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PubMed1987

Hemostatic derangement in dengue haemorrhagic fever.

Forty children, aged 1/2-14 years, with serologically proven dengue haemorrhagic fever were daily studied for hemostatic tests. There were 4, 20 and 16 cases of grade I, II III respectively. Hemostatic derangements in DHF is a multifactorial mechanism. Vasculopathy, thrombocytopenia, platelet dysfunction were found in most cases. Mild to moderate degree of prothrombin complex deficiency was observed in 15% and 50% of grade II and grade III respectively while laboratory evidence of consumptive coagulopathy was noted in 30% of shock cases and 10% of non-shock cases. Hypofibrinogenemia and increased PTT are commonly seen in grade III reflect the presence of stimulation of intrinsic coagulation pathway probably from immunologic reaction. Frank DIC is very rarely observed. FDP is slightly increased but not as high as in classical DIC. Further study on the role of platelet-endothelial interaction should be elucidated including the efficient management to stop bleeding in severe shock cases.

Adolescent↗
PubMed1980

Acquired von Willebrand's syndrome during autoimmune disorder.

A case with evidence of acquired von Willebrand's syndrome associated with systemic lupus erythmatosus and Sjögren's syndrome is described. The patient, who had no family history of bleeding, presented a haemorrhagic diathesis of recent origin, the bleeding time was prolonged, procoagulant Factor-VIII and von Willebrand factor levels were low and platelet aggregation was decreased with different concentrations of Ristocetin. No improvement was seen after the tranfusion of cryoprecipitates, and there was no increase in procoagulant Factor-VIII. Clinical improvement resulted after treatment with corticosteroids, and later, the laboratory abnormalities characteristic of von Willebrand's disease became normal. The level of procoagulant factor-VIII reached the very high level of 810%.

Adult↗
PubMed1996

[Factor XI deficiency: do patients with hemorrhagic diathesis also have hemostasis defects?].

It is well known that the extent of bleeding in patients with a deficiency of factor XI does not parallel the residual factor activity. Therefore, additional hemostatic aspects must be taken into consideration. 27 patients of 18 different families--6 with severe (FXI < 0.01 to 0.09 U/ml) and 21 with moderate (FXI 0.20 to 0.252 U/ml) factor XI deficiency--were reinvestigated regarding hemostasis including bleeding time and platelet function. 16 had an enhanced bleeding tendency, while the others--including 3 with severe FXI deficiency of < 0.01 U/ml--never suffered from bleeding complications despite delicate surgery in some. All 16 of the symptomatic patients had, besides the reduction of factor XI activity to various extents, an additional hemostatic defect: 3 had a moderate alpha/delta storage pool detect of the platelets, 11 a platelet anomaly mainly characterized by reduced ADP aggregation and 2 an isolated prolonged bleeding time of unknown cause. Synthesis of platelet thromboxane was unimpaired in all patients as tested by formation of malondialdehyde after stimulation with N-ethyl maleimide. Hence, in patients with a known factor XI deficiency diagnostic and prophylactic measures before surgery should concentrate on such additional findings. Preoperative administration of desmopressin, and not replacement of factor XI, will be the treatment of choice in these cases.

Adult↗
PubMed1990

Bleeding time and other laboratory tests to monitor the safety and efficacy of thrombolytic therapy.

Widespread use of thrombolytic agents in a variety of settings has highlighted the need for measures of safety and efficacy. Previously used laboratory parameters, such as decreasing levels of fibrinogen and increasing levels of fibrin(ogen) degradation products (FDPs), have failed to correlate consistently with hemorrhagic events and have not yet been useful in predicting patients at risk for bleeding. Although the bleeding time (BT) has been considered primarily to reflect platelet function, it also reflects the interaction of platelets with vessel wall and coagulation pathways. Recently, the BT has been considered as a potential predictor of clinical bleeding during thrombolysis. The BT, as a measure of in vivo hemostatic competence, may be particularly well-suited for this application. Serial BTs during thrombolytic therapy may provide valuable information regarding safety and efficacy, but further studies are needed to confirm preliminary findings.

