[The influence of citoflavin on molecular mechanisms of hypertensive encephalopathy development in patients with systolic arterial hypertension].

The molecular pharmacological effects of cytoflavin in patients with hypertensive encephalopathy (HE) and isolated systolic arterial hypertension (ISAH) have been investigated using the following methods: assessment of complaints, 24-hour arterial pressure monitoring, ultrasound diagnostics including echocardiography, measurement of lipid profiles and coagulograms, and molecular phenotyping by MALDI-TOF/TOF-MS. A combination of cytoflavin administration with standard therapy of HE and ISAH led to the most expressed return development of clinical symptoms, restoration of the hemodynamic, structural, and geometrical parameters of cardiovascular system, and normalization of the indices of lipid profiles and coagulograms in comparison to patients with HE and ISAH, which accepted only standard therapy. Molecular mechanisms of cytoflavin action have been revealed, which include control of the activity of cellular signaling pathways by means of intermolecular interactions. The optimized therapy of HE and ISAH is recommended for clinical application, which assumes a combined use of standard therapy and cytoflavin and provides a geroprotective action upon the cardiovascular system.

[Cognitive impairment in elderly patients with acute hypertensive encephalopathy].

Acute hypertensive encephalopathy in elderly patients appears reversible mild cognitive impairment. The erythrocyte sedimentation rate and blood creatinine measured during a hypertensive crisis are predictors of decline of visual-spatial orientation after two weeks of treatment.

[The peculiarities of serum levels of S100b protein and antibodies to it in patients with crisis and stable essential hypertension].

The article covers the results of research into the levels of S100b protein and antibodies to it in the serum of patients with crisis and stable essential hypertension. The results show that neutrophic protein dysmetabolism plays an important role in the pathogenesis of hypertonic dyscirculatory encephalopathy and the forming of cognitive disorder syndrome. The data obtained suggest that hypertensive crises lead to pathologic changes in hematoencephalic barrier permeability and the development of autoimmune reactions with participation of neutrophic proteins.

Plasma concentrations of atrial and brain natriuretic peptides in a case with hypertensive encephalopathy.

Hemodynamic mechanism for brain edema forrmation in patients with hypertensive encephalopathy is unclear. Potential roles of natriuretic peptides in the pathogenesis of hypertensive encephalopathy are discussed. A 32-year-old man presented with slight left hemiparesis. He was slightly confused, and his blood pressure was extremely high. Cranial plain computerized tomography scans revealed diffuse brain edema mainly in the supratentorial white matter region. Blood examination revealed that plasma concentrations of atrial and brain natriuretic peptides were significantly high. His left hemiparesis disappeared within a day, but he tended to be agitated. His altered mental status, however, resolved with control of blood pressure. Serial magnetic resonance imagings demonstrated that the magnitude of brain edema was attenuated in proportion to decline in plasma concentrations of natriuretic peptides. This case suggests that significant elevation of plasma concentrations of natriuretic peptides may contribute to an acute rise in blood pressure, and that these peptides potentially play an important role in development of brain edema in hypertensive encephalopathy.

Low doses of liquorice can induce hypertension encephalopathy.

Prolonged ingestion of liquorice is a well-known cause of hypertension due to hypermineralocorticoidism. We describe 2 cases of hypertension encephalopathy (in addition to the classical symptoms of hypertension, hypokalemia and suppression of the renin-aldosterone system) which resulted in pseudohyperaldosteronism syndrome due to the regular daily intake of low doses of liquorice. Glycyrrhizic acid, a component of liquorice, produces both hypermineralocorticism and the onset of encephalopathy through the inhibition of 11beta-hydroxysteroid dehydrogenase. Hypertension encephalopathy due to the daily intake of low doses of liquorice, however, has not been previously documented. It is proposed that some people could be susceptible to low doses of glycyrrhizic acid because of a 11beta-hydroxysteroid dehydrogenase deficiency.