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Bemiparin

A Review of its Use in the Prevention of Venous Thromboembolism and Treatment of Deep Vein Thrombosis

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Summary

Abstract

Bemiparin (bemiparin sodium; Hibor®, Ivor®, Zibor®, Badyket®) is a low molecular weight heparin (LMWH) with a lower mean molecular weight (3600D) and a higher anti-Xa/IIa ratio (8:1) than other LMWHs.

Bemiparin was effective as thromboprophylaxis in surgical patients in well controlled clinical trials. No cases of venous thromboembolism (VTE) were reported in low- to moderate-risk patients receiving prophylaxis with bemiparin 2500 anti-Xa IU/day for 7 days or unfractionated heparin (UFH) 5000 anti-XaIU twice daily for 7 days. In high-risk patients, bemiparin 3500 anti-Xa IU/day for ≥8 days was more effective than UFH 5000 anti-XaIU twice daily for ≥8 days in the prevention of VTE in patients undergoing total hip replacement. Postoperative bemiparin 3500 anti-Xa IU/day for 10 days was as effective as enoxaparin 4000 anti-Xa IU/day for 10 days commenced 12 hours before surgery in high-risk patients undergoing total knee replacement.

As a short-term treatment for acute established deep vein thrombosis (DVT), bemiparin 5000–10 000 anti-Xa IU/day (dependent on bodyweight) for 7 or 10 days was more effective than intravenous UFH (5000 anti-XaIU bolus followed by 30 000 or 40 000 anti-Xa IU/day for 7 days) in reducing thrombus size from baseline. Bemiparin 3500 anti-Xa IU/day was also as effective as oral warfarin (10 mg/day for the first 3 days, then adjusted to achieve an international normalised ratio between 2 and 3) for the long-term (12 weeks) treatment of DVT, although data are limited.

Subcutaneous bemiparin was generally well tolerated. The most commonly reported adverse events in clinical trials were postoperative bleeding complications (similar incidence to that with UFH or enoxaparin in high-risk patients, lower incidence in low- to moderate-risk patients).

Conclusions: Bemiparin is a new LMWH which has shown efficacy in a small number of well controlled trials in the prevention of postoperative VTE in low- to moderate- and high-risk patients and in the treatment of established DVT. It can be initiated pre- or post-operatively, whereas recommendations for other LMWHs in Europe primarily involve preoperative initiation. Additional comparative studies would be beneficial in determining the overall place of bemiparin, particularly with respect to the relative incidence of bleeding complications. In the meantime, available data suggest that bemiparin is an effective and useful addition to the available range of LMWHs for the prevention of VTE and treatment of DVT.

Pharmacodynamic Properties

Bemiparin is obtained by the chemical depolymerisation (β elimination) and fractionation of porcine mucosal unfractionated heparin (UFH). With a mean molecular weight of 3600D and approximately 85% of its polysaccharide chains under 6000D, bemiparin has been referred to as a ‘second-generation’ low molecular weight heparin (LMWH).

Bemiparin has anti-Xa activity of 80–120 IU/mg and an anti-IIa activity of 5–20 IU/mg. The anti-Xa/IIa ratio of approximately 8: 1 is higher than that of other LMWHs, including enoxaparin (3.8: 1), dalteparin (2.7: 1), reviparin (3.5: 1) and tinzaparin (1.9: 1). It is thought that the high anti-Xa/IIa ratio of bemiparin may lead to greater antithrombotic activity without increasing the risk of bleeding.

In healthy volunteers and patients at risk of venous thromboembolism (VTE), subcutaneous bemiparin significantly increased anti-Xa activity; however, anti-IIa activity and levels of antithrombin were generally not affected. The anti-Xa activity of bemiparin was reduced by protamine sulfate.