Bleeding Time↗
PubMed2001

[New laboratory tests for detecting platelet abnormalities].

Platelets play important roles in thrombosis and hemostasis, and their abnormalities lead to hemostatic disorders or thrombotic diseases. The development of new tests for assessing platelet disorders is awaited. In this article, the measurement of blood thrombopoietin levels and detection of platelet aggregates with a particle counting method using light scattering are described as candidates for new laboratory tests for detecting platelet abnormalities.

Animals↗
PubMed1992

[Prevalence of lupus anticoagulant, autoimmune hemolysis, thrombocytopenia and disorders of platelet function in unselected patients with SLE].

Prevalence of lupus anticoagulant (LA) in patients with systemic lupus erythematosus (SLE) and clinical manifestations vary widely between different clinical series. We investigated the relation between LA, autoimmune hemolytic anemia (AIHA), thrombocytopenia and platelet dysfunction in 80 unselected patients with SLE. AIHA was found in 6 patients (7.5%) and thrombocytopenia in 10 patients (12.5%), which was not related to platelet aggregation abnormalities. Compared to controls, patients with SLE showed significantly prolonged aPTT and kaolin clotting time (KCT), but platelet aggregation induced by both collagen and thrombin was not impaired. LA activity as defined by Rosner et al. (index for LA/ICA) was found in 15 patients (18.9%). Only 7 of these patients showed a positive platelet neutralization test (Triplett) and 9a positive tissue thromboplastin inhibition test (Schleider). In our SLE patients 23.7% have suffered from at least one thrombotic complication. In patients with LA activity thromboembolic complications were increased (p < 0.05). Thrombocytopenia was found in 6% of LA-negative but in 20% of LA-positive patients.

Abortion, Spontaneous↗
PubMed1997

Effects of chronic exercise and deconditioning on platelet function in women.

To investigate the effects of chronic exercise and deconditioning on platelet function in women, 16 healthy sedentary women were divided into control and exercise groups. The exercise group cycled on an ergometer at 50% maximal oxygen consumption for 30 min/day, 5 days/wk, for two consecutive menstrual cycles and then were deconditioned for three menstrual cycles. During this period, platelet adhesiveness on a fibrinogen-coated surface, ADP-induced platelet aggregation and intracellular calcium concentration elevation, guanosine 3',5'-cyclic monophosphate (cGMP) content in platelets, and plasma nitric oxide metabolite levels were measured before and immediately after a progressive exercise test in the midfollicular phase. Our results indicated that, after exercise training, 1) resting heart rates and blood pressures were reduced, and exercise performance was improved; 2) resting platelet function was decreased, whereas plasma nitrite and nitrate levels and platelet cGMP contents were enhanced; and 3) the potentiation of platelet function by acute strenuous exercise was decreased, whereas the increases in plasma nitrite and nitrate levels and platelet cGMP contents were enhanced by acute exercise. Furthermore, deconditioning reversed these training effects. This implies that training-induced platelet functional changes in women in the midfollicular phase may be mediated by nitric oxide.

Adult↗
PubMed2001

The effects of hydroxyethyl starches of varying molecular weights on platelet function.

We evaluated the effect of various hydroxyethyl starch (HES) solutions on platelet function. Blood was obtained before and after the IV infusion (10 mL/kg) of saline (n = 10), HES 70/0.5--0.55 (molecular weight in kD/degree of substitution; n = 10), HES 130/0.38--0.45 (n = 10), HES 200/0.6--0.66 (n = 10), or HES 450/0.7--0.8 (n = 10) in otherwise healthy patients scheduled for elective surgery. Collagen and epinephrine were used as agonists for assessment of platelet function analyzer closure times. Flow cytometry was used to assess agonist-induced expression of activated glycoprotein IIb/IIIa complex and P-selectin. Infusion of HES 450/0.7--0.8, HES 200/0.6--0.66, and HES 70/0.5--0.55 prolonged closure times and reduced glycoprotein IIb/IIIa expression, whereas saline and HES 130/0.38--0.45 had no significant effect on platelet variables. P selectin expression was not affected by any solution tested. In vitro experiments demonstrated a less inhibiting effect of HES 130/0.38--0.45 on closure times when compared with other HES solutions. This study shows that HES 450/0.7--0.8, HES 200/0.6--0.66, and HES 70/0.5--0.55 inhibit platelet function by reducing the availability of the functional receptor for fibrinogen on the platelet surface. Our data indicate that fluid resuscitation with HES 130/0.38--0.45 may reduce the risk of bleeding associated with synthetic colloids of higher molecular weight and degree of substitution.

