Search Results
Search for other papers by Ying Hua in
Google Scholar
PubMed
Search for other papers by Jinqiong Fang in
Google Scholar
PubMed
Search for other papers by Xiaocong Yao in
Google Scholar
PubMed
Department of Clinical Research Center, The First People's Hospital of Xiaoshan District, Xiaoshan Affiliated Hospital of Wenzhou Medical University, Hangzhou, Zhejiang, China
Search for other papers by Zhongxin Zhu in
Google Scholar
PubMed
Background
Obesity and osteoporosis are major public health issues globally. The prevalence of these two diseases prompts the need to better understand the relationship between them. Previous studies, however, have yielded controversial findings on this issue. Therefore, our aim in this study was to evaluate the independent association between waist circumference (WC), as a marker of obesity, and the bone mineral density (BMD) of the lumbar spine among middle-aged adults using data from the National Health and Nutrition Examination Survey (NHANES).
Methods
Our analysis was based on NHANES data from 2011 to 2018, including 5084 adults, 40–59 years of age. A weighted multiple linear regression analysis was used to evaluate the association between WC and lumbar BMD, with smooth curve fitting performed for non-linearities.
Results
After adjusting for BMI and other potential confounders, WC was negatively associated with lumbar BMD in men (β = −2.8, 95% CI: −4.0 to −1.6) and premenopausal women (β = −2.6, 95% CI: −4.1 to −1.1). On subgroup analysis stratified by BMI, this negative association was more significant in men with a BMI ≥30 kg/m2 (β = −4.1, 95% CI: −6.3 to −2.0) and in pre- and postmenopausal women with a BMI <25 kg/m2 (premenopausal women: β= −5.7, 95% CI: −9.4 to−2.0; postmenopausal women: β=−5.6, 95% CI: −9.7 to −1.6). We further identified an inverted U-shaped relationship among premenopausal women, with a point of inflection at WC of 80 cm.
Conclusions
Our study found an inverse relationship between WC and lumbar BMD in middle-aged men with BMI ≥30 kg/m2, and women with BMI <25 kg/m2.
Search for other papers by Kathrin R Frey in
Google Scholar
PubMed
Search for other papers by Tina Kienitz in
Google Scholar
PubMed
Search for other papers by Julia Schulz in
Google Scholar
PubMed
Search for other papers by Manfred Ventz in
Google Scholar
PubMed
Search for other papers by Kathrin Zopf in
Google Scholar
PubMed
Search for other papers by Marcus Quinkler in
Google Scholar
PubMed
Context
Patients with primary adrenal insufficiency (PAI) or congenital adrenal hyperplasia (CAH) receive life-long glucocorticoid (GC) therapy. Daily GC doses are often above the physiological cortisol production rate and can cause long-term morbidities such as osteoporosis. No prospective trial has investigated the long-term effect of different GC therapies on bone mineral density (BMD) in those patients.
Objectives
To determine if patients on hydrocortisone (HC) or prednisolone show changes in BMD after follow-up of 5.5 years. To investigate if BMD is altered after switching from immediate- to modified-release HC.
Design and patients
Prospective, observational, longitudinal study with evaluation of BMD by DXA at visit1, after 2.2 ± 0.4 (visit2) and after 5.5 ± 0.8 years (visit3) included 36 PAI and 8 CAH patients. Thirteen patients received prednisolone (age 52.5 ± 14.8 years; 8 women) and 31 patients received immediate-release HC (age 48.9 ± 15.8 years; 22 women). Twelve patients on immediate-release switched to modified-release HC at visit2.
Results
Prednisolone showed significantly lower Z-scores compared to HC at femoral neck (−0.85 ± 0.80 vs −0.25 ± 1.16, P < 0.05), trochanter (−0.96 ± 0.62 vs 0.51 ± 1.07, P < 0.05) and total hip (−0.78 ± 0.55 vs 0.36 ± 1.04, P < 0.05), but not at lumbar spine, throughout the study. Prednisolone dose decreased by 8% over study time, but no significant effect was seen on BMD. BMD did not change significantly after switching from immediate- to modified-release HC.
Conclusions
The use of prednisolone as hormone replacement therapy results in significantly lower BMD compared to HC. Patients on low-dose HC replacement therapy showed unchanged Z-scores within the normal reference range during the study period.
