Search Results
You are looking at 1 - 10 of 118 items for :
- Abstract: Calcium x
- Abstract: Menopause x
- Abstract: Osteo* x
K.G. Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Search for other papers by Elinor Chelsom Vogt in
Google Scholar
PubMed
Department of Gynecology and Obstetrics, Haukeland University Hospital, Bergen, Norway
Search for other papers by Francisco Gómez Real in
Google Scholar
PubMed
K.G. Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Search for other papers by Eystein Sverre Husebye in
Google Scholar
PubMed
Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Stockholm, Sweden
Search for other papers by Sigridur Björnsdottir in
Google Scholar
PubMed
Department of Sleep, Landspitali University Hospital Reykjavík, Reykjavik, Iceland
Search for other papers by Bryndis Benediktsdottir in
Google Scholar
PubMed
Search for other papers by Randi Jacobsen Bertelsen in
Google Scholar
PubMed
Search for other papers by Pascal Demoly in
Google Scholar
PubMed
Search for other papers by Karl Anders Franklin in
Google Scholar
PubMed
Search for other papers by Leire Sainz de Aja Gallastegui in
Google Scholar
PubMed
Search for other papers by Francisco Javier Callejas González in
Google Scholar
PubMed
Allergy and Lung Health Unit, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Victoria, Australia
Search for other papers by Joachim Heinrich in
Google Scholar
PubMed
Search for other papers by Mathias Holm in
Google Scholar
PubMed
Search for other papers by Nils Oscar Jogi in
Google Scholar
PubMed
Search for other papers by Benedicte Leynaert in
Google Scholar
PubMed
Search for other papers by Eva Lindberg in
Google Scholar
PubMed
Search for other papers by Andrei Malinovschi in
Google Scholar
PubMed
Albacete Faculty of Medicine, Castilla-La Mancha University, Albacete, Spain
Search for other papers by Jesús Martínez-Moratalla in
Google Scholar
PubMed
Search for other papers by Raúl Godoy Mayoral in
Google Scholar
PubMed
Search for other papers by Anna Oudin in
Google Scholar
PubMed
Search for other papers by Antonio Pereira-Vega in
Google Scholar
PubMed
Search for other papers by Chantal Raherison Semjen in
Google Scholar
PubMed
The National Research Center for the Working Environment, Copenhagen, Denmark
Search for other papers by Vivi Schlünssen in
Google Scholar
PubMed
Search for other papers by Kai Triebner in
Google Scholar
PubMed
K.G. Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Search for other papers by Marianne Øksnes in
Google Scholar
PubMed
Objective
To investigate markers of premature menopause (<40 years) and specifically the prevalence of autoimmune primary ovarian insufficiency (POI) in European women.
Design
Postmenopausal women were categorized according to age at menopause and self-reported reason for menopause in a cross-sectional analysis of 6870 women.
Methods
Variables associated with the timing of menopause and hormone measurements of 17β-estradiol and follicle-stimulating hormone were explored using multivariable logistic regression analysis. Specific immunoprecipitating assays of steroidogenic autoantibodies against 21-hydroxylase (21-OH), side-chain cleavage enzyme (anti-SCC) and 17alpha-hydroxylase (17 OH), as well as NACHT leucine-rich-repeat protein 5 were used to identify women with likely autoimmune POI.
Results
Premature menopause was identified in 2.8% of women, and these women had higher frequencies of nulliparity (37.4% vs 19.7%), obesity (28.7% vs 21.4%), osteoporosis (17.1% vs 11.6%), hormone replacement therapy (59.1% vs 36.9%) and never smokers (60.1% vs 50.9%) (P < 0.05), compared to women with menopause ≥40 years. Iatrogenic causes were found in 91 (47%) and non-ovarian causes in 27 (14%) women, while 77 (39%) women were classified as POI of unknown cause, resulting in a 1.1% prevalence of idiopathic POI. After adjustments nulliparity was the only variable significantly associated with POI (odds ratio 2.46; 95% CI 1.63–3.42). Based on the presence of autoantibodies against 21 OH and SCC, 4.5% of POI cases were of likely autoimmune origin.
