Thromb Haemostasis
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Acquired factor V(FV) inhibitors as a rare bleeding disorder, poses a formidable challenge to treating physicians with limited evidence to guide its management. We systematically reviewed our experience in Singapore and the published literature to determine possible answers to clinical questions formulated on the manifestation and best management of non-bovine thrombin and non-congenital acquired FV inhibitors. The incidence in Singapore was 0.09 cases per million person years (3 cases over 10 years). ⋯ Steroids as single agent IET was effective in the majority of patients. Logical management approaches may be drawn but are limited by small sample size, heterogeneity of reports, and potential publication bias. The inception of a comprehensive registry will provide more reliable data that may verify our findings.
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Review Meta Analysis
VIDAS D-dimer in combination with clinical pre-test probability to rule out pulmonary embolism. A systematic review of management outcome studies.
Clinical outcome studies have shown that it is safe to withhold anticoagulant therapy in patients with suspected pulmonary embolism (PE) who have a negative D-dimer result and a low pretest probability (PTP) either using a PTP model or clinical gestalt. It was the objective of the present study to assess the safety of the combination of a negative VIDAS D-dimer result in combination with a non-high PTP using the Wells or Geneva models to exclude PE. A systematic literature search strategy was conducted using MEDLINE, EMBASE, the Cochrane Register of Controlled Trials and all EBM Reviews. ⋯ PE was ruled out by a negative D-dimer test in 2,248 (40%, 95% confidence intervals [CI] 38.7 to 41.3%) of them. The three-month thromboembolic risk in patients left untreated on the basis of a low/intermediate or unlikely PTP and a negative D-dimer test was 3/2,166 (0.14%, 95% CI 0.05 to 0.41%). In conclusion, the combination of a negative VIDAS D-dimer result and a non-high PTP effectively and safely excludes PE in an important proportion of outpatients with suspected PE.
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Coronary heart disease (CHD) is the leading cause of death globally. Following an acute coronary artery occlusion, timely myocardial reperfusion using either primary percutaneous coronary intervention (PCI) or thrombolytic therapy remains the most effective treatment strategy for reducing myocardial infarct size, preventing left ventricular remodelling, preserving left ventricular systolic function and improving clinical outcomes. However, the full benefits of myocardial reperfusion are not realised, given that the actual process of reperfusing ischaemic myocardium can independently induce cell death - a phenomenon termed lethal reperfusion injury. ⋯ Experimental studies demonstrate that this stuttered form of myocardial reperfusion improves myocardial perfusion, maintains endothelial function, attenuates apoptotic cell death, reduces myocardial infarct size, preserves left ventricular systolic function and reduces mortality. The mechanisms underlying the cardioprotective effect of ischaemic postconditioning are the subject of intense investigation. In this article we review the signalling pathways which have been implicated as potential mediators of ischaemic postconditioning, the identification of which have provided novel pharmacological targets of cardioprotection capable of recapitulating the protective benefits of ischaemic postconditioning.
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The concept of 'Compensatory anti-inflammatory response syndrome' (CARS) was proposed in 1997 by Roger Bone (1941-1997) to qualify the consequences of the counter-regulatory mechanisms initiated to limit the overzealous inflammatory process in patients with infectious (sepsis) or non-infectious systemic inflammatory response syndrome (SIRS). One major consequence of CARS is the modification of the immune status that could favour the enhanced susceptibility of intensive care patients to nosocomial infections. Indeed, most animal 'two-hit' models illustrate an enhanced sensitivity to infection after a first insult. ⋯ However, this is rather a reprogramming of circulating leukocytes, since there is not a global defect of the immune cells functions. Furthermore, within tissues, leukocytes are rather primed or activated than immunosuppressed. Thus, CARS may be considered as an adapted compartmentalized response with the aim to silence some acute proinflammatory genes, and to maintain the possible expression of certain genes involved in the anti-infectious process.