Factors which Influence the Bleeding Time

1962 ◽  
Vol 08 (03) ◽  
pp. 511-523
Author(s):  
G. J. H den Ottolander ◽  
A Bleijenberg

SummaryA prolonged bleeding time can be due to a vascular, plasmatic, or thrombocytic cause. On the basis of investigations in 8 patients with a prolonged bleeding time, these different forms are discussed.There appeared to be at least two plasmatic factors one of which is the bleeding factor of Nilsson. The demonstration of a thrombocytic cause is sometimes only possible with transfusions of normal platelet suspensions. A patient is described with a prolonged bleeding time due to an acquired thrombo-pathia, resulting from excessive haemorrhages and exchange transfusions.

1992 ◽  
Vol 68 (05) ◽  
pp. 495-499 ◽  
Author(s):  
E Orlando ◽  
S Cortelazzo ◽  
M Marchetti ◽  
R Sanfratello ◽  
T Barbui

SummaryPlatelet adhesion to collagen under flow conditions was studied in 18 patients with lupus anticoagulant, seven of which showed a prolonged bleeding time in the presence of a normal platelet count. The effect of patient plasma, IgG and purified anticardiolipin antibodies on platelet adhesion was also examined. We found a significant reduction of platelet adhesion in patients with lupus anticoagulant, which was more evident in patients with prolonged bleeding time. This platelet adhesion defect could be attributed to a plasma factor. In fact, patients' platelets regained normal adhesion when mixed with normal plasma, whereas controls' platelets showed abnormal adhesion in the presence of patient plasma. A causative role of antiphospholipid antibodies was demonstrated in experiments using purified immunoglobulins and anticardiolipin antibodies.


Blood ◽  
1992 ◽  
Vol 79 (6) ◽  
pp. 1466-1471 ◽  
Author(s):  
H Deckmyn ◽  
E Van Houtte ◽  
J Vermylen

We studied a 5-year-old girl presenting with a markedly prolonged bleeding time. Her platelets were refractory to collagen stimulation, but the response to other agonists was normal. There were no coagulation abnormalities as measured by standard tests. Two- dimensional electrophoresis showed no abnormalities of the patient's platelet membrane glycoproteins. When the patient's plasma or purified plasma IgG was mixed with normal platelets, collagen-induced platelet aggregation was blocked. Western blotting showed the presence of an antibody in the patient's plasma directed against a protein of molecular weight 85 to 90 Kd under both reducing and nonreducing conditions. This protein comigrated with glycoprotein (GP) IV immunoprecipitated by OKM5 from 125I-labeled platelets. Immunoprecipitation of 125I-labeled normal platelet glycoproteins with the patient's IgGs also yielded an 85- to 90-Kd protein that migrated on the diagonal following nonreduced/reduced two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Despite similarities in electrophoretic behavior, the antigen was not demonstrated to be GPIV, since purified GPIV was not recognized by the antibody.


Blood ◽  
1992 ◽  
Vol 79 (6) ◽  
pp. 1466-1471 ◽  
Author(s):  
H Deckmyn ◽  
E Van Houtte ◽  
J Vermylen

Abstract We studied a 5-year-old girl presenting with a markedly prolonged bleeding time. Her platelets were refractory to collagen stimulation, but the response to other agonists was normal. There were no coagulation abnormalities as measured by standard tests. Two- dimensional electrophoresis showed no abnormalities of the patient's platelet membrane glycoproteins. When the patient's plasma or purified plasma IgG was mixed with normal platelets, collagen-induced platelet aggregation was blocked. Western blotting showed the presence of an antibody in the patient's plasma directed against a protein of molecular weight 85 to 90 Kd under both reducing and nonreducing conditions. This protein comigrated with glycoprotein (GP) IV immunoprecipitated by OKM5 from 125I-labeled platelets. Immunoprecipitation of 125I-labeled normal platelet glycoproteins with the patient's IgGs also yielded an 85- to 90-Kd protein that migrated on the diagonal following nonreduced/reduced two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Despite similarities in electrophoretic behavior, the antigen was not demonstrated to be GPIV, since purified GPIV was not recognized by the antibody.


