scholarly journals Novel venous thromboembolism mouse model to evaluate the role of complete and partial factor XIII deficiency in pulmonary embolism risk

2021 ◽  
Author(s):  
Sravya Kattula ◽  
Yaqiu Sang ◽  
Gustaaf de Ridder ◽  
Anna C. Silver ◽  
Emma G. Bouck ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Venous Thromboembolism ◽  
Mouse Model ◽  
Factor Xiii ◽  
Factor Xiii Deficiency ◽  
Partial Factor

Prevention Of Shwartzman’S Phenomenon In Factor XIII Deficiency

1981 ◽  
Author(s):  
Soo Young Lee ◽  
Sung Keun Chang ◽  
Soo II Chung
Keyword(s):  
Factor Xiii ◽  
Rabbit Platelet ◽  
Factor Xiii Deficiency ◽  
Platelet Factor ◽  
Cortical Necrosis ◽  
Rate Of Increase ◽  
Shwartzman Reaction

Cross-linked clots formed in vitro are reported to be more resistant to fibrinolysis but the relevance of these observations to the situation in vivo is uncertain. The possible role of Factor XIII in the formation of diffuse intravascular fibrin deposition was examined in experimentally induced Factor XIII deficient rabbits. Factor XIII deficiency was induced by intravenous infusion of IgG isolated from goat anti-rabbit platelet Factor XIII. Control received normal goat IgG. The Shwartzman reaction was produced by two injections of bacterial endotoxin given 24 hours apart.The most striking histological differences were observed after 48 hours. A large number of glomerular loops were enlarged and engorged with red blood cells and platelet- fibrin thrombi; extensive bilateral cortical necrosis was observed in 8 out of 10 endotoxin injected control rabbits but none in the Factor XIII deficient group.Fibrinogen levels in control rabbits were increased 3-4 fold (1.1g/100 ml), at 24 hours and slightly decreased at 48 hours after endotoxin injection, whereas in Factor XIII deficient animals, the rate of increase was slower but reached similar levels at 48 hours. Fibrinolytic activity in vivo, studied by the degradation of infused 125I-fibrinogen, was significantly increased in both endotoxin injected groups, irrespective of Factor XIII levels.These results strongly suggest that cross-linked thrombi are more resistant to fibrinolysis in vivo as well as in vitro.

scholarly journals Impact and role of pulmonary embolism response teams in venous thromboembolism associated with COVID-19

2021 ◽  
pp. jim-2021-001856
Author(s):  
Mateo Porres-Aguilar ◽  
Victor F Tapson ◽  
Belinda N Rivera-Lebron ◽  
Parth M Rali ◽  
David Jiménez ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Venous Thromboembolism ◽  
Critical Role ◽  
Prothrombotic State ◽  
Common Goal ◽  
Optimal Patient Care ◽  
Response Team ◽  
The Common ◽  
Therapeutic Decision Making

Venous thromboembolism associated with COVID-19, particularly acute pulmonary embolism, may represent a challenging and complex clinical scenario. The benefits of having a multidisciplinary pulmonary embolism response team (PERT) can be important during such a pandemic. The aim of PERT in the care of such patients is to provide fast, appropriate, multidisciplinary, team-based approach, with the common goal to tailor the best therapeutic decision making, prioritizing always optimal patient care, especially given lack of evidence-based clinical practice guidelines in the setting of COVID-19, which potentially confers a significant prothrombotic state. Herein, we would like to briefly emphasize the importance and potential critical role of PERT in the care of patients in which these two devastating illnesses are present together.

Prevention and Treatment of Venous Thromboembolism and Pulmonary Embolism: The Role of Novel Oral Anticoagulants

2012 ◽  
Vol 7 (3) ◽  
pp. 175-194 ◽  
Author(s):  
Spyridon Deftereos ◽  
Georgios Hatzis ◽  
Charalambos Kossyvakis ◽  
Georgios Bouras ◽  
Vasiliki Panagopoulou ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Venous Thromboembolism ◽  
Oral Anticoagulants ◽  
Novel Oral Anticoagulants ◽  
Prevention And Treatment

Role of blood coagulation factor XIII in patients with acute pulmonary embolism. Correlation of factor XIII antigen levels with pulmonary occlusion rate, fibrinogen, D-dimer, and clot firmness

