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PubMed1984

Platelet-type von Willebrand's disease.

Platelet-type von Willebrand's disease is a recently described disorder of primary hemostasis, possessing attributes both of von Willebrand's disease and of a qualitative platelet abnormality. This article discusses the clinical features, laboratory aspects, pathophysiology, and treatment of platelet-type von Willebrand's disease.

Blood Coagulation Tests↗
PubMed2006

Using the Platelet Function Analyzer-100 for monitoring aspirin therapy.

INTRODUCTION: The aim of the study was to evaluate the test characteristics of the Platelet Function Analyzer-100 (PFA-100) in patients treated with aspirin. METHODS AND RESULTS: The study consisted of two sub-studies. In study 1, 10 patients with ischemic heart disease (IHD) and 10 controls had platelet function assessed by optical platelet aggregation and the PFA-100 method in two 5-week periods. Patients with IHD were treated with aspirin 150 mg/day (first 5-week period), and 300 mg/day (second 5-week period), whereas the controls only received aspirin (150 mg/day) during the second 5-week period. From the results of study 1, we found that a cut-off value for the PFA-100 collagen/epinephrine cartridge <165 s identified patients not taking aspirin (sensitivity 0.91, specificity 1.00). A good agreement between the PFA-100 method and optical platelet aggregation was found. Within-subject variation for the PFA-100 collagen/epinephrine cartridge was +/-28%, as compared to +/-17% for the optical platelet aggregation. Study 2 included 298 aspirin treated patients who were admitted with symptoms suggestive of an acute myocardial infarction. Platelet function was assessed in duplicate by the PFA-100 collagen/epinephrine cartridge, and a 95% Limit of Agreement interval at [-65%, 65%] indicated a limited precision. CONCLUSION: We defined a cut-off value below which patients not taking aspirin can be identified. However, due to imprecision of the PFA-100 method repeated duplicate assessment of the collagen/epinephrine Closure Time is recommended.

Aged↗
PubMed2007

Platelet function in whole-blood donors is impaired: the effects of painkillers.

BACKGROUND: Aspirin (ASA) or non-aspirin-like nonsteroidal anti-inflammatory drugs (NSAIDs) influence platelet (PLT) function by inhibiting cyclooxygenase enzymes. In this study, the aim was to address the use of ASA or NSAIDs before donation and the effect on PLT function. STUDY DESIGN AND METHODS: Donors were asked questions about recent use of ASA or NSAIDs. Furthermore, PLT function was evaluated by measurement of the closure time (CT) in a PLT function analyzer (PFA-100, Dade Behring) and by aggregometry (response to ADP or arachidonic acid [AA]). RESULTS: Of 100 questioned donors, 22 percent had used ASA (n = 4), NSAIDs (n = 6), or paracetamol (n = 12) before donation. Upon assessment of the PLT function in the PFA-100, 27 donors showed values of greater than 180 seconds, indicative of impaired PLT function. Of these, only 7 had used pain killers before donation. Furthermore, 15 of 22 users had normal CTs. Aggregation after stimulation with AA was absent in 33 PLT-rich samples. Again only 8 had reported use of ASA (3), NSAIDs (1), or paracetamol (4). Of the 22 users, 14 had normal AA aggregation responses. All donor samples showed ADP-induced aggregation, indicating PLT integrity. There was no difference between the group of donors who reported the intake of ASA or NSAIDs and the group of donors who did not with respect to the tested PLT function assays. CONCLUSION: It is concluded that there is a considerable group of donors that use PLT-influencing medication before donation. A relation between the reported use and impaired PLT function in blood donors could not be established, however. Impaired PLT function as tested may have other causes than intake of ASA or NSAIDs.

Acetaminophen↗
PubMed1995

Half-dose aprotinin preserves hemostatic function in patients undergoing bypass operations.

High-dose aprotinin reduces bleeding in cardiac operations but with potential side-effects and increased cost. It is therefore mandatory that the effectiveness of a low dose be investigated. Half of the Hammersmith regimen was studied in cardiac surgical patients to find out how it could reduce bleeding. Blood fibrinolysis parameters were studied in 40 elective patients undergoing coronary artery bypass grafting in a double-blind, placebo-controlled study design. The plasma activities of tissue plasminogen activator, plasminogen activator inhibitor, alpha 2-antiplasmin, plasminogen, fibrinogen, and D-dimer as well as platelet number, bleeding times, activated clotting time, and aprotinin plasma concentrations were assessed before, during, and after the operation. Fibrinolysis was inhibited by aprotinin as evidenced by decreased D-dimer (p = 0.0001) and tissue plasminogen activator (p = 0.0432) levels and increased plasminogen activator inhibitor (p = 0.0105) and alpha 2-antiplasmin (p = 0.0002) levels during the operation. A postoperative abnormal bleeding time occurred 38% more frequently in the placebo group (p < 0.05). Aprotinin plasma concentrations reached adequate levels to inhibit plasmin and plasma kallikrein. This study showed that half-dose aprotinin significantly inhibits fibrinolysis and prevents postoperative abnormal bleeding time in cardiac surgical patients.

