Present study was aimed to investigate sympathetic responses to mental stress with hypothesis that the presence of obesity in patients with hypertension has a modifying effect. Young male subjects, 8 with hypertension grade I, with BMI<25 kg/m2 (HT), 10 with hypertension grade I, and BMI>30 kg/m2 (HT OB), 14 healthy controls with BMI<30 kg/m2 (OB), and 13 healthy controls with BMI<25 kg/m2 (C) underwent the Stroop test. ECG was recorded continuously to evaluate heart rate variability (HRV). Blood pressure (BP) and catecholamine concentrations were measured at baseline, at the end of mental stress test and 15 min thereafter. Patients with HT demonstrated increased adrenaline concentrations and enhanced stress-induced noradrenaline release compared to that in healthy controls. In obese subjects, stress-induced increase of systolicBP was lower compared to lean individuals. Stress exposure induced a significant rise in the low frequency power component of HRV, however the increase was lower in the HT OB group compared to C. Obesity in patients with hypertension did not lead to a different reaction in comparison with lean hypertensive subjects. The present data demonstrate higher sympathoadrenal activity in early-stage of hypertension. Obesity is connected with higher resting systolicBP and modifies the HRV response to mental stress., A. Garafova, A. Penesova, E. Cizmarova, A. Marko, M. Vlcek, D. Jezova., and Obsahuje bibliografii
Chronic systemic inflammation is associated with increased cardiovascular mortality in patients with rheumatoid arthritis (RA). The aim of our study was to investigate association of glucose metabolism and inflammatory markers in a group of patients with rheumatoid arthritis free of other metabolic risk factors. Twenty-two premenopausal RA females (11 patients on low-dose GC (<8.5 mg/day of prednisone or equivalent), 11 patients without glucocorticoid therapy) and 15 age- and BMImatched healthy females underwent the oral glucose tolerance test. The insulin sensitivity indices according Matsuda (ISIMAT) and Cederholm (ISICED) as well as HOMA2 %S were calculated. Cytokines, lipid profile, non-esterified fatty acids (NEFA) and plasminogen activator inhibitor-1 (PAI-1) were measured in baseline blood samples. Despite elevated interleukin IL-6 and TNF alpha, glucose, insulin and C-peptide responses to oral glucose load as well as ISIMAT, ISICED, PAI-1 and NEFA were comparable in both RA groups and healthy controls. HOMA 2 %S correlated with disease activity. In conclusions, low-dose glucocorticoid treatment does not lead to glucose metabolism impairment in RA patients without other metabolic risk factors. Increased cardiovascular mortality and morbidity is probably due to a direct effect of systemic inflammation on myocardium and/or blood vessels., A. Penesová, ... [et al.]., and Obsahuje seznam literatury
The aim of our study was to investigate adrenocortical function in the context of disease activity and inflammatory status in premenopausal RA females. Adrenal glucocorticoid and androgen responses to the 1 μg ACTH 1-24 test were investigated in 23 premenopausal RA and in 15 age- and BMI-matched healthy females. Twelve RA patients were on low-dose prednisone (<8.5 mg/day). Patients with DAS28>3.2 had lower (p<0.05) total plasma cortisol, 17-hydroxyprogesterone, dehydroepiandrosterone and androstenedione responses in the ACTH test compared to healthy controls. Patients with DAS28>3.2 had lower (p<0.05) dehydroepiandrosterone response in the ACTH test compared to patients with DAS28≤3.2. C-reactive protein (CRP), DAS28, and interleukin (IL)-6 negatively correlated with androstenedione response to ACTH 1-24. Responses of all measured adrenal steroids were lower (p<0.05) in patients on low-dose glucocorticoids compared to healthy controls. RA patients not treated with glucocorticoids had lower total cortisol response (p=0.038) but did not differ in free plasma cortisol in the ACTH test. The results indicate an association of increased disease activity with a decrease in adrenal androgen production in RA and normal cortisol bioavailability in patients not treated with glucocorticoids., R. Imrich, M. Vlcek, J. Kerlik, M. Vogeser, F. Kirchhoff, A. Penesova, Z. Radikova, J. Lukac, J. Rovensky., and Obsahuje bibliografii
Multiple sclerosis (MS) is a chronic inflammatory and demyelinating disease of the central nervous system. In addition to the genetic, epigenetic and immunological components, various other factors, e.g. unhealthy dietary habits, play a role in the MS pathogenesis. Dietary intervention is a highly appealing approach, as it presents a simple and relatively low risk method to potentially improve outcomes in patients with brain disorders in order to achieve remission and improvement of clinical status, well-being and life expectancy of patients with MS. The importance of saturated fat intake restriction for the clinical status improvement of MS patients was pointed for the first time in 1950s. Recently, decreased risk of first clinical diagnosis of CNS demyelination associated with higher intake of omega-3 polyunsaturated fatty acids particularly originating from fish was reported. Only few clinical trials have been performed to address the question of the role of dietary intervention, such is e.g. low saturated fat diet in MS treatment. This review summarizes current knowledge about the effect of different dietary approaches (diets low in saturated fat and dietary supplements such as fish oil, lipoic acid, omega-3 polyunsaturated fatty acids, seeds oils, high fiber diet, vitamin D, etc.) on neurological signs, patient’s well-being, physical and inflammatory status. So far the results are not conclusive, therefore much more research is needed to confirm and to understand the effectiveness of these dietary interventions in the long term and well defined studies., A. Penesová, Z. Dean, B. Kollár, A. Havranová, R. Imrich, M. Vlček, Ž. Rádiková., and Obsahuje bibliografii