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PubMed1985

A method of testing platelet aggregation in native whole blood.

A method of testing collagen induced platelet aggregation and ATP release in native (= non anticoagulated) whole blood by monitoring the electrical impedance in the Chrono Log Whole Blood Aggregometer is reported. It is the first simple method by which aggregation of human platelets can be measured in their natural environment. In normal individuals lower threshold collagen concentrations could induce platelet aggregation as determined with this method than in the other tested methods (impedance method with citrated blood, optical method in platelet rich plasma). The aggregation response was not inhibited by hirudin or heparin in therapeutic dose. The luminescence channel of the Whole Blood Aggregometer permits measurements of ATP release in native whole blood.

Adult↗
PubMed1989

Budd-Chiari syndrome and thrombosis of other abdominal vessels in the chronic myeloproliferative diseases.

Of 501 patients with chronic myeloproliferative diseases (c-MPD) 18 developed thrombosis of major abdominal vessels including 6 with hepatic vein thrombosis (Budd-Chiari syndrome). The complication was seen in 14 of 140 (10%) patients with polycythemia vera (PV), 3 of 23 (13%) patients with essential thrombocythemia (ET), 1 of 106 (1%) patients with idiopathic myelofibrosis (IMF), and none of 232 patients with chronic myelogenous leukemia (CML). Leading symptoms and signs were abdominal pain, progressive splenomegaly, widening abdominal girth, ascites, venous collaterals, and nausea and vomiting. The diagnostic modalities with highest specificity were angiography and explorative laparotomy. A causal relationship between the thrombotic event and hematocrit, thrombocyte count, or hemostatic abnormalities at the time of diagnosis could not be established. Detailed laboratory tests of platelet function and coagulation and fibrinolytic parameters of 5 surviving patients did not show any specific defect. Despite medical and surgical intervention, 39% of the patients died within 2 months after diagnosis of the thrombosis. The majority of the survivors developed further complications like liver cirrhosis with portal hypertension and esophageal varices or the short bowel syndrome after extensive bowel resection for mesenterial infarction.

Blood Coagulation Tests↗
PubMed1984

Clinical significance of accelerated fibrinolysis in liver disease.

We compared site and severity of bleeding in 46 patients with cirrhosis of the liver and accelerated fibrinolysis (defined as a dilute whole-blood clot lysis time less than 2 h) to 44 patients with cirrhosis of the liver and normal fibrinolysis (dilute whole-blood clot lysis time greater than 4 h). Patients with accelerated fibrinolysis had a significantly higher incidence of severe soft-tissue bleeding after trauma and a trend toward increased intracranial bleeding. Mucosal, postoperative, and gastrointestinal bleeding were equally frequent in the two groups. The median partial thromboplastin time was significantly longer, and the median bilirubin and fibrin/fibrinogen degradation product levels were significantly higher in the group with accelerated fibrinolysis, but median prothrombin time, platelet count, and levels of fibrinogen and serum albumin were comparable. The fibrinolytic inhibitor epsilon-aminocaproic acid successfully controlled bleeding in 4 of 6 cases used. Accelerated fibrinolysis may predispose patients with cirrhosis to soft-tissue and intracranial bleeding.

Bilirubin↗
PubMed1991

[Changes in thrombocytic hemostasis in patients with diabetic glomerulosclerosis].

Indices of thrombocytic hemostasis were determined in 40 patients with diabetic glomerulosclerosis. It was found that patients suffering of diabetic glomerulosclerosis with chronic renal insufficiency showed signs of hypercoagulemia while changes of the thrombocytic hemostasis become of diverse values. There was a high correlation of hemostasis changes and clinical manifestations of diabetes mellitus and diabetic glomerulosclerosis. Three tests are recommended for treatment choice: hemolysate-aggregation test, determination of soluble complexes of monomer fibrin and fibrin-splitting product.

Adult↗
PubMed2001

Laboratory diagnosis of von Willebrand disorder (vWD) and monitoring of DDAVP therapy: efficacy of the PFA-100 and vWF:CBA as combined diagnostic strategies.

