Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Platelet Function Tests”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 613 records · Page 34Linked to original sources
PubMed1977

Abnormalities in platelet function and morphology in a case of thrombocythemia.

A patient with "life-long" bleeding problems and thrombocythemia had normal results on routine coagulation and fibrinolysis tests, but platelet function tests, including bleeding time, platelet adhesiveness, aggregation, and uptake and release of labeled serotonin were markedly altered. In addition, several types of ultrastructural abnormalities not reported previously were observed in some of the patient's platelets. The relationship between thrombocythemia, platelet dysfunction, and abnormal morphology is discussed.

Adenosine Diphosphate↗
PubMed1996

The effects of time interval after venipuncture and of anticoagulation on platelet adhesion and aggregation.

Abnormal platelet function plays an important role in atherosclerosis and thrombotic disorders. Simple in vitro testing of platelet function is preferable to other techniques, and adhesion measurement is especially important because it reflects an immediate platelet response. The time lapse after venipuncture and the anticoagulant may affect platelet function in an as yet unknown way. A method for determining platelet adhesion under controlled whole blood flow conditions and an aggregation study were used. Platelet adhesion and aggregation changed significantly with time elapsed since venipuncture, peaking after 60 min (P < 0.05): a plateau was reached only after more than 120 min. Platelet adhesion was directly suppressed by the use of sodium citrate as an anticoagulant, and surface density decreased from 14.2 to 8.8 (P < 0.001). To prevent the effect of time after venipuncture on platelet function, testing should be performed at the plateau phase.

Adenosine Diphosphate↗
PubMed2003

Haemostatic profile of small children during and following cardiopulmonary bypass.

OBJECTIVE: We evaluated changes of the haemostatic system during pediatric cardiac surgery during and after cardiopulmonary bypass (CPB). METHOD: Twenty-five children under 15 kg of body weight undergoing open-heart surgery were divided into three groups; 9 patients (Group A), no bank blood was used throughout the surgery; 8 patients (Group B), packed red cells were used in the priming of CPB circuit; 8 patients (Group C) in cyanotic condition, for whom surgery was performed without bank blood. CPB caused a significant decrease of platelet counts in all three groups, the levels of which remained similar next morning. RESULTS: Platelet counts decreased more significantly in Group C (59+/-27 k/mm3) than in Group A (119+/-42 k/mm3) and B (104+/-27 k/mm3). Platelet function-platelet activating factor test (HemoSTATUS) did not significantly decrease throughout the perioperative period in Group A. HemoSTATUS value decreased during CPB and recovered after CPB in Group B and C. Prothrombin time international ratio (PT-INR) and activated partial thromboplastin time were significantly prolonged just after CPB and recovered until next morning in all three groups. PT-INR was more prolonged in Group C (2.92+/-0.62) than in Group A (2.08+/-0.27) and B (2.42+/-0.42). There was no significant difference in postoperative bleeding for the first 12 hours among the three groups. CONCLUSION: Although extreme hemodilution during CPB significantly impairs the coagulation and platelet system, these changes are usually transient and tolerable with minimal postoperative hemorrhage. However, a prolonged CPB and preoperative cyanotic condition may induce a critical decrease of platelet counts and increase postoperative bleeding.

Blood Coagulation Tests↗
PubMed1994

[Effect of HPA-1a(PLA1) and HLA antibodies on platelet function, measured with the in vitro bleeding test].

The influence of platelet-specific and HLA antibodies on primary hemostasis was investigated by the in vitro bleeding test (IVBT). Seven of 12 plasmas with HPA-1a (PLA1) antibodies and two with antibodies against glycoprotein Ib/IX significantly inhibited the IVBT of normal cross-match-positive donor blood. This correlated with an increase of GMP-140 on the platelets determined by flow cytometry. Therefore the inhibition of the IVBT was interpreted to be due to rapid platelet activation by platelet-specific antibodies followed by an irreversible loss of function. In contrast, with HLA antibodies neither activation nor inhibition of the platelet function could be proven.

Antigens, Human Platelet↗
PubMed2001

Comparison of GP IIB/IIIA inhibitors and their activity as measured by aggregometry, flow cytometry, single platelet counting, and the rapid platelet function analyzer.