In vitro, bemiparin, dalteparin and UFH significantly increased the expression, release and activity of tissue factor pathway inhibitor (TFPI) in static endothelial cells to similar extents. However, in endothelial cells under arterial shear stress in vitro, bemiparin increased the secretion and cell surface activity of TFPI while UFH and dalteparin did not increase the production of TFPI.

Bemiparin, UFH, enoxaparin and nadroparin all reduced mean red cell aggregability to a similar extent.

Bemiparin does not appear to have any clinically significant effect on the activated partial thromboplastin time and the thrombin time. The effects of bemiparin on the production of tissue-plasminogen activator (t-PA) in human umbilical vein endothelial cells (HUVECs) in vitro was similar to that of control cells. In contrast, UFH induced a 3-fold increase in t-PA. Bemiparin and UFH increased levels of the inhibitor of t-PA (plasminogen activator inhibitor-1) in HUVECs in vitro to a similar extent. However, unlike UFH, bemiparin had no effect on the production of tissue factor in HUVECs in vitro.

Bemiparin suppressed markers of hypercoagulability (e.g. D-dimer, thrombin-antithrombin complexes and factor VII:c) and increased levels of protein C in 100 patients with congestive heart failure.

In vitro the binding of bemiparin to dead leucocytes was lower than that of UFH. In addition, heparin binding proteins were less effective at blocking the antithrombin activity of bemiparin than that of UFH.

Pharmacokinetic Profile

After a single subcutaneous administration of bemiparin 2500–12 500 anti-XaIU to healthy volunteers the anti-Xa activity increased in a dose-dependent manner; however, maximum anti-Xa activity (Emax) was reached within 2–6 hours, regardless of dose. Subcutaneous bemiparin had high bioavailability in healthy volunteers and the mean volume of distribution of anti-Xa after intravenous administration of bemiparin 5000 anti-XaIU to healthy volunteers was 5.1L.

Bemiparin undergoes linear elimination via the renal route. A single dose of subcutaneous bemiparin 2500–12 000 has a long elimination half-life (4–5 hours) and MRT (>7 hours). The mean total clearance of anti-Xa activity after intravenous administration of bemiparin to healthy volunteers was 0.90 L/h (15.5 mL/ min).

The pharmacokinetic profile of bemiparin 3500 anti-XaIU was generally similar to that of enoxaparin 4000 anti-XaIU; however, the area under the effect-time curve was significantly greater after administration of bemiparin than enoxaparin (3.78 vs 3.42 IU · h/mL; p < 0.05). Bemiparin 3500 anti-XaIU exerted a significantly more rapid and greater anti-Xa activity than tinzaparin 4500 anti-XaIU (p < 0.005 for all comparisons).

Establishing the pharmacokinetic profile of the TFPI effect is important because potent anticoagulant synergism results in vitro when both the anti-Xa amidolytic and TFPI effects occur simultaneously. The effect of bemiparin on the release of TFPI was not dose dependent. The Emax of the TFPI effect was reached earlier than the Emax of the anti-Xa effect after subcutaneous administration of bemiparin 2500–12 500 anti-XaIU to healthy volunteers. Bemiparin and enoxaparin had a similar effect on the release of TFPI; however, the Emax of the TFPI effect was significantly lower after administration of bemiparin than after tinzaparin in healthy volunteers (94.05 vs 128.92 ng/mL; p < 0.01).

Clinical Efficacy

The efficacy of subcutaneous bemiparin in the prevention of venous thromboembolism (VTE) in low- to moderate-patients after abdominal surgery or high-risk patients after orthopaedic surgery has been established in three randomised, double-blind, multicentre comparative trials with UFH or enoxaparin and three noncomparative trials.

