scholarly journals Management of suspected and confirmed recurrent venous thrombosis while on anticoagulant therapy. What next?

2019 ◽  
Vol 180 ◽  
pp. 105-109
Author(s):  
Marc A. Rodger ◽  
Sebastien Miranda ◽  
Aurelien Delluc ◽  
Marc Carrier
Blood ◽  
1991 ◽  
Vol 78 (9) ◽  
pp. 2194-2197
Author(s):  
C Demers ◽  
JS Ginsberg ◽  
P Brill-Edwards ◽  
A Panju ◽  
TE Warkentin ◽  
...  

In order to determine the efficacy and safety of ancrod, a rapid acting defibrinogenating drug, for patients with heparin-induced thrombocytopenia, 11 consecutive patients who required anticoagulant therapy because of venous thromboembolism and who developed acute heparin-induced thrombocytopenia or had a history of heparin-induced thrombocytopenia were treated with ancrod. Heparin therapy was discontinued (in patients receiving heparin) and ancrod started at a dose of 1 to 2 U/kg every 24 hours with subsequent daily doses adjusted to maintain fibrinogen levels between 0.5 and 1.0 g/L. Ancrod was continued until warfarin had become effective. The platelet count increased to more than 150 x 10(9)/L within 2 to 10 days in all thrombocytopenic patients. Two patients with a history of heparin- induced thrombocytopenia maintained normal platelet counts while receiving ancrod. Two patients had recurrent venous thrombosis while receiving warfarin, 10 days after ancrod was discontinued: one of these patients had metastatic pancreatic carcinoma and developed phlegmasia cerulea dolens and the other patient developed a venographically proven extension of her deep venous thrombosis. One patient suffered a bleeding episode into the thigh with a 16-g/L decrease in her hemoglobin level while receiving ancrod therapy. No other side effects were noted. Our experience indicates that ancrod therapy is a reasonable approach for patients with heparin-induced thrombocytopenia who require anticoagulant therapy.


Blood ◽  
1991 ◽  
Vol 78 (9) ◽  
pp. 2194-2197 ◽  
Author(s):  
C Demers ◽  
JS Ginsberg ◽  
P Brill-Edwards ◽  
A Panju ◽  
TE Warkentin ◽  
...  

Abstract In order to determine the efficacy and safety of ancrod, a rapid acting defibrinogenating drug, for patients with heparin-induced thrombocytopenia, 11 consecutive patients who required anticoagulant therapy because of venous thromboembolism and who developed acute heparin-induced thrombocytopenia or had a history of heparin-induced thrombocytopenia were treated with ancrod. Heparin therapy was discontinued (in patients receiving heparin) and ancrod started at a dose of 1 to 2 U/kg every 24 hours with subsequent daily doses adjusted to maintain fibrinogen levels between 0.5 and 1.0 g/L. Ancrod was continued until warfarin had become effective. The platelet count increased to more than 150 x 10(9)/L within 2 to 10 days in all thrombocytopenic patients. Two patients with a history of heparin- induced thrombocytopenia maintained normal platelet counts while receiving ancrod. Two patients had recurrent venous thrombosis while receiving warfarin, 10 days after ancrod was discontinued: one of these patients had metastatic pancreatic carcinoma and developed phlegmasia cerulea dolens and the other patient developed a venographically proven extension of her deep venous thrombosis. One patient suffered a bleeding episode into the thigh with a 16-g/L decrease in her hemoglobin level while receiving ancrod therapy. No other side effects were noted. Our experience indicates that ancrod therapy is a reasonable approach for patients with heparin-induced thrombocytopenia who require anticoagulant therapy.


1985 ◽  
Vol 54 (04) ◽  
pp. 744-745 ◽  
Author(s):  
R Vikydal ◽  
C Korninger ◽  
P A Kyrle ◽  
H Niessner ◽  
I Pabinger ◽  
...  

