TNL, as well as the soluble AM concentrations in plasma and CSF, were increased during the acute IBD phase and progressive in relation to the severeness of the disease, so that they might have been the indicators of CNS inflammatory reaction intensity. Furthermore, the results indicated their role in IBD pathogenesis and offered the possibility of researching the application of antagonists and/or activity modulators of some of them in IBD therapy.
The main potentially protective effect of the increased CSF cortisol concentration in patients with completed stroke in the acute phase could be the decrease of deleterious effects of lipid peroxidation reactions induced by ischemia. This mechanism could be the attempt of organism to compensate ischemia-disturbed homeostasis.
Ischemic brain disease (IBD) represents clinical entity participating with almost 80% in all vascular brain diseases. Ethiopatogenesis and pathophysiology of the ischemic brain disease are apparently most complex in human medicine. In addition to the significant progression in understanding of ethiopatogenesis and pathophysiology of the ischemic brain disease, we are currently aware of the fact that in one third of these patients the source--the disorder or the disease of crucial importance for this sequence of events in the opposing direction cannot be diagnosed with certainty. This case report presents a 32-year-old patient with the verified ischemic lesion of brain parenchyma, in whom the lowered concentrations of protein S were registered by comprehensive clinical and biochemical examinations. The lower concentrations of protein S are a significant co-factor of anticoagulant system, in the absence of other significant diseases, disorders or abnormalities which could ethiopatogenetically be significant for IBD.
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