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  • br Conclusions Symptoms from bilateral thalamic edema caused


    Conclusions Symptoms from bilateral thalamic edema caused by increased venous hypertension can be reversed with appropriate management of the inciting vascular lesion. This case demonstrates a rare patient with decreased CBF in the thalamus in SPECT and completely recovered after factor Xa inhibitor administration. If a patient presents with focal neurological deficits, headache, and neuropsychological symptoms such as somnolence, DCVT might be the underlying condition. As in DCVT in other locations, early recognition of this clinical entity and treatment are prerequisites for a favorable outcome. Although this is a case report, factor Xa inhibitor may show a similar clinical benefit as vitamin K antagonist in the treatment of DCVT. Further systematic prospective evaluation is warranted.
    Introduction Under physiological conditions, the endothelial layer acts as one of the regulators of the haemostatic mechanism, acting as a barrier between the blood and the underlying thrombogenic tissue. However, this barrier is dynamic and is regulated to conform to the requirements of the local vasculature. Alterations in endothelial permeability are essential in the maintenance of the correct homeostatic functions but also, are often central in the pathogenesis of inflammatory and vascular disorders. Following injury, the responses by the vasculature limits blood flow and then allows seepage into the sub-endothelial layer. Protease activated receptors are G-protein coupled receptors which act as sensors for the presence of active proteases, in particular those that are involved in the coagulation mechanism [1,2]. The endothelial Epinephrine HCl express PAR1 and PAR2 which mediate numerous outcomes that include changes to endothelial permeability [[3], [4], [5]]. PAR2 signalling is induced following the proteolysis by coagulation factor Xa (fXa), tissue factor-factor VIIa (TF-fVIIa) complex as well as by trypsin I, II and IV, tryptase, acrosin, granzyme A and kallikrein 2, 4, 6 and 14, in a canonical manner, and by elastase, proteinase 3 and cathepsins G and S in a non-canonical system [6,7]. The activation of PAR2 has also been associated with inflammatory responses during chronic disorders [2,8] and suggested as a cause of vascular complications associated with various diseases [4,9]. Endothelial cells are connected to each other by a complex set of junction proteins [[10], [11], [12], [13]]. Under normal conditions, inter-endothelial junctions open to permit the passage of molecules and surveillance cells in a dynamic and size-selective manner [[14], [15], [16]]. Moreover, a number of inflammatory agents including thrombin and VEGF, are able to stretch out these junctions permitting contact between plasma and the sub-endothelial layer [[17], [18], [19]]. It has been shown that endothelial cells respond to coagulation by altering the vascular permeability [20]. However, little is known of the endothelial responses under conditions of coagulation, when the proteases are simultaneously generated. Furthermore, the overall response is likely to also be dependent on the magnitude of coagulation activation, which in turn would be dependent on the extent of the injury incurred. The role of PAR2 in the alteration of vascular permeability has not been defined. Current reports equally ascribe the activation of PAR2 signalling to increases in endothelial permeability [8,21,22], and refute such a response [23,24]. In addition, it has been suggested that PAR2 acts in conjunction with PAR1 to desensitize subsequent cellular responses to thrombin [5]. In this study we have examined the ability of fXa and TF-fVIIa to influence the permeability of endothelial monolayers. In addition, by inhibiting fXa activity and blocking PAR2 activation, the role of these proteins in the regulation of endothelial permeability is further clarified.
    Material and methods
    Results To ensure that the endothelial monolayers were not affected for the duration of the assay by the lack of serum, the presence of blue dextran or the inclusion of DMSO, initially the Transwell-monolayers were monitored over 2 h and confirmed to remain intact (not shown). Incubation of the monolayer without any stimulus resulted a gradual increase in the transfer of dextran blue as expected, but this was not significant over the period of analysis (Fig. 1) and therefore deemed to be a stable model.