We have coevaluated a combination of test processes for diagnosing von Willebrand disease (vWD) and monitoring deamino-delta-D-arginine vasopressin (DDAVP) therapy. Using normal controls (n = 23), closure time (CT) ranges measured by PFA-100(R) were (mean +/- 2SD): (i) collagen/ADP cartridge (C/ADP): 67-127 s (ii) collagen/epinephrine (C/Epi): 94-162 s. From a panel of 125 patients undergoing evaluation for clinical haemostatic defects, 29/30 samples from patients with vWD [17/18 type 1, 1/1 type 3, 3/3 type 2A, 7/7 type 2B and 1/1 pseudo-vWD] gave prolonged CTs using C/Epi. The C/ADP was less sensitive, being normal in 7/18 of the type 1 vWD individuals, with higher sensitivity to more severe vWD. Individuals with haemophilia (six factor VIII-deficient, one factor XI-deficient) gave normal CTs, while those with clinical thrombocytopenia (n=13) gave normal or prolonged CTs, somewhat dependent on platelet count. The PFA-100 was also evaluated as a part of the laboratory monitoring procedure in patients with either vWD or haemophilia undergoing a DDAVP trial as a therapeutic management process. For vWD, correction of an initially prolonged CT by DDAVP, accompanied by normalization of von Willebrand factor (vWF) measurable by von Willebrand factor antigen, vWF collagen binding activity and vWF ristocetin cofactor assays (vWF:Ag, vWF:CBA and vWF:RCof), was achieved in type 1 vWD (n=5). In an individual with type 2A vWD, DDAVP normalized vWF:Ag and vWF:RCof, but had no apparent effect on the baseline maximally prolonged CT. In an individual with type 2B vWD, factor VIII/vWF concentrate also normalized vWF:Ag and vWF:RCof, but similarly had no apparent effect on the baseline maximally prolonged CT. vWF:CBA did not normalize for either of these individuals, potentially suggesting that normalization of vWF:CBA might be required for normalization of CT. This concept is supported by correlation analysis undertaken between CT and various vWF parameters. Among these, vWF:CBA held the strongest relationship in our data set, which showed an inverse progressive rise in CT for falling vWF:CBA. Based on these results, we would conclude that the PFA-100 is highly sensitive to the presence of vWD, and may thus provide a valuable screening test for vWD. Furthermore, the combined utility of the PFA-100 and vWF:CBA as markers of DDAVP responsiveness may prove to be simple, quick but powerful, predictors for its clinical efficacy.

Blood Protein Disorders↗
PubMed1983

Characterization of the effect of plasma lipoproteins on platelet function in vitro.

Thrombin-induced platelet activation is enhanced by very low and low density lipoproteins but decreased by high density lipoprotein. Plasma lipoproteins maximally affect platelet aggregation and 14C-serotonin release in a gel-filtered platelet preparation within 10 min of incubation at 37 degrees C. This effect is saturable and physiologic concentrations of lipoproteins are required in order to attain this saturation. When no aggregating agent is added to the incubation medium, the lipoproteins alone did not alter platelet aggregation. However, 14C-serotonin release is increased by very-low- and low-density lipoproteins alone more than by high density lipoprotein. On removal of the lipoproteins after incubation with the platelets, and subsequent testing of platelet function, minimal influence of these lipoproteins on the platelet function remains. Arachidonic acid causes similar results to thrombin when added to the platelet suspension after incubation with the lipoprotein. Our results further emphasize the 'opposing effects' of very low and low density lipoproteins as compared to high density lipoproteins on platelets and/or platelet-thrombin interaction.

Arachidonic Acid↗
PubMed1996

Leukocyte and platelet depletion protects the liver from damage induced by cholestasis and ischemia-reperfusion in the dog.

BACKGROUND: Ischemia-reperfusion injury has been studied in various organs. The effects of leukocyte and platelet depletion on cholestasis and ischemia-reperfusion-induced liver damage were evaluated in the dog liver. METHODS: The left hepatic duct was ligated for 4 weeks to create a cholestatic lobe. An ischemic condition was produced for 60 min by stopping the peristaltic pump supplying blood to the liver. The metabolism of substances modulated in the liver during cholestasis and I-R was assessed in non-treated and in leukocyte- and platelet-depleted animals. RESULTS: The extraction rate of insulin and indocyanine green decreased during cholestasis and ischemia-reperfusion. Cholestasis accelerated the release of thromboxane A2 but not prostaglandin I2 after ischemia-reperfusion. Ischemia-reperfusion accelerated the release of prostaglandin I2 and thromboxane A2 from the liver. Further, ischemia-reperfusion increased the ratio of thromboxane A2 to prostaglandin I2. Cholestasis promoted an increase in the level. Ischemia-reperfusion caused an increase in the lipid peroxide level, and no change in the alpha-tocopherol level. Ischemia-reperfusion caused an increase in the lipid peroxide level, a decrease in the alpha-tocopherol level, and no change in the glutathione level. Depletion of leukocytes and platelets reduced these changes during cholestasis and ischemia-reperfusion. CONCLUSIONS: Depletion of leukocytes and platelets thus appears to protect liver function from cholestasis and ischemia-reperfusion injury by reducing peroxidation of lipids composing the cell membrane and the rate of thromboxane A2 prostaglandin I2, which predicts cellular damage, and by increasing the levels of alpha-tocopherol and glutathione, believed to be free radical scavengers.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