Conclusion
Idiopathic POI affects 1.1% of all women and almost half of the women with premature menopause. Autoimmunity explains 4.5% of these cases judged by positive steroidogenic autoantibodies.
Department of Nutrition, Institute of Life Sciences, Federal University of Juiz de Fora, Governador Valadares, Minas Gerais, Brazil
Department of Nutrition, Faculty of Health and Medical Sciences, University of Surrey, University of Surrey, Guildford, UK
Search for other papers by Marcela Moraes Mendes in
Google Scholar
PubMed
Search for other papers by Patricia Borges Botelho in
Google Scholar
PubMed
Search for other papers by Helena Ribeiro in
Google Scholar
PubMed
Vitamin D enhances calcium absorption and bone mineralisation, promotes maintenance of muscle function, and is crucial for musculoskeletal health. Low vitamin D status triggers secondary hyperparathyroidism, increases bone loss, and leads to muscle weakness. The primary physiologic function of vitamin D and its metabolites is maintaining calcium homeostasis for metabolic functioning, signal transduction, and neuromuscular activity. A considerable amount of human evidence supports the well-recognised contribution of adequate serum 25-hydroxyvitamin D concentrations for bone homeostasis maintenance and prevention and treatment strategies for osteoporosis when combined with adequate calcium intake. This paper aimed to review the literature published, mainly in the last 20 years, on the effect of vitamin D and its supplementation for musculoskeletal health in order to identify the aspects that remain unclear or controversial and therefore require further investigation and debate. There is a clear need for consistent data to establish realistic and meaningful recommendations of vitamin D status that consider different population groups and locations. Moreover, there is still a lack of consensus on thresholds for vitamin D deficiency and optimal status as well as toxicity, optimal intake of vitamin D, vitamin D supplement alone as a strategy to prevent fractures and falls, recommended sun exposure at different latitudes and for different skin pigmentations, and the extra skeletal effects of vitamin D.
Search for other papers by Gabriella Oliveira Lima in
Google Scholar
PubMed
Search for other papers by Alex Luiz Menezes da Silva in
Google Scholar
PubMed
Search for other papers by Julianne Elba Cunha Azevedo in
Google Scholar
PubMed
Search for other papers by Chirlene Pinheiro Nascimento in
Google Scholar
PubMed
Search for other papers by Luana Rodrigues Vieira in
Google Scholar
PubMed
Search for other papers by Akira Otake Hamoy in
Google Scholar
PubMed
Search for other papers by Luan Oliveira Ferreira in
Google Scholar
PubMed
Search for other papers by Verônica Regina Lobato Oliveira Bahia in
Google Scholar
PubMed
Search for other papers by Nilton Akio Muto in
Google Scholar
PubMed
Search for other papers by Dielly Catrina Favacho Lopes in
Google Scholar
PubMed
Search for other papers by Moisés Hamoy in
Google Scholar
PubMed
Low plasma levels of vitamin D causes bone mineral change that can precipitate osteopenia and osteoporosis and could aggravate autoimmune diseases, hypertension and diabetes. The demand for vitamin D supplementation becomes necessary; however, the consumption of vitamin D is not without risks, which its toxicity could have potentially serious consequences related to hypervitaminosis D, such as hypercalcemia and cerebral alterations. Thus, the present study describes the electroencephalographic changes caused by supraphysiological doses of vitamin D in the brain electrical dynamics and the electrocardiographic changes. After 4 days of treatment with vitamin D at a dose of 25,000 IU/kg, the serum calcium levels found were increased in comparison with the control group. The electrocorticogram analysis found a reduction in wave activity in the delta, theta, alpha and beta frequency bands. For ECG was observed changes with shortened QT follow-up, which could be related to serum calcium concentration. This study presented important evidence about the cerebral and cardiac alterations caused by high doses of vitamin D, indicating valuable parameters in the screening and decision-making process for diagnosing patients with symptoms suggestive of intoxication.
