Therapeutic doses of low molecular weight heparin previous to the standard prophylaxis for hip replacement: a pilot study

1993 ◽  
Vol 70 ◽  
pp. S13
2001 ◽  
Vol 85 (06) ◽  
pp. 979-985 ◽  
Author(s):  
David Kuter ◽  
Jennifer Brown

SummaryAlthough heparin is widely used as an antithrombotic agent, its multiple mechanisms of action are not fully defined. Recent work has suggested that tissue factor pathway inhibitor (TFPI) may contribute to the antithrombotic activity of heparin by inhibiting the extrinsic pathway of coagulation. We have investigated the effect of heparin on TFPI and have found that when unfractionated heparin is given by continuous intravenous infusion to hospitalized inpatients, TFPI levels increase 2.3-fold and remain high as long as heparin is continued, but return to baseline levels soon after the infusion is stopped. In contrast, therapeutic doses of the low molecular weight heparin, dalteparin, resulted in significantly less TFPI induction. Given the increasing number of studies establishing the clinical efficacy of low molecular weight heparins as antithrombotic agents, these results suggest that TFPI may not be a major contributor to the antithrombotic effect of heparin.


Author(s):  
GIOVANA BADAN MARTINS ◽  
ANA ELIZA DURãES DE FARIA ◽  
AMANDA KIMURA LUCCHESI REIS ◽  
MARCUS VINíCIUS BUENO ◽  
MARIA PAULA SIQUEIRA DE MELO PERES ◽  
...  

2003 ◽  
Vol 23 (03) ◽  
pp. 131-134 ◽  
Author(s):  
J. Bösiger ◽  
F. Demarmels Biasiutti

SummaryRecurrent thromboembolism despite oral anticoagulation is primarily suspicious of overt or occult neoplasia. We report on a man (age: 67 years) who presented with severe thrombophilia which was only controlled when the patient was set on a combined anticoagulation with low molecular weight heparin in supratherapeutic dosage and phenprocoumon with a target INR of 2.0. Despite repeated evaluation over about two years, a malignant tumour could never be demonstrated. However, the patient suffered in addition to a protein S deficiency from an antiphosphospholipid syndrome and a chronic myelomonocytic leukaemia.We postulate that the accepted strong thrombogenicity of antiphosphospholipid syndrome was further increased by protein S deficiency and a possibly procoagulatory effect of the abnormal monocytes explaining the severe thrombophilia resistant to standard therapeutic anticoagulation with a vitamin K antagonist and usual therapeutic doses of low molecular weight heparin, respectively.


1999 ◽  
Vol 22 (3) ◽  
pp. 213-217 ◽  
Author(s):  
Anna Vittoria Mattioli ◽  
Emma Tarabini Castellani ◽  
Lavinia Goedecke ◽  
Luca Sormani ◽  
Sabina Sterneri ◽  
...  

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1244-1244
Author(s):  
Giorgia Saccullo ◽  
Alessandra Malato ◽  
Lucio Lo Coco ◽  
Ilenia Barbello ◽  
Clementina Caracciolo ◽  
...  

Abstract Abstract 1244 Introduction. We tested the efficacy and safety of fixed doses of Low-Molecular Weight Heparin (LMWH) in cancer patients requiring interruption of Vitamin-k Antagonist (VKA) because of invasive procedures (defined as major and non major surgery) or chemotherapy inducing platelets depletion. Methodology. Cancer patients were defined to be at high (atrial fibrillation [AF] with previous stroke, prosthetic mitralic valves and venous thromboembolism [VTE] lasting < 3months) or low risk of thrombosis (AF without previous stroke, VTE lasted > 3 months, and prosthetic aortic valves). They discontinued VKA 5 + 1days before surgery or chemotherapy; in those at low-risk for thrombosis, LMWH was given at a prophylactic dosage of 3.800 U.I. (nadroparin) or 4.000 U.I. (enoxaparin) anti-FXa once daily the night before the procedure or the beginning of chemotherapy. In patients at high-risk for thrombosis, LMWH was started early after VKA cessation (when an INR < 1.5) and given at fixed sub-therapeutic doses (3.800 or 4.000 UI anti-FXa twice daily) until procedure or beginning of chemotherapy. In patients undergoing procedures, LMWH was reinitiated 12 hours after procedure while VKA the day after; in patients receiving chemotherapy, LMWH was reinitiated 12 h after a stable platelet count > 30.000 mmc3 and VKA 12 h after a stable platelet count > 50.000 mmc3. Heparin was continued until a therapeutic INR value was reached. The primary efficacy endpoints were the incidence of thromboembolism and major bleeding from VKA suspension to 30 + 2 days post-procedure or next chemotherapy. Results. A total of 156 patients (68, 53.9% at low-risk and 58, 46.1% at high-risk for thrombosis) were enrolled (Table 1); 44 (28.2%) underwent major surgery, 53 (33.9%) non-major surgery and 29 (18.5%) chemotherapy. Overall, thromboembolic events occurred in 5 patients (3.2%, 95% confidence intervals 0.5–5.9), 4 belonging to high-risk and 1 to low-risk group. Overall, major bleeding occurred in 5 patients (3.2%, 95 CI 0.5–5.9), all belonging to high-risk group (3 during major surgery and 2 during chemotherapy). The mean time of anticoagulation with LMWH was 7.5 days in patients underwent procedures and 13.2 days in those who received chemotherapy. Conclusion. LMWH given at fixed sub-therapeutic doses appears to be a feasible and relatively safe approach for bridging therapy in chronic anticoagulated cancer patients requiring VKA interruption. Disclosures: No relevant conflicts of interest to declare.


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