Subcutaneous bemiparin provided effective prophylaxis for the prevention of VTE in both low- to moderate-risk and high-risk patients undergoing surgery. In low- to moderate-risk patients undergoing abdominal surgery, the efficacy of bemiparin 2500 anti-Xa IU/day administered for 7 days with the first dose administered 2 hours prior to surgery was similar to that of subcutaneous UFH 5000 anti-XaIU twice daily also for 7 days. However, in high-risk patients undergoing hip replacement, bemiparin 3500 anti-Xa IU/day for >8 days was more effective than UFH 5000 anti-XaIU twice daily for the same duration in the prevention of VTE, with fewer bemiparin recipients experiencing VTE or deep vein thrombosis (DVT). Furthermore, in an extended follow-up (56 days after surgery) in this trial, only one patient receiving bemiparin experienced a VTE event; in the same period four UFH recipients developed a VTE event.

Bemiparin 3500 anti-XaIU for 10 ± 2 days with the initial dose administered postoperatively (6 hours after surgery) was as effective for the prophylaxis of VTE as enoxaparin 40 mg/day for 10 ± 2 days commenced preoperatively (12 hours prior to surgery) in high-risk patients, 94% of whom underwent neuraxial blockade; however, this trial was not powered to demonstrate statistical superiority of one regimen over another.

The results of noncomparative studies in moderate- or high-risk patients supported data reported in the comparative studies.

In a randomised, nonblind, multicentre trial, bemiparin had better efficacy than UFH in the immediate treatment of acute established DVT. Significantly more patients receiving bemiparin (500 anti-Xa IU/day if bodyweight <50kg, 7500 anti-Xa IU/day if bodyweight 50–70kg and 10 000 anti-Xa IU/day if bodyweight >70kg) for 7 or 10 days experienced venographic reduction in thrombus size between baseline and day 14 than those receiving UFH (a 5000 anti-XaIU bolus followed by a continuous infusion of 40 000 anti-Xa IU/day in patients at low risk of bleeding and 30 000 anti-Xa IU/day in patients at high risk of bleeding) for 7 days (72%, 72% and 52%, respectively; p < 0.005 for both comparisons), as assessed by Marder score. However, there was no significant difference between the treatment groups for the long-term (12 week) treatment of DVT, as assessed by the percentage of patients with partial or complete recanalisation of the involved veins and the incidence of recurrent VTE events.

Tolerability

Clinical trials have shown that subcutaneous bemiparin is well tolerated when used for the prophylaxis of VTE or treatment of DVT. Bleeding complications including blood loss, wound haematomas and haematomas at the injection site were the most common adverse events in clinical trials.

In high-risk patients, bemiparin was associated with a similar incidence of major bleeding complications to that of UFH. Similarly, the incidence of major or minor bleeding complications associated with postoperative bemiparin was similar to that of enoxaparin with the initial dose administered preoperatively. However, the incidence of haematoma and other local reactions at the injection site was significantly lower in patients receiving bemiparin compared with enoxaparin recipients (22.7% vs 32.5%; p = 0.03). Of note, no neuraxial complications were reported for patients receiving postoperative bemiparin and enoxaparin started preoperatively with neuraxial blackade.

In low- to moderate-risk patients, no major bleeding events were reported with bemiparin prophylactic therapy; however, 3.7% of patients receiving UFH experienced required transfusion with more than two units of red blood cells and 2.4% required reoperation because of major bleeding events. The incidence of wound haematoma (6% vs 18%; p = 0.015) and the mean number and size of haematomas at the injection site (data not reported; p = 0.004 and p = 0.017) were significantly lower in patients receiving bemiparin than in UFH recipients.

In patients receiving treatment for established DVT, the incidence of major or minor bleeding complications was similar for patients receiving short-term UFH plus long-term warfarin, short-term bemiparin plus long-term warfarin or long-term bemiparin (time of assessment not reported).

The total incidence of unspecified adverse events was similar for patients receiving bemiparin, UFH or enoxaparin in high-risk patients.

