Bone and Mineral Metabolism
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Branch of National Clinical Research Centre for Metabolic Diseases,
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Branch of National Clinical Research Centre for Metabolic Diseases,
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Department of Endocrinology, Endocrine and Metabolic Disease Medical Center, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University,
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Department of Endocrinology, Endocrine and Metabolic Disease Medical Center, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University,
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Branch of National Clinical Research Centre for Metabolic Diseases,
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Introduction
The aim of this study was to investigate the relationship between the AST/ALT ratio and osteopenia or osteoporosis in patients with type 2 diabetes mellitus (T2DM).
Methods
A total of 589 patients with T2DM were divided into two groups based on T-score: T-score ≥ −1.0 group, normal bone mineral density and T-score < −1.0 group, osteopenia or osteoporosis (OP). The association between the AST/ALT ratio and osteopenia/OP was evaluated by multivariate analyses. The receiver operating characteristic (ROC) curves were used to estimate the diagnostic performance according to the area under the ROC curve (AUC).
Results
The patients in the T-score < −1.0 group showed significantly higher AST/ALT level than those in the T-score ≥ −1.0 group (0.93 ± 0.16 vs 1.17 ± 0.24, P < 0.001). According to the interquartile range of the AST/ALT ratio, the participants were divided into four groups: Q1 (0.650, 0.874), Q2 (0.875, 0.999), Q3 (1.000, 1.173) and Q4 (1.174, 1.917). After adjustment for confounding factors, compared with Q1 of the AST/ALT level, subjects in Q3 and Q4 remained more likely to have osteopenia or osteoporosis (Q3, OR 3.478, 95% CI 1.641–7.411; Q4, OR 15.278, 95% CI 6.377–36.837). The AST/ALT ratio provided an AUC value of 0.81 (95% CI 0.77–0.84) for osteopenia or osteoporosis in patients with T2DM.
Conclusion
An elevated AST/ALT ratio is associated with the evaluated risk of osteopenia/OP in patients with T2DM. The AST/ALT ratio, a practical and cost-effective biomarker, may be a potential predictor of osteopenia/OP in patients with T2DM.
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MVZ endokrinologikum Göttingen,
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Purpose
Fracture risk determination is essential when recommending treatment in osteoporosis management. We calculated the risk probabilities of major osteoporotic and hip fractures using the DVO score established in German-speaking countries and the FRAX tool.
Methods
We retrospectively analysed data from 555 female patients (mean age 64.2 ± 10.3 years) evaluated for osteoporosis. As suggested by DVO guidelines before 2023, we set the therapy threshold of >30% for vertebral and hip fractures. Major osteoporotic fracture (MOF) and hip fracture risk (HF) were calculated based on corresponding FRAX scores. We applied the internationally most common therapy threshold of ≥20% for MOF and ≥3% for HF and determined the ‘DVO-equivalent risk levels’ for FRAX-based assessment.
Results
The DVO score identified 52.8% of women as having a 10-year risk of hip and vertebral fractures >30%. FRAX score for HF ≥ 3% without bone mineral density (BMD) identified the highest number of patients (56%). The proportion of female patients identified for treatment only by DVO score (14.6%) were more likely to present spinal fractures (38.3 vs 18.6%), whereas the 10.6% of patients only identified by FRAX including BMD presented more peripheral fractures (40.7 vs 29.6%). The thresholds for this ‘DVO-equivalent risk level’ for ‘FRAX with BMD’ would be ≥10% for MOF and ≥2.6% for HF.
Conclusion
Given the differences in the DVO and FRAX scores, we highly recommend considering both scores when assessing individual women for treatment.
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Objective
Hypercalcaemia is often considered as an emergency because of a potential risk of life-threatening arrhythmias or coma. However, there is little evidence, apart from case studies, that hypercalcaemia can be immediately life-threatening. The aim of our study was to prospectively assess whether hypercalcaemia (Ca ≥ 3 mmol/L) was associated with immediately life-threatening complications.
Design and methods
We conducted a prospective observational study aiming to include the first one hundred patients aged ≥18 who had a calcium concentration ≥3 mmol/L, admitted to the emergency department (ED). The primary outcome was the number of life-threatening cardiac arrhythmias (ventricular tachycardia, ventricular fibrillation, sinus arrest and second- or third-degree atrioventricular blocks) or neurological complications defined by a Glasgow Coma Scale score <9 during the stay in the ED. The secondary outcomes were correlation between calcium concentrations and ECG (electrocardiogram) QTc intervals, Glasgow Coma Scale scores and mortality during the following 12-month follow-up period.