Faculté de Chirurgie Dentaire, Université de Toulouse III, Toulouse, France
Search for other papers by Emmanuelle Noirrit in
Google Scholar
PubMed
Search for other papers by Mélissa Buscato in
Google Scholar
PubMed
Search for other papers by Marion Dupuis in
Google Scholar
PubMed
CHU de Toulouse, Laboratoire d’Hématologie, Toulouse, France
Search for other papers by Bernard Payrastre in
Google Scholar
PubMed
Search for other papers by Coralie Fontaine in
Google Scholar
PubMed
Search for other papers by Jean-François Arnal in
Google Scholar
PubMed
Faculté de Chirurgie Dentaire, Université de Toulouse III, Toulouse, France
Search for other papers by Marie-Cécile Valera in
Google Scholar
PubMed
Estrogen–progestin therapy was previously considered as the standard of care for managing bothersome symptoms associated with menopause, but it increases risks of breast cancer and of thromboembolism. The combination of conjugated estrogen (CE) with bazedoxifene (BZA) named tissue-selective estrogen complex (TSEC) was designed to minimize or even abrogate the undesirable effects on breast, while maintaining the beneficial effects such as prevention of osteoporosis and suppression of climacteric symptoms. The risk on thromboembolism associated with TSEC is unknown, although the clinical available data are reassuring. The aim of this study was to define the impact of a chronic administration of CE, BZA or CE + BZA on hemostasis and thrombosis in ovariectomized mice. As expected, CE, but not BZA neither CE + BZA, induced uterine and vagina hypertrophy. As previously demonstrated for 17β-estradiol (E2), we found that CE (i) increased tail-bleeding time, (ii) prevented occlusive thrombus formation in injured carotid artery and (iii) protected against collagen/epinephrine-induced thromboembolism. Thus, whereas BZA antagonized CE action on reproductive tissues, it had no impact on the effect of CE on hemostasis, thromboembolism and arterial thrombosis in mice. CE + BZA shared the anti-thrombotic actions of CE in these mouse models. If a similar process is at work in women, CE combined with BZA could contribute to minimize the risk of thrombosis associated with hormone replacement therapy.
Search for other papers by Keina Nishio in
Google Scholar
PubMed
Search for other papers by Akiko Tanabe in
Google Scholar
PubMed
Search for other papers by Risa Maruoka in
Google Scholar
PubMed
Search for other papers by Kiyoko Nakamura in
Google Scholar
PubMed
Search for other papers by Masaaki Takai in
Google Scholar
PubMed
Search for other papers by Tatsuharu Sekijima in
Google Scholar
PubMed
Search for other papers by Satoshi Tunetoh in
Google Scholar
PubMed
Search for other papers by Yoshito Terai in
Google Scholar
PubMed
Search for other papers by Masahide Ohmichi in
Google Scholar
PubMed
Objective
Although surgical menopause may increase the risks of osteoporosis, few studies have investigated the influence of chemotherapy and radiation therapy. The aim of this study is to evaluate the effects of treatments for gynecological malignancies on bone mineral density (BMD).
Methods
This study enrolled 35 premenopausal women (15 ovarian cancers (OCs), 9 endometrial cancers (ECs), and 11 cervical cancers (CCs)) who underwent surgical treatment that included bilateral oophorectomy with or without adjuvant platinum-based chemotherapy in OC and EC patients, or concurrent chemo-radiation therapy (CCRT) in CC patients according to the established protocols at the Osaka Medical College Hospital between 2006 and 2008. The BMD of the lumbar spine (L1–L4) was measured by dual-energy X-ray absorptiometry, and urine cross-linked telopeptides of type I collagen (NTx) and bone alkaline phosphatase (BAP) were assessed for evaluation of bone resorption and bone formation respectively. These assessments were performed at baseline and 12 months after treatment.
Results
Although the serum BAP was significantly increased only in the CC group, a rapid increase in the bone resorption marker urinary NTx was observed in all groups. The BMD, 12 months after CCRT was significantly decreased in the CC group at 91.9±5.9% (P<0.05 in comparison to the baseline).
Conclusion
This research suggests that anticancer therapies for premenopausal women with gynecological malignancies increase bone resorption and may reduce BMD, particularly in CC patients who have received CCRT. Therefore, gynecologic cancer survivors should be educated about these potential risks and complications.
