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Ross I Baker

Publications and source records attributed to Ross I Baker.

8 recordsLinked to original sources

Randomized comparison of low molecular weight heparin and coumarin derivatives on the survival of patients with cancer and venous thromboembolism.

PURPOSE: Experimental studies and indirect clinical evidence suggest that low molecular weight heparins may have antineoplastic effects. We investigated the influence of a low molecular weight heparin dalteparin on the survival of patients with active cancer and acute venous thromboembolism. PATIENTS AND METHODS: Survival data were examined in a posthoc analysis in patients with solid tumors and venous thromboembolism who were randomly assigned to dalteparin or a coumarin derivative for 6 months in a multicenter, open-label, randomized, controlled trial. All-cause mortality at 12 months was compared between treatment groups in patients with and without metastatic malignancy. The effect of dalteparin on survival was compared between the two patient subgroups. RESULTS: During the 12-month follow-up period, 356 of 602 patients with solid tumors and acute venous thromboembolism died. Among patients without metastatic disease, the probability of death at 12 months was 20% in the dalteparin group, as compared with 36% in the oral anticoagulant group (hazard ratio, 0.50; 95% CI, 0.27 to 0.95; P = .03). In patients with metastatic cancer, no difference in mortality between the treatment groups was observed (72% and 69%, respectively; hazard ratio, 1.1; 95% CI, 0.87 to 1.4; P = .46). The observed effects of dalteparin on survival were statistically significantly different between patients with and without metastatic disease (P = .02). CONCLUSION: The use of dalteparin relative to coumarin derivatives was associated with improved survival in patients with solid tumors who did not have metastatic disease at the time of an acute venous thromboembolic event. Additional studies are warranted to investigate these findings.

Acute Disease↗

Once-daily enoxaparin in the outpatient setting versus unfractionated heparin in hospital for the treatment of symptomatic deep-vein thrombosis.

BACKGROUND: Once- and twice-daily low-molecular-weight heparin administered in hospital have been shown to be effective and safe for treating deep-vein thrombosis. The aim of this study was to compare the efficacy and safety of deep-vein thrombosis treatment using once-daily subcutaneous enoxaparin in the outpatient setting with intravenous unfractionated heparin in hospital. METHODS: This randomized, parallel-group, open-label study was conducted in 18 centers in 4 countries. In total, 298 patients with symptomatic deep-vein thrombosis who were eligible for home treatment were randomized to treatment with enoxaparin in the outpatient setting (1.5 mg/kg subcutaneously once-daily) or unfractionated heparin in hospital (5000 IU bolus and 1250 IU/hour intravenous infusion) for > or =5 days. Clinical endpoints were assessed during a 6-month follow-up period. RESULTS: Among all patients treated with enoxaparin, there was a trend towards fewer recurrent deep-vein thromboses (1.3% vs. 5.4%; p = 0.060) and pulmonary emboli (1.3% vs. 4.1%; p = 0.17) compared with patients treated with unfractionated heparin. When considering a post-hoc combined endpoint of deep-vein thrombosis and pulmonary embolism, significantly fewer events occurred in the enoxaparin group than in the unfractionated-heparin group (2.7% vs. 8.8%; p = 0.026). The incidences of bleeding events and adverse events in the enoxaparin and unfractionated-heparin groups were similar. CONCLUSIONS: Once-daily subcutaneous enoxaparin in the outpatient setting is at least as effective and as well tolerated as in-hospital intravenous unfractionated heparin for treatment of deep-vein thrombosis.

Adult↗

Warfarin reversal: consensus guidelines, on behalf of the Australasian Society of Thrombosis and Haemostasis.

For most warfarin indications, the target maintenance international normalised ratio (INR) is 2-3. Risk factors for bleeding complications with warfarin use include age, history of past bleeding and specific comorbid conditions. To reverse the effects of warfarin, vitamin K(1) can be given. Immediate reversal is achieved with a prothrombin complex concentrate (PCC) and fresh frozen plasma (FFP). Vitamin K(1) is essential for sustaining the reversal achieved by PCC and FFP. When oral vitamin K(1) is used for warfarin reversal, the injectable formulation of vitamin K(1) is preferable to tablets because of its flexible dosing; this formulation can be given orally or injected. To temporarily reverse the effect of warfarin when there is a need to continue warfarin therapy, vitamin K(1) should be given in a dose that will quickly lower the INR to a safe, but not subtherapeutic, range and will not cause resistance once warfarin is reinstated. Prothrombinex-HT is the only PCC approved in Australia and New Zealand for warfarin reversal. It contains factors II, IX and X, and low levels of factor VII. FFP should be added to Prothrombinex-HT as a source of factor VII when used for warfarin reversal. Simple dental or dermatological procedures may not require interruption to warfarin therapy. If necessary, warfarin therapy can be withheld 5 days before elective surgery, when the INR usually falls to below 1.5 and surgery can be conducted safely. Bridging anticoagulation therapy for patients at high risk for thromboembolism should be undertaken in consultation with the relevant experts.

Administration, Oral↗

Endothelial and platelet activation in acute ischemic stroke and its etiological subtypes.