In comparative trials, bemiparin prophylaxis generally did not result in any significant changes to haematological or biochemical parameters. Platelet counts were similar between bemiparin and its comparators. In one trial, a mild and transient decrease in platelet count was reported in 3.2% of high-risk patients receiving bemiparin and 2.6% of enoxaparin recipients. In another trial, 2.0%, 1.9% and 3.2% of patients receiving UFH plus long-term warfarin, short-term bemiparin plus long-term warfarin and long-term bemiparin as treatment for established DVT experienced heparin-induced thrombocytopenia. However, none of these patients developed further thrombotic or bleeding complications.

Pharmacoeconomic Considerations

Data from a cost-analysis and cost-minimisation evaluation of a small prospective, nonrandomised pharmacoeconomic study from a Spanish institutional perspective suggest that although bemiparin has a lower acquisition cost than that of other LMWHs (enoxaparin or dalteparin) [4589 vs 10 174 pesetas; p < 0.0001, 1 peseta ≈ 0.006 Euro] there were no significant differences between treatment groups for total costs, hospitalisation costs, costs of other treatments or outpatient prophylaxis (currency year not reported).

Results of a cost-minimisation analysis showed that treatment with bemiparin resulted in a mean saving of 2146–5585 pesetas per patient when only drug costs were considered (significance not reported) and a mean cost saving of 13 601–33 471 pesetas per patient when total costs were considered; however, this was not significant.

Dosage and Administration

Bemiparin is approved in a number of European countries for the prevention of VTE in patients undergoing general surgery (moderate-risk patients) or orthopaedic surgery (high-risk patients) and for the treatment of established DVT. It is recommended that bemiparin be administered by subcutaneous injection via the abdomen. Bemiparin should not be administered intramuscularly.

Patients at moderate risk of postsurgical VTE should receive subcutaneous bemiparin 2500 anti-Xa IU/day and patients at high risk should receive 3500 anti-Xa IU/day until they are completely mobile. The first dose should be administered 2 hours before surgery or within 6 hours after surgery.

The dosage of bemiparin for the treatment of acute established DVT is dependent on the patient’s bodyweight (5000 anti-Xa IU/day if body weight <50kg; 7500 anti-Xa IU/day if bodyweight 50–70kg; 10 000 anti-Xa IU/day if bodyweight >70kg).

Caution should be exercised when bemiparin is to be administered to patients with uncontrolled hypertension, increased risk of bleeding, ulceration of the stomach or intestine, acute bacterial endocarditis, cerebral vascular accident or renal or hepatic impairment. There have been no clinical studies on bemiparin in pregnant or lactating women.

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  1. Use of tradenames is for product identification purposes only and does not imply endorsement.

References

  1. Anderson FA, Spencer FA. Risk factors for venous thromboembolism. Circulation 2003; 107: 19–116

    Article  Google Scholar 

  2. White RH. The epidemiology of venous thromboembolism. Circulation 2003; 107: 14–8

    Article  Google Scholar 

  3. Scottish Intercollegiate Consensus Guidelines Network. Prophylaxis of venous thromboembolism: a national clinical guideline [online]. Available from URL: http://www.sign.ac.uk/pdf/sign62.pdf [Accessed 2003 Sep 16]

  4. Vaughn P, Gardner J, Peters F, et al. Risk factors for venous thromboembolism in general surgical patients. Isr Med Assoc J 2002; 4: 1037–9

    Google Scholar 

  5. Geerts WH, Heit JA, Clagett GP, et al. Prevention of venous thromboembolism. Chest 2001 Jan; 119 (1 Suppl.): 132S–75S

    Article  PubMed  CAS  Google Scholar 

  6. Morris TA. Heparin and low molecular weight heparin: background and pharmacology. Clin Chest Med 2003; 24: 39–47

    Article  PubMed  Google Scholar 

  7. Hirsh J, Warkentin TE, Shaughnessy SG, et al. Heparin and low-molecular-weight heparin: mechanisms of action, pharmacokinetics, dosing, monitoring, efficacy, and safety. Chest 2001; 119: 64S–94S

