Biomedical subjects

Dominique Lasne

Publications and source records attributed to Dominique Lasne.

7 recordsLinked to original sources

PubMed2006

From normal to pathological hemostasis.

PURPOSE: To review the evolution of knowledge on physiological hemostasis and the main abnormalities that may interfere with hemostasis in the perioperative period. METHODS: Narrative review of the literature, including relevant papers published in English. PRINCIPAL FINDINGS: Physiological hemostasis controls blood fluidity and rapidly induces hemostatic plug formation in order to stop or limit bleeding. The three distinct phases of the hemostatic process, primary hemostasis, coagulation and fibrinolysis are closely linked to each other and precisely regulated in order to efficiently close vessel wounds, promote vascular healing and maintain vessel patency. Primary hemostasis is the result of complex interactions between the vascular wall, platelets and adhesive proteins. Initiation of the coagulation pathway in vivo is secondary to the exposure of tissue factor (TF) and the formation of TF/VIIa complex which can activate both FIX and FX. This initiation phase is followed by a propagation phase with amplification of thrombin generation. Several control mechanisms exist for localizing fibrin formation to the site of injury including tissue factor pathway inhibitor, protein C system, antithrombin, and glycosaminoglycans on the vessel wall. Fibrinolysis is also a highly regulated system that controls fibrin dissolution. Both constitutive and acquired hemostasic defects exist. The consequences of these abnormalities are highly variable according to the type of defect, and to the genetic and environmental background. CONCLUSION: Hemostasis is one of the most complex physiological self-defence systems, not only involved in control of blood fluidity but also interfering in major physiopathological processes. The evolution of our knowledge of the physiology of hemostasis has numerous implications for therapy.

Animals↗

PubMed2006

Minimizing perioperative blood loss and transfusions in children.

PURPOSE: To summarize the physiology and pathophysiology relevant to perioperative blood loss in children. Strategies to reduce blood losses are reviewed. METHODS: The literature was reviewed using the electronic library PUBMED and the Cochrane Database of Systematic Reviews. Relevant studies published in English or French with an English abstract are included. The following keywords were used: children, blood transfusion, surgical blood loss, erythropoietin, autologous blood, red blood cell saver, normovolemic hemodilution, desmopressin, aminocaproic acid, tranexamic acid, aprotinin, cardiac surgery, liver transplantation and scoliosis surgery. MAIN FINDINGS: For patients with idiopathic scoliosis, predonation with or without the addition of erythropoietin is a safe and effective way to avoid the use of allogenic blood products. For open heart procedures: whole blood of less than 48 hr is helpful for children of less than two years of age undergoing complex procedures; tranexamic acid may be helpful for cyanotic heart disease and, to a lesser degree, for reoperations; while anti-kallikrein blood levels of aprotinin may both reduce the need for allogenic blood transfusions and improve postoperative oxygenation in infants. CONCLUSION: Reducing perioperative allogenic blood transfusions is possible in pediatric patients provided that prophylactic measures are adapted to age, disease and type of surgery.

Animals↗

PubMed2006

Diagnosis and management of heparin-induced thrombocytopenia.

PURPOSE: To review recent developments in the pathogenesis, clinical features, laboratory testing and treatment of heparin-induced thrombocytopenia (HIT). METHODS: Narrative review of the literature, including relevant papers published in English or French. PRINCIPAL FINDINGS: Although the prevalence of HIT has decreased with the widespread use of low molecular weight heparin in the past ten years, HIT remains a life-threatening prothrombotic state. This immune adverse event due to heparin-dependent antibodies that bind to chemokines (such as platelet factor 4) induces platelet activation and hypercoagulability. Heparin-induced thrombocytopenia can be complicated by thrombosis even after withdrawing heparin, explaining why substituting heparin with an alternative anticoagulant (danaparoid, lepirudin, argatroban) is always necessary. However, management of these alternative treatments is difficult, and in some patients there is the risk of withdrawing heparin without taking the time to diagnose HIT properly on the basis of clinical and laboratory findings (evolution of platelet count, laboratory testing such as antigen assays and platelet activation tests). CONCLUSIONS: Management of HIT has become easier in recent years with the development of more specific and sensitive laboratory tests and new antithrombotic drugs. However, the diagnosis of HIT is often difficult, and it remains very important to investigate this adverse reaction systematically in every patient treated with heparin who develops thrombocytopenia.

Anticoagulants↗

PubMed2004

The homozygous FcgammaRIIIa-158V genotype is a risk factor for heparin-induced thrombocytopenia in patients with antibodies to heparin-platelet factor 4 complexes.

We hypothesized that Fcgamma receptor IIIa (FcgammaRIIIa), a polymorphic receptor for the Fc portion of immunoglobulin G (IgG) other than FcgammaRIIa, was involved in heparin-induced thrombocytopenia (HIT). FcgammaRIIa-131 and FcgammaRIIIa-158 genotypes were determined in 102 patients with definite HIT and in 2 control groups of patients treated by heparin (86 subjects without detectable antibodies [Abs] to heparin-platelet factor 4 [H/PF4], Ab(-) group; 84 patients with Abs to H/PF4 without HIT, Ab(+) group). There were no significant differences in genotype distribution or allele frequencies between the 3 groups for FcgammaRIIa-131H/R polymorphism. In contrast, FcgammaRIIIa-158V homozygotes were more frequent in the HIT group than in the Ab(+) group (P = .02), a difference that was more pronounced in patients with high levels of anti-H/PF4 Abs (P = .01). Since anti-H/PF4 Abs are mainly IgG1 and IgG3, clearance of sensitized platelets may be increased in patients homozygous for the FcgammaRIIIa-158V allotype, thus contributing to the development of thrombocytopenia.

