Browsing by Author "Lambrinoudaki, Irene (6601969370)"

Osteoporosis and the resulting fractures are major public health issues as the world population is ageing. Various therapies such as bisphosphonates, strontium ranelate and more recently denosumab are available. This clinical guide provides the evidence for the clinical use of selective estrogen modulators (SERMs) in the management of osteoporosis in postmenopausal women. © 2011 Elsevier Ireland Ltd.

Osteoporosis and the resulting fractures are major public health issues as the world population is ageing. Various therapies such as bisphosphonates, strontium ranelate and more recently denosumab are available. This clinical guide provides the evidence for the clinical use of selective estrogen modulators (SERMs) in the management of osteoporosis in postmenopausal women. © 2011 Elsevier Ireland Ltd.

Introduction: Venous thromboembolism (VTE), including deep venous thrombosis (DVT) and pulmonary embolism (PE), is a serious cardiovascular event whose incidence rises with increasing age. Aims: To formulate a position statement on the management of the menopause in women with a personal or family history of VTE. Material and methods: Literature review and consensus of expert opinion. Results and conclusions: Randomized controlled trials have shown an increased risk of VTE in oral hormone therapy (HT) users. There are no randomized trial data on the effect of transdermal estrogen on VTE. Recent observational studies and meta-analyses suggest that transdermal estrogen does not increase VTE risk. These clinical observations are supported by experimental data showing that transdermal estrogen has a minimal effect on hepatic metabolism of hemostatic proteins as the portal circulation is bypassed. A personal or family history of VTE, especially in individuals with a prothrombotic mutation, is a strong contraindication to oral HT but transdermal estrogen can be considered after careful individual evaluation of the benefits and risks. Transdermal estrogen should be also the first choice in overweight/obese women requiring HT. Observational studies suggest that micronized progesterone and dydrogesterone might have a better risk profile than other progestins with regard to VTE risk. Although these findings should be confirmed by randomized clinical trials, they strongly suggest that both the route of estrogen administration and the type of progestin may be important determinants of the overall benefit-risk profile of HT. © 2011 Elsevier Ireland Ltd. All rights reserved.

Introduction: Venous thromboembolism (VTE), including deep venous thrombosis (DVT) and pulmonary embolism (PE), is a serious cardiovascular event whose incidence rises with increasing age. Aims: To formulate a position statement on the management of the menopause in women with a personal or family history of VTE. Material and methods: Literature review and consensus of expert opinion. Results and conclusions: Randomized controlled trials have shown an increased risk of VTE in oral hormone therapy (HT) users. There are no randomized trial data on the effect of transdermal estrogen on VTE. Recent observational studies and meta-analyses suggest that transdermal estrogen does not increase VTE risk. These clinical observations are supported by experimental data showing that transdermal estrogen has a minimal effect on hepatic metabolism of hemostatic proteins as the portal circulation is bypassed. A personal or family history of VTE, especially in individuals with a prothrombotic mutation, is a strong contraindication to oral HT but transdermal estrogen can be considered after careful individual evaluation of the benefits and risks. Transdermal estrogen should be also the first choice in overweight/obese women requiring HT. Observational studies suggest that micronized progesterone and dydrogesterone might have a better risk profile than other progestins with regard to VTE risk. Although these findings should be confirmed by randomized clinical trials, they strongly suggest that both the route of estrogen administration and the type of progestin may be important determinants of the overall benefit-risk profile of HT. © 2011 Elsevier Ireland Ltd. All rights reserved.

