The influence of acetaldehyde and glycosaminoglycans upon Factor Xa- and Factor X-deficient plasma

2002 ◽  
Vol 80 (9) ◽  
pp. 879-886 ◽  
Author(s):  
Arthur S Brecher ◽  
Eric L Hommema
Keyword(s):  
Blood Coagulation ◽  
Partial Thromboplastin Time ◽  
Factor Xa ◽  
Activated Partial Thromboplastin Time ◽  
Clotting Factor ◽  
Factor X ◽  
Chondroitin Sulfates ◽  
Prolonged Aptt ◽  
Subsequent Addition ◽  
Three Components

The comparative effects of glycosaminoglycans and acetaldehyde (AcH) – glycosaminoglycan (GAG) mixtures upon Factor Xa- (FXa) and Factor X-deficient plasma (FXDP) have been studied by activated partial thromboplastin time (APTT) studies. Heparin at 0.025, 0.030, 0.04, and 0.05 U statistically prolonged the APTT when pre-incubated with FXa at 37°C for 3 min prior to addition to FXDP and subsequent addition of Ca2+. Upon addition of 0.25, 0.375, and 0.5 µg heparin-6000 (H6k) to FXa, significant increases in APTT were observed. Similarly, profound increases in APTT were observed when 0.5, 0.75, and 1.0 µg heparin-3000 (H3k) was added to FXa. The chondroitin sulfates (CSA, CSB, CSC) had far less impact upon APTT with the FXa–FXDP system. In examining the effects of AcH–GAG mixtures upon the clotting factor, it was observed that 44.3 and 443 mM AcH synergistically prolonged the APTT in a statistically significant manner regardless of the order of premixing the three components. Hence, AcH may play a role in prolonging APTT in alcoholics. It synergistically prolonged APTT in concert with GAGs and FXa at the AcH levels used in this study. The effect of the GAGs upon FXDP is far less than its effect upon FXa.Key words: Factor Xa, acetaldehyde, heparin, glycosaminoglycans, blood coagulation.

Group Analysis Of Abnormal Factor X Molecules

1981 ◽  
Author(s):  
D S Fair ◽  
T S Edgington
Keyword(s):  
Prothrombin Time ◽  
Blood Coagulation ◽  
Partial Thromboplastin Time ◽  
Random Distribution ◽  
Group Analysis ◽  
Activated Partial Thromboplastin Time ◽  
Clot Formation ◽  
Structural Defects ◽  
Factor X ◽  
Molecular Associations

Factor X lies central in blood coagulation being the point of convergence of the intrinsic and extrinsic pathways and in its activated form is the initial enzyme in the final stages of clot formation. The interaction of Factor X with its activators, cofactors and substrates suggest that there are multiple structural loci present on the surface of this molecule available for these molecular associations. Hence, abnormal molecules may reflect different specific structural defects resulting in decreased function. We analyzed 28 abnormal Factor X plasmas by four parameters: 1) antigen (Ag) measured in radioimmunoassay and activity as measured by: 2) prothrombin time (PT), 3) Russell’s viper venom time (RVV), and 4) activated partial thromboplastin time (APTT). Abnormal Factor X plasmas were from congenital (16), transient (2) and amyloid associated (10) deficiencies. In order to objectively determine groups of abnormal molecules we evaluated their distributions in the following manner: (1) PT activity vs Ag concentration; (2) RVV activity vs PT/Ag; and (3)APTT activity vs RVV/(PT/Ag).A non-random distribution of plasmas was observed which could be grouped into ten classes and subclasses of abnormal Factor X molecules. These data suggest that the groups of abnormal molecules may reflect common structural defects shared among its members located at specific structural loci involved in either the activation or the function of these Factor X molecules.

scholarly journals A Rare Cause of Isolated Prolonged Activated Partial Thromboplastin Time: An Overview of Prekallikrein Deficiency and the Contact System