Aged↗
PubMed1989

Impaired fibrinolysis in patients with thrombotic or haemostatic defects.

In a retrospective study of the 47 patients examined for thrombotic defects, 34 had prolonged euglobulin lysis times (ELT) with 27 of these also having elevated tissue-plasminogen activator inhibitor (t-PAI) activity. Twenty three of the 57 patients examined for possible bleeding problems had prolonged ELT with 15 of this group also having raised levels of t-PAI. There was a statistically greater (P less than 0.005) incidence of elevated t-PAI in the thrombotic group. The incidence of 40% patients with prolonged ELT in the haemostasis group was surprising and perhaps represents some compensatory mechanism to combat bleeding. Thus in vitro tests showed that a reduced capacity for fibrinolysis was present in diametrically opposed groups.

Adolescent↗
PubMed1985

Comparison of two simple tests for the lupus anticoagulant.

Mixtures of various patient lupus inhibitor-containing plasmas and normal plasma were tested concurrently with the dilute tissue thromboplastin inhibition (DTTI) test and the kaolin clotting time (KCT). The KCT was found to be more sensitive to the presence of the lupus inhibitor than the DTTI. The principle of reducing the platelet phospholipid content in the KCT test plasma to enhance sensitivity for the lupus inhibitor was extended by using plasmas filtered through 0.22-micron cellulose acetate filters.

Blood Coagulation Factors↗
PubMed2006

Recombinant factor VIIa reverses the inhibitory effect of aspirin or aspirin plus clopidogrel on in vitro thrombin generation.

BACKGROUND: Antiplatelet drugs constitute the therapy of choice for acute coronary syndromes, but bleeding can be a side-effect requiring treatment. Restoration of normal platelet activity is also mandatory before urgent surgery. This study investigated: (a) whether a regimen of aspirin or clopidogrel plus aspirin significantly inhibited platelet thrombin generation (TG); and (b) the reversal of this inhibition by recombinant activated factor VII (rFVIIa). METHODS AND RESULTS: TG was evaluated by the lag time, time to peak, peak of TG, and area under the curve after 35 min of assay (AUC(0 --> 35 min)). These measures were examined by the calibrated automated thrombography method in 22 healthy volunteers, 22 volunteers after a 100 mg day(-1) aspirin intake (200 mg first day) for 5-7 days, and 22 healthy volunteers after aspirin 100 mg day(-1) (200 mg first day) plus clopidogrel 75 mg day(-1) (300 mg first day) for 4-7 days. The TG parameters were measured under basal conditions and after platelet stimulation by sodium arachidonate (AA), adenosine 5'-diphosphate (ADP), collagen and rFVIIa in normal non-aspirinated as well as in vivo aspirinated platelet-rich plasma (PRP) or aspirin plus clopidogrel PRP. Lag time was shorter (P < 0.05), and peak of TG and AUC(0 --> 35 min) were significantly greater (P < 0.01 for both), in PRP activated with ADP, collagen, AA or FVIIa than in non-activated PRP from normal subjects. Both non-activated PRP and activated PRP prepared from platelets obtained from volunteers after aspirin intake showed significant prolongation of the time parameters but there was less effect on peak of TG and AUC(0 --> 35 min). For most parameters, aspirin plus clopidogrel administration showed to be more effective compared with the effect obtained by aspirin alone. When rFVIIa was added to ASA-PRP or ASA + Clop PRP, lag time (P < 0.001 for all) and time to peak (P < 0.001-0.017) were significantly shortened, indicating that rFVIIa reverses the inhibitory effect of these anti-aggregating agents. CONCLUSION: Platelets activated by AA, ADP, collagen or FVIIa triggered TG. This effect was inhibited by aspirin plus clopidogrel, suggesting an additional benefit of this drug combination for preventing thrombosis. rFVIIa reverses the inhibitory effect of aspirin or aspirin plus clopidogrel, and could be useful for bleeding complications or when acute surgery is needed during treatment with these antiplatelet drugs.

Adult↗
PubMed1990

Comparative studies on properties of unfractionated and low molecular weight heparin.