Introduction: Premature ovarian failure (also known as premature menopause) is defined as menopause before the age of 40. It can be "natural" or "iatrogenic" such as after bilateral oophorectomy. It may be either primary or secondary. In the majority of cases of primary POF the cause is unknown. Chromosome abnormalities (especially X chromosome), follicle-stimulating hormone receptor gene polymorphisms, inhibin B mutations, enzyme deficiencies and autoimmune disease may be involved. Secondary POF is becoming more important as survival after treatment of malignancy through surgery, radiotherapy and chemotherapy continues to improve. Aim: To formulate a position statement on the management of premature ovarian failure. Materials and methods: Literature review and consensus of expert opinion. Results and conclusions: Diagnosis should be confirmed with an elevated FSH greater than 40 IU/L and an estradiol level below 50 pmol/L in the absence of bilateral oophorectomy. Further assessment should include thyroid function tests, autoimmune screen for polyendocrinopathy, karyotype (less than 30 years of age) and bone mineral density. Untreated early ovarian failure increases the risk of osteoporosis, cardiovascular disease, dementia, cognitive decline and Parkinsonism. The mainstay of treatment is hormone therapy which needs to be continued until the average age of the natural menopause. With regard to fertility, while spontaneous ovulation may occur the best chance of achieving pregnancy is through donor oocyte in vitro fertilization. It is essential that women are provided with adequate information as they may find it a difficult diagnosis to accept. It is recommended that women with POF are seen in a specialist unit able to deal with their multiple needs. © 2010 Elsevier Ireland Ltd. All rights reserved.

Introduction: Premature ovarian failure (also known as premature menopause) is defined as menopause before the age of 40. It can be "natural" or "iatrogenic" such as after bilateral oophorectomy. It may be either primary or secondary. In the majority of cases of primary POF the cause is unknown. Chromosome abnormalities (especially X chromosome), follicle-stimulating hormone receptor gene polymorphisms, inhibin B mutations, enzyme deficiencies and autoimmune disease may be involved. Secondary POF is becoming more important as survival after treatment of malignancy through surgery, radiotherapy and chemotherapy continues to improve. Aim: To formulate a position statement on the management of premature ovarian failure. Materials and methods: Literature review and consensus of expert opinion. Results and conclusions: Diagnosis should be confirmed with an elevated FSH greater than 40 IU/L and an estradiol level below 50 pmol/L in the absence of bilateral oophorectomy. Further assessment should include thyroid function tests, autoimmune screen for polyendocrinopathy, karyotype (less than 30 years of age) and bone mineral density. Untreated early ovarian failure increases the risk of osteoporosis, cardiovascular disease, dementia, cognitive decline and Parkinsonism. The mainstay of treatment is hormone therapy which needs to be continued until the average age of the natural menopause. With regard to fertility, while spontaneous ovulation may occur the best chance of achieving pregnancy is through donor oocyte in vitro fertilization. It is essential that women are provided with adequate information as they may find it a difficult diagnosis to accept. It is recommended that women with POF are seen in a specialist unit able to deal with their multiple needs. © 2010 Elsevier Ireland Ltd. All rights reserved.

Introduction: There is emerging evidence on the widespread tissue effects of vitamin D. Aims: To formulate a position statement on the role of vitamin D in postmenopausal women. Materials and methods: Literature review and consensus of expert opinion. Results and conclusions: Epidemiological and prospective studies have related vitamin D deficiency with not only osteoporosis but also cardiovascular disease, diabetes, cancer, infections and neurodegenerative disease. However the evidence is robust for skeletal but not nonskeletal outcomes where data from large prospective studies are lacking. The major natural source of vitamin D is cutaneous synthesis through exposure to sunlight with a small amount from the diet in animal-based foods such as fatty fish, eggs and milk. Vitamin D status is determined by measuring serum 25-hydroxyvitamin D [25(OH)D] levels. Optimal serum 25(OH)D levels are in the region of 30-90 ng/mL (75-225 nmol/L) though there is no international consensus. Levels vary according to time of the year (lower in the winter), latitude, altitude, air pollution, skin pigmentation, use of sunscreens and clothing coverage. Risk factors for low serum 25(OH)D levels include: obesity, malabsorption syndromes, medication use (e.g. anticonvulsants, antiretrovirals), skin aging, low sun exposure and those in residential care. Fortified foods do not necessarily provide sufficient amounts of vitamin D. Regular sunlight exposure (without sunscreens) for 15 min, 3-4 times a week, in the middle of the day in summer generate healthy levels. The recommended daily allowance is 600 IU/day increasing to 800 IU/day in those aged 71 years and older. Supplementation can be undertaken with either vitamin D2 (ergocalciferol) or vitamin D3 (cholecalciferol) with monitoring depending on the dose used and the presence of concomitant medical conditions such as renal disease. © 2011 Elsevier Ireland Ltd. All rights reserved.

