Although produced largely in the periphery, gonadal steroids play a key role in regulating the development and functions of the central nervous system and have been implicated in several chronic neuropsychiatric disorders, with schizophrenia and Alzheimer's disease (AD) most prominent. Despite major differences in pathobiology and clinical manifestations, in both conditions, estrogen transpires primarily with protective effects, buffering the onset and progression of diseases at various levels. As a result, estrogen replacement therapy (ERT) emerges as one of the most widely discussed adjuvant interventions. In this review, we revisit evidence supporting the protective role of estrogen in schizophrenia and AD and consider putative cellular and molecular mechanisms. We explore the underlying functional processes relevant to the manifestation of these devastating conditions, with a focus on synaptic transmission and plasticity mechanisms. We discuss specific effects of estrogen deficit on neurotransmitter systems such as cholinergic, dopaminergic, serotoninergic, and glutamatergic. While the evidence from both, preclinical and clinical reports, in general, are supportive of the protective effects of estrogen from cognitive decline to synaptic pathology, numerous questions remain, calling for further research.

• Klíčová slova
• Adjuvant therapy, Animal models, Cognitive deficit, Menopause, Neuroprotection, Plasticity,
• MeSH
• Alzheimerova nemoc farmakoterapie   metabolismus   MeSH
• estrogenní substituční terapie metody   MeSH
• estrogeny metabolismus   farmakologie   MeSH
• lidé MeSH
• schizofrenie farmakoterapie   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• estrogeny MeSH

OBJECTIVE: To describe relations among postmenopause, hormonal therapy, lipid metabolism and risk of cardiovascular diseases. DESIGN: Search and analysis of relevant data from medical literature. METHODS: Analysis of the relation between serum lipid profile and postmenopausal changes, evaluation of positive and negative effects of estrogens on vascular wall and lipid metabolism, analysis of methods for the assessment of cardiovascular risk and evaluation of recent guidelines. RESULTS: Postmenopause is connected with significant changes in lipid metabolism, serum lipid profile and with increased risk of cardiovascular diseases. Deficit of estrogens influences lipid metabolism negatively. However, estrogen substitution has both positive and negative effects on vascular wall. Negative effects are: increased occurence of postprandial hyperlipidemia with increased triglycerides, generation of aterogenous small dense LDL particles, increased risk of inflammatory changes in vascular wall and procoagulation situation. CONCLUSION: Hormonal therapy can display some positive effects of vascular wall. However, recent data evaluate hormonal substitution with regard to atherosclerosis and cardiovascular problems as less benefitial or even risky.

• MeSH
• estrogenní substituční terapie * MeSH
• estrogeny fyziologie   MeSH
• kardiovaskulární fyziologické jevy * MeSH
• kardiovaskulární nemoci etiologie   patofyziologie   MeSH
• lidé MeSH
• metabolismus lipidů MeSH
• postmenopauza metabolismus   fyziologie   MeSH
• rizikové faktory MeSH
• Check Tag
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• estrogeny MeSH

• Klíčová slova
• ADRENOGENITAL SYNDROME/urine *, ESTROGENS/urine *,
• MeSH
• adrenogenitální syndrom moč   MeSH
• estrogeny moč   MeSH
• kongenery estradiolu * MeSH
• kongenitální adrenální hyperplazie * MeSH
• kontraceptiva ženská * MeSH
• lidé MeSH
• Check Tag
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• estrogeny MeSH
• kongenery estradiolu * MeSH
• kontraceptiva ženská * MeSH

OBJECTIVE: Presentation of a familiar incidence of complete androgen insensitivity syndrome. DESIGN: Case report with literature review. SETTING: Department of Gynecology and Obstetrics, Department of Pediatrics, Medical Faculty and University Hospital in Pilsen, Charles University in Prague. CONCLUSION: Androgen insensitivity syndrome is the most common male-hermaphroditism. Affected individuals have a male karyotype, but owing to the unresponsiveness of the cells to androgens a disruption in sexual development occurs. Clinical picture of the syndrome is very variable. Our case-report deals with a familiar incidence of complete androgen insensitivity syndrome, formerly incorrectly called "testicular feminization syndrome". The karyotype of these individuals is 46, XY. They have female external genitalia, male gonads, the uterus and fallopian tubes are missing and vagina is shorter. In this case, the complete androgen insensitivity syndrome was diagnosed in two sisters in childhood as a part of reduced growth investigation. The same syndrome was also detected in their mothers sister. Both girls already underwent laparoscopic gonadectomy. The older one started at the age of 11 with estrogen replacement therapy.

• MeSH
• dítě MeSH
• estrogenní substituční terapie metody   MeSH
• karyotypizace MeSH
• laparoskopie metody   MeSH
• lidé MeSH
• ovarektomie metody   MeSH
• syndrom rezistence na androgeny diagnóza   genetika   terapie   MeSH
• Check Tag
• dítě MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• kazuistiky MeSH
• přehledy MeSH

• MeSH
• estrogeny krev   MeSH
• lidé MeSH
• luteinizační hormon krev   MeSH
• syndrom rezistence na androgeny krev   MeSH
• testosteron krev   MeSH
• zpětná vazba MeSH
• Check Tag
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH
• Názvy látek
• estrogeny MeSH
• luteinizační hormon MeSH
• testosteron MeSH

OBJECTIVE: An increased rate of fractures has been reported in patients with Turner syndrome (TS). We aimed to assess bone geometry and volumetric bone mineral density (vBMD) at the radius in girls with TS and to evaluate the relationships between bone parameters and fracture history. METHODS AND DESIGN: Sixty-seven girls with TS aged 6-19 years treated currently or in the past with growth hormone (GH) and/or oestrogens were examined using peripheral quantitative computed tomography. Results were compared to reference data. RESULTS: Cortical area and cortical thickness were low in all age groups (all P<0·001). Height-adjusted total bone area at the diaphysis was increased in prepubertal and postpubertal girls (mean Z-score 1·0, P<0·05 for both) and normal in the pubertal group (mean Z-score 0·1). Cortical vBMD was decreased (mean age-specific Z-scores -2·0, -1·6 and -1·0 for prepubertal, pubertal and postpubertal groups, respectively, P<0·01 for all groups). Height- , age- and cortical thickness-adjusted cortical vBMD was positively correlated to the duration of GH therapy (P=0·012) and to oestrogen administration (P=0·047). Girls with a history of fractures had lower total vBMD at the metaphysis compared to nonfractured TS girls (mean Z-scores -1·7 vs-0·9, P=0·04). CONCLUSIONS: There is a cortical bone deficit in girls with TS characterized by low cortical area, thin cortex and probably decreased cortical vBMD. Early commencement of GH therapy, as well as oestrogen replacement, is associated with higher cortical vBMD. Further studies should investigate the potential causality of this relation.

• MeSH
• dítě MeSH
• dospělí MeSH
• estrogeny terapeutické užití   MeSH
• kosti a kostní tkáň anatomie a histologie   účinky léků   metabolismus   MeSH
• kostní denzita účinky léků   fyziologie   MeSH
• lidé MeSH
• lidský růstový hormon terapeutické užití   MeSH
• mladiství MeSH
• mladý dospělý MeSH
• puberta fyziologie   MeSH
• Turnerův syndrom farmakoterapie   metabolismus   patofyziologie   MeSH
• Check Tag
• dítě MeSH
• dospělí MeSH
• lidé MeSH
• mladiství MeSH
• mladý dospělý MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• estrogeny MeSH
• lidský růstový hormon MeSH