Results
The median calcium concentration was 3.3 mmol/L (3.1–3.7). Cancer was the first cause of hypercalcaemia. No patient presented a life-threatening cardiac arrhythmia during their stay in the ED. Three patients presented a life-threatening neurological complication. There was no correlation between calcaemia and QTc intervals or Glasgow Coma Scale score. Prognosis was poor, and 43 patients died during the 12 months.
Conclusions
We found no cases of immediately life-threatening cardiac arrhythmias. Three patients had indeed a life-threatening neurological complication but always had at least one other major factor that could severely alter mental status, such as profound metabolic acidosis.
Significance statement
This paper aims to revisit what most physicians, whether specialists or not, consider to be scientifically proven facts concerning the immediate threat caused by hypercalcaemia. Its novelty is threefold: first, this is the only prospective study that exists to date studying the life-threatening consequences of hypercalcaemia; second, having included one hundred patients, we found no life-threatening cardiac arrhythmias, which is not what would be expected if one reads guidelines concerning hypercalcaemia; and third, life-threatening neurological complications were very rare and only occurred in patients with at least one other major cause of altered neurological status, such as severe metabolic acidosis or hypernatraemia.
Research Program for Clinical and Molecular Metabolism (CAMM), Faculty of Medicine, University of Helsinki,
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Children’s Hospital, Pediatric Research Center, University of Helsinki and Helsinki University Hospital,
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Children’s Hospital, Pediatric Research Center, University of Helsinki and Helsinki University Hospital,
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Children’s Hospital, Pediatric Research Center, University of Helsinki and Helsinki University Hospital,
Folkhälsan Institute of Genetics,
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Children’s Hospital, Pediatric Research Center, University of Helsinki and Helsinki University Hospital,
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Children’s Hospital, Pediatric Research Center, University of Helsinki and Helsinki University Hospital,
Folkhälsan Institute of Genetics,
Department of Moecular Medicine and Surgery, Karolinska Institutet, and Clinical Genetics, Karolinska University Laboratory, Karolinska University Hospital,
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Children’s Hospital, Pediatric Research Center, University of Helsinki and Helsinki University Hospital,
Population Health Unit, National Institute for Health and Welfare (THL),
Clinical Medicine Research Unit, MRC Oulu, Oulu University Hospital and University of Oulu,
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Amino-terminal propeptide of type 1 procollagen (P1NP) and carboxy-terminal crosslinked telopeptide of type 1 collagen (CTX-I) are markers of bone metabolism. We examined the effect of vitamin D3 supplementation on these markers and their relationship with growth and bone parameters in 12-month-old infants. In a randomized, double-blinded, vitamin D intervention in infants (VIDI) study, 987 infants received daily vitamin D3 supplementation of 10 μg (group-10) or 30 μg (group-30) from age 2 weeks to 24 months. We conducted a secondary analysis of the original VIDI trial. At 12 months of age, P1NP (n = 812) and CTX-I (n = 786) concentrations were analyzed, and anthropometrics and total bone mineral content, volumetric bone mineral density, cross-sectional area and polar moment of inertia of tibia were measured by peripheral quantitative computed tomography. The growth rate in weight and length was calculated from birth to 12 months. The vitamin D dose did not influence mean (SD) levels of CTX-I (group-10: 0.90 (0.31); group-30: 0.89 (0.31) (P > 0.53)). The mean difference of P1NP (CI 95%) comparing group-10 with group-30 was 35 (−103, 33) ng/mL (P = 0.31) in boys and −63 (−4, 130) ng/mL (P = 0.064) in girls. In group-10, girls had higher mean (SD) value of P1NP (1509 (362) ng/mL) than boys (1407 (297) ng/mL) (P = 0.003); no sex differences were observed in group-30 (girls: 1446 (359); boys: 1442 (359), P = 0.91) or CTX-I. P1NP associated positively with the growth rate in length (B (CI 95%) 0.0003 (0.0001, 0.001), P = 0.022) in the whole cohort but not in subgroups divided by the intervention group or sex, adjusted for birth size and parental heights and corrected for multiple testing. P1NP associated positively with the growth rate in weight (0.01 (0.0003, 0.01), P < 0.001). An inverse association was observed between CTX-I and length (cm) in the whole cohort (−0.90 (−1.40, −0.40), P = 0.005) and in group-30 (−1.05 (−1.72, −0.39), P = 0.011). Furthermore, CTX-I associated negatively with weight (SDS) in the whole cohort (−0.33 (−0.55, −0.12), P = 0.015) and the growth rate in weight (−0.43 (−0.66, −0.20), P = 0.005), persisting in group-30 and in boys but not in group-10 or in girls. Neither marker was associated with bone parameters. The observed sex difference in P1NP might suggest that a higher vitamin D dose resulted in a small decrease in bone collagen matrix formation in girls but not in boys. P1NP and CTX-I associate with growth and body size but not with bone mineralization in infancy.
