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Results for “Platelet Function Tests”

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At least 631 records · Page 35Linked to original sources
PubMed1982

Inhibition of spontaneous platelet aggregation and adhesion by indobufen (K 3920). A randomized, double-blind crossover study on platelet, coagulation and fibrinolysis function tests.

In a randomized double-blind crossover study in 12 patients with atherosclerotic disease, the effect of 2 dosages (100 and 200 mg twice daily) of indobufen, a new synthetic inhibition of platelet aggregation, on some platelet functions, coagulation and fibrinolysis tests was investigated. Regardless of the dosage used, indobufen was shown to induce a prompt normalization of the enhanced platelet aggregation of these patients. The effect lasted for the entire period of drug administration and in 50% of patients a normal platelet aggregation was maintained until the fourth day after discontinuation of the drug. Indobufen was also able to reduce platelet adhesiveness and to lengthen bleeding time, especially when the higher dosage was used.

Aged↗
PubMed2001

Platelet function during pregnancy: an evaluation using the PFA-100 analyser.

In clinical practice, the only tests of platelet function are bleeding time and platelet number. Bleeding time lacks sensitivity and specificity but the PFA-100, an in vitro analyser of platelet function may be of value. This study aimed to evaluate any correlation between platelet number and function using the PFA-100 in pregnant women. During a 21-month period, platelet function was evaluated in whole blood as part of the pre-anaesthetic coagulation testing screen with the PFA-100 using collagen and epinephrine (PFA-EPI) or ADP (PFA-ADP) as platelet agonists. Thrombocytopenia was defined as a platelet number less than 150 G litre(-1). The patients were divided into four groups: Group I (n=110) normal pregnancy; Group II (n=38) thrombocytopenia of pregnancy; Group III (n=13) women with pre-eclampsia without thrombocytopenia; Group IV (n=19) women with pre-eclampsia and thrombocytopenia. Results are expressed as mean (SD). Platelet count was not statistically different between Groups II and IV (111.1 (23.1) vs 99.5 (28.0) G litre(-1)). PFA-EPI was statistically increased in Group II (124.0 (26.3) s), Group III (128.3 (17.9) s), and Group IV (143.6 (47.7) s) compared with normal pregnant patients (114.6 (27.3) s, P<0.05, Mann-Whitney U-test). PFA-ADP was statistically increased only in Group II compared with normal pregnant patients (90.5 (18.9) vs 80.2 (11.2) s, P<0.05). PFA values were increased above normal laboratory values in (four of 38) Group II patients and (six of 19) Group IV patients but in no patients in Group III. PFA-ADP results were correlated with platelet count only in Group IV (r=-0.74, P=0.0003). The increased PFA values and the correlation between PFA-ADP and platelet number in hypertensive thrombocytopenic women confirms that platelet function may be decreased in such patients. In patients with pregnancy-induced thrombocytopenia, platelet function may be preserved when the platelet count is as low as 60 G litre(-1).

Adolescent↗
PubMed1998

Neonatal platelet physiology and pathophysiology.

Platelets contribute to primary haemostatic events and are closely linked to plasmatic coagulation. Their function is highly dependent not only on their number but also on their integral physiology. In comparison with adults or children, the haemostasis of newborn infants, although physiological, is characterized by a reduced functional reserve capacity leading to the rapid occurrence of bleeding disorders especially in the presence of additional risk factors such as prematurity, asphyxia, or infection. Morphological and biochemical differences reflect an immature cellular stage which results in platelet hyporeactivity and contributes to the reduced capacity of the neonatal haemostatic system. Additionally acquired and inherited platelet disorders markedly affect platelet function. Hence assessment of neonatal platelet physiology may supply important information, however, no adequate screening tests are currently available, and technical difficulties of blood sampling limit the value of laboratory testing. Evaluation of the neonatal platelet function is highly dependent on individual laboratory results and it is advisable to perform complex diagnostic procedures with the collaboration of specialists experienced in neonatal haematology. With the advent of new technology such as platelet flow cytometry more adequate tools are available, although still reserved for specialized laboratories, thus awaiting their clinical significance. The role of maternal influences on neonatal platelet function must be always considered. Thus, neonatal platelet physiology and pathophysiology is complex and require more studies and experience.

Blood Platelet Disorders↗
PubMed2001

Laboratory diagnosis of heparin-induced thrombocytopenia: advantages of a functional flow cytometric test in comparison to the heparin-induced platelet-activation test.

