr/dt (Rsqu approximately 0.996), in spite of a 5-fold increase in the shear- and transport-rates of platelets. This can be explained by postulating the existence of a Pdel, which was estimated as 2.89 s for collagen/ADP and 4.62 s in collagen/epinephrine test cartridges. This new hypothesis explains for the first time the relative independence of in vivo and ex vivo bleeding time on blood platelet concentrations, a well known observation at platelet counts higher than 40,000/microl. If the described physical model is correct, platelet thrombus growth rate is strongly decreased as a consequence of Pdel in extreme arterial flow conditions. A preliminary report of these experiments has been published (Kratzer MAA, Platelets 2002; 13: 344).

Adenosine Diphosphate↗
PubMed2000

A global platelet test of thrombosis and thrombolysis detects a prothrombotic state in some patients with non-insulin dependent diabetes and in some patients with stroke.

Platelet aggregation and spontaneous thrombolytic activity were assessed in patients with non-insulin dependent diabetes and stroke using a shear-induced and agonist-induced platelet aggregation test. The Thrombotic Status Analyser (TSA), induces platelet-rich thrombus formation solely by shear forces, while whole blood platelet aggregometry measures platelet reactivity to different agonists. These tests were employed in the present study because in earlier studies they both demonstrated that platelet aggregability in healthy volunteers was unchanged with age. On the other hand, it is known that thrombolytic activity decreases with age in males, but not in females. In diabetic patients shear-induced platelet aggregability varied according to the stage of nephropathy but platelet aggregation to collagen was suppressed at all stages. Platelet reaction to shear stress was enhanced in stroke patients with haemorrhagic episodes but not in patients with lacunar infarction. In contrast, platelet reactivity to collagen was suppressed and changes in ADP-induced platelet aggregability were inconsistent. Suppressed thrombolysis was observed only in diabetes with minor renal defect. Fibrinogen was increased in diabetes with stage III and IV nephropathy. Fibrinopeptide A (FPA) and D-dimer were increased in stroke. Thus, the observed increase in fibrinogen, FPA and D-dimer is inconsistent with changes in platelet aggregability. Our present findings suggest that a shear-induced platelet aggregation test is superior to other tests such as agonist-induced platelet aggregation and thrombotic markers such as fibrinogen, FPA and D-dimer in detecting a prothrombotic state. It is concluded that elderly males may have a prothrombotic state not because of platelet hyper-aggregability but because of suppressed thrombolytic activity. On the other hand, a prothrombotic state in patients with non-insulin dependent diabetes and after stroke may be due to changes in age-independent platelet aggregability.

Adult↗
PubMed2001

Platelet aggregatory responses to low-dose collagen are maintained in hirudin-anticoagulated whole blood for 24 h when stored at room temperature.

Whole blood from 15 volunteers was anticoagulated with hirudin (200U/l) and the response to a known submaximal concentration of collagen (0.6 microg/ml) was tested by impedance aggregometry. In 8 volunteers platelet counts were also taken before and after the maximum aggregatory response. These tests were repeated when the samples had rested for 24 h at room temperature. The median [interquartile range] aggregatory response immediately after sampling was 17.3 [16.7-18.4] ohms. At 24 h it was 17.7 [15.8-19.3] ohms (p = 0.88) although variance was increased (p = 0.006). The immediate platelet count before collagen exposure was 438 [381-510] x 10(9)/l and 258 [227-297] x 10(9)/l post-collagen. At 24 h the platelet count was 448 [443-473] x 10(9)/l (p = 0.224 versus immediate count) but variance was not increased (p = 0.215). After full aggregation the count fell to 284 [234-304] x 10(9)/l (p = 0.592 versus early post-collagen). Variances were similar (p = 0.558). Aggregate response ratios increased non-significantly after 24 h from 0.59 [0.53-0.62] to 0.64 [0.51-0.68] although variance was increased (p = 0.021). Full macroaggregatory responses by impedance aggregometry were seen after 24h storage of whole blood with hirudin at room temperature. This suggests both that distant assessment of platelet function using a standardized method is possible and a potential role of thrombin inhibition for platelet storage.

