Postępowanie w chorobach tarczycy u kobiet w ciąży

The management of thyroid disorders during pregnancy is one of the most frequently disputed problems in modern endocrinology. It is widely known that thyroid dysfunction may result in subfertility, and, if inadequately treated during pregnancy, may cause obstetrical complications and influence fetal development. The 2007 Endocrine Society Practice Guideline endorsed with the participation of the Latino America Thyroid Association, the American Thyroid Association, the Asia and Oceania Thyroid Association and the European Thyroid Association, greatly contributed towards uniformity of the management of thyroid disorders during pregnancy and postpartum. Despite the tremendous progress in knowledge on the mutual influence of pregnancy and thyroid in health and disease, there are still important areas of uncertainty. There have been at least a few important studies published in the last 3 years, which influenced the thyroidal care of the expecting mother. It should also be remembered that guidelines may not always be universally applied in all populations with different ethnical, socio-economical, nutritional (including iodine intake) background or exposed to different iodine prophylaxis models. The Task Force for development of guidelines for thyroid dysfunction management in pregnant women was established in 2008. The expert group has recognized the following tasks: development of the coherent model of the management of thyroid dysfunction in pregnant women, identification of the group of women at risk of thyroid dysfunction, who may require endocrine care in the preconception period, during pregnancy and postpartum – that is in other words, the development of Polish recommendations for targeted thyroid disorder case finding during pregnancy, and the development of Polish trimester-specific reference values of thyroid hormones. Comprehensive Polish guidelines developed by the Task Force are to systematize the management of the thyroid disorders in pregnant women in Poland. (Pol J Endocrinol 2011; 62 (4): 362–381)Jednym z aktualnie szeroko dyskutowanych problemów współczesnej endokrynologii jest opieka tyreologiczna nad kobietą ciężarną. Powszechnie wiadomo, że dysfunkcja tarczycy może być przyczyną zaburzeń płodności, a nieleczona prawidłowo w czasie ciąży zwiększa ryzyko powikłań położniczych oraz ma wpływ na rozwój płodu. Opublikowane w 2007 roku wytyczne Towarzystwa Endokrynologicznego (Endocrine Society), opracowane przy współudziale Towarzystwa Tyreologicznego Ameryki Łacińskiej (LATS), Towarzystwa Tyreologicznego Azji i Oceanii (AOTA), Amerykańskiego Towarzystwa Tyreologicznego (ATA) oraz Europejskiego Towarzystwa Tyreologicznego (ETA), w dużym stopniu usystematyzowały zasady postępowania w chorobach tarczycy w czasie ciąży i w okresie poporodowym. Pomimo ogromnego postępu wiedzy na temat wzajemnego wpływu ciąży i funkcji gruczołu tarczowego w zdrowiu i chorobie, jaki osiągnięto w ciągu ostatnich kilkunastu lat, nadal pewne obszary wymagają dalszych badań. W ciągu 3 lat, które minęły od publikacji wytycznych, przybyło danych, które wpłynęły na niektóre zasady prowadzenia ciężarnej z chorobą tarczycy. Wytyczne nie zawsze mają charakter uniwersalny i nie mogą być w prosty sposób transponowane na społeczeństwa zróżnicowane etnicznie i ekonomicznie, o odmiennych zwyczajach dietetycznych, w tym w spożyciu nośników jodu, oraz stosujące odmienne modele profilaktyki jodowej. W 2008 roku powołano Zespół Ekspertów do spraw Opieki Tyreologicznej w Ciąży. Za cele prac Zespołu przyjęto: opracowanie modelu opieki nad ciężarną z zaburzeniami funkcji tarczycy, określenie grupy kobiet z ryzykiem zaburzeń funkcji tarczycy wymagających oceny tyreologicznej podczas planowania ciąży, w trakcie jej trwania oraz w okresie poporodowym — czyli przygotowanie polskich wskazań do badań przesiewowych oraz ustalenie wartości referencyjnych stężeń hormonów tarczycy w poszczególnych trymestrach ciąży. Opracowane przez Zespół wytyczne systematyzują zasady opieki tyreologicznej nad kobietą ciężarną w Polsce. (Endokrynol Pol 2011; 62 (4): 362–381

Matrix delivery transdermal 17beta-estradiol for the prevention of bone loss in postmenopausal women. The International Study Group.

