Biomedical subjects

Claire Bal Dit Sollier

Publications and source records attributed to Claire Bal Dit Sollier.

4 recordsLinked to original sources

PubMed2006

Interaction between paracetamol and warfarin in patients: a double-blind, placebo-controlled, randomized study.

BACKGROUND AND OBJECTIVES: Paracetamol (acetaminophen) has occasionally been reported to interact with warfarin. The primary end-point of this study was to investigate whether paracetamol initiation potentiates the anticoagulant effect of warfarin and the mechanism of the interaction. DESIGN AND METHODS: In a double-blind placebo-controlled, randomized, cross-over study, 20 patients on stable oral anticoagulant therapy with warfarin for at least 1 month were randomized to receive placebo or paracetamol 1g four times daily for 14 days. International Normalized Ratio (INR) and clotting factors activities were measured before the first administration and then on days 2, 4, 7, 9, 11,14. RESULTS: Mean INR rose rapidly after the start of paracetamol and was significantly increased within one week of paracetamol intake compared to placebo, p=0.0002. The INR values reached a mean maximum of 3.45+/-0.78 with paracetamol versus 2.66+/-0.73 with placebo (p=0.03), corresponding to a maximum increase from baseline of 1.20+/-0.62 with paracetamol versus 0.37+/-0.48 with placebo (p<0.001). Together with the rise in INR on paracetamol treatment there were significant reductions in the vitamin K-dependent clotting factors II, VII, IX and X. INTERPRETATION AND CONCLUSIONS: The most plausible hypothesis to explain the in vivo interaction is that paracetamol (or its metabolites) interfere with enzymes involved in vitamin K-dependent coagulation factor synthesis. Paracetamol at 4 g daily (a dose higher than that used in clinical practice) potentiates the anticoagulant response produced by warfarin. Clinicians should be aware of this clinically significant and underestimated interaction.

Acetaminophen↗

PubMed2004

Relationship between C reactive protein and pulse pressure is not mediated by atherosclerosis or aortic stiffness.

BACKGROUND: Pulse pressure (PP), C reactive protein (CRP) and soluble intercellular adhesion molecule-1 (sICAM-1) levels have been associated with cardiovascular prognosis. Interestingly, previous reports have shown that PP was associated both with CRP and sICAM-1. The mechanisms underlying these associations remain unknown. On the one hand, it has been shown that PP influences, via endothelial function, the expression of various molecules, which in turn may generate inflammation. On the other hand, inflammation-induced changes in the arterial wall, modifying the PP, may be the confounding factor of these relationships. The aim of the present study was to investigate the role played by the arterial structure and the aortic stiffness on these relationships. METHODS: In a cross-sectional population sample of 891 healthy subjects, carotid-femoral pulse wave velocity and blood pressure were measured in the supine position. The common carotid intima-media thickness and the presence of plaques were assessed by ultrasonography. CRP and sICAM-1 levels were measured by an immunonephelemetric method and an immunoenzymatic method, respectively. RESULTS: A positive relationship was found between PP and CRP (P < 0.001). This relationship remained after adjustment for classical cardiovascular risk factors, and successively for mean blood pressure, intima-media thickness, presence of plaques and pulse wave velocity (P < 0.05). No significant association was observed between PP and sICAM-1. CONCLUSIONS: The results of this study demonstrate that changes in arterial structure and in arterial stiffness are not confounding factors in the relationship between PP and CRP.

Adult↗

PubMed2003

Soluble CD14 and aortic stiffness in a population-based study.

OBJECTIVE: Soluble CD14 (sCD14), an effective mediator for the activation of monocytes by bacterial endotoxin is involved in the release of substances able to modify the characteristics of the arterial wall. The aim of this study was to investigate, in humans, the relationship of sCD14 with aortic stiffness and to analyse the influence of arterial structure and endothelial function on this relationship. DESIGN: Cross-sectional population-based study. PARTICIPANTS: One thousand and fifteen subjects randomly selected from the polling lists, were recruited by the Toulouse MONICA centre between 1995 and 1997. METHODS: Carotid-femoral pulse wave velocity (PWV) and blood pressure (BP) were measured in the supine position. Common carotid intima-media thickness (IMT) and the presence of plaques were assessed by ultrasonography. sCD14 was measured using an immunoenzymatic method. RESULTS: The results concern the 891 subjects with complete data for all the variables. In the bivariate analyses, PWV (P < 0.001), systolic BP (P < 0.05), pulse pressure (PP) (P < 0.01), IMT (P < 0.001), the number of plaques (P < 0.05) and von Willebrand factor activity (vWFa) (P < 0.001) were positively associated with sCD14, whereas no significant relationship was observed between sCD14 and diastolic BP. After adjustment for age and sex, no significant relationship remained between IMT, the number of plaques, SBP, PP and sCD14. A significant and positive relationship was observed between sCD14 and PWV (trend P < 0.05) after adjustment for numerous confounders. CONCLUSION: This population-based study yields first evidence that sCD14 is associated with aortic stiffness independently of age, BP and atherosclerosis in humans.

Adult↗

PubMed2002

Dissociation between fibrinogen and fibrin interaction with platelets in patients with different subtypes of Glanzmann's thrombasthenia: studies in an ex vivo perfusion chamber model.

To explore the possible role of a residual or variant alphaIIbbeta3 integrin (alphaIIbbeta3) in thrombogenesis, we used a new ex vivo perfusion chamber model to examine blood from patients with different subtypes of Glanzmann's thrombasthenia (GT). Non-anticoagulated blood was perfused through capillaries coated with type III collagen for 4.5 min (shear rate: 1600/s). Platelet deposition was quantified as platelet adhesion and mean thrombus size volume; fibrin and von Willebrand Factor (VWF) were specifically revealed by immunohistochemistry. In two patients with variant and in one patient with type II GT, platelet adhesion was maximal and we observed an unexpected formation of thrombi that were smaller than normal in size. These thrombi were surrounded by a thick meshwork that displayed a strong staining for fibrin and VWF. In two patients with heterozygous GT, platelet adhesion and thrombogenesis were normal. In two patients with type I GT, there was no thrombus formation, although platelet adhesion was also maximal. These data suggest the existence of a substitute pathway for thrombogenesis mediated by fibrin and possibly alphaIIbbeta3 (alphaIIbbeta3 at a reduced level, as in type II, and/or abnormal) as this fibrin network was not observed in type I GT with no alphaIIbbeta3. These interactions might facilitate haemostasis and even lead to thrombosis under certain favourable conditions. Furthermore, these data might have pharmacological relevance to the development of anti-alphaIIbbeta3 antithrombotic agents.

Blood Platelets↗