Anticoagulants↗
PubMed1999

Heparin-induced thrombocytopenia in France, 1980-1998.

Due to the extensive use of unfractionated heparins in France, there is considerable experience with heparin-induced thrombocytopenia (HIT). It is recommended that platelet counts be performed twice a week for three weeks when patients are treated with any form of heparin. A drop in platelet counts can, however, occur not only in HIT patients but also for other unrelated reasons. For diagnosing HIT, all laboratories in France use platelet aggregometry inspite of poor sensitivity. Both false positive and false negative results are obtained. The serotonin release test is not used in France. The ELISA test for HIT does not always correlate with the platelet aggregation test and many patients with a positive ELISA test do not necessarily have other evidence for HIT. This is especially true in patients following cardiopulmonary bypass surgery. None of the available laboratory tests reliably identify patients with HIT. Patients with HIT should not be managed with low-molecular-weight heparins, but danaparoid, argatroban and ancrod are viable options. Also, recombinant hirudin has been employed. All have advantages and disadvantages. At present, the diagnosis and management of patients with HIT remains difficult and properly designed clinical studies are needed to obtain answers to several open questions.

Anticoagulants↗
PubMed2004

A randomized crossover comparative study of aspirin, cilostazol and clopidogrel in normal controls: analysis with quantitative bleeding time and platelet aggregation test.

The effects of three antiplatelet drugs, aspirin, clopidogrel and cilostazol, were examined and compared using a quantitative bleeding time (QBT) test apparatus. In 12 healthy adult male subjects, a QBT test and platelet aggregation test were performed before and after medication. Cilostazol was found to be as effective as aspirin and clopidogrel in inhibiting platelet aggregation. Following the oral administration of aspirin and clopidogrel for 7 days, the bleeding time was significantly prolonged. In contrast, none of these QBT parameters were altered by the cilostazol treatment. This suggests that cilostazol has potent efficacy in inhibiting platelet aggregation without prolonging the bleeding time and changing the bleeding pattern.

Adult↗
PubMed2006

Testing various fruits for anti-thrombotic effect: i. Mulberries.

Prevention of arterial thrombotic disease has high priority in developed countries. As inappropriate diet predispose to acute thrombotic events, regular intake of an antithrombotic diet may be a convenient and effective way of prevention. The present study was performed to examine antithrombotic effect of mulberry varieties. A shear-induced in vitro platelet reactivity/thrombolysis test (Gorog Thrombosis Test) was used to screen for antiplatelet and thrombolytic activities. In case of effectiveness, it was followed by an in vivo test of laser-induced thrombosis in mice. Antioxidant capacity was assessed by superoxide anion and radical scavenging activities. Total polyphenolics, anthocyanin and citrate contents were also measured. The tested varieties showed different effect in vitro on platelet reactivity and endogenous thrombolytic activity. Varieties inhibiting platelet reactivity were antithrombotic in vivo regardless inhibition or enhancement of thrombolysis. Those mulberry varieties, which enhanced platelet reactivity in vitro, were prothrombotic only if inhibitory activity on endogenous thrombolysis coexisted with the platelet effect. Antioxidant activities and polyphenolics content did not affect platelets and the overall thrombotic status. However, antioxidant activities and polyphenolics content significantly correlated with the endogenous thrombolytic activity. These data showed that mulberry varieties can be grouped into subclasses with either anti- or prothrombotic activities. Antioxidant activities and polyphenolic contents do not affect platelets but may enhance endogenous thrombolysis, thus causing an overall antithrombotic effect.

Animals↗
PubMedDate not supplied

Monitoring aspirin 100 mg and clopidogrel 75 mg therapy with the PFA-100 device in patients with peripheral arterial disease.

