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The aim of the study was to examine various haemostasis values to identify the most relevant biological indicators for detecting significant haemorrhage, to determine the effectiveness of fresh frozen plasma (FFP) transfusion. Our findings suggest that a low prothrombin time, elevated Von Willebrand Antigen, increased plasma fibrinogen, and reduced Ca2 + levels are associated with challenges in achieving proper haemostasis. However, measurements of factors II, V, VII, VIII, IX, X, XI, XIII, protein C, and protein S do not appear to be linked to difficulties in achieving adequate haemostasis. Additionally, the administration of FFP appears to impact factors V, VII, X, and II. Trial registration EudraCT number: 2019-002898-64. [ABSTRACT FROM AUTHOR]

Introduction: The STA R Max® 2 is a new coagulation analyser developed by Diagnostica Stago, able to perform clotting, chromogenic and immuno‐turbidimetric tests. A pre‐analytical module build into the cap‐piercing needle performs the sample integrity verification (sample tube filling and measurement of haemolysis, icterus, lipaemia). The STA R Max® 2 analyser incorporates an accreditation program tools to assist technical validation of the analyser. We assessed the analytical performance of the STA R Max® 2. Materials and methods: The following tests were assessed: prothrombin time, activated partial thromboplastin time, thrombin time, fibrinogen, factor V (FV), antithrombin (AT), D‐dimers (DDI) and von Willebrand factor antigen. The assay precisions were assessed using fresh plasma samples or internal quality controls. An inter‐analyser comparison was performed with a STA‐R Evolution® analyser or, for the FV, with a BCS® XP System. Haemolysis and icterus detection were also verified. Results: For the intra‐assay precision, the coefficients of variation (CV%) were all less than 5% and for DDI, the standard deviation (SD) was less than 0.1. For the inter‐assay study, all CV% were less than 5%, with the exception of FV and AT (FV: 6.68% and 5.27%; AT: 7% and 12.14% for normal and pathological values, respectively). SD was less than 0.1 for DDI. The inter‐analyser comparison demonstrated good results. Haemolysis and icterus were detected correctly for all our assessed samples. Conclusion: According to our methods validation's recommendations, the results demonstrated a good technical and analytical performance of the STA R Max® 2 analysers for the tests assessed. [ABSTRACT FROM AUTHOR]

Raloxifene (RLX), a selective oestrogen receptor modulator, has oestrogen-agonist effects on bone, lipoproteins, and homocysteine and oestrogen-antagonist activity in the breast and uterus, positioning it as a potential drug for long-term prevention of coronary heart disease in postmenopausal women. To further evaluate its influence on cardiovascular risk factors, we studied the effects of 60 mg/day RLX on serum lipid levels, inflammatory (high-sensitivity C-reactive protein, and coagulation (fibrinogen) markers, monocytes, and fibrinolysis in 15 healthy postmenopausal women. Markers were measured at baseline, after 1 month without treatment, and after 3 months of treatment. Fibrinolysis was evaluated using the euglobulin clot lysis time (ECLT) determined with a new semiautomatic optical method. Monocyte phenotype was determined by measurement of the expression of the antigens CD14, HLA-DR, and CD62-L using flow cytometry. After 3 months of RLX treatment, we observed a decrease in total cholesterol (p = 0.002), in low-density lipoprotein cholesterol (p <0.001), and in lipoprotein A (p = 0.01). Fibrinogen (p = 0.002) decreased significantly, and high-sensitivity C-reactive protein had a tendency to decrease, but this did not reach statistical significance (p = 0.06). RLX treatment had no effect on ECLT (p = 0.223) or on white blood cell, lymphocyte, and total monocyte counts (p = 0.313). Monocyte expression of HLA-DR, CD14, and CD62-L was not modified by the treatment. In conclusion, we confirm that RLX has beneficial short-term effects on levels of lipids and inflammatory markers, with no effect on fibrinolysis or monocyte phenotype. Le raloxifène (RLX), un modulateur sélectif du récepteur des œstrogènes, reproduit les effets agonistes des œstrogènes sur l’os, les lipoprotéines et l’homocystéine, et l’activité antagoniste des œstrogènes dans le sein et l’utérus, ce qui le positionne comme médicament potentiel de prévention de la coronaropathie à long terme chez les femmes postménopausées. Pour évaluer son influence sur les facteurs de risques cardiovasculaires, nous avons examiné les effets de 60 mg/jour de RLX sur les taux de lipides sériques, les marqueurs d’inflammation (protéine C-réactive à haute sensibilité) et de coagulation (fibrinogène), les monocytes et la fibrinolyse chez 15 femmes postménopausées en santé. Nous avons mesuré les marqueurs au début, après 1 mois sans traitement et après 3 mois de traitement. Nous avons évalué la fibrinolyse en utilisant le temps de lyse des euglobulines (TLE), déterminé par une nouvelle méthode optique semiautomatique. Nous avons déterminé le phénotype des monocytes en mesurant l’expression des antigènes CD14, HDLA-DR et CD62-L au moyen de la méthode de cytométrie en flux. Après 3 mois de traitement au RLX, nous avons observé une diminution du taux de cholestérol total (p = 0,002), des lipoprotéines de faible densité cholestérol (p < 0,001) et des lipoprotéines A (p = 0,01). Le taux de fibrinogène (p = 0,002) a diminué de manière significative et celui de la protéine C-réactive à haute sensibilité a eu tendance à diminuer, mais cette diminution n’a pas atteint une signification statistique (p = 0,006). Le traitement au RLX n’a pas eu d’effet sur le TLC (p = 0,223) ni sur les numérations leucocytaires, lymphocytaires ou monocytaires totales (p = 0,313). Le traitement n’a pas modifié l’expression monocytaire de HLA-DR, CD14 et CD62-L. Ainsi, nous confirmons que le RLX a des effets bénéfiques à court terme sur les taux des lipides et des marqueurs de l’inflammation, et qu’il n’a aucun effet sur la fibrinolyse ou le phénotype monocytaire. [ABSTRACT FROM AUTHOR]