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Section Endocrinology, Department of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands
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Division of Child Health, Wilhelmina Children’s Hospital/University Medical Center Utrecht, Utrecht, the Netherlands
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Department of Paediatrics, Emma Children's Hospital/Amsterdam University Medical Center, Amsterdam, the Netherlands
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Childhood cancer survivors are at increased risk of developing (long-term) skeletal adverse effects, such as osteonecrosis, impaired bone mineral density, and fractures. This paper provides an overview of the current understanding of bone health in these survivors, examining whether it represents a significant concern. It focusses on the challenges of assessing and managing bone health in childhood cancer survivors, highlighting diagnostic pitfalls, methods for accurately identifying those at high risk, and suggested strategies for the surveillance and management of osteonecrosis and impaired bone mineral density. The need for improved surveillance strategies, particularly for high-risk survivors, alongside potential prevention and management options, including pharmacological and lifestyle interventions, is emphasised. Given the lack of consensus on optimal prevention and treatment strategies, the paper emphasises the need for further research to optimise care and improve long-term outcomes for childhood cancer survivors with bone health impairments.
Faculty of Medicine, School of Medicine, National Yang-Ming Chiao Tung University, Taipei, Taiwan
Department of Family Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
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Division of Musculoskeletal Section, Department of Radiology, Taipei Veterans General Hospital, Taipei, Taiwan
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Faculty of Medicine, School of Medicine, National Yang-Ming Chiao Tung University, Taipei, Taiwan
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School of Medicine, College of Medicine, Fu Jen Catholic University, New Taipei, Taiwan
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Faculty of Medicine, School of Medicine, National Yang-Ming Chiao Tung University, Taipei, Taiwan
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
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Division of Gastroenterology and Hepatology, Department of Internal Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
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Faculty of Medicine, School of Medicine, National Yang-Ming Chiao Tung University, Taipei, Taiwan
Department of Family Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
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Faculty of Medicine, School of Medicine, National Yang-Ming Chiao Tung University, Taipei, Taiwan
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Division of Gastroenterology and Hepatology, Department of Internal Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
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Objective
Previous studies have suggested that body mass index (BMI) should be considered when assessing the relationship between fatty liver (FL) and osteoporosis. The aim of this study was to investigate future fracture events in people with FL, focusing on the effect of BMI in both sexes.
Methods
This retrospective cohort study, spanning from 2011 to 2019, enrolled 941 people, including 441 women and 500 men, aged 50 years or older who underwent liver imaging (ultrasound, computed tomography, or magnetic resonance image) and dual-energy X-ray absorptiometry (for bone mineral density measurements). The study examined predictors of osteoporosis in both sexes and the effect of different ranges of BMI (18.5–24, 24–27, and ≥27 kg/m2) on the risk of future fracture events in FL patients.
Results
The average follow-up period was 5.3 years for women and 4.2 years for men. Multivariate analysis identified age and BMI as independent risk factors of osteoporosis in both sexes. Each unit increase in BMI decreased the risk of osteoporosis by ≥10%. In both women and men with FL, a BMI of 24–27 kg/m2 offered protection against future fractures, compared to those without FL and with a BMI of 18.5–24 kg/m2.
Conclusion
The protective effect of a higher BMI against future fractures in middle-aged and elderly female and male patients with FL is not uniform and diminishes beyond certain BMI ranges.
