| 1. |
- Bagge, August, et al.
(författare)
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High-dose omega-3 fatty acids have no effect on platelet aggregation or coagulation measured with static and flow-based aggregation instruments and Sonoclot; an observational study in healthy volunteers
- 2018
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Ingår i: Scandinavian Journal of Clinical & Laboratory Investigation. - : Informa UK Limited. - 1502-7686 .- 0036-5513. ; 78:7-8, s. 539-545
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Tidskriftsartikel (refereegranskat)abstract
- The effect of omega-3 fatty acids on platelet aggregation and coagulation is highly unclear. Studies both support and refute the impacts of omega-3 fatty acids on prolonged bleeding time and platelet inhibition as well as its purported positive effects on cardiovascular disease. In a previous pilot study we suggested an inhibition of platelet aggregation measured with multiple electrode aggregometry. Following on that, the aim of the present study was to investigate the effects of supplementary high doses of omega-3 fatty acids on platelet aggregation and coagulation in a sample-size calculated number of healthy volunteers using Sonoclot, multiple electrode aggregometry, and flow-based Cellix instruments after 10 days of omega-3 fatty acid intake. Twelve healthy human volunteers ingested 2520 mg of supplementary omega-3 fatty acids per day for 10 days. Venous blood was sampled and platelet aggregation and coagulation were measured before and after the treatment period. The viscoelastic test instrument Sonoclot, multiple electrode aggregometry, and flow-based Cellix instruments with collagen-coated channels were used to evaluate platelet aggregation and coagulation. There were no differences in any of the measured variables after the treatment period as compared to before. In this well-powered study on healthy volunteers, no effects of high doses of omega-3 fatty acids after 10 days of intake could be demonstrated, either on coagulation or platelet function. Further studies are needed to clarify whether omega-3 fatty acids have a role in the regulation of the putative complex processes in vivo.
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| 2. |
- Dahlberg, Sofia, et al.
(författare)
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Detection of subclinical vitamin K deficiency in neurosurgery with PIVKA-II
- 2017
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Ingår i: Scandinavian Journal of Clinical and Laboratory Investigation. - : Informa UK Limited. - 0036-5513 .- 1502-7686. ; 77:4, s. 267-274
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Tidskriftsartikel (refereegranskat)abstract
- Vitamin K is known for supporting the carboxylation of hepatic coagulation proteins. Levels of proteins induced by vitamin K absence for factor II (PIVKA-II) reflect hypocarboxylated prothrombin and can be used to detect subclinical vitamin K deficiency. The aim of this study was to determine the prevalence of perioperative subclinical vitamin K deficiency among neurosurgical patients using PIVKA-II and investigate the existence of any correlation to standard coagulation assays. Also, the antitumor effects of vitamin K were reviewed. Thirty-five patients undergoing brain tumor resection were included. Blood samples were drawn preoperatively, at the end of surgery and in the morning after surgery. In addition to PIVKA-II, factor II and the Owren and Quick prothrombin times were analyzed. Seventeen of 35 patients had elevated PIVKA-II levels before surgery, which continued to be above normal range postoperatively. Median PIVKA-II and Owren prothrombin time (PT-INR) were increased on the morning day 1 postoperatively compared to before surgery, whereas Quick end-stage prothrombin time (EPT) decreased and factor II was unaffected. Postoperative complications were connected to high PIVKA-II increases. Positive correlations between PIVKA-II and factor II and body mass index (BMI) were found. In conclusion, PIVKA-II was increased in many patients preoperatively and then increased by the morning following surgery. Standard coagulation assays were largely non-pathological. Correlations were demonstrated between PIVKA-II and factor II and BMI. The effect of perioperative treatment with different vitamin K supplements should be investigated in future studies, as well as clinical trials evaluating their antitumor effects.
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| 3. |
- Jansohn, Erik, et al.
(författare)
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A pilot study on the applicability of thromboelastometry in detecting brain tumour-induced hypercoagulation
- 2017
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Ingår i: Scandinavian Journal of Clinical and Laboratory Investigation. - : Informa UK Limited. - 0036-5513 .- 1502-7686. ; 77:4, s. 289-294
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Tidskriftsartikel (refereegranskat)abstract
- Patients with intracranial tumours have an increased risk of venous thromboembolism, particularly during the first month after neurosurgery. A proposed explanation for this increased risk, are procoagulant tumour-derived substances, such as tissue factor, usually measured in peripheral blood. The aim of the present study is to investigate whether a rotational thromboelastometry (ROTEM) can measure the procoagulative activity of tumour tissue. The study included 21 patients who were undergoing a craniotomy and complete tumour resection after written consent and ethical approval were obtained. Tumour tissue was biopsied during surgery and used for in vitro spiking of patients own citrated whole blood. Blood samples with or without spiking were analyzed with ROTEM using different activating reagents. ROTEM clotting time significantly decreased (p < .001), indicating a hypercoagulative response on clot initiation that was strongest for glioma tumours. However, ROTEM clot formation time was significantly prolonged (p < .001), which was an opposite response that indicated poor initial clot propagation. ROTEM maximum lysis was increased in the tumour tissue-spiked samples (p < .001), indicating a strong fibrinolytic activity in brain tumour tissue. Tissue extracts from intracranial tumours have both procoagulant and fibrinolytic effects that are detectable with ROTEM. Glioma tumours had the strongest hypercoagulative response in our in vitro model. Larger studies are necessary to test the clinical relevance and accuracy of tumour extract spiked viscoelastic tests to predict the individual patient risk for developing a thrombotic complication.