Background: Recent reports have identified the apnoea and hypopnoea index (AHI) as an additional independent risk factor for cardiovascular morbidity and mortality. However, several studies reported contradictory results about the association between the serum C-reactive protein (CRP) level and the severity of apnoea. Objective: The purpose of this work is to study this association in patients referred to the sleep laboratory for clinical suspicion of sleep apnoea and presenting a wide range of AHI. Methods: Forty-nine consecutive patients were included in the study. The SigmaStat® software package (Jandle Scientific) was used. Multilinear regression analysis was tested using a stepwise backward selection of the explicative variables. The clinical characteristics (diabetes, hypertension, smoking habits, gender) were treated as dichotomous variables, while all other data (age, BMI, lipids, white blood cells) were continuous ones; high-sensitivity (hs)-CRP was the dependent variable. Results: In univariate analysis, AHI was correlated to hs-CRP: R = 0.43, p = 0.002. In multivariate analyses, we found an independent association between the AHI, adjusted for classical cardiovascular risk factors, and hs-CRP. Conclusion: In a sample of 49 patients, referred to the sleep laboratory for suspicion of sleep apnoea in routine practice, we observed an independent association between the AHI and hs-CRP. Copyright © 2006 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background-: Endothelial cell dysfunction may be implicated in the development of multiple organ failure (MOF) by a number of mechanisms. Among these, altered fibrinolysis promotes fibrin deposition, which may create microvascular alterations during inflammation. Elevated concentrations of C-reactive protein (CRP), especially when these persist over time, are correlated with an increased risk of MOF and death. CRP may inhibit fibrinolysis by inducing plasminogen activator inhibitor-1 (PAI-1) release from human aortic endothelial cells. Moreover, the administration of recombinant CRP in volunteers may increase circulating PAI-1 levels. In this study, we tested the hypothesis that CRP is associated with hypofibrinolysis in intensive care patients with and without sepsis. Methods-: We studied the association of inflammation and abnormal fibrinolysis in intensive care unit (ICU) patients with (n = 11) and without (n = 21) sepsis. The inflammatory response was assessed by serum concentration of C-reactive protein (CRP), a marker of the acute phase reaction, which increase rapidly in the inflammatory response, and the plasma fibrinolytic capacity was evaluated by the Euglobulin Clot Lysis Time (ECLT), determined by a new semi-automatic method. Results-: ECLT was significantly higher in septic than non-septic patients (1104 ± 439 vs 665 ± 275 min; p = 0.002) and was significantly correlated with CRP concentration (R2 = 0.45; p < 0.001). In a multivariate analysis, CRP was the strongest predictor of ECLT (R2 = 0.51, F = 25.6, p < 0.001). [ABSTRACT FROM AUTHOR]

Venous thromboembolism (VTE), including deep vein thrombosis and pulmonary embolism, is an important complication in patients hospitalized in intensive care units (ICU). Thromboprophylaxis is mainly performed with Low Molecular Weight Heparin (LMWH) and, in some specific patients, with Unfractionated Heparin (UFH). These intensive units are an environment where individual patient variability is extreme and where traditional antithrombotic protocols are frequently ineffective. This was known for a long time, but the hospitalization of many patients with COVID-19 inflammatory storms suddenly highlighted this knowledge. It is therefore reasonable to propose variable antithrombotic prevention protocols based initially on a series of individual criteria (weight, BMI, and thrombotic risks). Secondly, they should be adjusted by the monitoring of anticoagulant activity, preferably by measuring the anti-Xa activity. However, we still face unresolved questions, such as once- or twice-daily LMWH injections, monitoring at the peak and/or trough, and poorly defined therapeutic targets. Equally surprisingly, we observed a lack of standardization of the anti-Xa activity kits. [ABSTRACT FROM AUTHOR]