BACKGROUND: GP IIb/IIIa inhibitors have primarily been used short-term e.g., during PTCA. They failed to show clinical benefit during long-term therapy. One reason might be the absence of a method to monitor inhibitor activity. This study compared platelet aggregometry, the rapid platelet function analyzer (RPFA) test, single platelet counting, and flow cytometric determination of receptor occupancy to measure GP IIb/IIIa-receptor inhibitor activity. METHODS: Increasing doses of abciximab, tirofiban, and eptifibatide were added to whole blood in vitro. Whole blood was used for the RPFA, for single platelet counting and flow cytometry. Platelet rich plasma was prepared for aggregometry. RESULTS: The correlation between aggregometry and RPFA results was linear for abciximab and eptifibatide. Tirofiban was a stronger inhibitor with the RPFA (IC(50) 7.7nM) than with aggregometry (IC(50) 19.6nM). The single platelet counting technique showed that even supratherapeutic concentrations of all three inhibitors could not completely suppress microaggregation. Abciximab concentrations that were equipotent to tirofiban with aggregometry were less potent with regards to the inhibition of microaggregation. This difference was more pronounced with TRAP induced microaggregation than with ADP. The flow cytometric receptor occupancy test showed that occupancy was 95% with 5 microg/ml abciximab and almost 97% with 10 microg/ml. Tirofiban reached a maximum receptor occupancy of 56%, eptifibatide 64%. CONCLUSIONS: While aggregometry is time consuming the RPFA provides results fast and with little variability. There is still a discrepancy between aggregometry and RPFA results for tirofiban. The single platelet counting technique detects the inhibition of microaggregation the relevance of which for the clinical outcome is not known. The flow cytometric receptor occupancy assay is best suited for abciximab.

Dose-Response Relationship, Drug↗
PubMed2000

[Effect of a high single subcutaneous dose of unfractionated heparin on platelet function in dogs].

The influence of heparin on different tests of platelet function was investigated in 5 healthy dogs receiving subcutaneously 1000 I.E./kg BW of a commercial unfractionated Sodium heparin preparation. Blood samples were collected before and 4 hours after heparin injection. Besides plasma activity of heparin platelet count, capillary bleeding time with two different methods, platelet aggregation according to Breddin and to Born with the inductors ADP, collagen, and thrombin as well as in vitro bleeding time were measured. The activity of heparin four hours after the subcutaneous heparin application was 1.20 +/- 0.11 I.E./ml. Compared to the starting values no significant influence of this heparin level could be demonstrated on platelet count, platelet aggregation according to Born with the inductors ADP and collagen, platelet aggregation according to the Breddin method as well as in vitro bleeding time (p > 0.05). Only one of the two methods used for measuring the capillary bleeding time showed a slight prolongation compared to the starting value (mean = 77 sec) to 88 sec (p < 0.05). The most significant influence was seen on the platelet aggregation induced by 1 I.U./ml thrombin, whereby the aggregation maximum decreased from 92.0% (mean) to 12.2% (p < 0.001). Whereas the latter result has to be interpreted primarily as a consequence of the anti-thrombin effect of heparin, the results of the other tests in summary illustrate the clinical unimportant influence of heparin on platelet function in dogs.

Adenosine Diphosphate↗
PubMed2004

ADP induced platelet degranulation in healthy individuals is reduced by clopidogrel after pretreatment with atorvastatin.

Statins inhibit platelet reactivity and reduce blood thrombogenicity. The effectiveness of clopidogrel in inhibiting platelet reactivity was suggested to be reduced in the presence of atorvastatin due to shared enzymes in metabolism. Healthy individuals, 17 pretreated with atorvastatin (20 mg/d for 3 days) and 17 without pretreatment, as well as 15 patients with stable coronary artery disease (CAD) and concurrent atorvastatin therapy were started on clopidogrel (loading dose 300 mg, then 75 mg/d). P-selectin on platelet surface after stimulation with ADP or Thrombin Receptor Activating Peptide (TRAP) was flow cytometrically measured before and during clopidogrel administration. Whole blood platelet agglutination was tested by a platelet function assay.TRAP and - in trend - ADP induced p-selectin exposure was reduced by the atorvastatin pretreatment before clopidogrel was added. Combining clopidogrel with atorvastatin in the healthy individuals led to a further reduction in ADP-induced platelet p-selectin exposure. Clopidogrel also reduced platelet reactivity in CAD patients with concurrent atorvastatin medication. We conclude that pretreatment with atorvastatin reduces platelet reactivity before administration of clopidgrel. No drug interaction was seen, however, platelet inhibitory effects were observed during the treatment with clopidogrel and atorvastatin.

Adenosine Diphosphate↗
PubMed2002

The effects of drugs used in anaesthesia on platelet membrane receptors and on platelet function.