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| 4. |
- Kander, Thomas, et al.
(författare)
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Temperature effects on haemostasis in whole blood from ticagrelor- and aspirin-treated patients with acute coronary syndrome.
- 2015
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Ingår i: Scandinavian Journal of Clinical & Laboratory Investigation. - : Informa UK Limited. - 1502-7686 .- 0036-5513. ; 75:1, s. 27-35
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Tidskriftsartikel (refereegranskat)abstract
- Background. Comatose survivors after cardiac arrest are treated with mild induced hypothermia and potent platelet- inhibiting drugs after coronary stenting. Previous studies have shown an increased incidence of stent thrombosis during clopidogrel and aspirin treatment in conjunction with induced hypothermia. The aim of this study was to investigate the in vitro effect of induced hypo- and hyperthermia on blood from patients undergoing ticagrelor- and aspirin-mediated platelet inhibition. Methods. Whole blood from 15 patients with acute coronary syndrome who were treated with ticagrelor and aspirin and from eight healthy volunteers was incubated for 1 hour at 28, 33, 37, and 39°C. Results. In blood from patients with acute coronary syndrome, the activated clotting time (Sonoclot) was prolonged in mild hypothermic (33°C) compared to normothermic (37°C) samples. Sonoclot, clotting rate and platelet function were decreased in hypothermic compared to normothermic samples. Platelet-induced activation and aggregation (Multiplate(®)) was unchanged in mild hypothermic compared to normothermic samples. In contrast, mild hypothermia supported increased platelet activation as measured with flow cytometry with up-regulation of PAC-1 and P-selectin on the platelet surface. Conclusion. In acute coronary syndrome patients treated with ticagrelor and aspirin, in vitro hypothermia to 33°C markedly increased platelet activity measured with flow cytometry, whereas viscoelastic coagulation test (Sonoclot) revealed a hypocoagulative response. Prospective clinical trials studying platelet inhibition at different temperatures and correlating changes in platelet function to bleeding or stent occlusion are needed.
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| 5. |
- Pearson, Kevin, et al.
(författare)
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Desmopressin in vitro effects on platelet function, monitored with Multiplate, ROTEM and Sonoclot.
- 2016
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Ingår i: Scandinavian Journal of Clinical and Laboratory Investigation. - : Informa UK Limited. - 1502-7686 .- 0036-5513. ; :Feb 29, s. 282-290
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Tidskriftsartikel (refereegranskat)abstract
- Background and aims The vasopressin analogue desmopressin has demonstrated efficacy in decreasing bleeding time by increasing the circulating levels of coagulation factor VIII and von Willebrand factor, but also by direct effects on platelets. Previous studies have demonstrated contrasting results regarding the effect of desmopressin on platelets in vitro. The aim of this study was to investigate the dose-response effects of in vitro desmopressin in whole blood. Our hypothesis was that desmopressin could increase platelet function in anticoagulated whole blood being stored up to 4 hours. Methods Desmopressin was administered with up to four different concentrations to venous whole blood, sampled with standard vacutainer tubes from 10 healthy volunteers after consent. Platelet function was analyzed with three different point-of-care techniques: Multiplate platelet aggregometry with adenosine diphosphate, collagen, thrombin receptor activating peptide-6, ristocetin and arachidonic acid agonists, tissue factor-activated thromboelastometry and Sonoclot glass bead viscoelastic coagulation tests at baseline and 4 hours later using different activator reagents. Results Thromboelastometry and Sonoclot did not show any significant change between baseline and 4 h later. A significant decrease in area under curve (AUC) could be seen with the Multiplate between baseline and after 4 h. Desmopressin did not improve any of these tests at baseline or during a 4 h storage and incubation period. Conclusion In vitro administered desmopressin could not increase normal platelet function or coagulation being measured with thromboelastometry and Sonoclot. Multiplate indicated decreased platelet aggregation over time, without any effect of in vitro added desmopressin.
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