The Coagulation Defect in Hypervitaminosis A in Rats

1962 ◽  
Vol 07 (01) ◽  
pp. 159-168 ◽  
Author(s):  
L. G Israels ◽  
J Foerster ◽  
A Zipursky
Keyword(s):  
Vitamin A ◽  
Prothrombin Time ◽  
Marked Reduction ◽  
Factor Ix ◽  
Factor Vii ◽  
Factor V ◽  
Vitamin K1 ◽  
Hypervitaminosis A ◽  
Daily Feeding ◽  
Coagulation Defect

SummaryRats fed vitamin A, 70 000 u daily for a period of 28 days developed a hemorrhagic state characterized by a prolonged prothrombin time and stypven time, a marked reduction in prothrombin and the factor VII-complex, and an inconstant decrease in factor V activity. A serum defect in thromboplastin generation was also noted. The defects in the extrinsic system were prevented by the simultaneous daily feeding of 60 μg to 120 μg of vitamin K1 but this did not uniformly prevent the serum defect in thromboplastin generation which is thought to represent a depletion in factor IX.

Occult intravascular clotting by means of intravenous injection of thrombin

1959 ◽  
Vol 197 (4) ◽  
pp. 791-794 ◽  
Author(s):  
Armand J. Quick ◽  
Clara V. Hussey ◽  
John Harris ◽  
Kenneth Peters
Keyword(s):  
Factor Viii ◽  
Prothrombin Time ◽  
Intravenous Injection ◽  
Factor Ix ◽  
Capillary Network ◽  
Factor Vii ◽  
Factor V ◽  
Dilute Solution ◽  
Progressive Decrease ◽  
Stable Factor

On infusing a dilute solution of thrombin intravenously into a dog at a constant and carefully regulated rate, no massive thrombosis occurs and no evidence of a thrombo-embolic state is obtained. An occult type of intravascular clotting is produced which is characterized by a progressive decrease of the level of fibrinogen, thrombocytopenia, a prolonged prothrombin time and a poor consumption of prothrombin. Labile factor (factor V) and thromboplastinogen (factor VIII) are strikingly diminished. Prothrombin is moderately decreased while stable factor (factor VII) and PTC (factor IX) are not significantly affected. It is postulated that the adsorption of thrombin to the fibrin fibrils which are filtered off in the capillary network and destroyed, constitutes the principal means for preventing dangerous accumulation of thrombin in the blood.

The Effects of Leguminous Seed Extracts on Blood Coagulation

1962 ◽  
Vol 08 (02) ◽  
pp. 256-269
Author(s):  
R. J Speer ◽  
J. L Porter
Keyword(s):  
Factor Viii ◽  
Prothrombin Time ◽  
Blood Coagulation ◽  
Factor Ix ◽  
Factor Vii ◽  
Clot Lysis ◽  
Factor V ◽  
Leguminous Seed ◽  
Recalcification Time ◽  
Clot Time

SummaryThe saline extracts of one hundred leguminous seed were screened for their effect on blood coagulation by the following tests: thrombin clot time, recalcification time, Quick prothrombin time, clot lysis and clot retraction. Nineteen of these extracts, when reacted with normal plasma, gave a prolonged clot time in at least one of two tests: recalcification time and Quick prothrombin time. The eight which gave a prolonged Quick prothrombin time were tested for inhibition in the following assay systems: Factor V, factor VII-complex, and prothrombin. All nineteen, including the seventeen which prolonged the re-calcification time and the two which did not, were tested for their inhibitory action in the following assay systems: Factor VIII, factor IX, and plasma thromboplastin antecedent.The inhibition of prothrombin, factor V, and factor VII-complex was mild and not specific for any of these factors. Factor V activity was depressed more than the other two. By contrast, the inhibition of factor VIII, factor IX, and plasma thromboplastin antecedent was very strong and demonstrated a relatively high degree of specificity.