2021 ◽  
Vol 9 ◽  
pp. 232470962110121
Author(s):  
Ivy Riano ◽  
Klaorat Prasongdee
Keyword(s):  
Partial Thromboplastin Time ◽  
Normal Activity ◽  
Fresh Frozen Plasma ◽  
Activated Partial Thromboplastin Time ◽  
Recessive Trait ◽  
Bleeding Tendency ◽  
Contact Activation ◽  
Asymptomatic Patients ◽  
Prolonged Aptt ◽  
Fresh Frozen

Prekallikrein (PK) deficiency, also known as Fletcher factor deficiency, is a very rare disorder inherited as an autosomal recessive trait. It is usually identified incidentally in asymptomatic patients with a prolonged activated partial thromboplastin time (aPTT). In this article, we present the case of a 52-year-old woman, with no prior personal or family history of thrombotic or hemorrhagic disorders, who was noted to have substantial protracted aPTT through the routine coagulation assessment before a kidney biopsy. The patient had an uneventful biopsy course after receiving fresh frozen plasma (FFP). Laboratory investigations performed before the biopsy indicated normal activity for factors VIII, IX, XI, XII, and von Willebrand factor (vWF) as well as negative lupus anticoagulant (LA) screen. The plasma PK assay revealed low activity at 15% consistent with mild PK deficiency. The deficit of PK is characterized by a severely prolonged aPTT and normal prothrombin time (PT) in the absence of bleeding tendency. PK plays a role in the contact-activated coagulation pathway and the inflammatory response. Thus, other differential diagnoses of isolated prolonged aPTT include intrinsic pathway factor deficiencies and nonspecific inhibitors such as LA. We concluded that the initial evaluation of a prolonged aPTT with normal PT should appraise the measurement of contact activation factors and factor inhibitors. PK deficiency should be considered in asymptomatic patients with isolated aPTT prolongation, which corrects on incubation, with normal levels of the contact activation factors and factor inhibitors.

scholarly journals Discordance in activated partial thromboplastin time and anti-factor Xa levels in COVID-19 patients on heparin therapy

2021 ◽  
Vol 198 ◽  
pp. 79-82
Author(s):  
Matthew Lawlor ◽  
Aakriti Gupta ◽  
Lauren S. Ranard ◽  
Mahesh V. Madhavan ◽  
Jianhua Li ◽  
...  
Keyword(s):  
Partial Thromboplastin Time ◽  
Factor Xa ◽  
Heparin Therapy ◽  
Activated Partial Thromboplastin Time

Antihemostatic Effect of Hsien-Ho-T'sao (Agrimonia pilosa)

1984 ◽  
Vol 12 (01n04) ◽  
pp. 116-123 ◽  
Author(s):  
Jih-Pyang Wang ◽  
Mei-Feng Hsu ◽  
Che-Ming Teng
Keyword(s):  
Prothrombin Time ◽  
Blood Coagulation ◽  
Partial Thromboplastin Time ◽  
Bleeding Time ◽  
Fibrinogen Level ◽  
Platelet Rich Plasma ◽  
Water Extract ◽  
Activated Partial Thromboplastin Time ◽  
Thrombin Time

Bleeding time in rats was markedly prolonged after the adminstration of the water extract of Hsien-Ho-T'sao. This antihemostatic effect was more marked in the group of i.p. injection of the drug than in the group of p.o. administration for 2 to 7 consecutive days. Blood coagulation studies showed that plasma prothrombin time, activated partial thromboplastin time and stypven time were prolonged, while thrombin time adnd fibrinogen level were not changed. The thromboelastographic recording showed that reation time was prolonged and maximal elasticity of clot was decreased. In addition, ADP- and collagen- induced aggregations of platelet-rich plasma was suppressed. In conclusion, the prolongation of the bleeding time might be due to both anticoagulant and antiplatelet action of the drug.