Department of Endocrinology, University of Manchester, School of Medical Sciences, Manchester, UK
Search for other papers by Victoria Chatzimavridou-Grigoriadou in
Google Scholar
PubMed
Department of Endocrinology, University of Manchester, School of Medical Sciences, Manchester, UK
Search for other papers by Lisa H Barraclough in
Google Scholar
PubMed
Search for other papers by Rohit Kochhar in
Google Scholar
PubMed
Search for other papers by Lucy Buckley in
Google Scholar
PubMed
Search for other papers by Nooreen Alam in
Google Scholar
PubMed
Search for other papers by Claire E Higham in
Google Scholar
PubMed
Background
Radiotherapy-related insufficiency fractures (RRIFs) represent a common, burdensome consequence of pelvic radiotherapy. Their underlying mechanisms remain unclear, and data on the effect of osteoporosis are contradictory, with limited studies assessing bone mineral density (BMD) by dual-energy x-ray absorptiometry (DXA).
Methods
BMD by DXA (Hologic) scan and fracture risk following pelvic RRIF were retrospectively assessed in 39 patients (median age 68 years) at a tertiary cancer centre. Patient characteristics and treatment history are presented narratively; correlations were explored using univariate regression analyses.
Results
Additional cancer treatments included chemotherapy (n = 31), surgery (n = 20) and brachytherapy (n = 19). Median interval between initiation of radiotherapy and RRIF was 11 (7.5–20.8) and that between RRIF and DXA 3 was (1–6) months. Three patients had normal BMD, 16 had osteopenia and 16 osteoporosis, following World Health Organization classification. Four patients were <40 years at the time of DXA (all Z-scores > –2). Median 10-year risk for hip and major osteoporotic fracture was 3.1% (1.5–5.7) and 11.5% (7.1–13.8), respectively. Only 33.3% of patients had high fracture risk (hip fracture >4% and/or major osteoporotic >20%), and 31% fell above the intervention threshold per National Osteoporosis Guidelines Group (NOGG) guidance (2017). Higher BMD was predicted by lower pelvic radiotherapy dose (only in L3 and L4), concomitant chemotherapy and higher body mass index.
Conclusion
At the time of RRIF, most patients did not have osteoporosis, some had normal BMD and overall had low fracture risk. Whilst low BMD is a probable risk factor, it is unlikely to be the main mechanism underlying RRIFs, and further studies are required to understand the predictive value of BMD.
Search for other papers by Jiaxin Zhang in
Google Scholar
PubMed
Search for other papers by Jinlan Jiang in
Google Scholar
PubMed
Search for other papers by Yao Qin in
Google Scholar
PubMed
Search for other papers by Yihui Zhang in
Google Scholar
PubMed
Search for other papers by Yungang Wu in
Google Scholar
PubMed
Search for other papers by Huadong Xu in
Google Scholar
PubMed
Purpose
This study aims to investigate the associations of the systemic immune-inflammation index (SII) with bone mineral density (BMD) and osteoporosis in adult females from a nationally representative sample.
Methods
A cross-sectional study was performed among 4092 females aged ≥20 years from the National Health and Nutrition Examination Survey 2007–2010. Linear and logistic regressions were applied to explore the relationships of SII with BMD and the risk of osteoporosis, respectively.
Results
Linear regression analyses found that a doubling of SII levels was significantly correlated with a 1.39% (95% CI: 0.57%, 2.20%) decrease in total femur BMD, a 1.16% (95% CI: 0.31%, 2.00%) decrease in femur neck BMD, a 1.73% (95% CI: 0.78%, 2.66%) decrease in trochanter BMD, and a 1.35% (95% CI: 0.50%, 2.20%) decrease in intertrochanteric BMD among postmenopausal women, after adjusting for covariates. Logistic regression analyses showed that compared with postmenopausal women in the lowest SII quartile, those in the highest quartile had higher risks of osteoporosis in the total femur (odds ratio (OR) = 1.70, 95% CI: 1.04, 2.76), trochanter (OR = 1.86, 95% CI: 1.07, 3.38), intertrochanter (OR = 2.01, 95% CI: 1.05, 4.04) as well as overall osteoporosis (OR = 1.57, 95% CI: 1.04, 2.37). In contrast, there was no significant association between SII and BMD in premenopausal women.
Conclusions
SII levels were negatively associated with BMD levels in postmenopausal women but not in premenopausal women. Elevated SII levels could be a potential risk factor for osteoporosis in postmenopausal women.
Search for other papers by Ann-Kristin Picke in
Google Scholar
PubMed
Search for other papers by Graeme Campbell in
Google Scholar
PubMed
Division of Bone and Mineral Diseases, Washington University in St Louis, St Louis, Missouri, USA
Search for other papers by Nicola Napoli in
Google Scholar
PubMed
Search for other papers by Lorenz C Hofbauer in
Google Scholar
PubMed
Search for other papers by Martina Rauner in
Google Scholar
PubMed
The prevalence of type 2 diabetes mellitus (T2DM) is increasing worldwide, especially as a result of our aging society, high caloric intake and sedentary lifestyle. Besides the well-known complications of T2DM on the cardiovascular system, the eyes, kidneys and nerves, bone strength is also impaired in diabetic patients. Patients with T2DM have a 40–70% increased risk for fractures, despite having a normal to increased bone mineral density, suggesting that other factors besides bone quantity must account for increased bone fragility. This review summarizes the current knowledge on the complex effects of T2DM on bone including effects on bone cells, bone material properties and other endocrine systems that subsequently affect bone, discusses the effects of T2DM medications on bone and concludes with a model identifying factors that may contribute to poor bone quality and increased bone fragility in T2DM.