Introduction: There is emerging evidence on the widespread tissue effects of vitamin D. Aims: To formulate a position statement on the role of vitamin D in postmenopausal women. Materials and methods: Literature review and consensus of expert opinion. Results and conclusions: Epidemiological and prospective studies have related vitamin D deficiency with not only osteoporosis but also cardiovascular disease, diabetes, cancer, infections and neurodegenerative disease. However the evidence is robust for skeletal but not nonskeletal outcomes where data from large prospective studies are lacking. The major natural source of vitamin D is cutaneous synthesis through exposure to sunlight with a small amount from the diet in animal-based foods such as fatty fish, eggs and milk. Vitamin D status is determined by measuring serum 25-hydroxyvitamin D [25(OH)D] levels. Optimal serum 25(OH)D levels are in the region of 30-90 ng/mL (75-225 nmol/L) though there is no international consensus. Levels vary according to time of the year (lower in the winter), latitude, altitude, air pollution, skin pigmentation, use of sunscreens and clothing coverage. Risk factors for low serum 25(OH)D levels include: obesity, malabsorption syndromes, medication use (e.g. anticonvulsants, antiretrovirals), skin aging, low sun exposure and those in residential care. Fortified foods do not necessarily provide sufficient amounts of vitamin D. Regular sunlight exposure (without sunscreens) for 15 min, 3-4 times a week, in the middle of the day in summer generate healthy levels. The recommended daily allowance is 600 IU/day increasing to 800 IU/day in those aged 71 years and older. Supplementation can be undertaken with either vitamin D2 (ergocalciferol) or vitamin D3 (cholecalciferol) with monitoring depending on the dose used and the presence of concomitant medical conditions such as renal disease. © 2011 Elsevier Ireland Ltd. All rights reserved.

Aging and its underlying pathophysiological background has always attracted the attention of the scientific society. Defined as the gradual, time-dependent, heterogeneous decline of physiological functions, aging is orchestrated by a plethora of molecular mechanisms, which vividly interact to alter body homeostasis. The ability of an organism to adjust to these alterations, in conjunction with the dynamic effect of various environmental stimuli across lifespan, promotes longevity, frailty or disease. Endocrine function undergoes major changes during aging, as well. Specifically, alterations in hormonal networks and concomitant hormonal deficits/excess, augmented by poor sensitivity of tissues to their action, take place. As hypothalamic-pituitary unit is the central regulator of crucial body functions, these alterations can be translated in significant clinical sequelae that can impair the quality of life and promote frailty and disease. Delineating the hormonal signaling alterations that occur across lifespan and exploring possible remedial interventions could possibly help us improve the quality of life of the elderly and promote longevity. © 2017 European Society of Endocrinology Printed in Great Britain.

Aging and its underlying pathophysiological background has always attracted the attention of the scientific society. Defined as the gradual, time-dependent, heterogeneous decline of physiological functions, aging is orchestrated by a plethora of molecular mechanisms, which vividly interact to alter body homeostasis. The ability of an organism to adjust to these alterations, in conjunction with the dynamic effect of various environmental stimuli across lifespan, promotes longevity, frailty or disease. Endocrine function undergoes major changes during aging, as well. Specifically, alterations in hormonal networks and concomitant hormonal deficits/excess, augmented by poor sensitivity of tissues to their action, take place. As hypothalamic-pituitary unit is the central regulator of crucial body functions, these alterations can be translated in significant clinical sequelae that can impair the quality of life and promote frailty and disease. Delineating the hormonal signaling alterations that occur across lifespan and exploring possible remedial interventions could possibly help us improve the quality of life of the elderly and promote longevity. © 2017 European Society of Endocrinology Printed in Great Britain.

