Search Results
Search for other papers by June Young Choi in
Google Scholar
PubMed
Search for other papers by Jin Wook Yi in
Google Scholar
PubMed
Search for other papers by Jun Hyup Lee in
Google Scholar
PubMed
Search for other papers by Ra-Yeong Song in
Google Scholar
PubMed
Search for other papers by Hyeongwon Yu in
Google Scholar
PubMed
Search for other papers by Hyungju Kwon in
Google Scholar
PubMed
Search for other papers by Young Jun Chai in
Google Scholar
PubMed
Search for other papers by Su-jin Kim in
Google Scholar
PubMed
Search for other papers by Kyu Eun Lee in
Google Scholar
PubMed
The purpose of this study was to assess the relationship between vitamin D receptor gene (VDR) expression and prognostic factors in papillary thyroid cancer (PTC). mRNA sequencing and somatic mutation data from The Cancer Genome Atlas (TCGA) were analyzed. VDR mRNA expression was compared to clinicopathologic variables by linear regression. Tree-based classification was applied to find cutoff and patients were split into low and high VDR group. Logistic regression, Kaplan–Meier analysis, differentially expressed gene (DEG) test and pathway analysis were performed to assess the differences between two VDR groups. VDR mRNA expression was elevated in PTC than that in normal thyroid tissue. VDR expressions were high in classic and tall-cell variant PTC and lateral neck node metastasis was present. High VDR group was also associated with classic and tall cell subtype, AJCC stage IV and lower recurrence-free survival. DEG test reveals that 545 genes were upregulated in high VDR group. Thyroid cancer-related pathways were enriched in high VDR group in pathway analyses. VDR mRNA overexpression was correlated with worse prognostic factors such as subtypes of papillary thyroid carcinoma that are known to be worse prognosis, lateral neck node metastasis, advanced stage and recurrence-free survival.
Endocrinology Unit 2, University of Pisa, Pisa, Italy
Search for other papers by Federica Saponaro in
Google Scholar
PubMed
Laboratory of Clinical Pathology, University Hospital of Pisa, Pisa, Italy
Search for other papers by Alessandro Saba in
Google Scholar
PubMed
Search for other papers by Sabina Frascarelli in
Google Scholar
PubMed
Search for other papers by Concetta Prontera in
Google Scholar
PubMed
Search for other papers by Aldo Clerico in
Google Scholar
PubMed
Search for other papers by Marco Scalese in
Google Scholar
PubMed
Search for other papers by Maria Rita Sessa in
Google Scholar
PubMed
Search for other papers by Filomena Cetani in
Google Scholar
PubMed
Search for other papers by Simona Borsari in
Google Scholar
PubMed
Search for other papers by Elena Pardi in
Google Scholar
PubMed
Search for other papers by Antonella Marvelli in
Google Scholar
PubMed
Search for other papers by Claudio Marcocci in
Google Scholar
PubMed
Search for other papers by Claudio Passino in
Google Scholar
PubMed
Search for other papers by Riccardo Zucchi in
Google Scholar
PubMed
Objectives
The aims of this paper were to evaluate the levels of Vitamin D (VitD) in patients with heart failure (HF), compared to a control group, to assess the effects of VitD on HF outcome and to compare VitD measurement between LIAISON immunoassay and HPLC-MS-MS methods in this population.
Design and Methods
We collected clinical, biochemical and outcome data from 247 patients with HF and in a subgroup of 151 patients, we measured VitD both with LIAISON and HPLC-MS-MS.
Results
HF patients had statistically lower 25OHD levels (45.2 ± 23.7 nmol/L vs 58.2 ± 24.0 nmol/L, P < 0.001) and a statistically higher prevalence of VitD insufficiency (61.1% vs 39.5%, P < 0.001) and deficiency (24.7% vs 6.6%, P < 0.001), compared to healthy controls. There was a significant inverse relationship between baseline 25OHD and risk of HF-related death, with a HR of 0.59 (95% CI 0.37–0.92, P = 0.02), confirmed in a multivariate adjusted analysis. Kaplan–Meier survival analyses showed that VitD insufficiency was associated with reduced survival in HF patients (log rank P = 0.017). There was a good agreement between LIAISON and HPLC-MS-MS (Cohen’s kappa coefficient 0.70), but the prevalence of VitD insufficiency was significantly higher with the former compared to the latter method (58.3%, n = 88 vs 55.6%, n = 84, P < 0.001). LIAISON underestimated the 25OHD levels and showed a mean relative bias of −0.739% with 95% of limits of agreement (−9.00 to +7.52%), when compared to HPLC-MS-MS.