Two parallel prothrombin activator systems in Australian rough-scaled snake, Tropidechis carinatus

2005 ◽  
Vol 93 (01) ◽  
pp. 40-47 ◽  
Author(s):  
Md. Abu Reza ◽  
Sanjay Swarup ◽  
Manjunatha Kini
Keyword(s):  
Blood Coagulation ◽  
Blood Clotting ◽  
Cdna Sequence ◽  
Factor Xa ◽  
Coagulation Factor ◽  
Venom Gland ◽  
Factor X ◽  
Specific Expression ◽  
Life Saving ◽  
Sequence Encoding

SummaryIt is uncommon for similar pathways/systems to be involved in highly divergent functions within single organisms. Earlier, we have shown that trocarin D, a venom prothrombin activator, from the Australian rough-scaled snake Tropidechis carinatus, is structurally and functionally similar to the blood coagulation factor Xa (FXa). The presence of a haemostatic system in these snakes implies that they have two parallel prothrombin activating systems: one in the plasma, that participates in the life saving process of blood clotting and the other in their venom, where it acts as a toxin. Here, we report the complete cDNA sequence encoding the blood coagulation factor X (FX) from the liver of T. carinatus. Deduced T. carinatus FX sequence shows ~80% identity with trocarin D but ~50% identity with the mammalian FX. Our present study confirms the presence of two separate genes – one each for FX and trocarin D, that code for similar proteins in T. carinatus snake. These two genes have different expression sites and divergent uses suggesting that snake venom prothrombin activators have probably evolved by the duplication of the liver FX gene and subsequently marked for tissue-specific expression in the venom gland.

scholarly journals Clinical outcomes with unfractionated heparin monitored by anti‐factor Xa vs. activated partial Thromboplastin time

2019 ◽  
Vol 94 (9) ◽  
pp. 1015-1019 ◽  
Author(s):  
James C. Coons ◽  
Carlo J. Iasella ◽  
Megan Thornberg ◽  
Mary Grace Fitzmaurice ◽  
Kimberly Goehring ◽  
...  
Keyword(s):  
Unfractionated Heparin ◽  
Clinical Outcomes ◽  
Partial Thromboplastin Time ◽  
Factor Xa ◽  
Activated Partial Thromboplastin Time

Hypoxia alters blood coagulation during acute decompression in humans

1984 ◽  
Vol 56 (3) ◽  
pp. 666-670 ◽  
Author(s):  
H. M. O'Brodovich ◽  
M. Andrew ◽  
G. W. Gray ◽  
G. Coates
Keyword(s):  
Molecular Weight ◽  
Platelet Count ◽  
Blood Coagulation ◽  
High Molecular Weight ◽  
Plasma Protein ◽  
Partial Thromboplastin Time ◽  
Activated Partial Thromboplastin Time ◽  
Total Plasma ◽  
High Molecular Weight Kininogen ◽  
Total Plasma Protein

Acute decompression is associated with a shortening of the activated partial thromboplastin time (aPTT). This study was performed to examine whether this change in aPTT results from hypoxia or hypobaria. We exposed healthy adults on three separate occasions to 2 h of 1) hypoxic hypobaria (410 Torr, n = 5), 2) hypoxic normobaria (fractional inspired O2 tension = 0.11, n = 4), or 3) normoxic hypobaria (410 Torr breathing supplemental O2, n = 5). The aPTT shortened during hypoxic hypobaria and hypoxic normobaria (P less than 0.05) but was unchanged during normoxic hypobaria. The prothrombin and thrombin times, hematocrit, and concentrations of fibrinogen, total plasma protein, and fibrinogen-fibrin fragment E were unchanged. During hypoxic hypobaria biologic levels of prekallikrein, high-molecular-weight kininogen, and factors XII, XI, X, VII, V, and II were unchanged, but procoagulant VIII (VIII:C) increased 50% without an increase in VIII-related antigen levels (VIIIR:Ag). Fibrin monomer was not detected in any group. In one subject who became ill after 1.5 h of hypoxic normobaria aPTT shortened by 10 s; the platelet count decreased by 93,000/mm3; VIII:C increased fivefold, but VIIIR:Ag only increased three-fold. We conclude that it is the hypoxia which shortens aPTT during acute decompression to 410 Torr and speculate that it results from an increase in plasma VIII:C-like activity.

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