    Article  PubMed  CAS  Google Scholar 

  8. Weitz JI. Low-molecular-weight heparins. N Engl J Med 1997 Sep 4; 337(10): 688–98

    Article  PubMed  CAS  Google Scholar 

  9. Samama MM, Bara L, Gerotziafas GT. Mechanisms for the antithrombotic activity in man of low molecular weight heparins (LMWHs). Haemostasis 1994; 24: 105–17

    PubMed  CAS  Google Scholar 

  10. Rovi Pharmaceutical Laboratories. Hibor (bemiparin sodium): summary of product characteristics. Madrid: Rovi Pharmaceutical Laboratories, 2002 Jun

    Google Scholar 

  11. Kakkar VV, Howes J, Sharma V, et al. A comparative, doubleblind, randomised trial of a new second generation LMWH (bemiparin) and UFH in the prevention of post-operative venous thromboembolism. Thromb Haemost 2000 Apr; 83(4): 523–9

    PubMed  CAS  Google Scholar 

  12. Rovi Pharmaceutical Laboratories. Phivor 25,000 IU (bemiparin sodium): final proposed summary of product characteristics. Madrid: Rovi Pharmaceutical Laboratories, 2003 Mar

    Google Scholar 

  13. Falkon L, Saenz-Campos D, Antonijoan R, et al. Bioavailability and pharmacokinetics of a new low molecular weight heparin (RO-11) — a three way cross-over study in healthy volunteers. Thromb Res 1995; 78(1): 77–86

    Article  PubMed  CAS  Google Scholar 

  14. Falkon L, Gari M, Barbanoj M, et al. Tissue factor pathway inhibitor and anti-FXa kinetic profiles of a new low-molecularmass heparin, bemiparin, at therapeutic subcutaneous doses. Blood Coagul Fibrinolysis 1998 Mar; 9(2): 137–41

    Article  PubMed  CAS  Google Scholar 

  15. Falkon L, Bayes M, Frontera G, et al. Pharmacokinetics and tolerability of a new low molecular mass heparin (RO-11) in healthy volunteers — a dose-finding study within the therapeutical range. Thromb Haemost 1997 Jan; 77(1): 133–6

    PubMed  CAS  Google Scholar 

  16. Moreno Gonzalez E, Fontcuberta J, de la Llama F, et al. Prophylaxis of thromboembolic disease with RO-11 (ROVI), during abdominal surgery. Hepatogastroenterology 1996; 43: 744–7

    PubMed  CAS  Google Scholar 

  17. Falkon L, Gari M, Gich I, et al. In vitro and ex vivo neutralizing effect of protamine sulphate on the anticoagulant activity of a new low molecular mass heparin. Thromb Res 1998; 89:79–83

    Article  PubMed  CAS  Google Scholar 

  18. Antonijoan RM, Borrell M, Zsolt I, et al. Interaction between protamine sulfate and a new LMWH at therapeutic doses in healthy volunteers: bemiparin 7500 IU [abstract]. 18th Congress of the International Society of Thrombosis and Haemostasis; 2001 Jul 6–12; Paris

  19. Falkon L, Gari M, Saenz-Campos D, et al. Kinetic behaviour of the TFPI and anti-FXa effects, after the injection of a LMWH (RO-11) in healthy subjects. Thromb Haemost 1995 Apr; 73(4): 728–9

    PubMed  CAS  Google Scholar 

  20. Westmuckett AD, Kakkar VV, Hamuro T, et al. Bemiparin and fluid flow modulate the expression, activity and release of tissue factor pathway inhibitor in human endothelial cells in vitro. Thromb Haemost 2001 Dec; 86(6): 1547–54

    PubMed  CAS  Google Scholar 

  21. Martinez M, Vaya A, Lopez-Camacho C, et al. High and low molecular weight heparins do not modify red blood cell aggregability in vitro. Clin Haemorheol Microcirc 2000; 23: 67–70

