[Chronic stress is associated with increased levels of cortisol and catecholamines as well as with an enhanced activity of the sympathico-sensory nervous system. These neuroendocrine events influence both directly and indirectly the lipid and glucose metabolism as well as inflammatory immune reactions. Stress effects directly cause vascular damage and atherosclerosis via the renin-angiotensin system (RAS). Besides RAS, activities of monocytes/macrophages and the sympathico-sensory nervous system lead to local cardiovascular inflammation and cell hypertrophy. Transactivation between G-protein coupled adrenoceptors and tyrosine kinase receptors as well as the switching between β1- and β2- adrenergic receptors play an important role in the development of cardiac hypertrophy and heart failure. In all chronic neuroendocrine diseases that are associated with increased activity of the sympathetic nervous system, the development of cardiovascular damages needs to be considered.]

[INTRODUCTION - A number of diseases can cause hyperreninaemia and secondary hyperaldosteronism due to the stimulation of the renin-angiotensin system (RAS). The authors present a case of a patient suffering from a feeding disorder, whose secondary hyperaldosteronism verified by hormone examinations recovered after resolution of the feeding disorder. CASE REPORT - The authors found that the patient, who had been on an extreme vegetarian diet and avioded all forms of common salt as well as natural sodium intake for 8 years, had consistently normal electrolite levels, normal blood pressure, elevated plasma renin activity (PRA) and plasma aldosterone levels. Salt loading and postural tests verified secondary hyperaldosteronism. All known diseases that might lead to elevated RAS activity were excluded. After cessation of the salt-restricted diet, the patient’s PRA and plasma aldosteron levels returned to the normal range, which confirmed the possibility that the secondary hyperaldosteronism developed because of the feeding disorder. CONCLUSION - The authors have not found similar hormon alterations due to alimentary causes in humans in the literature. According to their hypothesis, the feeding disorder might lead to secondary hyperaldosteronism via affecting the system or systems that regulate RAS activity.]

[Polycystic ovary syndrome is an endemic disease, thus its treatment is of great importance. In polycystic ovary syndrome, metformin decreases androgen levels, improves menstrual irregularity, hirsutism, ovulation ratio, and the efficiency of lifestyle interventions on visceral obesity, endothelial function and LDL-cholesterol level. It seems plausible to suppose that metformin decreases the incidence of diabetes in this group of patients. Metformin is superior to oral contraceptives/antiandrogens in respect of its effect on triglyceride level and insulin sensitivity, however, it is less effective in decreasing androgen levels, normalisation of the menstrual cycle and supposedly in the prevention of endometrial cancer. Metformin therapy improves fertility, however, when infertility is the main problem, it is not indicated as the primary treatment. In this case, ovulation induction, ovary drilling, as well as in vitro fertilization are warranted that can be supported by metformin therapy is some cases.]