As type 2 diabetes mellitus (T2DM) is affected by both chronological and ovarian ageing, it is common in postmenopausal women. This review analyses and critically appraises the literature regarding the optimal therapeutic strategies for T2DM in women after menopause. Lifestyle interventions, including changes in dietary habits and physical exercise in everyday life targeting a modest weight loss (5%), represent the cornerstone of management. Limited intake of alcohol and sodium, as well as smoking cessation, are additional lifestyle changes for both endothelial and bone health. Regarding medications, postmenopausal women should be initially treated with metformin, concurrently with lifestyle intervention. If glycosylated haemoglobin (HbA1c) remains over the target level (usually ≥7%), dipeptidyl peptidase-4 inhibitors (DPP-4i) or glucagon-like peptide-1 receptor agonists (GLP-1RA) should be preferred. Thiazolidinediones (TZDs) and canagliflozin should be avoided in postmenopausal women with increased fracture risk. Insulin should be used with caution to avoid hypoglycaemia. Bariatric surgery is a well established and effective therapeutic option for both weight loss and glycaemic control in very obese patients with T2DM; however, metabolic benefits should be balanced against nutritional deficiencies that often present after surgery. Proper control of hypertension, with avoidance of hypotension, is of great importance as a measure against falls. Annual tests for retinopathy and neuropathy are crucial for the same reason. Menopausal hormone therapy (MHT) has a beneficial effect on glucose homeostasis, reduces the risk of new-onset T2DM and improves glucose control in women with T2DM. T2DM has been considered a cardiovascular disease equivalent, which meant that postmenopausal women with the disease could not take MHT but current evidence supports an individualised approach to this issue. Therapeutic strategies for women with T2DM after menopause should aim to maximise benefits for metabolic, cardiovascular and bone health with the minimum of adverse effects, bearing in mind that most women will spend more than one-third of their life being of postmenopausal status. © 2019 Elsevier B.V.

As type 2 diabetes mellitus (T2DM) is affected by both chronological and ovarian ageing, it is common in postmenopausal women. This review analyses and critically appraises the literature regarding the optimal therapeutic strategies for T2DM in women after menopause. Lifestyle interventions, including changes in dietary habits and physical exercise in everyday life targeting a modest weight loss (5%), represent the cornerstone of management. Limited intake of alcohol and sodium, as well as smoking cessation, are additional lifestyle changes for both endothelial and bone health. Regarding medications, postmenopausal women should be initially treated with metformin, concurrently with lifestyle intervention. If glycosylated haemoglobin (HbA1c) remains over the target level (usually ≥7%), dipeptidyl peptidase-4 inhibitors (DPP-4i) or glucagon-like peptide-1 receptor agonists (GLP-1RA) should be preferred. Thiazolidinediones (TZDs) and canagliflozin should be avoided in postmenopausal women with increased fracture risk. Insulin should be used with caution to avoid hypoglycaemia. Bariatric surgery is a well established and effective therapeutic option for both weight loss and glycaemic control in very obese patients with T2DM; however, metabolic benefits should be balanced against nutritional deficiencies that often present after surgery. Proper control of hypertension, with avoidance of hypotension, is of great importance as a measure against falls. Annual tests for retinopathy and neuropathy are crucial for the same reason. Menopausal hormone therapy (MHT) has a beneficial effect on glucose homeostasis, reduces the risk of new-onset T2DM and improves glucose control in women with T2DM. T2DM has been considered a cardiovascular disease equivalent, which meant that postmenopausal women with the disease could not take MHT but current evidence supports an individualised approach to this issue. Therapeutic strategies for women with T2DM after menopause should aim to maximise benefits for metabolic, cardiovascular and bone health with the minimum of adverse effects, bearing in mind that most women will spend more than one-third of their life being of postmenopausal status. © 2019 Elsevier B.V.