Adult↗
PubMed1981

Antithrombotic therapy: role of platelet-inhibitor drugs. I. Current concepts of thrombogenesis: role of platelets. (first of three parts).

Definite evidence has confirmed that platelets play a major role in thrombus formation and embolization, especially in the arterial system. In addition, increasing evidence has now shown that platelet deposition and thrombus formation can contribute to the growth and progression of atherosclerotic plaques. For these reasons, considerable attention has been focused recently on the question of whether drugs that inhibit certain platelet functions can prevent or modify the course of arterial thromboembolic disease and atherosclerotic disease in humans. In this first part, we review the current understanding of the role of platelets in thrombus formation, especially in the arterial system. This section comprises (1) the phases of arterial thrombus formation and its ultrastructural and biochemical basis, (2) the clinicopathologic presentation and fate of the arterial thrombus, and (3) the role of laboratory tests in its detection.

Animals↗
PubMed2002

Use of the bleeding time in the neonatal intensive care unit.

UNLABELLED: Impairments of primary hemostasis are frequently responsible for serious bleeding in sick infants in the neonatal intensive care unit (NICU). Therefore, a rational approach to these infants with hemorrhagic manifestations, in addition to an accurate medical history, a careful physical examination and routine screening coagulation tests, may include a bleeding time. The bleeding time is the traditional in vivo test for assessing primary hemostasis. It is a useful clinical tool to detect quantitative or qualitative platelet disorders or microvascular defectiveness. Its diagnostic value in neonates is controversial, mainly owing to limited experience in executing the test, which is performed uncommonly in the NICU. Using a template device expressly adapted for neonates (Surgicutt Newborn), a small incision 2.5 mm long and 0.5 mm deep provides a standardized, reproducible and sensitive bleeding time, with minimal scarring and pain. Various hereditary or acquired maternal and neonatal diseases, as well as some antepartum medications given to the mother or drugs commonly used to treat NICU patients, such as indomethacin, ibuprofen, penicillin compounds and theophylline, can impair primary hemostasis and consequently prolong the bleeding time in neonates. Furthermore, other factors distinctive to neonates, including gestational age, the increased von Willebrand factor concentration and function, high hematocrit, the large size of erythrocytes and platelet hyporeactivity in the first 10 d of life, affect platelet-vessel wall interaction and influence the interpretation of bleeding time results in newborn infants. Because the clinical evaluation of primary hemostasis consists of complex laboratory testing, largely reserved for specialized laboratories and currently not routinely performed in newborn infants, automated bleeding time devices specifically generated to make standardized and acceptably small incisions in newborn infants have become a surrogate. CONCLUSION: With awareness of its value and limitations, the bleeding time can be included in the baseline evaluation of neonates in the NICU, for guiding diagnosis and treatment of primary hemostatic disorders.

Bleeding Time↗
PubMed2005

Evidence based coagulation monitors: heparin monitoring, thromboelastography, and platelet function.