A total of 277 early postmenopausal women were enrolled in this placebo-controlled 2-year study to examine the efficacy of a matrix transdermal 17beta-estradiol system, at three different dosages (25, 50 and 75 mg/day) combined with sequential oral dydrogesterone 20 mg/day, in preventing bone loss. At 2 years, the difference from placebo in percentage change from baseline of L1-4 lumbar spine bone mineral density (BMD) (assessed by dual-energy X-ray absorptiometry) was 4.7% +/- 0.7% with estradiol 25 mg/day, 7.3% +/- 0.7% with estradiol 50 mg/day and 8.7% +/- 0.7% with estradiol 75 mg/day (all values mean +/- SEM). There were also significant increases in femoral neck, trochanter and total hip BMD with all doses of estradiol compared with placebo. Additionally, most patients had a significant gain (increase greater than 2.08%) in lumbar spine bone mass compared with placebo. Patients who received estradiol also experienced clinically significant and dose-related decreases in total serum osteocalcin, serum bone alkaline phosphatase and urinary C-telopeptide, with all three markers of bone turnover returning to premenopausal levels. Estradiol was well tolerated during the 2-year treatment period. Transdermal estradiol is effective and well tolerated at dosages between 25-75 mg/day in the prevention of bone loss in postmenopausal women; 25 mg/day offers an effective option for those women who cannot tolerate higher doses

Matrix delivery transdermal 17 beta-estradiol for the prevention of bone loss in postmenopausal women

A total of 277 early postmenopausal women were enrolled in this placebo-controlled 2-year study to examine the efficacy of a matrix transdermal 17β-estradiol system, at three different dosages (25, 50 and 75 μg/day) combined with sequential oral dydrogesterone 20 mg/day, in preventing bone loss. At 2 years, the difference from placebo in percentage change from baseline of L1-4 lumbar spine bone mineral density (BMD) (assessed by dual-energy X-ray absorptiometry) was 4.7% ± 0.7% with estradiol 25 μg/day, 7.3% ± 0.7% with estradiol 50 μg/day and 8.7% ± 0.7% with estradiol 75 μg/day (all values mean ± SEM). There were also significant increases in femoral neck, trochanter and total hip BMD with all doses of estradiol compared with placebo. Additionally, most patients had a significant gain (increase greater than 2.08%) in lumbar spine bone mass compared with placebo. Patients who received estradiol also experienced clinically significant and dose-related decreases in total serum osteocalcin, serum bone alkaline phosphatase and urinary C-telopeptide, with all three markers of bone turnover returning to premenopausal levels. Estradiol was well tolerated during the 2-year treatment period. Transdermal estradiol is effective and well tolerated at dosages between 25-75 μg/day in the prevention of bone loss in postmenopausal women; 25 μg/day offers an effective option for those women who cannot tolerate higher doses

Lipotoxicity, neuroinflammation, glial cells and oestrogenic compounds

The high concentrations of free fatty acids as a consequence of obesity and overweight have become risk factors for the development of different diseases including neurodegenerative ailments. Free fatty acids (FAs) are strongly related to inflammatory events, causing cellular and tissue alterations in the brain, including cell death, deficits in neurogenesis and gliogenesis and cognitive decline. It has been reported that people with a high body mass index have a higher risk of suffering from Alzheimer's disease. Hormones such as estradiol not only have beneficial effects on brain tissue but also exert some adverse effects on peripheral tissues including the ovary and breast. For this reason, some studies have evaluated the protective effect of estrogen receptor (ER) agonists with more specific tissue activities, such as the neuroactive steroid tibolone. Activation of ERs positively affects the expression of pro-survival factors and cell signaling pathways, thus promoting cell survival. This review aims to discuss the relationship between lipotoxicity and the development of neurodegenerative diseases. We also elaborate on the cellular and molecular mechanisms involved in neuroprotection induced by estrogens