Nearly one third of patients with heparin-induced thrombocytopenia (HIT) will progress to overt thrombosis. Owing to the severity of HIT, a reliable prompt diagnosis is mandatory. In this study 248 consecutive samples from patients referred to our laboratory for HIT diagnosis and 97 specimens from normal controls were prospectively evaluated in parallel using the heparin-induced platelet aggregation (HIPA) test and a flow cytometric (FC) test. The HIPA test resulted in 214 negative, 17 indeterminate and 17 positive samples of patients. The FC method detects activated platelets induced by heparin-immune complexes using the highly sensitive recombinant probe annexin V and pooled platelets from multiple donors. The criteria for positive FC test results included an increase in platelet activiation of at least 11% at 0.3 IU/mL heparin concentration in the tube, and a ratio of more than 1.5 between platelet activation at 0.3 and 200 IU/mL heparin. According to the cut-off level 17 patients who showed indeteminate HIPA test results had 14 negative and 3 indeterminate corresponding FC test results. Only one of these patients (HIPA test indeterminate, FC test indeterminate) had no other obvious medical cause for thrombocytopenia than HIT. Infections or inflammations did not show any association with the FC test results, whereas thromboembolic events displayed a significant patelet activation at pharmacological heparin concentration. Therefore the FC test is associated to the complications of HIT. In conclusion, the FC test, which is fast and practical, showed a good agreement with the HIPA test and may be an accurate and useful test for HIT.

Annexin A5↗
PubMed1992

Ticlopidine and platelet function in healthy volunteers.

The influence of a 4-weeks therapy with 500 mg ticlopidine daily on platelet function parameters was examined in 10 male healthy volunteers aged 20-33 years in order to extend the knowledge on the antiplatelet activity of this substance. Ticlopidine significantly (p less than 0.01) affected ex-vivo platelet aggregation induced by ADP and increased platelet sensitivity to the antiaggregatory action of PGI2. Generation of TXB2 from endogenous substrate during spontaneous clotting of blood (serum-TXB2), conversion of exogenous radiolabelled arachidonic acid into TXB2 and MDA-formation in isolated platelets were unaffected by the treatment. The TXB2-level in plasma of volunteers, however, was decreased, after administration of the drug. The diminished alpha-granule content liberation (beta-thromboglobulin: p less than 0.01; PDGF: p less than 0.01; PF4 not significant) indicates that ticlopidine induces a decrease in platelet activity. The beneficial effect on release reaction is not associated with a decrease in TXA2-formation. Our results demonstrate that ticlopidine inhibits platelet activity, especially the PDGF-release. These results confirm the value of this drug in the prevention of atherosclerosis and its thromboembolic complications.

Adult↗
PubMed1958

The uptake of adrenaline and noradrenaline by blood platelets of the pig.

Pig platelets contained 0.2 to 2.6 ng. adrenaline/10(8) platelets (4 experiments). Noradrenaline was not detected in them. When platelet-rich plasma was incubated at 37 degrees with 1 or 10mug. of added catechol amine/ml., the platelets continued to accumulate adrenaline for at least 120 min.; only about one-third as much noradrenaline as adrenaline was taken up. The concentrations of adrenaline taken up by different platelet samples at the end of incubation for 90 min. were proportional to the concentration of adenosine triphosphate in the platelets.

Adenosine Triphosphate↗
PubMed1986

Laboratory investigation of platelet function: a review of methodology.

Over the past decade interest in and knowledge about the role of platelets in the haemostatic process and in various pathological conditions has continued to grow. The scope of laboratory methodology to investigate platelet function in clinical haemorrhagic and thrombotic disorders in the specialised haemostasis unit has also proportionally widened. After highlighting the physiological processes of the role of platelets in the haemostatic mechanism this brief review comments critically on the available routine techniques used to study platelet function in patients who present primarily with a bleeding tendency.

Adenine Nucleotides↗
PubMed1983

New beta-lactam antibiotics and hemorrhagic diathesis: comparison of moxalactam and cefotaxime.

Two new beta-lactam antibiotics, moxalactam and cefotaxime, were administered to two groups of patients with clinical indications for cephalosporin therapy and bacteriologically confirmed infection. The ten patients receiving moxalactam included five patients with impaired renal function; the ten receiving cefotaxime included seven with impaired renal function (serum creatinine greater than 1.3 mg/dl). Antibiotics were administered for seven days in dosages adjusted to the level of renal function. Serum trough levels, measured by microbiological assay, were within the therapeutic range: moxalactam median, 3 micrograms/ml (range, 0.6-20 micrograms/ml) and cefotaxime median, 2.9 micrograms/ml (range, 0.5-16 micrograms/ml).

Adolescent↗
PubMed1993

[Platelet functions in atherosclerosis].

Recent advances on platelet functions involved in atherosclerosis and subsequent thromboembolic diseases are reviewed. Platelets show multiple roles in hemostasis/thrombosis, wound healing, allergy, inflammation, metastasis of malignant cells and vasospasms through aggregation/secretion reaction. In atheromatous plaque, migration and proliferation of vascular smooth muscle cells and macrophages are the most prominent findings. In this pathological state, platelet may play as an enhancer by the secretion of bioactive substances including platelet-derived growth factor, serotonin and platelet factor 4. Investigation on platelet dynamics must be carried out not only for monitoring but also for the assessment of progressive factors in atherosclerotic disease.

Arteriosclerosis↗