Antigens, CD↗

PubMed2004

Anti-prothrombin antibodies as a potential risk factor of recurrent venous thromboembolism.

The role of antiprothrombin (aPT) antibodies in the development of venous thromboembolism (VTE) is still uncertain. The aim of this study was to evaluate the potential role of aPT antibodies in the development of recurrent thromboembolism. Out of 236 consecutive symptomatic patients with an episode of acute VTE, antiphospholipid antibodies were found in 85 (36.0%), of whom 24 were carriers of aPT antibodies (10.2% of the entire cohort). A history of previous thromboembolism was identified in 56 patients (23.7%). The prevalence of previous thromboembolism was significantly higher in carriers than in non-carriers of antiphospholipid antibodies (OR=2.4; 95% CI, 1.3 to 4.4). Of the 24 patients with aPT antibodies, 12 had a history of previous thromboembolism. In a multivariate logistic regression analysis, in which the other categories of antiphospholipid antibodies were taken into account, as well as the patient's age, sex, and the modality of clinical presentation, it was found that the presence of aPT antibodies was significantly associated with the prevalence of prior thromboembolism (OR=3.3; 95% CI, 1.3 to 8.6). Since aPT antibodies are more commonly identifiable in patients with multiple thrombotic episodes, they are a likely risk factor for recurrent thromboembolism.

Adult↗

PubMed2004

Polymorphonuclear leukocyte and monocyte activation induced by plasma from patients with heparin-induced thrombocytopenia in whole blood.

Heparin-induced thrombocytopenia (HIT), a severe complication of heparin therapy, results from platelet activation by heparin-dependent antibodies. Previously, we have shown that plasma from patients with HIT (HIT plasma) induces leukocyteplatelet aggregation in blood. In this report, we examined leukocyte activation by HIT plasma and the contribution of heparin and platelets to this activation, in whole blood. Degranulation of leukocytes from HIT patients was evaluated as a leukocyte activation marker. We showed that polymorphonuclear leukocytes (PMN) and monocytes were the leukocyte subpopulations involved in platelet-leukocyte aggregation induced by HIT plasma in healthy donor blood. PMN and monocyte activation, reflected by increased surface expression of the CD11b adhesion molecule, was induced by HIT plasma in a heparin-dependent manner. The CD11b increase induced by HIT plasma was observed on PMN only when they were associated with platelets. Moreover, the increased CD11b expression on monocytes and PMN correlated strongly with the degree of platelet adhesion to these cells. Degranulation of leukocytes from HIT patients and control subjects (non-HIT heparin-treated patients and healthy subjects) was evaluated in vivo by measuring the plasma myeloperoxidase concentration. HIT plasma contained higher myeloperoxidase concentrations than control plasma, suggesting leukocyte degranulation during HIT. In conclusion, this study provides the first evidence that PMN activation is induced by HIT plasma. HIT plasma induced PMN and monocyte activation in a heparin-dependent manner. In whole blood, platelet association with monocytes and PMN, and the activation of these leukocytes by HIT plasma were interrelated. Finally, leukocyte degranulation could be involved in HIT physiopathology.

Adult↗

PubMedDate not supplied

Antiplatelet agents in the perioperative period: expert recommendations of the French Society of Anesthesiology and Intensive Care (SFAR) 2001--summary statement.

PURPOSE: Antiplatelet agents are administered to an increasing number of patients. Preoperative treatment with these agents represents a major problem for the anesthesiologist. The results of a French expert meeting on their perioperative management are reported. METHODS: Responses to questions formulated by the Organizing Committee were drafted by a group of experts and reviewed by a multidisciplinary. Reading Committee. Recommendations were classified (grade) according to the evidence level of the studies supporting them. PRINCIPAL FINDINGS: First, antiplatelet agents have a variable effect on hemostasis as far as bleeding risk is concerned. Aspirin and non-steroidal anti-inflammatory drugs (NSAIDs) increase intra- and postoperative bleeding moderately, but not transfusion requirements. Very few data are available on clopidogrel and ticlopidin. Anti-glycoprotein (GP) IIb/IIIa agents may increase bleeding when surgery is required in proximity with their administration. Second, the common practice of withdrawing antiplatelet agents is now challenged because an increased incidence of myocardial infarction has been reported in patients in whom treatment was interrupted. Third, aspirin should not be withdrawn for most vascular procedures and in several additional settings. When a definite increase in intraoperative bleeding is feared, or when surgical hemostasis is difficult, aspirin, clopidogrel or ticlopidine can be replaced by short-acting NSAIDS, given for a ten-day period and interrupted the day before surgery. Platelet transfusion should only be given when overt bleeding is observed. Postoperatively, antiplatelet treatment should be resumed immediately after surgery (first six hours). CONCLUSION: Anesthesiologists should be aware of the indications, potential complications and means of substitution of these agents.

Anesthesia↗