A tool to identify vascular patients who receive antiplatelet therapy nd to distinguish between responders and non-responders to antiplatelet therapy could be of clinical importance. The present observational study was designed to investigate whether the PFA-100 device (Dade Behring) is suitable to detect long-term therapy of aspirin (100 mg/d) and/or clopidogrel (75 mg/d) in a cohort of patients with peripheral arterial disease (PAD). A total of 150 consecutive patients with PAD were studied; 34 patients were excluded from the study due to irregular intake of antiplatelet therapy or due to method limitations. Of the remaining 116 patients, 42 had no antiplatelet therapy, 47 had daily aspirin (100 mg) intake, 19 were administered clopidogrel 75 mg daily, and 10 received a medication with 100 mg aspirin plus clopidogrel 75 mg daily, all for at least 10 days. Nonparametric Kruskal-Wallis test with post hoc comparisons showed that collagen plus epinephrine (CEPI) closure times of the patient group receiving aspirin and the group receiving aspirin plus clopidogrel were similar (p>0.05). In contrast, both patient groups exhibited prolonged CEPI values compared to patients without antiplatelet therapy and patients taking clopidogrel (p<0.001). Finally, both patients without antiplatelet therapy and patients with clopidogrel did not show marked differences with respect to their CEPI values (p>0.05). However, Kruskal-Wallis test results revealed that collagen plus adenosine-5'-diphosphate closure times were not significantly different in all four patient groups (p=0.257). In conclusion, the PFA-100 device may be a suitable tool for monitoring aspirin 100 mg therapy, but it is not appropriate for the detection of clopidogrel administration in its current setup. Although it appears plausible that patients with PAD could benefit from monitoring platelet inhibition, clear evidence for this concept is still lacking.

Adenosine Diphosphate↗
PubMed2004

Diagnosis and management of hemolysis, elevated liver enzymes, and low platelets syndrome.

Pregnancies complicated by hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome require a well-formulated management plan. The development of this syndrome after 34 weeks' gestation or with documentation of maternal or fetal compromise is an indication for delivery. Acute fatty liver of pregnancy, hemolytic uremic syndrome, and thrombotic thrombocytopenic purpura may present with signs, symptoms, and laboratory abnormalities that may be confused with HELLP syndrome. Thorough investigation is warranted because of the differences in proper management among these various complications of pregnancy. Expectant management in patients with HELLP syndrome remote from term and the use of corticosteroids to improve postpartum maternal outcome remain experimental.

Counseling↗
PubMed1997

[Effect of rhG-CSF on platelets using in vitro bleeding time and transcranial Doppler examination].

There is experimental evidence for recombinant human granulocyte colony-stimulating factor (rhG-CSF)-induced stimulation of hemostaseologic parameters including platelets. Using the closure time of the in vitro bleeding test (IVBT, Thrombostat 4000, VDG, Seeon) and different hemostaseologic parameters, our results are suggestive of a directly or indirectly induced in vivo stimulation of platelets following rhG-CSF stimulation in healthy stem cell donors. According to the negative transcranial Doppler microembolic monitoring of the middle cerebral artery, there is no evidence for clinically silent cerebral microembolism supporting a prothrombotic state facilitating the formation of arterial thrombi with subsequent cerebral embolization.

Adolescent↗
PubMed1984

An assessment of whole blood impedance aggregometry using blood from normal subjects and haemodialysis patients.

Impedance aggregometry allows the measurement of platelet responses in whole blood as well as in PRP. The variability of haematocrit values encountered when applying this technique to haemodialysis patients prompted an investigation of the effects of red cells on platelet aggregation in whole blood. Collagen induced aggregation was measured in both PRP and whole blood from haemodialysis patients and healthy controls. Platelets from haemodialysis patients were less aggregable than those from the controls when tested in PRP, but more aggregable when tested in whole blood. Blood samples with a range of haematocrit values were prepared by mixing PRP and autologous red cells, and used to study the effect of haematocrit on platelet aggregation. In blood from control subjects aggregation rate was reduced by rising haematocrit but no reduction of maximum aggregation occurred until haematocrit exceeded 40%. In contrast uraemic platelets showed increased responses in the presence of red cells. In a limited cross over study no significant difference was found in the effect on platelet aggregation of washed erythrocytes from uraemic and non-uraemic donors. It is concluded that red cell presence influences platelet aggregation by complex mechanisms during impedance aggregometry and that this effect must be considered when interpreting results.

Chronic Disease↗