The hemostatic management of patients undergoing cardiac surgery is a unique challenge. Since its inception, cardiopulmonary bypass (CPB) has required meticulous attention to maintaining adequate anticoagulation. New anticoagulants and alternative monitoring techniques present an opportunity to investigate potential advances in the area of anticoagulation for CPB. Hemostasis after CPB is still a vexing problem, and the addition of antiplatelet medication to the platelet defect already incurred during CPB has led to hemorrhagic complications in cardiac surgery. The two opposing processes of anticoagulation and hemostasis must be managed carefully and modified with respect to the patient's hematologic status and desired hemostatic outcome. Cardiac surgical patients consume a much larger fraction of perioperative blood transfusions than the percentage of the surgical population they represent. Thus, during CPB, careful attention must be paid to optimal anticoagulation, platelet quiescence, biocompatible circuitry and interventions, and to monitoring hemostasis. The multifactorial etiology of the CPB-induced hemostatic defect requires a multimodal approach to blood conservation and hemostasis monitoring, including heparin maintenance and sophisticated point-of-care hemostasis monitoring. Each technology has its own attributes and each may be suitable for different populations based upon the expected defects being measured. This article reviews the evidence supporting the use of point-of-care monitors in coagulation and hemostasis management in cardiac surgical patients.

Anticoagulants↗
PubMed1985

Effect of aspirin on serum thrombin time and bleeding time.

The present study describes and utilizes a novel method, the serum thrombin time (STT), as a measure of the time for fibrin clot formation in serum following addition of a supramaximal concentration of fibrinogen. The STT and bleeding time (BT) are selectively prolonged in male subjects 2 hours and 24 hours after ingestion of aspirin. In contrast, the STT is unchanged after aspirin ingestion by female subjects. These data indicate that inhibition of cyclooxygenase product formation by aspirin may alter the third stage of coagulation, specifically, endogenous thrombin activity. Furthermore, the ability of aspirin to prolong the STT appears to be sex-specific. Moreover, the STT may be a clinical reflection of endogenous thrombin activity in vivo as well as in vitro and may be of clinical value as a diagnostic probe in the assessment of medical and surgical disorders.

Adult↗
PubMed2001

Arginine inhibits hemostasis activation.

BACKGROUND: The diagnosis and the therapy of in vivo hemostasis activation is of great clinical importance. Artefactual changes of the hemostasis (i.e., coagulation or fibrinolysis) in vitro have to be prevented. Usual in vitro anticoagulation by sodium citrate does not fully inhibit coagulation--or fibrinolysis--activation. Therefore, there is need for a simple physiologic inhibitor of hemostasis activation both in diagnosis and therapy of hemostasis activation. METHODS: Whole blood clotting time (WBCT), prothrombin time (PT), activated partial thromboplastin time (APTT), in vitro bleeding test closure time (IVBT-CT), and whole blood aggregometry (WBA) were determined in normal human blood or plasma, supplemented with increasing concentrations of L-arginine or guanidine. RESULTS: Arginine in concentrations of 5-100 mM inhibited the WBCT, PT, APTT, IVBT-CT, and WBA. Arginine (50 mM) resulted in a two-fold prolongation of WBCT, PT, or IVBT-CT (the anti-epinephrine action is superior to the anti-ADP action), a four-fold prolongation of APTT or a 60% inhibition of WBA. CONCLUSION: L-Arginine (or guanidine) inhibited the activation of hemostasis. Arginine might be used as hemostasis stabilizer both in the diagnosis and therapy of hemostasis activation. The usage of arginine as an in vitro hemostasis inhibitor might be indicated in the diagnosis of hemostasis activation, as occurring in pharmacological thrombolysis or disseminated intravascular coagulation (DIC). The storage of blood or blood products might be improved by arginine stabilization. The amino acid (and nitric oxide precursor) L-arginine could be an interesting new pharmacologic agent to inhibit a pathologic hemostasis activation.

Arginine↗
PubMed2006

Laboratory monitoring of therapy in von Willebrand disease: efficacy of the PFA-100 and von Willebrand factor:collagen-binding activity as coupled strategies.

