DOES THE HORMONAL REPLACEMENT THERAPY INFLUENCE THE BRAIN FUNCTION?

DOES THE HORMONAL REPLACEMENT THERAPY INFLUENCE THE BRAIN FUNCTION?

S22 8th European Congress on Menopause (EMAS) / Maturitas 63, Supplement 1 (2009) S1–S136 81 Polish Menopause and Andropause Society: Hot Topics in...

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S22

8th European Congress on Menopause (EMAS) / Maturitas 63, Supplement 1 (2009) S1–S136

81

Polish Menopause and Andropause Society: Hot Topics in Menopausal Medicine

OSTEOPENIA - TO TREAT OR NOT TO TREAT. SYMPOSIUM OF POLISH MENOPAUSE AND ANDROPAUSE SOCIETY R. Spaczynski. Poznan University of Medical Sciences, Department of Gynecology and Obstetrics, Poznan, Poland

79 DOES TESTOSTERONE REPLACEMENT THERAPY INCREASE THE RISK OF PROSTATE CANCER? G. Jakiel. Medical University of Lublin, Reproduction and Andrology, Lublin, Poland Objectives: In 2005 ISA, ISSAM and EUA published the common recommendations about the investigation, treatment and monitoring of late onset hypogonadism in male. Testosterone replacement therapy is now, being prescribed more often for aging male, the same population in which cancer incidence increases. The hypothesis that high levels of circulating testosterone (especially exogenous) is a risk factor for prostate cancer is supported by the dramatic regression after castrations, of clinical symptoms in men with advanced prostate cancer, but the relationship between prostate cancer and testosterone is not completely understood. Methods: Review of published studies investigating the relationships between testosterone (circulating and prostate tissue containing) and prostate cancer risk. Results: It has been traditionally accepted (especially by urologists), that testosterone substitution in ageing males has the potential to harm the prostate. Recent publications have shown that testosterone replacement has little effect on prostate tissue androgen concentration and cellular function. The epidemiological data and clinical trials have shown no increase in prostate carcinoma rates in normal men or men with increased risk for prostate cancer and no reduction risk in men with low serum testosterone levels. Conclusions: The use of testosterone substitution is contraindicated in cases of known prostate cancer due to the permissive role of testosterone in malignancies of the prostate gland, but there is no good evidence to date suggesting that long-term use of testosterone in hypogonadal men promotes or induces prostate cancer per se. Keywords: LOH, prostate cancer, testosterone substitution.

80 DOES THE HORMONAL REPLACEMENT THERAPY INFLUENCE THE BRAIN FUNCTION? B. Meczekalski. Poznan University of Medical Sciences, Department of Gynecological Endocrinology, Poznan, Poland Estrogens exert an essential role in the brain function. They influence neurotransmitters and neuropeptides synthesis, synaptic plasticity and electrical excitability. Estrogen receptors are localized in numerous brain areas such as pituitary, hypothalamus, limbic system and cortex. Adequate estrogen levels normal during reproductive and premenopausal period can ensure physiological processes related to central nervous system function. There are evidences that estrogens deficiency during menopause period in important part impair brain function. It has been paid attention whether hormonal replacement therapy (HRT) influence the cognitive function, the risk of depression and Alzheimer disease. Clinical studies of estrogen replacement therapy (ERT) and cognitive function have reported controversial results, indicating a lack of efficacy of estrogens on cognition in post-menopausal women aged ≥65 years. There are controversies on the possible role of HRT in the decrease of the depression risk. Contemporary studies indicate, that routine therapeutic use of estrogens in women with Alzheimer disease is not justified but it may have a role in the prophylaxis of this disease. This field of gynecological endocrinology is particularly interesting and developing. Additional experimental and clinical studies are needed to explain HRT influence on brain function.

Low bone mass - osteopenia - is exclusively defined on the assessment of bone mineral density (BMD) that falls between -1,0 and -2,5 SD of that classified for young women. As long as nonpharmacologic interventions in osteopenia rise no controversy recommendations for pharmacologic management are inconsistent. All patients with osteopenia should be recommended nonpharmacologic actions to maintain their bone mass and limit potential development of osteoporotic fractures. These actions include: balanced diet with adequate supplementation of protein, calcium, vitamin D as well as regular weight bearing exercise. Further lifestyle modification should include reduction of excessive alcohol consumption and total elimination of tobacco smoking. Recommendations for therapy in osteopenic patients should be based on the assessment of absolute risk of fracture, including clinical risk factors combined with BMD measurements rather than on a fixed level of BMD. Selected authorities recommend pharmacologic treatment of all women with BMD below -2,0 SD and treatment of postmenopausal women with T-scores below -1,5 SD and one or more risk factors. Other expert organizations advice no treatment of osteopenia, unless at least one risk factor (including thinness, history of fragility fracture and hip fracture in a parent) is identified and then treatment should be instituted in women with T-scores below -2,0 SD. Pharmacologic therapy for selected osteopenic patients comprises bisphosphonates, selective estrogen receptor modulators and combined or estrogen alone hormone therapy. However it needs to be stressed that pharmacological therapy is only indicated in those osteopenic women assessed to be at increased fracture risk.

Asociación Española para el Estudio de la Menopausia - AEEM (Spanish Association for the Study of Menopause) 82 MENOPAUSE AND ANDROGENS S. Palacios. Palacios Institute of Woman’s Health, Madrid, Spain Objective: Tto review the data on androgens in menopausal women and the efficacy and security of the androgens treatment. Methods: This review is based upon the medical literature identified by searching in Medline for randomized clinical trials, meta-analysis and guidelines from several Medical Societies. Results: Circulating androgens are produced by the ovaries, the suprarenal glandules and the peripheral conversion. Postmenopausal women’s ovaries continue producing and secreting testosterone. No specific menopausal effect has been observed on circulating androgenic levels, although these levels decrease gradually with age and abruptly with surgical menopause. Androgen insufficiency syndrome is a controversial issue due to the existing difficulties when specifying the normal levels using current analytical methods. There are clear efficacy evidences on hypoactive sexual desire disorder with both oral and transdermic testosterone. Data show its benefits on bone remodelling, cognitive effects, musculature and body composition. Nevertheless, all the studies have been carried out in few patients. Adverse effects are related to the dose. With physiological doses only a study with increased hirsutism was found. Besides, most of the studies have 6-12 month-results. Conclusion: Nowadays, the treatment with testosterone patch 300 mg/day is only prescribed to women who have hypoactive sexual desire disorder and it causes personal distress. There are no evidences on other added benefits. Adverse effects are minimal or non-existent after a one-year treatment. More security data are needed in a longer term.