University of Ljubljana, Faculty of Medicine, Ljubljana, Slovenia
Search for other papers by Mojca Zerjav Tansek in
Google Scholar
PubMed
Search for other papers by Ana Bertoncel in
Google Scholar
PubMed
Search for other papers by Brina Sebez in
Google Scholar
PubMed
Search for other papers by Janez Zibert in
Google Scholar
PubMed
University of Ljubljana, Faculty of Medicine, Ljubljana, Slovenia
Search for other papers by Urh Groselj in
Google Scholar
PubMed
University of Ljubljana, Faculty of Medicine, Ljubljana, Slovenia
Search for other papers by Tadej Battelino in
Google Scholar
PubMed
University of Ljubljana, Faculty of Medicine, Ljubljana, Slovenia
Search for other papers by Magdalena Avbelj Stefanija in
Google Scholar
PubMed
Despite recent improvements in the composition of the diet, lower mineral bone density and overweight tendencies are incoherently described in patients with phenylketonuria (PKU). The impact of dietary factors and plasma phenylalanine levels on growth, BMI, body composition, and bone mineral density was investigated in our cohort of patients with hyperphenylalaninemia (HPA) with or without dietary treatment. The anthropometric, metabolic, BMI and other nutritional indicators and bone mineral density were compared between the group of 96 treated patients with PKU (58 classic PKU (cPKU) and 38 patients with moderate-mild PKU defined as non-classic PKU (non-cPKU)) and the untreated group of 62 patients with benign HPA. Having compared the treated and untreated groups, there were normal outcomes and no statistically significant differences in BMI, body composition, and bone mineral density. Lower body height standard deviation scores were observed in the treated as compared to the untreated group (P < 0.001), but the difference was not significant when analyzing patients older than 18 years; however, cPKU adults were shorter compared to non-cPKU treated adults (P = 0.012). Interestingly, the whole-body fat was statistically higher in non-cPKU as compared to cPKU patients. In conclusion, the dietary treatment ensured adequate nutrition without significant consequences in BMI, body composition, and bone mineral density. A low protein diet may have delayed the growth in childhood, but the treated patients gained a normal final height. Mild untreated hyperphenylalaninemia characteristic for benign HPA had no negative physiological effect on bone mineral density.
Department of Endocrinology, Jiading Branch of Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
Search for other papers by Lizhi Zhang in
Google Scholar
PubMed
Search for other papers by Jinwei He in
Google Scholar
PubMed
Search for other papers by Xiang Sun in
Google Scholar
PubMed
Search for other papers by Dongyue Pang in
Google Scholar
PubMed
Search for other papers by Jingjing Hu in
Google Scholar
PubMed
Search for other papers by Bo Feng in
Google Scholar
PubMed
We demonstrated previously that there is a correlation between glucagon-like peptide-1 (GLP-1) single-nucleotide polymorphism (SNP) and bone mineral density in postmenopausal women. Both GLP-1 and glucose-dependent insulinotropic peptide are incretins. The glucose-dependent insulinotropic peptide receptor (GIPR) SNP rs10423928 has been extensively studied. However, it is not clear whether GIPR gene mutations affect bone metabolism. The aim of this study was to investigate the association between rs10423928 and bone mineral density in postmenopausal women in Shanghai. rs10423928 was detected in 884 postmenopausal women in Shanghai, and the correlation between the GIPR SNP and bone mineral density was assessed. The dominant T/T genotype of rs10423928 was found to be related to the bone mineral density of the femoral neck (P = 0.035). Overall, our findings indicate that the dominant T/T genotype of rs10423928 in postmenopausal women is significantly associated with a higher bone mineral density and that the T/T genotype exerts a bone-protective effect.
