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  • 1
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    Plasma Levels of Leptin and Risk of Future Incident Venous Thromboembolism
    Georg Thieme Verlag KG ; 2022
    In:  Thrombosis and Haemostasis Vol. 122, No. 04 ( 2022-04), p. 560-569
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 122, No. 04 ( 2022-04), p. 560-569
    Kurzfassung: Background Circulating levels of leptin, an adipocyte-derived hormone, are frequently elevated in obesity. Leptin has been reported to upregulate prothrombotic hemostatic factors in vitro and could potentially mediate venous thromboembolism (VTE) risk in obesity. However, whether leptin is associated with VTE remains uncertain. Objective This article investigates the association between plasma leptin and risk of incident VTE, and the potential of leptin to mediate VTE risk in obesity. Methods A population-based nested case–control study with 416 VTE cases and 848 age- and sex-matched controls was derived from the Tromsø Study. Logistic regression was used to calculate odds ratios (ORs) with 95% confidence intervals (CIs) for VTE across leptin quartiles. Analyses were performed separately in men and women using sex-specific quartile cut-offs determined in controls. Results In the age-adjusted model, the VTE risk increased across leptin quartiles, particularly in men. Compared with the lowest quartile, the ORs for VTE in the highest quartile were 1.70 (95% CI 1.04–2.79) in men and 1.36 (95% CI 0.85–2.17) in women. However, with additional adjustment for body mass index (BMI), risk estimates were markedly attenuated in men (OR 1.03, 95% CI 0.55–1.93) and women (OR 0.82, 95% CI 0.45–1.48). The ORs for VTE were increased in obese men and women (BMI ≥ 30 kg/m2) and were only marginally affected after adjustment for leptin. Conclusion Our results indicate that the apparent association between plasma leptin levels and VTE risk is confounded by BMI and that leptin is not a relevant mediator for VTE risk in obesity.
    Materialart: Online-Ressource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1055/s-0041-1732295
    Sprache: Englisch
    Verlag: Georg Thieme Verlag KG
    Publikationsdatum: 2022
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
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    Impact of a Vancomycin-Induced Shift of the Gut Microbiome in a Gram-Negative Direction on Plasma Factor VIII:C Levels: Results from a Randomized Controlled Trial
    Georg Thieme Verlag KG ; 2022
    In:  Thrombosis and Haemostasis Vol. 122, No. 04 ( 2022-04), p. 540-551
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 122, No. 04 ( 2022-04), p. 540-551
    Kurzfassung: Background Inflammation is present in several conditions associated with risk of venous thromboembolism. The gut microbiome might be a source of systemic inflammation and activation of coagulation, by translocation of lipopolysaccharides from gram-negative bacteria to the systemic circulation. Objective To investigate whether a vancomycin-induced shift of the gut microbiome in a gram-negative direction influences systemic inflammation and plasma factor (F) VIII procoagulant activity (FVIII:C). Methods and Results We performed a randomized controlled trial including 43 healthy volunteers aged 19 to 37 years. Twenty-one were randomized to 7 days of oral vancomycin intake and 22 served as controls. Feces and blood were sampled at baseline, the day after the end of intervention, and 3 weeks after intervention. Gut microbiome composition was assessed by amplicon sequencing. FVIII:C was measured using an activated partial thromboplastin time-based assay, cytokines were measured using multiplex technology, complement activation was measured using the enzyme-linked immunosorbent assay, and high-sensitivity C-reactive protein (CRP) was measured by an immunoturbidimetric assay. Vancomycin intake reduced gut microbiome diversity and increased the abundance of gram-negative bacteria. Change in FVIII:C in the intervention group was +4 IU/dL versus −6 IU/dL (p = 0.01) in the control group. A similar change was observed for log-transformed CRP (+0.21 mg/dL vs. −0.25 mg/dL, p = 0.04). The cytokines and complement activation markers remained similar in the two groups. Conclusion The found slight increases in FVIII:C and CRP levels might support the hypothesis that a vancomycin-induced gram-negative shift in the gut microbiome could induce increased systemic inflammation and thereby a procoagulant state.