Search for other papers by Alessandro Brancatella in
Google Scholar
PubMed
Search for other papers by Claudio Marcocci in
Google Scholar
PubMed
Thyroid hormones stimulate bone turnover in adults by increasing osteoclastic bone resorption. TSH suppressive therapy is usually applied in patients with differentiated thyroid cancer (DTC) to improve the disease outcome. Over the last decades several authors have closely monitored the potential harm suffered by the skeletal system. Several studies and meta-analyses have shown that chronic TSH suppressive therapy is safe in premenopausal women and men. Conversely, in postmenopausal women TSH suppressive therapy is associated with a decrease of bone mineral density, deterioration of bone architecture (quantitative CT, QCT; trabecular bone score, TBS), and, possibly, an increased risk of fractures. The TSH receptor is expressed in bone cells and the results of experimental studies in TSH receptor knockout mice and humans on whether low TSH levels, as opposed to solely high thyroid hormone levels, might contribute to bone loss in endogenous or exogenous thyrotoxicosis remain controversial. Recent guidelines on the use of TSH suppressive therapy in patients with DTC give value not only to its benefit on the outcome of the disease, but also to the risks associated with exogenous thyrotoxicosis, namely menopause, osteopenia or osteoporosis, age >60 years, and history of atrial fibrillation. Bone health (BMD and/or preferably TBS) should be evaluated in postmenopausal women under chronic TSH suppressive therapy or in those patients planning to be treated for several years. Antiresorptive therapy could also be considered in selected cases (increased risk of fracture or significant decline of BMD/TBS during therapy) to prevent bone loss.
Search for other papers by Nancy Martini in
Google Scholar
PubMed
Search for other papers by Lucas Streckwall in
Google Scholar
PubMed
Search for other papers by Antonio Desmond McCarthy in
Google Scholar
PubMed
In post-menopausal women, aged individuals, and patients with diabetes mellitus or chronic renal disease, bone mineral density (BMD) decreases while the vasculature accumulates arterial calcifications (ACs). AC can be found in the tunica intima and/or in the tunica media. Prospective studies have shown that patients with initially low BMD and/or the presence of fragility fractures have at follow-up a significantly increased risk for coronary and cerebrovascular events and for overall cardiovascular mortality. Similarly, patients presenting with abdominal aorta calcifications (an easily quantifiable marker of vascular pathology) show a significant decrease in the BMD (and an increase in the fragility) of bones irrigated by branches of the abdominal aorta, such as the hip and lumbar spine. AC induction is an ectopic tissue biomineralization process promoted by osteogenic transdifferentiation of vascular smooth muscle cells as well as by local and systemic secreted factors. In many cases, the same regulatory molecules modulate bone metabolism but in reverse. Investigation of animal and in vitro models has identified several potential mechanisms for this reciprocal bone–vascular regulation, such as vitamin K and D sufficiency, advanced glycation end-products–RAGE interaction, osteoprotegerin/RANKL/RANK, Fetuin A, oestrogen deficiency and phytooestrogen supplementation, microbiota and its relation to diet, among others. Complete elucidation of these potential mechanisms, as well as their clinical validation via controlled studies, will provide a basis for pharmacological intervention that could simultaneously promote bone and vascular health.
Search for other papers by E M Winter in
Google Scholar
PubMed
Search for other papers by A Ireland in
Google Scholar
PubMed
Search for other papers by N C Butterfield in
Google Scholar
PubMed
Search for other papers by M Haffner-Luntzer in
Google Scholar
PubMed
Search for other papers by M-N Horcajada in
Google Scholar
PubMed
Jan van Goyen Medical Center, Department of Internal Medicine, Amsterdam, the Netherlands
Search for other papers by A G Veldhuis-Vlug in
Google Scholar
PubMed
Department of Epidemiology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands
Search for other papers by L Oei in
Google Scholar
PubMed
Search for other papers by G Colaianni in
Google Scholar
PubMed
Search for other papers by N Bonnet in
Google Scholar
PubMed
In this review we discuss skeletal adaptations to the demanding situation of pregnancy and lactation. Calcium demands are increased during pregnancy and lactation, and this is effectuated by a complex series of hormonal changes. The changes in bone structure at the tissue and whole bone level observed during pregnancy and lactation appear to largely recover over time. The magnitude of the changes observed during lactation may relate to the volume and duration of breastfeeding and return to regular menses. Studies examining long-term consequences of pregnancy and lactation suggest that there are small, site-specific benefits to bone density and that bone geometry may also be affected. Pregnancy- and lactation-induced osteoporosis (PLO) is a rare disease for which the pathophysiological mechanism is as yet incompletely known; here, we discuss and speculate on the possible roles of genetics, oxytocin, sympathetic tone and bone marrow fat. Finally, we discuss fracture healing during pregnancy and lactation and the effects of estrogen on this process.