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In this review, we discuss the definition, prevalence, and etiology of sporadic multiglandular disease (MGD), with an emphasis on its preoperative and intraoperative predictors. Primary hyperparathyroidism (PHPT) is the third-most common endocrine disorder, and multiglandular parathyroid disease (MGD) is a cause of PHPT. Hereditary MGD can be definitively diagnosed with detailed family history and genetic testing, whereas sporadic MGD presents a greater challenge in clinical practice, and parathyroidectomy for MGD is associated with a higher risk of surgical failure than single gland disease (SGD). Therefore, it is crucial to be able to predict the presence of sporadic MGD in a timely manner, either preoperatively or intraoperatively. Various predictive methods cannot accurately identify all cases of sporadic MGD, but they can greatly optimize the management of MGD diagnosis and treatment and optimize the cure rate. Future research will urge us to investigate more integrative predictive models as well as increase our understanding of MGD pathogenesis.
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Objectives
It has not been established whether vitamin D deficiency is associated with anthropometric state; therefore, this systematic review examined the relationship between serum vitamin D levels with anthropometrics and adiposity across different ages.
Methods
Studies that examined vitamin D deficiency with adiposity measures in different age groups were searched in the PubMed, Scopus, Embase, and Google Scholar databases until November 2023. Two investigators independently reviewed titles and abstracts, examined full-text articles, extracted data, and rated the quality in accordance with the Newcastle–Ottawa criteria.
Results
Seventy-two studies, with a total of 59,430 subjects, were included. Of these studies, 27 cross-sectional studies and one longitudinal study (with 25,615 participants) evaluated the possible link between 25(OH)D serum concentrations and anthropometric/adiposity indices in the pediatric population. Forty-two cross-sectional studies and two cohort investigations (with 33,815 participants) investigated the relationship between serum 25(OH)D levels and adiposity measures in adults and/or the elderly population. There is evidence supporting links between vitamin D deficiency and obesity, and revealed an inverse association between vitamin D and adiposity indicators, specifically in female subjects. However, the effects of several confounding factors should also be considered.
Conclusion
Most published studies, most of which were cross-sectional, reported a negative association between vitamin D and female adiposity indicators. Therefore, serum vitamin D levels should be monitored in overweight/obese individuals.
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The link between obesity and low bone strength has become a significant medical concern. The canonical Wnt signaling pathway is a key regulator of mesenchymal stem cell differentiation into either osteoblasts or adipocytes with active Wnt signaling promoting osteoblastogenesis. Our previous research indicated that Dickkopf-1 (Dkk1), a Wnt inhibitor, is upregulated in bone tissue in obesity and that osteoblast-derived Dkk1 drives obesity-induced bone loss. However, Dkk1 is also produced by adipocytes, but the impact of adipogenic Dkk1 on bone remodeling and its role in obesity-induced bone loss remain unclear. Thus, in this study, we investigated the influence of adipogenic Dkk1 on bone homeostasis and obesity-induced bone loss in mice. To that end, deletion of Dkk1 in adipocytes was induced by tamoxifen administration into 8-week-old male Dkk1fl/fl;AdipoQcreERT2 mice. Bone and fat mass were analyzed at 12 and 20 weeks of age. Obesity was induced in 8-week-old male Dkk1fl/fl;AdipoQcre mice with a high-fat diet (HFD) rich in saturated fats for 12 weeks. We observed that 12-week-old male mice without adipogenic Dkk1 had a significant increase in trabecular bone volume in the vertebrae and femoral bones. While histological and serological bone formation markers were not different, the number of osteoclasts and adipocytes was decreased in the vertebral bones of Dkk1fl/fl;AdipoQcre-positive mice. Despite the increased bone mass in 12-week-old male mice, at 20 weeks of age, there was no difference in the bone volume between the controls and Dkk1fl/fl;AdipoQcre-positive mice. Also, Dkk1fl/fl;AdipoQcre-positive mice were not protected from HFD-induced bone loss. Even though mRNA expression levels of Sost, another important Wnt inhibitor, in bone from Dkk1-deficient mice fed with HFD were decreased compared to Dkk1-sufficient mice on an HFD, this did not prevent the HFD-induced suppression of bone formation. In conclusion, adipogenic Dkk1 may play a transient role in bone mass regulation during adolescence, but it does not contribute to bone homeostasis or obesity-induced bone loss later in life.
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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.
