scholarly journals S2220 It’s the Bloody Gallbladder! Spontaneous Gallbladder Hemorrhage Following Factor Xa Inhibition

2020 ◽  
Vol 115 (1) ◽  
pp. S1175-S1176
Author(s):  
Mohammad U. Azam ◽  
Isaac E. Perry ◽  
Muaz A. Ibrahim ◽  
Amanda Barrett ◽  
Steven B. Ellison ◽  
...  
Keyword(s):  
Factor Xa ◽  
Factor Xa Inhibition

Effect of Depolymerized Holothurian Glycosaminoglycan (DHG) on Tissue Factor Pathway Inhibitor: In Vitro and In Vivo Studies

1997 ◽  
Vol 78 (02) ◽  
pp. 864-870 ◽  
Author(s):  
Hideki Nagase ◽  
Kei-ichi Enjyoji ◽  
Yu-ichi Kamikubo ◽  
Keiko T Kitazato ◽  
Kenji Kitazato ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Tissue Factor Pathway Inhibitor ◽  
Factor Xa ◽  
Free Form ◽  
Initial Reaction ◽  
Extrinsic Pathway ◽  
Factor Xa Inhibition ◽  
Tissue Factor Pathway

SummaryDepolymerized holothurian glycosaminoglycan (DHG) is a glycosaminoglycan extracted from the sea cucumber Stichopus japonicusSelenka. In previous studies, we demonstrated that DHG has antithrombotic and anticoagulant activities that are distinguishable from those of heparin and dermatan sulfate. In the present study, we examined the effect of DHG on the tissue factor pathway inhibitor (TFPI), which inhibits the initial reaction of the tissue factor (TF)-mediated coagulation pathway. We first examined the effect of DHG on factor Xa inhibition by TFPI and the inhibition of TF-factor Vila by TFPI-factor Xa in in vitro experiments using human purified proteins. DHG increased the rate of factor Xa inhibition by TFPI, which was abolished either with a synthetic C-terminal peptide or with a synthetic K3 domain peptide of TFPI. In contrast, DHG reduced the rate of TF-factor Vila inhibition by TFPI-factor Xa. Therefore, the effect of DHG on in vitroactivity of TFPI appears to be contradictory. We then examined the effect of DHG on TFPI in cynomolgus monkeys and compared it with that of unfractionated heparin. DHG induced an increase in the circulating level of free-form TFPI in plasma about 20-fold when administered i.v. at 1 mg/kg. The prothrombin time (PT) in monkey plasma after DHG administration was longer than that estimated from the plasma concentrations of DHG. Therefore, free-form TFPI released by DHG seems to play an additive role in the anticoagulant mechanisms of DHG through the extrinsic pathway in vivo. From the results shown in the present work and in previous studies, we conclude that DHG shows anticoagulant activity at various stages of coagulation reactions, i.e., by inhibiting the initial reaction of the extrinsic pathway, by inhibiting the intrinsic Xase, and by inhibiting thrombin.

Combined coagulation phase-directed factor Xa inhibition with heparin compounds and DX-9065a - A direct and selective antagonist

2004 ◽  
Vol 92 (12) ◽  
pp. 1229-1231
Author(s):  
John Alexander ◽  
You Li ◽  
Edwin Bovill ◽  
Frederick Spencer ◽  
Thomas Robertson ◽  
...  
Keyword(s):  
Factor Xa ◽  
Selective Antagonist ◽  
Factor Xa Inhibition ◽  
Heparin Compounds

scholarly journals FXa Inhibition and Coagulation Changes During DVT Prophylaxis by Enoxaparin Over the Course of a 15-Day Follow-Up in Septic Patients

2009 ◽  
Vol 16 (5) ◽  
pp. 584-590 ◽  
Author(s):  
Zuzana Zenáhlíková ◽  
Jan Kvasnička ◽  
Zuzana Kudrnová ◽  
Magda Sudrová ◽  
Radka Brzežková ◽  
...  
Keyword(s):  
Severe Sepsis ◽  
Protein C ◽  
Factor Xa ◽  
Inclusion Criteria ◽  
C Reactive Protein ◽  
Once Daily ◽  
Reactive Protein ◽  
Factor Xa Inhibition ◽  
The Mean