Clinical management of von Willebrand disease (or von Willebrand disorder [vWD]) often involves factor replacement or desmopressin acetate (DDAVP) therapy to control (potential) bleeding. Laboratory monitoring involves testing patient samples prior to therapy and at discreet time points after therapy. Classical testing generally comprises assays for factor VIII:coagulant activity, von Willebrand factor (vWF):antigen and vWF:ristocetin cofactor activity. The PFA-100 (platelet function analyser) is a relatively new tool for the investigation of primary hemostasis, and studies have shown its potential utility in identifying both vWD and platelet disorders, and in monitoring DDAVP therapy in these patients. However, the PFA-100 has limited utility in monitoring factor replacement therapy. The collagen-binding activity (vWF:CB) assay is a relatively new functional vWF assay and studies have also shown its utility in identifying vWD, and in monitoring both DDAVP and factor replacement therapy in these patients. This review assesses the laboratory monitoring of therapy for vWD with a special focus on the combined potential utility of the PFA-100 and a vWF:CB assay sensitive for the presence or absence of large vWF multimers. This review should be of value to both hemostasis scientists and clinical specialists.

Chemistry, Clinical↗
PubMed1985

Thrombocytopenia and lupus-like anticoagulant in a patient with peripheral vascular disease: response to infusion of prostacyclin.

A 46 year old man with intermittent claudication due to severe peripheral vascular disease had a circulating lupus like anticoagulant (LLAC), thrombocytopenia (79 X 109/1), markedly reduced platelet survival and a normal bone marrow. He was treated with intravenous prostacyclin (PGI2) infusions which resulted in improvement of the patient's exercise tolerance and normalisation of his platelet count (300 X 109/1) and platelet aggregation could then be assessed. The platelets were markedly hyperaggregable and generated supranormal quantities of thromboxane A2. A diagnosis of consumptive thrombocytopenia secondary to peripheral vascular disease and platelet hyperaggregability was made. Despite therapy with aspirin and dipyridamole, gradual and progressive reduction in platelet count followed and his exercise tolerance declined over the next three months. Immunoglobulin prepared from the patient's serum did not inhibit vascular PGI2 synthesis in vitro. To our knowledge this is the first reported case of consumptive thrombocytopenia due to severe peripheral vascular disease and platelet hyperaggregability. PGI2 administration caused a transient resolution of these features which was not sustained by aspirin and dipyridamole.

Arteriosclerosis Obliterans↗
PubMed1994

Nafamostat mesilate reduces blood cell adhesion to cardiopulmonary bypass circuits: an in-vitro study.

Nafamostat mesilate (FUT-175) is a protease inhibitor, working as an inactivator of coagulation, fibrinolysis and platelet aggregation. Although FUT-175 directly blocks contact factors in coagulation, it also may decrease activation of humoral cascade systems when used in cardiopulmonary bypass circuits. We performed an in vitro study using fresh human blood in the following cardiopulmonary bypass circuits: standard circuit (C), biosurfaced circuit (B) and standard circuit containing FUT-175 (F). Each circuit was primed with 500 ml of electrolyte solution and 500 ml of fresh blood. Cardiopulmonary bypass was performed using a roller pump for four hours in two sets of each circuit configuration. Platelet factors (platelet count and beta-thromboglobulin), coagulation factors (thrombin-antithrombin III complex and fibrinopeptide A), fibrinolysis factors (alpha 2-plasmin inhibitor complex and alpha 2-plasmin inhibitor), complement factors (C3a, C4a), free hemoglobin, and granulocyte elastase were measured at the beginning and end of the study. Hemocytograms were measured concurrently. The FUT-175 group showed significantly lower levels of the measured indices than the biosurfaced group in thrombin-antithrombin III complex (7.4 +/- 2.1 vs. 54.9 +/- 38.1 ng/ml), fibrinopeptide A (7.2 +/- 2.0 vs. 20.2 +/- 14.6 ng/ml), beta-thromboglobulin (1940 +/- 250 vs. 2438 +/- 314 ng/ml) and free hemoglobin (25.2 +/- 14.3 vs. 73.8 +/- 18.4 mg/dl). There were no significant differences between Group F and Group B in platelet count, C3a, C4a and granulocyte elastase, although these indices were significantly lower in Groups F and B when compared to Group C.(ABSTRACT TRUNCATED AT 250 WORDS)

Benzamidines↗