    CAS  Google Scholar 

  22. Perez-Ruiz A, Montes R, Carrasco P, et al. Effects of a low molecular weight heparin, bemiparin, and unfractionated heparin on hemostatic properties of endothelium. Clin Applied Thromb Hemost 2002; 8(1): 65–71

    Article  CAS  Google Scholar 

  23. De Lorenzo F, Newberry D, Scully M, et al. Low molecular weight heparin (bemiparin sodium) and the coagulation profile of patients with heart failure. Am Heart J 2002 Apr; 143(4): 689–94

    PubMed  Google Scholar 

  24. Morita S, Gebska MA, Kakkar AK, et al. High affinity binding of heparin by necrotic tumour cells neutralises anticoagulant activity: implications for cancer related thromboembolism and heparin therapy. Thromb Haemost 2001; 86: 616–22

    PubMed  CAS  Google Scholar 

  25. Gebska MA, Titley I, Paterson HF, et al. High-affinity binding sites for heparin generated on leukocytes during apoptosis arise from nuclear structures segregated during cell death. Blood 2002 Mar 15; 99(6): 2221–7

    Article  PubMed  CAS  Google Scholar 

  26. Borrell M, Antonijoan RM, Ortin R, et al. Pharmacokinetic profiles of two LMWH: bemiparin 3500 IU and enoxaparin 4000 IU after subcutaneous administration in healthy volunteers [abstract]. 18th Congress of the International Society of Thrombosis and Haemostasis; 2001 Jul 6–12; Paris

  27. Depasse F, Gonzalez de Suso MJ, Lagoutte I, et al. Comparative study of the pharmacokinetic profiles of two LMWHs — bemiparin (3500 IU, anti-Xa) and tinzaparin (4500 IU, anti-Xa) — administered subcutaneously to healthy male volunteers. Thromb Res 2003; 109: 109–17

    Article  PubMed  CAS  Google Scholar 

  28. Hidalgo M, Figueroa JM. Prophylaxis of venous thromboembolism in abdominal wall surgery. Hernia 2000; 4: 242–7

    Article  Google Scholar 

  29. Fenollosa J, Seminario P. Efficacy and safety of bemiparin in the prophylaxis of venous thromboembolism in orthopedic surgery [in Spanish]. Revista De Ortopedia y Traumatologia 2001; 45(6): 460–5

    Google Scholar 

  30. Planes A, Vochelle N, Gonzalez De Suso MJ, et al. Prophylactic antithrombotic therapy after orthopedic surgery with bemiparin, a second-generation low molecular weight heparin (in Spanish]. Rev Esp Anestesiol Reanim 2001; 48(6): 258–63

    PubMed  CAS  Google Scholar 

  31. Navarro-Quilis A, Castellet E, Rocha E, et al. Efficacy and safety of bemiparin compared with enoxaparin in the prevention of venous thromboembolism after total knee arthroplasty: a randomized, double-blind clinical trial. J Thromb Haemost 2003; 1: 425–32

    Article  PubMed  CAS  Google Scholar 

  32. Bonal J, Gisbert R. Pharmacoeconomic analysis of prophylaxis for thromboembolic disease in hip replacement patients [in Spanish]. Rev Espa Farmacoecon 2000 Mar, 17-26

  33. Kakkar VV, Gebska M, Kadziola Z, et al. Low-molecularweight heparin in the acute and long-term treatment of deep vein thrombosis. Thromb Haemost 2003; 89: 674–80

    PubMed  CAS  Google Scholar 

  34. Ferriols-Lisart R, Ferriols-Lisart F, Jimenez-Torres V. Effectiveness and safety of bemiparin versus low-molecular weight heparins in orthopaedic surgery. Pharm World Sci 2002 Jun; 24(3): 87–94