The bleeding time as a preoperative screening test.

To examine the benefit of determination of the bleeding time as a preoperative screening test, the medical records of all patients who had a prolonged bleeding time during a six-month period were reviewed. At Northwestern Memorial Hospital, where the bleeding time test is part of the presurgical panel, 1,941 bleeding time determinations were performed during six months. Prolonged bleeding times were recorded in 110 preoperative patients, of whom 83 (75 percent) had bleeding risk factors, including drug ingestion, thrombocytopenia, and azotemia. In these patients, the bleeding time ranged unpredictably from 10 to more than 20 minutes. However, of the 27 patients without apparent risk factors, only two had bleeding times of more than 20 minutes. This small number probably does not justify the routine use of the test in all preoperative patients. Rather, the test should be used selectively for those subjects who, on the basis of history or laboratory evidence, are suspected of being at risk of hemorrhage. Moreover, even in these patients, prolongation of the bleeding time may not always be associated with excessive surgical blood loss.

Aspirin↗
PubMed1985

[Fundamental and clinical studies on aztreonam in pediatrics].

Fundamental and clinical results of AZT in pediatrics were as follows. Pharmacokinetics of AZT was studied for 1 case with resulting high serum concentration and a half-life of approximate 1 hour. AZT was administered to 10 patients with bacterial infections with 100% clinical efficacy and 62.5% bacterial elimination. Side effect was 1 case of diarrhea. There were no abnormal laboratory or coagulation test findings nor vitamin K deficiency, platelet hypofunction or effects on intestinal bacterial flora. AZT was considered to be high in safety. The administration of 20 mg/kg AZT 3 times a day was considered to be an effective treatment for pediatric Gram-negative infections.

Adolescent↗
PubMed1984

Association between bleeding time and platelet adherence to artery subendothelium.

The efficacy of five different factor VIII-von Willebrand factor (FVIII-VWF) preparations in mediating adherence of blood platelets to damaged vessel walls was tested in an annular perfusion chamber utilizing human arteries and reconstituted blood. FVIII-VWF-purified by Sepharose CL-4B chromatography and von Willebrand factor prepared from this preparation by dissociation with 0.25 M CaCl2 followed by Sepharose CL-6B chromatography were equally effective in mediating platelet adherence as FVIII-VWF in cryoprecipitate and in plasma from normal subjects. A commercial concentrate of FVIII-VWF (Hemofil, Hyland) used for the treatment of haemophiliacs did not mediate platelet adherence at normal levels of FVIII-VWF related properties. A recently developed high-purity FVIII-VWF preparation (Concentrate II) containing multimers of high molecular weight normalized the platelet adherence. Platelet adherence in plasma obtained from two patients with von Willebrand's disease (VWD) was impaired, but plasma samples obtained following treatment with Concentrate II mediated normal platelet adherence. The normalization of platelet adherence paralleled the normalization of the bleeding time. This platelet adherence assay offers an inexpensive and efficient in vitro tool to test the efficacy of FVIII-VWF preparations designed for VWD patients. Preparations such as cryoprecipitate and Concentrate II mediated the platelet adherence and normalized the bleeding time. The commercial preparation did not mediate platelet adherence and had no effect on the bleeding time.

Antigens↗
PubMed2002

The minimum concentration of fibrinogen needed for platelet aggregation using ADP.

