scholarly journals Probable causes of blood clotting driven by SARS-CoV-2

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Md Safiuddin
Keyword(s):  
1988 ◽  
Vol 60 (02) ◽  
pp. 205-208 ◽  
Author(s):  
Paul A Kyrle ◽  
Felix Stockenhuber ◽  
Brigitte Brenner ◽  
Heinz Gössinger ◽  
Christian Korninger ◽  
...  

SummaryThe formation of prostacyclin (PGI2) and thromboxane A2 and the release of beta-thromboglobulin (beta-TG) at the site of platelet-vessel wall interaction, i.e. in blood emerging from a standardized injury of the micro vasculature made to determine bleeding time, was studied in patients with end-stage chronic renal failure undergoing regular haemodialysis and in normal subjects. In the uraemic patients, levels of 6-keto-prostaglandin F1α (6-keto-PGF1α) were 1.3-fold to 6.3-fold higher than the corresponding values in the control subjects indicating an increased PGI2 formation in chronic uraemia. Formation of thromboxane B2 (TxB2) at the site of plug formation in vivo and during whole blood clotting in vitro was similar in the uraemic subjects and in the normals excluding a major defect in platelet prostaglandin metabolism in chronic renal failure. Significantly smaller amounts of beta-TG were found in blood obtained from the site of vascular injury as well as after in vitro blood clotting in patients with chronic renal failure indicating an impairment of the a-granule release in chronic uraemia. We therefore conclude that the haemorrhagic diathesis commonly seen in patients with chronic renal failure is - at least partially - due to an acquired defect of the platelet a-granule release and an increased generation of PGI2 in the micro vasculature.


1966 ◽  
Vol 15 (03/04) ◽  
pp. 591-602 ◽  
Author(s):  
R. G Macfarlane
Keyword(s):  

1968 ◽  
Vol 20 (01/02) ◽  
pp. 078-087 ◽  
Author(s):  
H. C Hemker ◽  
A. D Muller

SummaryPIVKA, the circulating anticoagulant protein found in vitamin K deficiency can, on kinetical grounds, be recognized as an analogue of factor X. The existence of analogues of other vitamin K-dependent clotting factors cannot be ruled out, but need not be assumed to explain the experimental results.


1968 ◽  
Vol 19 (03/04) ◽  
pp. 364-367 ◽  
Author(s):  
H. C Hemker ◽  
P. W Hemker

SummaryThe enzyme kinetics of competitive inhibition under conditions prevailing in clotting tests are developed and a method is given to measure relative amounts of a competitive inhibitor by means of the t — D plot.


1964 ◽  
Vol 11 (02) ◽  
pp. 485-496 ◽  
Author(s):  
B. J Koszewski ◽  
H Vahabzadeh

SummaryA case of hypercoagulability syndrome in a 35 years old male is reported. An abnormal heparin resistance was found which could be defined by means of a heparin clot-inhibition test as a deficiency in heparin co-factor. The required anticoagulant doses of heparin were forty times as high as in cases with intact heparin co-factor. The factor seemed to be used up in the process of coagulation, as plasma, but not serum, was able to correct the deficiency in vitro. Plasma infusions were helpful for four days, but a complete recovery was achieved only after an intensive course of fever therapy.The phenomenon of blood clotting should be regarded as a dynamic process which is facilitated by an array of clot promoting factors and opposed by a system of natural anticoagulants.


1967 ◽  
Vol 18 (03/04) ◽  
pp. 634-646 ◽  
Author(s):  
N Thurnherr

SummaryBlood clotting investigations have been executed in 25 patients who have undergone open heart surgery with extracorporeal circulation. A description of alterations in the activity of blood clotting factors, the fibrinolytic system, prothrombin consumption and platelets during several phases of the operation is given.


1981 ◽  
Vol 46 (04) ◽  
pp. 752-756 ◽  
Author(s):  
L Zuckerman ◽  
E Cohen ◽  
J P Vagher ◽  
E Woodward ◽  
J A Caprini

SummaryThrombelastography, although proven as a useful research tool has not been evaluated for its clinical utility against common coagulation laboratory tests. In this study we compare the thrombelastographic measurements with six common tests (the hematocrit, platelet count, fibrinogen, prothrombin time, activated thromboplastin time and fibrin split products). For such comparisons, two samples of subjects were selected, 141 normal volunteers and 121 patients with cancer. The data was subjected to various statistical techniques such as correlation, ANOVA, canonical and discriminant analysis to measure the extent of the correlations between the two sets of variables and their relative strength to detect blood clotting abnormalities. The results indicate that, although there is a strong relationship between the thrombelastographic variables and these common laboratory tests, the thrombelastographic variables contain additional information on the hemostatic process.


1982 ◽  
Vol 47 (03) ◽  
pp. 236-238 ◽  
Author(s):  
J H Winter ◽  
B Bennett ◽  
F McTaggart ◽  
A S Douglas

SummaryPlasma and serum antithrombin levels were measured in functional (initial rate measurement) and immunological assays together with serum lipid levels in normal subjects and patients with coronary artery disease. Specific antithrombin activity in plasma showed a negative correlation with triglyceride levels. The consumption of antithrombin activity during blood clotting was negatively correlated with both serum total triglyceride and heparin precipitable lipoprotein and positively correlated with serum high density lipoprotein cholesterol. Different blood lipoprotein fractions may influence the activity of the antithrombin III molecule.


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