1975 ◽  
Vol 33 (02) ◽  
pp. 278-285 ◽  
Author(s):  
Şeref Inceman ◽  
Yücel Tangün

SummaryA constitutional platelet function disorder in a twelve-year-old girl characterized by a lifelong bleeding tendency, prolonged bleeding time, normal platelet count, normal clot retraction, normal platelet factor 3 activity and impaired platelet aggregation was reported.Platelet aggregation, studied turbidimetrically, was absent in the presence of usual doses of ADP (1–4 μM), although a small wave of primary aggregation was obtained by very large ADP concentrations (25–50 μM). The platelets were also unresponsive to epinephrine, thrombin and diluted collagen suspensions. But an almost normal aggregation response occurred with strong collagen suspensions. The platelets responded to Ristocetin. Pelease of platelet ADP was found to be normal by collagen and thrombin, but impaired by kaolin. Platelet fibrinogen content was normal.The present case, investigated with recent methods, confirms the existence of a type of primary functional platelet disorder characterized solely by an aggregation defect, described in 1955 and 1962 under the name of “essential athrombia.”


Blood ◽  
1960 ◽  
Vol 15 (6) ◽  
pp. 807-829 ◽  
Author(s):  
GIOVANNI RACCUGLIA ◽  
JAMES V. NEEL ◽  
Ruth T. Davidson ◽  
Mary Jane Ussery

Abstract 1. A kindred of 311 individuals, many members of which are affected by a hemorrhagic diathesis, has been described. 2. The variability in the manifestations of this diathesis is extreme. In its fullest expression the disease is characterized by a prolonged bleeding time with evidence of a morphologic defect in the platelets, and a deficiency in antihemophilic globulin. Some possibly affected individuals exhibit only a prolonged bleeding time, while, on the other hand, the clinically most severely affected individual, with AHF levels on several occasions of 5 to 10 per cent, has not been observed by us to have a prolonged bleeding time, although his platelets are morphologically abnormal. 3. Genetic analysis suggests that the hemorrhagic tendency is determined by a single dominant gene of variable penetrance and expressivity. 4. No satisfactory explanation can be developed on the basis of these studies for the association between platelet abnormality and AHF deficiency. More specifically, it is impossible to conclude whether the platelet defect is precursor to the AHF deficiency, or whether—as on a priori grounds seems less likely—this is an example of true genetic pleiotropy. 5. The terminologic chaos which afflicts the literature on hemorrhagic diatheses characterized by a prolonged bleeding time is discussed in the light of the findings in this one large kindred, and suggestions are advanced for minimizing confusion based on terminology alone.


1999 ◽  
Vol 81 (03) ◽  
pp. 378-381 ◽  
Author(s):  
Frank Brosstad ◽  
Thore Egeland ◽  
Tor Egge ◽  
Erik Schrumpf ◽  
Kirsten Boberg

SummaryBleeding time determination is not advised as a general preoperative hemostasis screening test, but it might be useful in some patient groups. Patients referred for liver biopsy frequently have coagulation disturbances and are at risk of hemorrhage. In this prospective study 219 liver biopsies were carried out regardless of a prolonged bleeding time, but with minimum requirements for hemoglobin concentration, platelet count, and tests of the internal and external coagulation pathways. The bleeding time was prolonged in the case of 48 (22%) of the biopsies. Significant bleeding as defined by a hemoglobin decrease of ≥2.0 g/dl occurred in nine patients. Three of these patients were bone marrow transplanted. Patients with a prolonged bleeding time carried a five times higher risk of bleeding (odds ratio = 5.0; confidence interval = 1.1-21.8; p = 0.019). We conclude that the bleeding time may give additional information on the risk of bleeding in some patient groups undergoing liver biopsy.


1999 ◽  
Vol 30 (3) ◽  
pp. 456-460 ◽  
Author(s):  
Liliana Albornoz ◽  
Juan Carlos Bandi ◽  
Juan Carlos Otaso ◽  
Oscar Laudanno ◽  
Ricardo Mastai

Sign in / Sign up

Export Citation Format

Share Document