Changes Occurring During Coagulation in Glass. I. Normal Human Blood

1960 ◽  
Vol 4 (01) ◽  
pp. 001-016
Author(s):  
Jessica H. Lewis ◽  
Paul Didisheim ◽  
John H. Ferguson ◽  
Kenichi Hattori
Keyword(s):  
Coagulation Factors ◽  
Factor Ix ◽  
Factor Vii ◽  
Sodium Oxalate ◽  
Factor V ◽  
Rapid Rise ◽  
Rapid Fall ◽  
Glass Tubes ◽  
Normal Human ◽  
The Individual

SummaryNormal whole blood was allowed to stand in glass tubes at 37° C, and the clotting process stopped at various intervals by the addition of sodium oxalate. During the first 15 minutes a marked acceleration of clotting activity was found. Study of the individual coagulation factors showed the following changes: a sustained and rapid fall in platelet count, a sustained and rapid rise in PTC (factor IX), a steady fall in fibrinogen, a more gradual fall in AHF (factor VIII), a rapid rise and subsequent fall in proaccelerin (factor V) activity, a somewhat lesser and slower rise and fall in proconvertin (factor VII) activity, and a slow fall in prothrombin concentration. No changes were noted in Hageman factor or PTA activities.

Letters to the Editor

PEDIATRICS ◽  
1957 ◽  
Vol 19 (6) ◽  
pp. 1151-1151
Author(s):  
ARMAND J. QUICK
Keyword(s):  
Prothrombin Time ◽  
Vitamin K ◽  
Factor Vii ◽  
Factor V ◽  
Letters To The Editor ◽  
Time Determination

I wish to call your attention to a matter concerning the article of Fresh et al., "Blood Prothrombin, Proconvertin and Proaccelerin in Normal Infancy: Questionable Relationships of Vitamin K" which appeared in Pediatrics (19:241, 1957). On page 248 the following statement occurs: "Notwithstanding the insufficiently substantiated claims of Quick et al., that the simple `prothrombin time' determination is uninfluenced by an excess of factor V or factor VII,...." I consider such a statement inexcusable. While they could have said that "we regard the claims to be insufficiently substantiated, etc.," they made their statement to appear as a fact, which is not justified.

Prothrombin Activation Is Increased among Asymptomatic Carriers of the Prothrombin G20210A and Factor V Arg506Gln Mutations

2000 ◽  
Vol 84 (09) ◽  
pp. 396-400 ◽  
Author(s):  
Steve Humphries ◽  
Belinda Smillie ◽  
Lily Li ◽  
Jacqueline Cooper ◽  
Samad Barzegar ◽  
...  
Keyword(s):  
Factor Viia ◽  
Conclusive Evidence ◽  
Factor Ix ◽  
Factor Vii ◽  
Prothrombin G20210a ◽  
Factor V ◽  
Factor X ◽  
Coagulation Proteins ◽  
Prothrombin Activation

SummaryThe risk of venous thrombosis is increased in individuals who carry specific genetic abnormalities in blood coagulation proteins. Among Caucasians, the prothrombin G20210A and factor V Arg506Gln (FV R506Q) mutations are the most prevalent defects identified to date. We evaluated their influence on markers of coagulation activation among participants in the Second Northwick Park Heart Study, which recruited healthy men (aged 50–61 years) from nine general medical practices in England and Wales. They were free of clinical vascular disease and malignancy at the time of recruitment. Genotypes for the two mutations were analyzed using microplate array diagonal gel electrophoresis, and coagulation markers (factor XIIa; activation peptides of factor IX, factor X, and prothrombin; fibrinopeptide A) were measured by immunoassay. Factor VII coagulant activity and factor VIIa levels were determined by a functional clotting assay. Among 1548 men genotyped for both mutations, 28 (1.8%) and 52 (3.4%) were heterozygous for prothrombin G20210A and FV R506Q, respectively. The only coagulation marker that was significantly associated with the two mutations was prothrombin activation fragment F1+2 [mean ± SD, 0.88 ± 0.32 nmol/L in men with prothrombin G20210A (p = 0.002) and 0.89 ± 0.30 in men with FV R506Q (p = 0.0001) versus 0.72 ± 0.24 among non-carriers for either mutation]. This data provides conclusive evidence that heterozygosity for the prothrombin G20210A as well as the FV R506Q mutations in the general population leads to an increased rate of prothrombin activation in vivo.