2003 ◽  
Vol 90 (09) ◽  
pp. 434-438 ◽  
Author(s):  
Nils Kucher ◽  
Verena Schroeder ◽  
Hans Kohler
Keyword(s):  
Pulmonary Embolism ◽  
Factor Xiii ◽  
Acute Pulmonary Embolism ◽  
Coagulation Factor ◽  
Helical Computed Tomography ◽  
Coagulation Factor Xiii ◽  
A Subunit ◽  
Occlusion Rate ◽  
D Dimer

SummaryIn patients with acute pulmonary embolism (PE), pulmonary occlusion rate is directly related to D-dimer and inversely related to fibrinogen levels. The role of coagulation factor XIII (FXIII) levels in acute venous thromboembolism is not known. A total of 120 consecutive patients with suspected PE and VIDAS D-dimer levels >500 μg/L were investigated by helical computed tomography (CT). Pulmonary occlusion rate was assessed by CT using the modified Miller index. D-dimer, fibrinogen, and FXIII A- and B-subunit antigen levels were taken on admission. Thrombelastography (TEG) was performed in a subset of patients (n=12).The 71 patients with PE had lower FXIII A-subunit levels than the 49 patients with excluded PE (78.6±24.5% vs. 91.3±28.8%, p=0.01). In both groups, FXIII A-subunit was inversely related to D-dimer levels. FXIII A-subunit correlated with fibrinogen levels in patients with PE but not in patients without PE. FXIII A-subunit decreased with increasing pulmonary occlusion rate. The risk of PE was increased in the presence of A-subunit levels < 60% (OR 7.0 [95% CI 1.4-35.3], p=0.019). Clot firmness determined by TEG was lower in patients with PE than in patients without PE.In patients with PE, circulating FXIII A-subunit is decreased compared to patients with suspected but excluded PE. The higher the clot burden within the pulmonary arteries the lower the FXIII antigen. In these patients, direct relation of FXIII A-subunit to fibrinogen levels argues for significant consumption of these coagulation factors in PE. This consumption of FXIII can also be detected by a global coagulation test like TEG.

Venous thromboembolism in a general hospital. An update with low molecular weight heparin prophylaxis

VASA ◽  
2007 ◽  
Vol 36 (1) ◽  
pp. 17-22
Author(s):  
Schulz ◽  
Kesselring ◽  
Seeberger ◽  
Andresen
Keyword(s):  
Molecular Weight ◽  
Pulmonary Embolism ◽  
Venous Thromboembolism ◽  
Low Molecular Weight ◽  
Trauma Patients ◽  
Vte Prophylaxis ◽  
Vein Thrombosis ◽  
Patients At Risk ◽  
Hospital Stays ◽  
Event Rates

Background: Patients admitted to hospital for surgery or acute medical illnesses have a high risk for venous thromboembolism (VTE). Today’s widespread use of low molecular weight heparins (LMWH) for VTE prophylaxis is supposed to have reduced VTE rates substantially. However, data concerning the overall effectiveness of LMWH prophylaxis is sparse. Patients and methods: We prospectively studied all patients with symptomatic and objectively confirmed VTE seen in our hospital over a three year period. Event rates in different wards were analysed and compared. VTE prophylaxis with Enoxaparin was given to all patients at risk during their hospital stay. Results: A total of 50 464 inpatients were treated during the study period. 461 examinations were carried out for symptoms suggestive of VTE and yielded 89 positive results in 85 patients. Seventy eight patients were found to have deep vein thrombosis, 7 had pulmonary embolism, and 4 had both deep venous thrombosis and pulmonary embolism. The overall in hospital VTE event rate was 0.17%. The rate decreased during the study period from 0.22 in year one to 0,16 in year two and 0.13 % in year three. It ranged highest in neurologic and trauma patients (0.32%) and lowest (0.08%) in gynecology-obstetrics. Conclusions: With a simple and strictly applied regimen of prophylaxis with LMWH the overall rate of symptomatic VTE was very low in our hospitalized patients. Beside LMWH prophylaxis, shortening hospital stays and substantial improvements in surgical and anasthesia techniques achieved during the last decades probably play an essential role in decreasing VTE rates.

New Families with Hereditary Hemorrhagic Trait due to Deficiency of Fibrin Stabilizing Factor (F. XIII)

1968 ◽  
Vol 20 (03/04) ◽  
pp. 534-541 ◽  
Author(s):  
O Egeberg
Keyword(s):  
Factor Xiii ◽  
Family Members ◽  
Recessive Inheritance ◽  
Factor Xiii Deficiency ◽  
History Of ◽  
Congenital Factor

SummarySevere hemorrhagic disorder due to congenital factor XIII deficiency is described in two unrelated Norwegian girls.Plasma cephalin time was for both patients extraordinarily short during episodes of bleeding and hematomas. No such hyperactivity reaction was demonstrable in unaffected condition some months later.Estimations of blood factor XIII levels revealed a partial defect in the parents of both children, and also in some other family members, consistent with an autosomal incompletely recessive inheritance of the defect. Some of the presumptive heterozygotes had a history of light bleeding phenomenons; whether this was related to their partial lack of factor XIII is so far uncertain.