OBJECTIVE: Determine the minimum concentration of plasma fibrinogen needed to stimulate the aggregation of platelets, collected from normal subjects, using ADP. DESIGN: Platelet rich plasmas (300 x 10(9) platelets/L) were made and adjusted to final fibrinogen concentrations of 75, 19, 5, and 0 mg/dL using fibrinogen free serum. Each fibrinogen concentration in all twelve subjects was aggregated with ADP SETTING: Research laboratory in the Department of Clinical Laboratory Science at Saint Louis University. PARTICIPANTS: Twelve healthy volunteers of both genders, between the ages of 18 and 60 years who were not pregnant and weighed at least 110 pounds were included in the study. Subjects were excluded from the study if they had ingested aspirin within one week prior to blood collection. In addition, subjects with a history of bleeding disorders such as afibrinogenemia, hypofibrinogenemia, von Willebrand disease, and Bernand-Soulier disease were rejected from the study. MAIN OUTCOME MEASURES: Platelet aggregation tracings were analyzed for amplitude and compared across plasma fibrinogen concentrations. In addition, the type of curve (monophasic vs. biphasic), smoothness and aggregation stability were also noted. RESULTS: The results show that aggregation occurred with every dilution of fibrinogen tested and that the amplitude of the aggregation curves appears not to be dependent on plasma fibrinogen. CONCLUSIONS: The results indicate that platelets from healthy individuals previously exposed to normal fibrinogen levels will aggregate equally well in decreasing plasma fibrinogen concentrations and even in the absence of plasma fibrinogen using ADP as the aggregator.

Adenosine Diphosphate↗
PubMed1998

Pluronic F-68 inhibits agonist-induced platelet aggregation in human whole blood in vitro.

The effects have been studied of Pluronic F-68 at 0.04% (w/v) on platelet aggregation in hirudin (50 micrograms ml-1)-anticoagulated, human whole blood in vitro in response to the following aggregation agonists: (i) phorbol 12-myristate 13-acetate (PMA; 0.05, 0.1 or 0.15 microgram ml-1), (ii) collagen (0.125, 0.25 or 0.5 microgram ml-1), or (iii) ristocetin (0.3, 0.6 or 1.2 micrograms ml-1). Pluronic F-68 significantly (P < 0.05) inhibited platelet aggregation that followed the addition of all agonists at their lowest concentration tested. Pluronic F-68 had markedly less pronounced inhibitory effects on the platelet aggregation that occurred in response to 0.15 microgram ml-1 PMA, where the mean % aggregation after 8 min was 67% of control (P < 0.05). Pluronic F-68 did not alter platelet aggregation in blood treated with 0.25 or 0.5 microgram ml-1 of collagen.

Collagen↗
PubMed1987

Comparison of bleeding times performed on the arm and the leg.

The standardized bleeding time (SBT) is used to assess hemostatic function in patients suspected of having coagulation disorders. Because injury to the arm or the presence of intravascular cannulae often preclude the determination of SBTs on the upper extremity, the authors compared the SBT on the arm with the bleeding time on the leg to ascertain the efficacy of the lower extremity for this test. Thirty healthy volunteers were enrolled in the study. Bleeding times were performed on the forearm and on the medial aspect of the calf. The subjects then ingested 650 mg of aspirin, and the tests were repeated two hours later on the contralateral extremities. The mean preaspirin SBT (5.6 +/- 1.7 minutes did not differ significantly from the mean bleeding time on the leg (5.8 +/- 2.3 minutes) (P greater than 0.50), nor was there a significant difference between the mean postaspirin bleeding time on the arm (10.2 +/- 4.3 minutes) and that on the leg (9.9 +/- 3.7 minutes) (P greater than 0.50). On the basis of this study, the authors conclude that the arm and leg are equally reliable sites for determining bleeding times in normal persons and are equally sensitive for detection of aspirin-induced prolongation of bleeding.

Adult↗
PubMed1998

Cone and platelet analyser (CPA): a new test for the prediction of bleeding among thrombocytopenic patients.