Multidimensional Similarity of Letters

1969 ◽  
Vol 28 (1) ◽  
pp. 3-12 ◽  
Author(s):  
Teodor Kuennapas ◽  
Anne-Jeanette Janson
Keyword(s):  
Factor Viii ◽  
Factor Ix ◽  
Factor Vii ◽  
Similarity Analysis ◽  
Factor V ◽  
Factor I ◽  
Considerable Portion ◽  
Lower Case ◽  
Factor Ii

28 lower-case letters of the Swedish alphabet were studied by the method of multidimensional similarity analysis. 57 Ss participated in the experiment. 9 factors were found. Factor I is called ‘t’ or ‘Vertical linearity,’ Factor II: ‘o’ or ‘Roundness,’ Factor III: ‘n’ or ‘Parallel vertical linearity,’ Factor IV: ‘i’ or “Vertical linearity with dot,’ Factor V: ‘p’ or ‘Roundness attached to vertical linearity,’ Factor VI: ‘k’ or ‘Vertical linearity with crossness,’ Factor VII: ‘a’ or ‘Roundness attached to a hook,’ Factor VIII: V or ‘Angularity open upward’ and Factor IX: ‘z’ or ‘Zigzaggedness.’ ‘Vertical linearity’ and ‘Roundness’ are the most important of these factors and account for a considerable portion of the similarity among many letters.

Factor VII Activity and Antigen in Haemophilia B Variants

1980 ◽  
Vol 43 (01) ◽  
pp. 016-019 ◽  
Author(s):  
M G Mazzucconi ◽  
R M Bertina ◽  
D Romoli ◽  
M Orlando ◽  
G Avvisati ◽  
...  
Keyword(s):  
Prothrombin Time ◽  
Vitamin K ◽  
Normal Values ◽  
Factor Ix ◽  
Factor Vii ◽  
Confidence Limits ◽  
Vitamin K Deficiency ◽  
Haemophilia B ◽  
K Deficiency ◽  
Mild Deficiency

SummaryTwenty three patients belonging to 18 different pedigrees of Haemophilia B were studied with regard to ox-brain prothrombin time and its correlation to factor VII.Eleven among them were B-negative (no detectable factor IX antigen), five were B-reduced (factor IX antigen detectable but below the normal values) and seven were B-positive (normal levels of factor IX antigen).Ox-brain prothrombin time was found prolonged (≥ x̄ + 2.5 SD:99% confidence limits) in nine patients. Factor VII Activity (VII: C) was found reduced in 1/11 B-negative, in 2/5 B-reduced and in 4/7 B-positive patients. Factor VII Antigen (VII: Ag) was found normal in all but one patient.The ratio VII:C/VII:Ag was abnormal in eight patients independently from the variant of Haemophilia B. The underlying defect which causes the prolongation of Ox-brain prothrombin time due to factor VII: C mild deficiency is heterogeneous. Age, a mild Vitamin K deficiency, the presence of an inhibitor of Factor VII activation and other unknown causes, may be responsible for this pattern.

A Case of FVII Inhibitor.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3655-3655
Author(s):  
Michael Joshua Levitt ◽  
Arthur A. Topilow ◽  
William Lerner ◽  
Peter Mencel ◽  
Carl Henningson ◽  
...  
Keyword(s):  
Research Funding ◽  
Immunosuppressive Treatment ◽  
Factor Ix ◽  
Factor Vii ◽  
Factor V ◽  
First Line ◽  
Immunosuppressive Medications ◽  
Factor Ii ◽  
Plasma Factor ◽  
History Of