BACKGROUND AND PURPOSE: Activation of endothelial cells and platelets is an important mediator of atherothrombosis. Markers of endothelial cell and platelet activation such as soluble adhesion molecules can be measured in plasma. We hypothesized that patients with acute ischemic stroke would have increased blood concentrations of soluble E-selectin and von Willebrand factor (vWF), primarily reflecting activation of endothelial cells, and increased concentrations of soluble P-selectin and platelet-derived microvesicles (PDM), primarily reflecting activation of platelets, compared with healthy controls. We also hypothesized that these markers would be differentially elevated in ischemic stroke caused by large- and small-artery atherothrombosis compared with cardiogenic embolism. METHODS: We conducted a case-control study of 200 hospital-referred cases of first-ever ischemic stroke and 205 randomly selected community controls stratified by age, sex, and postal code. Using established criteria, we classified cases of stroke by etiological subtype in a blinded fashion. The prevalence of vascular risk factors and blood concentrations of E-selectin, P-selectin, vWF antigen, and PDM were determined in stroke cases within 7 days and at 3 to 6 months after stroke and in controls. RESULTS: Mean blood concentrations of soluble E-selectin, P-selectin, and PDM within 7 days of stroke onset were all significantly higher in cases compared with controls. At 3 to 6 months after stroke, the mean blood concentrations of E-selectin and P-selectin fell significantly below that of controls, and PDM concentrations remained elevated. There was a strong, graded, and independent (of age, sex, and vascular risk factors) association between increasing blood concentrations of E-selectin during the acute phase and all etiological subtypes of ischemic stroke, particularly ischemic stroke caused by large-artery atherothrombosis. There was also a significant, graded, and independent association between increasing blood concentrations of vWF during the acute phase and ischemic stroke caused by large-artery atherothrombosis. CONCLUSIONS: We have demonstrated significant associations between acute elevation of blood markers of endothelial cell and platelet activation and ischemic stroke and between acute elevation of blood markers of endothelial cell activation and ischemic stroke caused by large-artery atherothrombosis. Persistent elevated blood concentrations of PDM may be a marker of increased risk of ischemic stroke.

Acute Disease↗

Low-molecular-weight heparin versus a coumarin for the prevention of recurrent venous thromboembolism in patients with cancer.

BACKGROUND: Patients with cancer have a substantial risk of recurrent thrombosis despite the use of oral anticoagulant therapy. We compared the efficacy of a low-molecular-weight heparin with that of an oral anticoagulant agent in preventing recurrent thrombosis in patients with cancer. METHODS: Patients with cancer who had acute, symptomatic proximal deep-vein thrombosis, pulmonary embolism, or both were randomly assigned to receive low-molecular-weight heparin (dalteparin) at a dose of 200 IU per kilogram of body weight subcutaneously once daily for five to seven days and a coumarin derivative for six months (target international normalized ratio, 2.5) or dalteparin alone for six months (200 IU per kilogram once daily for one month, followed by a daily dose of approximately 150 IU per kilogram for five months). RESULTS: During the six-month study period, 27 of 336 patients in the dalteparin group had recurrent venous thromboembolism, as compared with 53 of 336 patients in the oral-anticoagulant group (hazard ratio, 0.48; P=0.002). The probability of recurrent thromboembolism at six months was 17 percent in the oral-anticoagulant group and 9 percent in the dalteparin group. No significant difference between the dalteparin group and the oral-anticoagulant group was detected in the rate of major bleeding (6 percent and 4 percent, respectively) or any bleeding (14 percent and 19 percent, respectively). The mortality rate at six months was 39 percent in the dalteparin group and 41 percent in the oral-anticoagulant group. CONCLUSIONS: In patients with cancer and acute venous thromboembolism, dalteparin was more effective than an oral anticoagulant in reducing the risk of recurrent thromboembolism without increasing the risk of bleeding.

Acenocoumarol↗

Venous thromboembolism in travellers: can we identify those at risk?

To assess the prevalence of clinical and laboratory risk factors in patients who develop venous thromboembolism following travel. The design was a case series of 58 consecutive patients presenting with venous thromboembolism within 30 days of travel. The setting was a major metropolitan teaching hospital and an affiliated private practice. The main outcome measures were prevalence of clinical and laboratory risk factors for venous thromboembolism, time to presentation, mode and duration of travel. Forty-eight [83%; 95% confidence interval (CI), 71-91%] of 58 patients developed venous thromboembolism following air travel. Thirty-four (59%; 95% CI, 45-71%) patients had travelled for more than 8 h and most patients were diagnosed with venous thromboembolism within 1 week of completing their journey. Pulmonary embolism occurred in 24 patients (41%; 95% CI, 29-55%), proximal deep vein thrombosis in 23 patients (40%; 95% CI, 27-53%), calf vein thrombosis in four patients (7%; 95% CI, 2-17%), and superficial thrombophlebitis in seven patients (12%; 95% CI, 5-23%). At least one clinical or laboratory risk factor (other than travel) was found in 49 patients (84%; 95% CI, 73-93%) and two or more risk factors were found in 30 patients (52%; 95% CI, 38-65%). The most common risk factors were oestrogens (24%; 95% CI, 14-37%), a past history of thrombosis (24%: 95% CI, 14-37%), and factor V Leiden (24%: 95% CI, 14-37%). These retrospective uncontrolled data suggest that at least one clinical or laboratory risk factor is present prior to travel in more than 80% of patients who develop venous thromboembolism within 30 days of travel. In most cases these risk factors can be identified by the clinical history alone, without recourse to laboratory testing. Whether patients with known risk factors for venous thromboembolism prior to travel should be targeted with specific thromboprophylaxis requires randomized evaluation.

Adolescent↗

Haematology.

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Australia↗