Conclusions
25OHD levels adequately measured by HPLC-MS-MS showed to be low in HF population and to be correlated with HF-related risk of death.
Search for other papers by Kristin Godang in
Google Scholar
PubMed
Search for other papers by Karolina Lundstam in
Google Scholar
PubMed
Search for other papers by Charlotte Mollerup in
Google Scholar
PubMed
Search for other papers by Stine Lyngvi Fougner in
Google Scholar
PubMed
Search for other papers by Ylva Pernow in
Google Scholar
PubMed
Search for other papers by Jörgen Nordenström in
Google Scholar
PubMed
Search for other papers by Thord Rosén in
Google Scholar
PubMed
Search for other papers by Svante Jansson in
Google Scholar
PubMed
Search for other papers by Mikael Hellström in
Google Scholar
PubMed
Faculty of Medicine, University of Oslo, Oslo, Norway
Search for other papers by Jens Bollerslev in
Google Scholar
PubMed
Faculty of Medicine, University of Oslo, Oslo, Norway
Search for other papers by Ansgar Heck in
Google Scholar
PubMed
Search for other papers by the SIPH Study Group in
Google Scholar
PubMed
Context
Mild primary hyperparathyroidism has been associated with increased body fat mass and unfavorable cardiovascular risk factors.
Objective
To assess the effect of parathyroidectomy on fat mass, glucose and lipid metabolism.
Design, patients, interventions, main outcome measures
119 patients previously randomized to observation (OBS; n = 58) or parathyroidectomy (PTX; n = 61) within the Scandinavian Investigation of Primary Hyperparathyroidism (SIPH) trial, an open randomized multicenter study, were included. Main outcome measures for this study were the differences in fat mass, markers for lipid and glucose metabolism between OBS and PTX 5 years after randomization.
Results
In the OBS group, total cholesterol (Total-C) decreased from mean 5.9 (±1.1) to 5.6 (±1.0) mmol/L (P = 0.037) and LDL cholesterol (LDL-C) decreased from 3.7 (±1.0) to 3.3 (±0.9) mmol/L (P = 0.010). In the PTX group, the Total-C and LDL-C remained unchanged resulting in a significant between-group difference over time (P = 0.013 and P = 0.026, respectively). This difference was driven by patients who started with lipid-lowering medication during the study period (OBS: 5; PTX: 1). There was an increase in trunk fat mass in the OBS group, but no between-group differences over time. Mean 25(OH) vitamin D increased in the PTX group (P < 0.001), but did not change in the OBS group. No difference in parameters of glucose metabolism was detected.
Conclusion
In mild PHPT, the measured metabolic and cardiovascular risk factors were not modified by PTX. Observation seems safe and cardiovascular risk reduction should not be regarded as a separate indication for parathyroidectomy based on the results from this study.
Search for other papers by Huda M Elsharkasi in
Google Scholar
PubMed
Search for other papers by Suet C Chen in
Google Scholar
PubMed
Search for other papers by Lewis Steell in
Google Scholar
PubMed
Paediatric Neurosciences Research Group, Royal Hospital for Children, NHS Greater Glasgow & Clyde, Glasgow, UK
Search for other papers by Shuko Joseph in
Google Scholar
PubMed
Search for other papers by Naiemh Abdalrahaman in
Google Scholar
PubMed
Search for other papers by Christie McComb in
Google Scholar
PubMed
Search for other papers by Blair Johnston in
Google Scholar
PubMed
Search for other papers by John Foster in
Google Scholar
PubMed
Search for other papers by Sze Choong Wong in
Google Scholar
PubMed
Search for other papers by S Faisal Ahmed in
Google Scholar
PubMed
Objective
The aim of this study is to investigate the role of 3T-MRI in assessing musculoskeletal health in children and young people.
Design
Bone, muscle and bone marrow imaging was performed in 161 healthy participants with a median age of 15.0 years (range, 8.0, 30.0).
Methods
Detailed assessment of bone microarchitecture (constructive interference in the steady state (CISS) sequence, voxel size 0.2 × 0.2 × 0.4 mm3), bone geometry (T1-weighted turbo spin echo (TSE) sequence, voxel size 0.4 × 0.4 × 2 mm3) and bone marrow (1H-MRS, point resolved spectroscopy sequence (PRESS) (single voxel size 20 × 20 × 20 mm3) size and muscle adiposity (Dixon, voxel size 1.1 × 1.1 × 2 mm3).