Platelet Accumulation on Fibrin-coated Polyethylene: Role of Platelet Activation and Factor XIII

1995 ◽  
Vol 73 (05) ◽  
pp. 850-856 ◽  
Author(s):  
F D Rubens ◽  
D W Perry ◽  
M W C Hatton ◽  
P D Bishop ◽  
M A Packham ◽  
...  
Keyword(s):  
Factor Xiii ◽  
Cross Linking ◽  
Internal Diameter ◽  
Static System ◽  
Graft Occlusion ◽  
Platelet Binding ◽  
Coated Surface ◽  
Platelet Accumulation ◽  
Polyethylene Tubing

SummaryPlatelet accumulation on small- and medium-calibre vascular grafts plays a significant role in graft occlusion. We examined platelet accumulation on the surface of fibrin-coated polyethylene tubing (internal diameter 0.17 cm) during 10 min of flow (l0ml/min) at high wall shear rate (764 s-1). Washed platelets labelled with 51Cr were resuspended in Tyrode solution containing albumin, apyrase and red blood cells (hematocrit 40%). When the thrombin that was used to form the fibrin-coated surface was inactivated with FPRCH2C1 before perfusion of the tubes with the platelet:red blood cell suspension, the accumulation of platelets was 59,840 ± 27,960 platelets per mm2, whereas accumulation on fibrin with residual active thrombin was 316,750 ± 32,560 platelets per mm2 (n = 4). When the fibrin on the surface was cross-linked by including recombinant factor XIII (rFXIII) in the fibrinogen solution used to prepare the fibrin-coated surface, platelet accumulation, after thrombin neutralization, was reduced by the cross-linking from 46,974 ± 9702 to 36,818 ± 7964 platelets per mm2 (n = 12, p <0.01). Platelet accumulation on tubes coated with D-dimer was ten times less than on tubes coated with D-domain; this finding also supports the observation that cross-linking of fibrin with the formation of γ-γ dimers reduces platelet accumulation on the fibrin-coated surface. Thrombin-activated platelets themselves were shown to cross-link fibrin when they had adhered to it during perfusion, or in a static system in which thrombin was used to form clots from FXIII-free fibrinogen in the presence of platelets. Thus, cross-linking of fibrin by FXIII in plasma or from platelets probably decreases the reactivity of the fibrin-containing thrombi to platelets by altering the lysine residue at or near the platelet-binding site of each of the γ-chains of the fibrinogen which was converted into the fibrin of these thrombi.

Determination of Factor XIII Activity and of Factor XIII Inhibitors Using an Ammonium-Sensitive Electrode

1983 ◽  
Vol 50 (02) ◽  
pp. 563-566 ◽  
Author(s):  
P Hellstern ◽  
K Schilz ◽  
G von Blohn ◽  
E Wenzel
Keyword(s):  
Factor Xiii ◽  
Normal Subjects ◽  
The Other ◽  
Activity Measurement ◽  
Factor Xiii Deficiency ◽  
Assay Procedure ◽  
Stabilization Factor ◽  
Release Method ◽  
Sensitive Electrode

SummaryAn assay for rapid factor XIII activity measurement has been developed based on the determination of the ammonium released during fibrin stabilization. Factor XIII was activated by thrombin and calcium. Ammonium was measured by an ammonium-sensitive electrode. It was demonstrated that the assay procedure yields accurate and precise results and that factor XIII-catalyzed fibrin stabilization can be measured kinetically. The amount of ammonium released during the first 90 min of fibrin stabilization was found to be 7.8 ± 0.5 moles per mole fibrinogen, which is in agreement with the findings of other authors. In 15 normal subjects and in 15 patients suffering from diseases with suspected factor XIII deficiency there was a satisfactory correlation between the results obtained by the “ammonium-release-method”, Bohn’s method, and the immunological assay (r1 = 0.65; r2= 0.70; p<0.01). In 3 of 5 patients with paraproteinemias the values of factor XIII activity determined by the ammonium-release method were markedly lower than those estimated by the other methods. It could be shown that inhibitor mechanisms were responsible for these discrepancies.

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