Search for other papers by Panagiotis Anagnostis in
Google Scholar
PubMed
Search for other papers by Irene Lambrinoudaki in
Google Scholar
PubMed
Search for other papers by John C Stevenson in
Google Scholar
PubMed
Search for other papers by Dimitrios G Goulis in
Google Scholar
PubMed
Cardiovascular disease (CVD) is of major concern in women entering menopause. The changing hormonal milieu predisposes them to increased CVD risk, due to a constellation of risk factors, such as visceral obesity, atherogenic dyslipidemia, dysregulation in glucose homeostasis, non-alcoholic fatty liver disease and arterial hypertension. However, an independent association of menopause per se with increased risk of CVD events has only been proven for early menopause (<45 years). Menopausal hormone therapy (MHT) ameliorates most of the CVD risk factors mentioned above. Transdermal estrogens are the preferable regimen, since they do not increase triglyceride concentrations and they are not associated with increased risk of venous thromboembolic events (VTE). Although administration of MHT should be considered on an individual basis, MHT may reduce CVD morbidity and mortality, if commenced during the early postmenopausal period (<60 years or within ten years since the last menstrual period). In women with premature ovarian insufficiency (POI), MHT should be administered at least until the average age of menopause (50–52 years). MHT is contraindicated in women with a history of VTE and is not currently recommended for the sole purpose of CVD prevention. The risk of breast cancer associated with MHT is generally low and is mainly conferred by the progestogen. Micronized progesterone and dydrogesterone are associated with lower risk compared to other progestogens.
Search for other papers by A Chinoy in
Google Scholar
PubMed
Search for other papers by M Skae in
Google Scholar
PubMed
Search for other papers by A Babiker in
Google Scholar
PubMed
Search for other papers by D Kendall in
Google Scholar
PubMed
Search for other papers by M Z Mughal in
Google Scholar
PubMed
Search for other papers by R Padidela in
Google Scholar
PubMed
Background
Hypoparathyroidism is characterised by hypocalcaemia, and standard management is with an active vitamin D analogue and adequate oral calcium intake (dietary and/or supplements). Little is described in the literature about the impact of intercurrent illnesses on calcium homeostasis in children with hypoparathyroidism.
Methods
We describe three children with hypoparathyroidism in whom intercurrent illnesses led to hypocalcaemia and escalation of treatment with alfacalcidol (1-hydroxycholecalciferol) and calcium supplements.
Results
Three infants managed with standard treatment for hypoparathyroidism (two with homozygous mutations in GCMB2 gene and one with Sanjad-Sakati syndrome) developed symptomatic hypocalcaemia (two infants developed seizures) following respiratory or gastrointestinal illnesses. Substantial increases in alfacalcidol doses (up to three times their pre-illness doses) and calcium supplementation were required to achieve acceptable serum calcium concentrations. However, following resolution of illness, these children developed an increase in serum calcium and hypercalciuria, necessitating rapid reduction to pre-illness dosages of alfacalcidol and oral calcium supplementation.
Conclusion
Intercurrent illness may precipitate symptomatic hypocalcaemia in children with hypoparathyroidism, necessitating increase in dosages of alfacalcidol and calcium supplements. Close monitoring is required on resolution of the intercurrent illness, with timely reduction of dosages of active analogues of vitamin D and calcium supplements to prevent hypercalcaemia, hypercalciuria and nephrocalcinosis.