The objective of our study was to examine the changes in coagulation parameters and inflammatory reaction over the course of 15 days in patients with severe sepsis. We tried to identify mechanisms by which sepsis-induced pathophysiological changes may influence the effectiveness of subcutaneously (SC) administered enoxaparin 40 mg once daily. A total of 16 patients (8 men, 8 women; age 35-83 years) meeting the inclusion criteria of severe sepsis were enrolled in this study. The follow-up was performed on days 1, 2, 3, 6, 9, 12, and 15 of hospitalization at the intensive care unit (ICU). Blood coagulation (activated partial thromboplastin time [aPTT], prothrombin time [PT], fibrinogen, antithrombin (AT), protein C [PC], D-dimer, fragment 1.2 [F1.2], factor Xa [FXa] inhibition) and inflammatory reactants (interleukin 6 [IL-6], C-reactive protein [CRP], orosomucoid, α-1-antitrypsin) were tested. The mean FXa inhibition was 0.17 (±0.17) IU/mL. The arbitrarily established range of FXa inhibition for prophylaxis, 0.2 to 0.4 IU/mL, was reached in 22 cases (20%), while in 74 cases (68%), it was below and in 13 cases (12%) above the aforementioned range. Factor Xa inhibition positively correlated with AT (r = .42; P < .001) and PC (r = .45; P < .001) activities. A negative correlation was found between the FXa inhibition and α-1-antitrypsin concentrations (r = —.33; P = .01) but only in the subgroup with α-1-antitrypsin concentrations ≥2.2 g/L. We confirmed that in most patients with sepsis, the prophylaxis with enoxaparin did not lead to the required FXa inhibition. The inhibition of FXa by enoxaparin depends mainly on the AT and PC activities.

scholarly journals Determination of factor Xa inhibition doses of low-molecular heparin, nadroparin and reviparin in urological patients

2007 ◽  
Vol 64 (8) ◽  
pp. 538-542
Author(s):  
Svetlana Pavlovic ◽  
Sladjana Zivkovic ◽  
Goran Koracevic
Keyword(s):  
Factor Xa ◽  
Surgical Operation ◽  
Moderate Risk ◽  
Statistical Parameters ◽  
Nadroparin Calcium ◽  
The People ◽  
Factor Xa Inhibition ◽  
Significant Difference ◽  
Higher Doses

Background/Aim. The inhibition of factor Xa (FX) by the use of low-molecular heparin (LMH) is important clinical procedure in patients with moderate and high risk for the developament of venous thromboembolism (VTE) and pulmonary embolism (PE). The aim of this study was to determine the level of inhibition of FXa by the use of prophylactic doses of LMH nadroparin-calcium and reviparine-sodium which were applied in urological patients with moderate risk for VTE and PE. Methods. The examination included 80 urological patients divided into 4 groups after urological, uroradiological and anesthesiological preoperative preparation and categorization of anesthesiological risk according to the ASA III classification. The first two groups, of 20 patients each, received the recommended doses of LMH in accordance with the preoperative risk, and an inhibition of FXa 48 hours after the surgical operation and four hours after the administration of LMH was determined. Heptest and homogenous anti-Xa test were used for monitoring of FXa inhibition. Since the obtained anti-Xa values were not satisfactory, two more groups were formed and given double the recommended doses. In these new groups, inhibition of FXa was in recommended range. Standard descriptive statistical parameters were used for describing the charateristics of the people from the formed groups. Results. All the patients examined were clinically estimated as patients of moderate risk, for VTE and PE. There were no statistically singificant difference in body weight of the patients who received nadroparin-calcium 0.3 ml and reviparine-sodium 0.25 ml and those who received their double doses, respectively. The level of FXa inhibition in the group in which the dose of nadroparin-calcium of 0.6 ml was applied was statistically significantly higher than in the group which received the dose of 0.3 ml (Mann-Whitney U test: Z = 5.416; p < 0.0001). The level of FXa in the group given reviparine-sodium 0.5 ml was significantly higher than in the group which received the half of this dose (Mann-Whitney U test: Z = 5.416; p < 0.0001). This research did not confirm a statistically significant difference in the levels of FXa inhibition in patients who received nadroparincalcium as VTE and PE prophilaxis in the dose of 0.6 ml and those who received reviparin-sodium 0.5 ml (in two doses of 0.25 ml) (Mann-Whitney U test: Z = 0.163; p > 0.05). Conclusion. According to biochemical monitoring, the recommended doses of LMH are insufficient for the prophylactic inhibition of FXa in urological pateints with moderate risk for VTE and PE, so the higher doses which inhibit FXa are recommended. .

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