Abstract Abstract 3655 Acquired inhibitors of coagulation are bleeding disorders that require prompt recognition, diagnosis, and management. Antibodies against factor VII are extremely rare with only a few cases reported in the literature. We present a case of a patient with an acquired Factor VII inhibitor. This is an 87 year old female with a past medical history of breast cancer, hypertension, and hyperlipidemia who presented to the emergency room with right flank pain and hematuria. A CT scan of the abdomen and pelvis showed bilateral hydronephrosis with no evidence of nephrolithiasis. The patient denied hematemesis or hematochezia but was noted to have hemoccult positive stools. The patient denied any anticoagulant use. Admission laboratories revealed a coagulopathy with a normal partial thromboplastin time (PTT) of 28 seconds and prolonged prothrombin time (PT) of greater than 50 seconds and INR of 19.59. The patient received vitamin K without improvement in coagulation parameters. A mixing study revealed a markedly prolonged PT that did not correct with 1:1 (18.9 seconds) and 4:1 (27.3 seconds) mix normal plasma. Factor assays shows an abnormal Factor VII level of less than 1%, and normal Factor II 121%, Factor V 140%, Factor VIII 201%, Factor IX 99%, and Factor XI 126% levels. A FVII inhibitor was 1.66 Bethesda units per milliliter. Immunosuppressive treatment was initiated with prednisone 1 milligram per kilogram daily and cyclophosphamide 200 milligrams daily. Factor VII levels normalized without evidence of inhibitor. The patient clinically improved and immunosuppressive medications were gradually tapered off. This case emphasizes the importance of prompt recognition in a patient with a rare acquired inhibitor of coagulation. Treatment with immunosuppressive therapy consisting of corticosteroids and cyclophosphamide resulted in normalization of factor VII levels and resolution of bleeding symptoms and should be considered as first-line management for such patients. Disclosures: Philipp: Baxter: Research Funding; Wyeth: Research Funding; Octapharma: Research Funding.

Coagulation Assays as Diagnostic Markers of Hepatocellular Carcinoma

1988 ◽  
Vol 60 (03) ◽  
pp. 468-470 ◽  
Author(s):  
J J Lefrère ◽  
J Conard ◽  
P Mavier ◽  
L Bettan ◽  
M Beaugrand ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Prothrombin Time ◽  
Alpha Fetoprotein ◽  
Factor V ◽  
Thrombin Time ◽  
Vitamin K1 ◽  
Normal Value ◽  
Coagulation Assays ◽  
Cirrhotic Patients ◽  
Time Test

SummaryWith the aim of improving the biological diagnosis of hepatocellular carcinoma (HCC), alpha-fetoprotein (AFP), des-gamma-carboxyprothrombin (DCP) and factor V levels were assayed in 119 patients with HCC and 60 cirrhotic patients without HCC. Among the patients with HCC, increased levels of AFP (>300 ng/ml) and of DCP (>15 mU/ml) vveie ubseived in 36% and 69% of the cases, respectively. None of the 60 patients without TTCC had increased AFP, and one had abnormal DCP; in this patient, DCP level returned to normal value after vitamin K1 injection. No significant correlation was found between increased AFP and DCP, thus indicating that the two tests complement each other for the diagnosis. A factor V level higher than expected from the reduced prothrombin time test of the patient was detected in 50% of patients with HCC and only 7% of those without HCC. No correlation was found between increased factor V and abnormal AFP or DCP The thrombin time, fibrinogen activity to antigen ratio, and polymerization index failed to differentiate between cirrhosis and HCC. We conclude that AFP, DCP and factor V may give complementary informations in the diagnosis of HCC, one of these markers at least being positive in 88% of the patients.

Studies on the Fate of Coagulation Factors during the Clotting of Normal and Pathological Blood

1959 ◽  
Vol 03 (04) ◽  
pp. 578-587
Author(s):  
Cecil Hougie
Keyword(s):  
Blood Coagulation ◽  
Hemophilia A ◽  
Coagulation Factors ◽  
Factor Ix ◽  
Hemophilia B ◽  
Factor Vii ◽  
Normal Blood ◽  
Modern Concept ◽  
Factor V ◽  
Mild Case

SummaryIn a mild case of Stuart factor (SF) deficiency and in a patient with hemophilia B (factor IX deficiency) consumption of AHF (factor VIII) was normal but was abnormal in more severe examples of these diseases. This finding reconciles previously conflicting reports. Factor V utilisation was abnormal in moderately severe cases of SF deficiency, hemophilia A and hemophilia B but normal in mild cases of SF deficiency and hemophilia B. A mild case of hemophilia A was not studied. These findings would be expected from the modern concept of blood coagulation. However, the findings with respect to AHF are equally well explained if AHF is destroyed by some intermediate product of blood coagulation, such as thrombin, appearing at the time of the appearance of fibrin.The concentration of SF was found to remain constant during the clotting of both normal blood and blood deficient in factor VILThe concentration of factor VII during the coagulation of normal blood remained constant until the appearance of fibrin. The concentration then increased, but this finding was not consistently obtained. No abnormality in the fate of factor VII during the clotting of blood deficient in SF was found.

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