Results
There was an inverse association of apparent bone volume/total volume (appBV/TV) with age (r = −0.5, P < 0.0005). Cortical area, endosteal and periosteal circumferences and muscle cross-sectional area showed a positive association to age (r > 0.49, P < 0.0001). In those over 17 years of age, these parameters were also higher in males than females (P < 0.05). This sex difference was also evident for appBV/TV and bone marrow adiposity (BMA) in the older participants (P < 0.05). AppBV/TV showed a negative correlation with BMA (r = −0.22, P = 0.01) which also showed an association with muscle adiposity (r = 0.24, P = 0.04). Cortical geometric parameters were highly correlated with muscle area (r > 0.57, P < 0.01).
Conclusions
In addition to providing deep insight into the normal relationships between bone, fat and muscle in young people, these novel data emphasize the role of MRI as a non-invasive method for performing a comprehensive and integrated assessment of musculoskeletal health in the growing skeleton.
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 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.
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.
Search for other papers by Sofya Gronskaia in
Google Scholar
PubMed
Search for other papers by Galina Melnichenko in
Google Scholar
PubMed
Search for other papers by Liudmila Rozhinskaya in
Google Scholar
PubMed
Search for other papers by Tatiana Grebennikova in
Google Scholar
PubMed
Search for other papers by Elizaveta Mamedova in
Google Scholar
PubMed
Search for other papers by Ekaterina Pigarova in
Google Scholar
PubMed
Search for other papers by Elena Przhialkovskaya in
Google Scholar
PubMed
Search for other papers by Larisa Dzeranova in
Google Scholar
PubMed
Search for other papers by Ivan Dedov in
Google Scholar
PubMed
Search for other papers by Valentin Fadeyev in
Google Scholar
PubMed
Search for other papers by Maria Luisa Brandi in
Google Scholar
PubMed
Search for other papers by Zhanna Belaya in
Google Scholar
PubMed
Hypoparathyroidism and pseudohypoparathyroidism are rare endocrine disorders, characterized by low serum calcium due to inappropriate parathyroid hormone (PTH) levels or resistance to its action. There is little epidemiological information regarding chronic hypoparathyroidism in Russia. This study aims to build a registry database of Russian patients with chronic hypoparathyroidism who were referred for hospital treatment in order to conduct initial analysis of clinical presentations and hospital management. The Italian registry model was taken to be able to integrate our data in the future. Two hundred patients with hypoparathyroidism (n = 194) and pseudohypoparathyroidism (n = 6) were enrolled over 2 years (2017–2019). The most frequent cause of hypoparathyroidism was neck surgery (82.5%, mostly females), followed by idiopathic hypoparathyroidism (10%), syndromic forms of genetic hypoparathyroidism (4.5%) and forms of defective PTH action (3%). Calcium supplements and alfacalcidol were prescribed in most cases. However, a minority of patients (n = 6) needed to receive teriparatide as the only way to maintain calcium levels and to prevent symptoms of hypocalcemia. Consequently, substitution treatment with parathyroid hormone should be available in certain cases of hypoparathyroidism. This database will be useful to estimate the potential requirement for recombinant PTH in Russia and standards for clinical and therapeutic approaches.
Search for other papers by Kaiyu Pan in
Google Scholar
PubMed
Search for other papers by Chengyue Zhang in
Google Scholar
PubMed
Search for other papers by Xiaocong Yao in
Google Scholar
PubMed
Search for other papers by Zhongxin Zhu in
Google Scholar
PubMed
Aim
Ensuring adequate calcium (Ca) intake during childhood and adolescence is critical to acquire good peak bone mass to prevent osteoporosis during older age. As one of the primary strategies to build and maintain healthy bones, we aimed to determine whether dietary Ca intake has an influence on bone mineral density (BMD) in children and adolescents.
Methods
We conducted a cross-sectional study composed of 10,092 individuals from the National Health and Nutrition Examination Survey (NHANES). Dietary Ca intake and total BMD were taken as independent and dependent variables, respectively. To evaluate the association between them, we conducted weighted multivariate linear regression models and smooth curve fittings.
Results
There was a significantly positive association between dietary Ca intake and total BMD. The strongest association was observed in 12–15 year old whites, 8–11 year old and 16–19 year old Mexican Americans, and 16–19 year old individuals from other race/ethnicity, in whom each quintile of Ca intake was increased. We also found that there were significant inflection points in females, blacks, and 12–15 year old adolescents group, which means that their total BMD would decrease when the dietary Ca intake was more than 2.6–2.8 g/d.
Conclusions
This cross-sectional study indicated that a considerable proportion of children and adolescents aged 8–19 years would attain greater total BMD if they increased their dietary Ca intake. However, higher dietary Ca intake (more than 2.6–2.8 g/d) is associated with lower total BMD in females, blacks, and 12–15 year old adolescents group.
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.