Search for other papers by Martine Cohen-Solal in
Google Scholar
PubMed
Search for other papers by Thomas Funck-Brentano in
Google Scholar
PubMed
Department of Renal Physiology, Necker Hospital, Université de Paris, Paris, France
Search for other papers by Pablo Ureña Torres in
Google Scholar
PubMed
Mineral and bone diseases (MBD) are predominant in patients with chronic kidney disease (CKD) and lead to several bone manifestations, from pain to skeletal fractures. Cumulative traditional clinical risk factors, such as age and gender, in addition to those related to CKD, enhance the risk of comorbidity and mortality related to fractures. Despite great advances in understanding MBD in CKD, clinical and biological targets are lacking, which leads to under-management of fractures. Optimal PTH control results in a net improvement in defining the levels of bone remodeling. In addition, circulating biomarkers such as bone-specific alkaline phosphatase and cross-linked collagen type I peptide will also provide additional information about remodeling rate, bone mineralization and the evaluation of fracture risk. Imaging techniques identify patients at risk by measurement of bone mineral density by DEXA or by high peripheral QCT, which allow the discrimination of trabecular and cortical bone. Here, we have reviewed the literature related to epidemiology and the pathophysiological role of mineral and biochemical factors involved in CKD-MBD with a special focus on fracture risk. We also provide an algorithm that could be used for the management of bone diseases and to guide treatment decisions. Finally, the combined expertise of clinicians from various disciplines is crucial for the best prevention of fractures.
Search for other papers by Veronica Kieffer in
Google Scholar
PubMed
Search for other papers by Kate Davies in
Google Scholar
PubMed
Search for other papers by Christine Gibson in
Google Scholar
PubMed
Search for other papers by Morag Middleton in
Google Scholar
PubMed
Search for other papers by Jean Munday in
Google Scholar
PubMed
Search for other papers by Shashana Shalet in
Google Scholar
PubMed
Search for other papers by Lisa Shepherd in
Google Scholar
PubMed
Search for other papers by Phillip Yeoh in
Google Scholar
PubMed
This competency framework was developed by a working group of endocrine specialist nurses with the support of the Society for Endocrinology to enhance the clinical care that adults with an endocrine disorder receive. Nurses should be able to demonstrate that they are functioning at an optimal level in order for patients to receive appropriate care. By formulating a competency framework from which an adult endocrine nurse specialist can work, it is envisaged that their development as professional practitioners can be enhanced. This is the second edition of the Competency Framework for Adult Endocrine Nursing. It introduces four new competencies on benign adrenal tumours, hypo- and hyperparathyroidism, osteoporosis and polycystic ovary syndrome. The authors and the Society for Endocrinology welcome constructive feedback on the document, both nationally and internationally, in anticipation that further developments and ideas can be incorporated into future versions.
Department of Clinical Science, Department of Medicine, Department of Medicine, Pediatric Department, University of Bergen, Bergen, Norway
Search for other papers by Marianne C Astor in
Google Scholar
PubMed
Department of Clinical Science, Department of Medicine, Department of Medicine, Pediatric Department, University of Bergen, Bergen, Norway
Search for other papers by Kristian Løvås in
Google Scholar
PubMed
Search for other papers by Anette S B Wolff in
Google Scholar
PubMed
Search for other papers by Bjørn Nedrebø in
Google Scholar
PubMed
Search for other papers by Eirik Bratland in
Google Scholar
PubMed
Search for other papers by Jon Steen-Johnsen in
Google Scholar
PubMed
Department of Clinical Science, Department of Medicine, Department of Medicine, Pediatric Department, University of Bergen, Bergen, Norway
Search for other papers by Eystein S Husebye in
Google Scholar
PubMed
Primary hypomagnesemia with secondary hypocalcemia (HSH) is an autosomal recessive disorder characterized by neuromuscular symptoms in infancy due to extremely low levels of serum magnesium and moderate to severe hypocalcemia. Homozygous mutations in the magnesium transporter gene transient receptor potential cation channel member 6 (TRPM6) cause the disease. HSH can be misdiagnosed as primary hypoparathyroidism. The aim of this study was to describe the genetic, clinical and biochemical features of patients clinically diagnosed with HSH in a Norwegian cohort. Five patients in four families with clinical features of HSH were identified, including one during a national survey of hypoparathyroidism. The clinical history of the patients and their families were reviewed and gene analyses of TRPM6 performed. Four of five patients presented with generalized seizures in infancy and extremely low levels of serum magnesium accompanied by moderate hypocalcemia. Two of the patients had an older sibling who died in infancy. Four novel mutations and one large deletion in TRPM6 were identified. In one patient two linked homozygous mutations were located in exon 22 (p.F978L) and exon 23 (p.G1042V). Two families had an identical mutation in exon 25 (p.E1155X). The fourth patient had a missense mutation in exon 4 (p.H61N) combined with a large deletion in the C-terminal end of the gene. HSH is a potentially lethal condition that can be misdiagnosed as primary hypoparathyroidism. The diagnosis is easily made if serum magnesium is measured. When treated appropriately with high doses of oral magnesium supplementation, severe hypomagnesemia is uncommon and the long-term prognosis seems to be good.