SummaryAntithrombin-III activity was determined in 752 patients with a history of venous thrombosis and/or pulmonary embolism. 54 patients (7.18%) had an antithrombin-III activity below the normal range. Among these were 13 patients (1.73%) with proven hereditary deficiency. 14 patients were judged to have probable hereditary antithrombin-III deficiency, because they had a positive family history, but antithrombin-III deficiency could not be verified in other members of the family. In the 27 remaining patients (most of them with only slight deficiency) hereditary antithrombin-III deficiency was unlikely. The prevalence of hereditary antithrombin-III deficiency was higher in patients with recurrent venous thrombosis.


2017 ◽  
Vol 1 (1) ◽  
pp. 112-119 ◽  
Author(s):  
Sigrid K. Braekkan ◽  
Camila Caram-Deelder ◽  
Bob Siegerink ◽  
Astrid van Hylckama Vlieg ◽  
Saskia le Cessie ◽  
...  

1970 ◽  
Vol 13 (1) ◽  
pp. 100-102
Author(s):  
Aparna Das ◽  
AKM Aminul Hoque ◽  
Ratan Dasgupta ◽  
Ahmedul Kabir ◽  
Gobinda Banik ◽  
...  

A 50- year-old female was presented with recurrent venous thrombosis with ischemic stroke due to protein S deficiency. Other causes of recurrent venous thrombosis were excluded by different investigations. We only found low level of protein S. In most of the cases, thrombophilia screening is not usaally done. So, this report will illustrate the importance of thrombophlia screening in patient having recurrent venous thrombosis. DOI: http://dx.doi.org/10.3329/jom.v13i1.10085 JOM 2012; 13(1): 100-102


2019 ◽  
Vol 13 (4) ◽  
pp. 37-45
Author(s):  
V. V. Dmitriev ◽  
A. S. Fedorova ◽  
N. V. Lipay ◽  
I. V. Begun ◽  
I. A. Dunaev ◽  
...  

Objective of the study was to compare blood clotting parameters in lymphoma patients with or without venous thrombosis (VT), as well as to analyze the duration and outcome of anticoagulant therapy in children, adolescents and young adults with lymphoma, whose program treatment was complicated by VT.Materials and methods . The analysis included 28 patients with lymphoma (Hodgkin lymphoma – 5, non-Hodgkin lymphoma – 23), aged from 2 to 25 years (median – 16.0 years), whose program treatment in 2005–2017 was complicated by VT. The case-control study was carried out to compare the parameters of blood coagulation. The control group consisted of 22 patients, aged from 2 to 20 years (median – 15.5 years) with the same diagnosis, age, therapy protocol and phase of treatment who had no thrombotic complications. The comparison group consisted of 35 healthy children aged from 3 to 18 years (median – 14.0 years).Results . There was no difference in majority of blood clotting parameters in lymphoma patients with or without VT. Hyperfibrinogenemia and an increased D-dimers level distinguished patients with lymphoma, regardless of the presence or absence of thrombosis, from healthy children of the same age (р<0.05). Anticoagulant therapy up to 3 months received 10 patients, for 4–6 months – 4, for 7–12 months – 12, up to 18 months – 2. One adult patient with a homozygous mutation 20210G>A gene of the factor II takes warfarin continuously for a long time after relapse of VT. Complete recanalization of the thrombosed vessel occurred within the first 3 months in 9 patients, within 4–6 months – in 1, within 7–12 months ‒ in 4. Partial recanalization within 3–12 months was confirmed in 8 patients. Vein obliteration, mainly the internal jugular vein, as the outcome of VT occurred in 6 patients within 4–12 months.Conclusion . Detection of routine blood clotting parameters does not allow identifying patients with thrombosis among children, adolescents and young adults with lymphoma. Fibrinogen and D-dimers levels were significantly higher in lymphoma patients, than in healthy children. Anticoagulant therapy for 3–12 months led to the complete or partial recanalization of VT in 79 % of patients. To detect blood clotting parameters by thrombosis development, as well as to reveal and monitor transient and permanent risk factors are necessary to specify the cause of VT and to determine the appropriate anticoagulant therapy.


The Lancet ◽  
2010 ◽  
Vol 376 (9757) ◽  
pp. 2032-2039 ◽  
Author(s):  
Paul Alexander Kyrle ◽  
Frits R Rosendaal ◽  
Sabine Eichinger

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