The risk of bleeding among thrombocytopenic patients was evaluated using our new cone and platelet analyser (CPA) test. Using this test, adherence of platelets was quantitated on extracellular matrix and expressed as percent of surface coverage (SC) and the average size (AS) of aggregates. 42 thrombocytopenic patients with ITP (n=23), post chemotherapy (n= 12) and others (n= 7) were tested over a total of 82 visits. On each visit, complete blood count and CPA tests were performed and patients were evaluated for evidence of bleeding (found in 40 visits). Bleeding patients had significantly lower platelet counts (27.4 +/- 22.0 v 47.1 +/- 21.0 x 10(9)/l), lower haematocrit values (30.2 +/- 8.1 v 35.2 +/- 6.6%), lower MPV (6.83 +/-1.89 v 8.98 +/- 1.13 fl), and lower SC (4.87 +/- 3.95 v 10.33 +/-5.48%) and AS (33.99 +/- 14.94 v 52.9 +/- 24.34 microm2). Univariate analysis yielded platelet count < or =20.0 x 10(9)/l, MPV < or =8 fl, haematocrit <35%, SC <5%, AS< or =40 microm2 as significantly associated with bleeding, whereas only MPV and SC were associated with bleeding (OR 6.95, CI 2.25-21.46 and OR 4.27, CI 1.29-14.16, respectively) by multivariate analysis. When taken together, 21/22 of patients (95%) with both low SC (<5%) and low MPV (<8.0 fl) had bleeding symptoms, whereas only 9/43 (21%) patients with both these parameters above these values experienced bleeding symptoms. We conclude that the CPA test and the parameter SC (<5%) together with MPV (< or =8 fl) might be used as independent predictors of bleeding in the management of thrombocytopenic patients.

Adolescent↗
PubMedDate not supplied

Platelet reactivity in spontaneously diabetic rats is independent from blood glucose and insulin levels.

Diabetes is associated with thrombotic disorders. Chemically induced and spontaneously induced diabetic animals and various in vitro tests have been used to reveal the prothrombotic state of diabetic patients. However, the results are not consistent. In the present study, platelet reactivity of spontaneously diabetic Goto-Kakizaki rats in vivo and in vitro was evaluated by laser-induced and shear-induced thrombosis models, which are physiologically relevant to thrombosis. Both results showed platelet hyperreactivity.

Animals↗
PubMed1990

[Evaluation of the hemostyptic properties of a collagen preparation].

In vitro tests were carried out to determine whether the haemostyptic properties of a collagen monomer were lost during the manufacturing process. An increased recalcification time and thromboplastin time as well as failure of the thrombocytes to adhere to the collagen fibres were observed. This indicates that blood coagulation can be attributed only to mechanical irritation of the blood corpuscles and not to the properties of the collagen molecules.

Collagen↗
PubMed1996

Use of enoxaparin in patients with heparin-induced thrombocytopenia syndrome.

PURPOSE: To determine whether low molecular weight heparin (LMWH) can be an alternative to unfractionated heparin (UH) for patients with heparin-induced thrombocytopenia syndrome (HIT). METHODS: The diagnosis of HIT was established in 126 patients by platelet aggregometry with UH (1 U/ml). These plasma samples were also tested for the ability to aggregate platelets in the presence of the LMWH enoxaparin (1 U/ml). Two patients with the HIT syndrome, after negative platelet aggregometry testing with enoxaparin, were anticoagulated with enoxaparin. RESULTS: Fifteen plasma samples that tested negative to UH also tested negative to enoxaparin. Forty-three of 126 (34%) UH-positive plasma samples aggregated platelets in the presence of enoxaparin. Twenty-two of 102 (22%) plasma samples with limited positive aggregation responses (minimal or no change in optical density) aggregated platelets in the presence of enoxaparin. However, 21 of 24 (88%) strongly positive plasma samples (30% to 60% change in optical density at 3 to 27 minutes) also aggregated platelets in the presence of enoxaparin. Two patients with HIT who received enoxaparin after aggregation testing demonstrated no cross-reactivity to enoxaparin achieved adequate anticoagulation and did not develop HIT. CONCLUSIONS: Thirty-four percent of plasma samples from patients with HIT (88% of those strongly positive) aggregated platelets in the presence of enoxaparin. Patients with HIT may safely receive enoxaparin if their plasma does not aggregate platelets in the presence of enoxaparin.

Aged↗
PubMed1972

Effects of progestogen oral contraception with norethisterone on blood clotting and platelets.

The effects on clotting tests and platelet function of six months' continuous administration of the 19-norsteroid, progestogen-only contraceptive, norethisterone, have been studied in four groups of women. In a group of women who have not previously taken oral contraceptive no acceleration of clotting or platelet factors was found, but in contrast a tendency to reduced coagulability was observed. Women who had previously been taking combined oestrogen-progestogen preparations showed reduced clotting and platelet parameters when norethisterone was substituted. No changes in clotting or platelets were found in women who changed from 17-acetoxysteroid progestogen chloramadinone acetate or in a group of women started postpartum.

Blood Coagulation↗