LMW heparin (FR-860) produced by depolymerization of unfractionated heparin with dinitric acid was used to investigate clinical effects in healthy volunteers. The results were as follows: 1. Subjective symptoms, physiologic studies, blood examinations, blood chemistry, and urinary chemistry tests were not changed. 2. Two of five volunteers who received unfractionated heparin (H-25) and two of five who received LMW heparin (F-50) manifested petechiae at the injection sites. These bleedings were dose dependent. 3. The effect on APTTs and thrombin times was less evident with F-25 and F-35 than with H-25; F-50 showed greater prolongation than H-25. 4. The half-life of LMW heparin was 1.5 to 1.8 hours; unfractionated heparin had 0.68 hours. 5. No changes were observed in the levels of AT III, fibrinogen, and FDP. 6. Platelet aggregation rates induced by 1.0 microM ADP were less affected by LMW heparin than by unfractionated heparin. 7. Platelet factor 4 levels increased markedly, but to a lesser extent with LMW heparin than with unfractionated heparin. These results are due to its mobilization from the vessel wall. No changes were observed in beta-thromboglobulin levels. 8. Fatty acid analysis (LPL and HTGL) was less affected by LMW heparin than by unfractionated heparin.

Adult↗
PubMed1994

Heparin-induced thrombocytopenia: a survey of tests employed and attitudes in haematology laboratories. Groupe d'Etude sur l'Hémostase et la Thrombose (GEHT) de la Société Française d'Hématologie.

A survey was carried out of the attitudes adopted in French laboratories with regard to the diagnosis of heparin-induced thrombocytopenia (HIT). The platelet aggregation assay is used in 100% of laboratories, aggregation being measured by light transmission in an aggregometer (3/4). Blood is drawn either in emergency (1/4) or after heparin discontinuation (1/4). The nature of the samples for testing is a fresh citrated plasma (100%) although frozen plasma is occasionally employed, while 40% of laboratories use less than 3 control platelet donors. Platelet response is verified in the presence of a non immune agonist (18%) or an immune challenge (known positive plasma or platelet activating monoclonal antibody) (13%). Heparin is of the same type as received by the patient and is tested at two or more concentrations of approximately 0.5 and 1.0 IU/ml, but rarely at high concentration (100 IU/ml). The platelet count is adjusted to 250-350 x 10(9)/l (18%), the ratio of patient plasma to PRP is 1:1 (59%), the time of observation is about 20 min (50%) and control platelets are tested with heparin to rule out any false positive results (9/10). Standardization is nevertheless required if the platelet aggregation assay is to be considered as a reference test.

Artifacts↗
PubMed1982

Changes in platelet function, blood coagulation and fibrinolysis during insulin-induced hypoglycaemia in juvenile diabetics and normal subjects.

Haemostatic parameters were assessed before insulin induced hypoglycaemia and 0, 1 and 2 hr after discontinuation of insulin infusion in 7 non-diabetics, aged 28 (22-31) years (mean and range), and 8 juvenile diabetics, aged 31 (27-35) years, with a mean duration of diabetes of 4 years. The patients were normoglycaemic for at least 10 hr before the study. Platelet aggregation in vitro was induced by lower adenosine diphosphate (ADP) concentrations in the diabetics than in the controls before hypoglycaemia and 0 and 60 min after insulin infusion. Platelet counts decreased significantly in the diabetics after hypoglycaemia, whereas no changes were seen in the control group. The activated partial thromboplastin time (APTT) was reduced in both groups and significantly lower in the diabetics than in the controls 120 min after insulin infusion. Fibrinogen and factor VIII R:Ag increased after insulin infusion; highest values were seen in the diabetics. The euglobulin clot lysis time (ELT) was reduced in both groups during insulin infusion; 120 min after end of insulin infusion ELT was significantly longer in the diabetics than in the control group.

Adult↗
PubMed1978

Demonstration of a platelet bypass mechanism in the clotting system using an acquired anticoagulant.

A lupus-type anticoagulant which causes strong inhibition of the partial thromboplastin time with kaolin (PTTK), the stypven time, and the thrombin generation tests has been investigated. All tests for platelet function were normal, as were all specific coagulation factor assays with the exception of a slightly reduced factor XI in this patient. A diethylaminoethyl-cellulose-immunoglobulin (DEAE-cellulose-IgG) fractionation of the patient's plasma produced two peaks containing inhibitory activity in the PTTK test. The first of these peaks had a cloudy appearance, suggesting the presence of immunoglobulin aggregates. Studies with IgG aggregates prepared from normal IgG and from the patient's IgG demonstrated that such aggregates were not the cause of inhibition. It was possible to neutralize the inhibitory activity of the purified IgG but not platelet-poor plasma (PPP) with a rabbit anti-IgG. The inhibition of the patient's PPP in the thrombin generation, the contact product, and the stypven time tests were corrected by the inclusion in the test system of platelets activated either by aggregation due to adenosine diphosphate (ADP) or formalin fixation and washing. These studies lend support to earlier findings that platelets interact at several sites in the coagulation cascade.

Antibodies↗