Platelet dysfunctions are known origins of perioperative bleeding disorders which are a major concern in the management of surgical patients. Among multiple factors, interactions of drugs used in anaesthesia with platelets have been implicated to aggravate the risk of haemorrhagic complications. This paper reviews in vitro and in vivo studies which have examined the effects of inhalational, intravenous, and local anaesthetics, opioids, and muscle relaxants on platelets. A brief summary of platelet physiology, function tests, and flow cytometric assessment of membrane receptors is included. Although the results of many studies have been conflicting, it appears that halothane, sevoflurane, and propofol inhibit platelet function in a reversible and dose-related manner at concentrations used clinically. Ilalothane affects the intracellular activating second messenger inositol triphosphate, platelet calcium homeostasis, thromboxane A2 formation, and the inhibiting signal transduction pathway including cyclic adenosine monophosphate. The proposed platelet inhibiting mechanism of sevoflurane involves the suppression of thromboxane A2 formation. Propofol appears to cause platelet dysfunctions by inhibiting calcium mobilisation upon agonist stimulation. Nitrous oxide causes a modest suppression of calcium mobilisation. An interaction of local anaesthetics with components in the platelet membrane appears to account for their inhibiting effect, but only at concentrations far higher than that found during clinical use. A clinically relevant antithrombotic effect of regional anaesthesia has been observed, though. Isoflurane, enflurane, desflurane, barbiturates, etomidate, opioids, and muscle relaxants seem to have negligible effects on platelets at therapeutic concentrations. Anaesthetists should be aware of the potential impairment of the coagulation profile by anaesthetic agents.

Anesthesia↗
PubMed2005

[Case of uremic platelet dysfunction].

The present case was a 59-year-old woman who underwent a right nephrectomy at 30 years of age, and in whom renal dysfunction occurred at 51 years of age. In November 199X, when her creatinine level reached 7 mg/dl, renal replacement therapy was recommended. She refused this therapy and began her own diet therapy, which consisted of taking only supplement beverage, but no food. Afterwards she became unable to do daily work, and entered our hospital in July of the next year. On admission, her bleeding time was over 10 minutes, but coagulation function tests showed normal values. Platelet function tests showed that coagulation with the addition of ADP was mildly decreased and that coagulation with the addition of aggregation was severely decreased. These data and her bleeding tendency improved with hemodialysis. Therefore, a diagnosis of aggregation non-responsive uremic platelet dysfunction was made. On admission, we were not able to insert a catheter for hemodialysis because of her severe bleeding tendency. A platelet transfusion was made so that we could insert the catheter without severe bleeding. However, this hemostatic effect lapsed after about five to six hours. Six hours after insertion of the catheter, oozing from the orifice of the catheter was seen and a red blood transfusion was necessary. Three days after beginning hemodialysis, the bleeding tendency was no longer seen. Her platelet function and coagulation test results also improved. We can make two conclusions regarding this case. The first is when the physician's medical strategy cannot be carried out due to uremic platelet dysfunction, a platelet transfusion can temporarily eliminate the bleeding tendency. The second is that the pathophysiology of uremic platelet dysfunction involves suppression of the primary step of platelet aggregation with collagen. Experience with the present case revealed the appropriate therapeutic strategy for the pathophysiology of uremic platelet dysfunction.

Blood Platelet Disorders↗
PubMed1998

Storage and quality assessment of platelets.

Platelet concentrates stored for 5 days under currently optimal conditions at 22 C demonstrate approximately a 20-30% loss of viability as determined by CCI measurements in thrombocytopenic patients and radiolabeling studies with healthy volunteers. The functionality of platelets is substantially lost during storage. This loss appears, for most part, to be reversible upon infusion. In view of this, stored platelets should be acceptable for prophylactic treatment of thrombocytopenic patients in whom immediate hemostatic function is not critical. However, whether stored platelets are functionally adequate for immediate arrest of perioperative bleeding in surgical patients remain uncertain. Currently, a fully adequate and appropriate test that evaluates the hemostatic function of a stored platelet product is not available. In view of this, a desired goal in research and development of new platelet products may then be to attain a platelet product that is similar to fresh platelets in various haemostatic functions. Whether this is an obtainable or relevant goal remains to be seen.

Adult↗
PubMed1981

[Effect of body weight reduction on platelet function and serum lipoproteins in obese children (author's transl)].

In 11 obese children aged 11,9 +/- 1,3 years total cholesterol (C), triglycerides (TG), HDL-C, LDL-C and apolipoprotein B (Apo B) were estimated in serum after 3 weeks of hypocaloric diet (800 kcal, kJ). In vitro platelet function was evaluated using the tests of ADP-induced aggregation and platelet sensitivity to prostacyclin. The in vivo platelet activity was judged by estimating plasma levels of beta-thromboglobuline (beta-TG) and platelet factor 4 (PF4). A mean weight loss of 5,7 +/- 1,8 kg was observed. Before diet, serum-C, TG and lipoprotein-C concentrations were found to be within the so called "normal range". After three weeks of diet we observed a significant decrease of total-C, which could be accounted for by a decline in the atherogenic LDL-C; furthermore Apo B levels significantly decreased. Concerning the tests of platelet function only for beta-TG and PF 4 a marked decline (to about 50% of the initial values) could be seen. These preliminary results and changes in the lipoprotein are discussed in connection with a possible reduction of the risk for the development of atherosclerotic lesions.

Adolescent↗