    Article  PubMed  CAS  Google Scholar 

  35. Rovi Pharmceutical Laboratories. Data on file. 2003

  36. Prandoni P. The treatment of venous thromboembolic disorders: new challenges and opportunities. Haematologica 2003 May; 88(5): 610–3

    PubMed  Google Scholar 

  37. Brown DFM. Treatment options for deep venous thrombosis. Emerg Med Clin North Am 2001 Nov; 19(4): 913–23

    Article  PubMed  CAS  Google Scholar 

  38. Hyers TM, Agnelli G, Hull RD, et al. Antithrombotic therapy for venous thromboembolic disease. Chest 2001; 119: 176S–93S

    Article  PubMed  CAS  Google Scholar 

  39. Institute for Clinical Systems Improvement. ICSI health care guideline: venous thromboembolism [online]. Available from URL: http://www.icsi.org/knowledge/detail.asp?catID=29&itemid=202 [Accessed 2003 Jul 11]

  40. Prandoni P. Heparins and venous thromboembolism: current practice and future directions. Thromb Haemost 2001 Jul; 86(1): 488–98

    PubMed  CAS  Google Scholar 

  41. McKay GA, Paterson KR. Low molecular weight heparins — a safer option than unfractionated heparin? Adv Drug Reactions Toxicol Rev 2001; 20(4): 256–76

    CAS  Google Scholar 

  42. Lumpkin MM. FDA public health advisory. Anesthesiology 1998; 88: 27A-8A

    Article  Google Scholar 

  43. Tryba M. European practice guidelines: thromboembolism prophylaxis and regional anesthesia. Reg Anesth Pain Med 1998; 23 (6 Suppl. 2): 178–82

    PubMed  CAS  Google Scholar 

  44. British Medical Association and the Royal Pharmaceutical Society of Great Britain. British national formulary (BNF). London: British Medical Association and the Royal Pharmaceutical Society of Great Britain, 2003

  45. Sweetman SC. Martindale: The complete drug reference. 33rd ed. London: Pharmaceutical Press, 2002

    Google Scholar 

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Correspondence to Therese M. Chapman.

Additional information

Various sections of the manuscript reviewed by: F. Depasse, Clinical Research Department, LCL Laboratory, Ivry-sur-Seine, France; S. Haas, Institut fur Experimentelle Onkologie and Therapieforshung der Technischen Universitat, Munich, Germany; A. Planès, Clinique Radio-Chirurgicale du Mail, La Rochelle, France; E. Rocha, Haematology Service, University Clinic of Navarra, Pamplona, Spain; A.G.G. Turpie, General Division, Hamilton Health Sciences, Hamilton, Ontario, Canada; G.J. Vanscoy, University Pharmacotherapy Associates-LLC, Monroeville, Pennsylvania, USA; A.D. Westmuckett, Thrombosis Research Institute, London, England.

Data Selection

Sources: Medical literature published in any language since 1980 on bemiparin, identified using Medline and EMBASE, supplemented by AdisBase (a proprietary database of Adis International). Additional references were identified from the reference lists of published articles. Bibliographical information, including contributory unpublished data, was also requested from the company developing the drug.

Search strategy: Medline search terms were ‘bemiparin’. EMBASE search terms were ‘bemiparin’. AdisBase search terms were ‘bemiparin’ or ‘bemiparin sodium’ or ‘RO-11’. Searches were last updated 15 September, 2003.

Selection: Studies in patients at risk of thromboembolism or with established deep vein thrombosis who received bemiparin. Inclusion of studies was based mainly on the methods section of the trials. When available, large, well controlled trials with appropriate statistical methodology were preferred. Relevant pharmacodynamic and pharmacokinetic data are also included.

Index terms: Bemiparin, venous thromboembolism, deep vein thrombosis, DVT, pharmacodynamics, pharmacokinetics, therapeutic use.

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Chapman, T.M., Goa, K.L. Bemiparin. Drugs 63, 2357–2377 (2003). https://doi.org/10.2165/00003495-200363210-00009

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