Heparin and Low-Molecular-Weight Heparin Therapy for Venous Thromboembolism: Will Unfractionated Heparin Survive?

2004 ◽  
Vol 30 ◽  
pp. 11-23 ◽  
1998 ◽  
Vol 4 (2) ◽  
pp. 126-128 ◽  
Author(s):  
Bruno Girolami ◽  
Paolo Prandoni ◽  
Laura Rossi ◽  
Antonio Girolami

The purpose of this study was to evaluate the in cidence of transaminase elevation in patients treated with un fractionated (UFH) or low molecular weight heparin (LMWH). Patients receiving UFH, nadroparin, or reviparin for venous thromboembolism and with normal baseline transaminase val ues were evaluated for serum transaminase levels 10-14 days after the start of heparin therapy or at the end of treatment. The incidence of high transaminase was 4.7% overall (95% CI, 2.2 to 7.3), while it was 2.9% (95% CI, 0.1 to 5.6) and 6.7% (95% CI, 2.5 to 11.0) with UFH and LMWH treated patients, respec tively. The difference was equal to -3.8% (95% CI, -8.9 to 1.2) and the common odds ratio was equal to 0.38 (95% CI, 0.12 to 1.16, p = .09). Nadroparin treated patients showed a 5.7% (95% CI, 1.3 to 10.2) incidence of high transaminase levels, while reviparin treated patients presented a 10.3% incidence (95% CI, -0.7 to 21.4). The comparison with UFH showed a mild trend in favor of UFH when compared with nadroparin, but not with reviparin. In conclusion, the incidence of trans aminase increase during heparin treatment for a venous throm boembolic event is equal to 3%, 6%, and 10% in UFH-, na droparin-, and reviparin-treated patients, respectively. LMWHs showed a slightly higher average incidences of hypertransami nasemia as compared with UFH. Differences did not reach statistical significance. Key Words: Unfractionated heparin— Low molecular weight heparin—Hypertransaminasemia.


Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 2197-2197
Author(s):  
Stephan Moll ◽  
Charles S. Abrams ◽  
Lawrence Rice ◽  
Richard C. Becker ◽  
Peter B. Berger ◽  
...  

Abstract Background : Thrombocytopenia in the patient on heparin can have various etiologies, including benign reversible causes and serious, potentially life-threatening ones, such as heparin induced thrombocytopenia (HIT). Knowledge about the prevalence of and timecourse of thrombocytopenia in heparin-treated patients may be helpful to develop systems of alerting clinicians to possible HIT and determining how frequently to check blood counts to detect thrombocytopenia that may be heralding HIT. Methods : The CATCH registry is a prospective registry of inpatients enrolled between March 2003 and April 2004 at over 50 US hospitals in 3 strata: [1] receiving > 96 hours of unfractionated heparin (UFH) or low molecular weight heparin (LMWH), [2] developing thrombocytopenia (platelets >50% reduction from baseline or <150,000/mm3) in the cardiac care unit and [3] patients on whom HIT tests were ordered. Here we present the data of the prolonged heparin stratum. Results : 1,121 and 861 patients received UFH and LMWH, respectively, for > 96 hours. A platelet count decrease of > 50 % from baseline was seen more frequently in patients on UFH than in patients on LMWH (10.7% and 7.9 %, respectively; p = 0.03). The parameters that predicted development of thrombocytopenia in the UHF group were length of heparin therapy, body mass index, and admission to a cardiac service; the only parameter predicting thrombocytopenia in the LMWH group was length of LMWH treatment. Of the patients with decreased platelet count by > 50 % from baseline (for UFH n = 120; for LMWH n = 68), this drop occurred in the UFH group at a median of 3.0 days after initiation of heparin and at a median of 4.0 days in the LMWH group. The difference in timing between the 2 groups was not statistically significant (p = 0.205). The platelet nadir was reached after a median /mean of 4.0 / 7.4 days in the UFH group, and 8.0 / 11.4 days in the LMWH group. This was statistically significantly different between the 2 groups (p-value = 0.0025). Conclusions : A platelet count decrease of > 50 % from baseline occurs frequently in inpatients treated with prolonged heparin. It occurs slightly more frequently on UFH than on LMWH. The median time to onset of thrombocytopenia (> 50 % decrease from baseline) occurs early, at 3–4 days. Daily platelet count checks in the first few days of heparin therapy may be helpful to rapidly discover thrombocytopenia that may then prompt HIT testing.


JAMA ◽  
2006 ◽  
Vol 296 (8) ◽  
pp. 935 ◽  
Author(s):  
Clive Kearon ◽  
Jeffrey S. Ginsberg ◽  
Jim A. Julian ◽  
James Douketis ◽  
Susan Solymoss ◽  
...  

2007 ◽  
Vol 14 (4) ◽  
pp. 385-392 ◽  
Author(s):  
Jawed Fareed ◽  
Walter Jeske ◽  
Daniel Fareed ◽  
Melaine Clark ◽  
Rakesh Wahi ◽  
...  

Low molecular weight heparins are replacing unfractionated heparin in a number of clinical indications because of their improved subcutaneous bioavailability and more predictable antithrombotic response. Clinical trials have demonstrated that low molecular weight heparins are at least as safe and effective as unfractionated heparin for the initial treatment of venous thromboembolism, and unfractionated heparin and warfarin for primary and secondary thromboprophylaxis. The mechanism behind the antithrombotic action of low molecular weight heparins is not fully understood but is likely to involve inhibition of coagulation factors Xa and IIa (thrombin), release of tissue-factor-pathway inhibitor, and inhibition of thrombin activatable fibrinolytic inhibitor. Different low molecular weight heparins have been shown to have various effects on coagulation parameters. Seven low molecular weight heparins are currently marketed worldwide, each demonstrated distinct chemical entities with unique pharmacokinetic and pharmacodynamic profiles. Each low molecular weight heparin is approved for specific indications based on the available efficacy and safety data for that product. The relative efficacy and safety of the low molecular weight heparins are unclear because there have been very few direct comparisons in randomized clinical trials. While recommending low molecular weight heparins for the prevention and treatment of venous thromboembolism, clinical guidelines have not specified individual agents. National and international organizations recognize that low molecular weight heparins are distinct entities and that they should not be used interchangeably in clinical practice. Each low molecular weight heparin should be used at the recommended dose when efficacy and safety data exist for the condition being treated. When these data are not available, the dosing and administration of low molecular weight heparins must be adapted from existing data and recommendations.


Sign in / Sign up

Export Citation Format

Share Document