    Materialart: Online-Ressource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1055/s-0041-1733906
    Sprache: Englisch
    Verlag: Georg Thieme Verlag KG
    Publikationsdatum: 2022
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
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    Increased circulating resistin is associated with insulin resistance, oxidative stress and platelet activation in type 2 diabetes mellitus
    Georg Thieme Verlag KG ; 2016
    In:  Thrombosis and Haemostasis Vol. 116, No. 12 ( 2016-11), p. 1089-1099
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 116, No. 12 ( 2016-11), p. 1089-1099
    Kurzfassung: Resistin is an adipokine that promotes inflammation and insulin resistance by targeting several cells including platelets. We hypothesised that in type 2 diabetes (T2DM), resistin may foster in vivo oxidative stress, thromboxane-dependent platelet activation and platelet-derived inflammatory proteins release, key determinants of atherothrombosis. A cross-sectional comparison of circulating resistin, sCD40L, as a marker of platelet-mediated inflammation, asymmetric dimethylarginine (ADMA), endothelial dysfunction marker, Dickkopf (DKK)-1, reflecting the inflammatory interaction between platelets and endothelial cells, and urinary 8-iso-PGF2α and 11-dehydro-TxB2, reflecting in vivo lipid peroxidation and platelet activation, respectively, was performed between 79 T2DM patients and 30 healthy subjects. Furthermore, we investigated the effects of the α-glucosidase inhibitor acarbose and the PPARγ agonist rosiglitazone, targeting hyperglycaemia or insulin resistance, versus placebo, in 28 and 18 T2DM subjects, respectively. Age- and gender-adjusted serum resistin levels were significantly higher in patients than in controls. HOMA (β=0.266, p=0.017) and 11-dehydro-TXB2 (β=0.354, p=0.002) independently predicted resistin levels. A 20-week treatment with acarbose was associated with significant reductions (p=0.001) in serum resistin, DKK-1, urinary 11-dehydro-TXB2 and 8-iso-PGF2α with direct correlations between the change in serum resistin and in other variables. A 24-week rosiglitazone treatment on top of metformin was associated with significant decreases in resistin, DKK-1, 11-dehydro-TXB2 and 8-iso-PGF2α, in parallel with HOMA decrease. In conclusion, resistin, antagonising insulin action in part through PPARγ activation, may favour insulin resistance and enhance oxidative stress, endothelial dysfunction and platelet activation. The adipokine-platelet interactions may be involved in platelet insulin resistance and their consequent pro-aggregatory phenotype in this setting.
    Materialart: Online-Ressource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1160/TH16-06-0471
    Sprache: Deutsch
    Verlag: Georg Thieme Verlag KG
    Publikationsdatum: 2016
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
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    Chemokines in cardiovascular risk prediction
    Georg Thieme Verlag KG ; 2007
    In:  Thrombosis and Haemostasis Vol. 97, No. 05 ( 2007), p. 748-754
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 97, No. 05 ( 2007), p. 748-754
    Kurzfassung: In consideration of the important role of inflammation in plaque progression and stability, recent work has focused on whether plasma markers of inflammation can non-invasively diagnose and predict coronary artery disease (CAD) and other forms of atherosclerotic disorders. Although several studies support an important pathogenic role of chemokines in atherogenesis and plaque destabilization, potentially representing attractive therapeutic targets in atherosclerotic disorders,this does not necessarily mean that chemokines are suitable parameters for risk prediction. In fact, the ability to reflect up-stream inflammatory activity, stable levels in individuals and high stability of the actual protein (e.g. long half-life and negligible circadian variation), are additional important criteria for an ideal biomarker in cardiovascular disease. Although plasma/serum levels of certain chemokines (e.g. interleukin 8 and monocyte chemoattractant protein- 1) have been shown to be predictive for future cardiac events in some studies, independent of traditional cardiovascular risk factors and C-reactive protein,and although certain gene polymorphisms of chemokines/chemokine receptors (e.g. fractalkine receptor) have been shown to be predictive of future atherosclerotic disease, further prospective studies, including a larger number patients,are needed to make any firm conclusion. While the demonstrations of an association between chemokines and CAD are a necessary first step, such studies do not establish the full clinical utility of a biomarker, which is a more demanding process that requires validation in multiple cohorts, and clear demonstration of incremental prognostic value over traditional risk models. If successful, such new biomarker will be a useful indicator for better risk assessment,diagnosis,and prognosis, as well as monitoring pharmacological treatments for atherosclerosis.
    Materialart: Online-Ressource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1160/TH07-01-0029
    Sprache: Englisch
    Verlag: Georg Thieme Verlag KG
    Publikationsdatum: 2007
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
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    Increased Concentrations of Soluble CD40 Ligand, RANTES and GRO-α in Preeclampsia – Possible Role of Platelet Activation
    Georg Thieme Verlag KG ; 2001
    In:  Thrombosis and Haemostasis Vol. 86, No. 11 ( 2001), p. 1272-1276
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 86, No. 11 ( 2001), p. 1272-1276
    Kurzfassung: Activated platelets may release inflammatory mediators that activate leukocytes and trigger inflammatory reactions in endothelial cells. We examined the concentrations of soluble CD40 ligand (sCD40L) and the chemokines RANTES and GRO-α in platelet-free plasma (PFP), and unstimulated and SFLLRN-stimulated platelet-rich plasma (PRP), as well as in platelet pellets before stimulation using enzyme immunoassays. Nineteen women with normal and twenty-one with preeclamptic pregnancies were studied, and several differences between these two groups of pregnancies were revealed (1). Women with preeclampsia had significantly increased concentrations of sCD40L and GRO-α in PFP (2). Platelets from these patients spontaneously released larger quantities of CD40L and RANTES ex vivo (3). When further activated ex vivo by SFLLRN, platelets from preeclamptic women released lower amounts per platelet of CD40L, RANTES and GRO-α (4). The platelet pellets in preeclamptic women contained decreased amounts of CD40L, RANTES and GRO-α per platelet. Our findings suggest enhanced platelet activation in vivo during preeclampsia resulting in increased release of inflammatory mediators, possibly contributing to inflammation, leukocyte activation and endothelial dysfunction in this disorder.
    Materialart: Online-Ressource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1055/s-0037-1616061
    Sprache: Englisch
    Verlag: Georg Thieme Verlag KG
    Publikationsdatum: 2001
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
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    The Effect of Protease-Activated Receptor-1 (PAR-1) Inhibition on Endothelial-Related Biomarkers in Patients with Coronary Artery Disease
    Georg Thieme Verlag KG ; 2023
    In:  Thrombosis and Haemostasis Vol. 123, No. 05 ( 2023-05), p. 510-521
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 123, No. 05 ( 2023-05), p. 510-521
    Kurzfassung: Background Vorapaxar has been shown to reduce cardiovascular mortality in post-myocardial infarction (MI) patients. Pharmacodynamic biomarker research related to protease-activated receptor-1 (PAR-1) inhibition with vorapaxar in humans has short follow-up (FU) duration and is mainly focused on platelets rather than endothelial cells. Aim This article assesses systemic changes in endothelial-related biomarkers during vorapaxar treatment compared with placebo at 30 days' FU and beyond, in patients with coronary heart disease. Methods Local substudy patients in Norway were included consecutively from two randomized controlled trials; post-MI subjects from TRA2P-TIMI 50 and non-ST-segment elevation MI (NSTEMI) patients from TRACER. Aliquots of citrated blood were stored at –80°C. Angiopoietin-2, angiopoietin-like 4, vascular endothelial growth factor, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, von Willebrand factor, thrombomodulin, and plasminogen activator inhibitor-1 and -2 were measured at 1-month FU and at study completion (median 2.3 years for pooled patients). Results A total of 265 consecutive patients (age median 62.0, males 83%) were included. Biomarkers were available at both FUs in 221 subjects. In the total population, angiopoietin-2 increased in patients on vorapaxar as compared with placebo at 1-month FU (p = 0.034). Angiopoietin-like 4 increased (p = 0.028) and plasminogen activator inhibitor-2 decreased (p = 0.025) in favor of vorapaxar at final FU. In post-MI subjects, a short-term increase in E-selectin favoring vorapaxar was observed, p = 0.029. Also, a short-term increase in von Willebrand factor (p = 0.032) favoring vorapaxar was noted in NSTEMI patients. Conclusion Significant endothelial biomarker changes during PAR-1 inhibition were observed in post-MI and NSTEMI patients.
    Materialart: Online-Ressource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1055/s-0042-1760256
    Sprache: Englisch
    Verlag: Georg Thieme Verlag KG
    Publikationsdatum: 2023
    Standort Signatur Einschränkungen Verfügbarkeit
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