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- Abstract: Hypoparathyroidism x
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- Abstract: Skeleton x
Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
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Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
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Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
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Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
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Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
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Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
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Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
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Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
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Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
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Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
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Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
Service d'Endocrinologie et Diabétologie de l'Enfant, Service de Pédiatrie générale – Consultation de rhumatologie, Service d'Endocrinologie et des Maladies de la Reproduction, Service d'ORL et chirurgie cervico-maxillo-faciale, Université Paris 11, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphore, Service d'Odontologie-Maladies Rares Hôpital Bretonneau 2 rue Carpeaux, Université Paris Descartes 12 Rue de l'École de Médecine, Service Rhumatologie B Hôpital Cochin, Centre de Référence des Maladies Rares des Maladies Auto-Inflammatoires Rares de l'Enfant, Service d'explorations fonctionnelles rénales, Service de Chirurgie infantile orthopédique, Association de patients RVRH-XLH, Hôpital Bicêtre, APHP, 78 rue du Général Leclerc, 94270 Le Kremlin Bicêtre, France
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In children, hypophosphatemic rickets (HR) is revealed by delayed walking, waddling gait, leg bowing, enlarged cartilages, bone pain, craniostenosis, spontaneous dental abscesses, and growth failure. If undiagnosed during childhood, patients with hypophosphatemia present with bone and/or joint pain, fractures, mineralization defects such as osteomalacia, entesopathy, severe dental anomalies, hearing loss, and fatigue. Healing rickets is the initial endpoint of treatment in children. Therapy aims at counteracting consequences of FGF23 excess, i.e. oral phosphorus supplementation with multiple daily intakes to compensate for renal phosphate wasting and active vitamin D analogs (alfacalcidol or calcitriol) to counter the 1,25-diOH-vitamin D deficiency. Corrective surgeries for residual leg bowing at the end of growth are occasionally performed. In absence of consensus regarding indications of the treatment in adults, it is generally accepted that medical treatment should be reinitiated (or maintained) in symptomatic patients to reduce pain, which may be due to bone microfractures and/or osteomalacia. In addition to the conventional treatment, optimal care of symptomatic patients requires pharmacological and non-pharmacological management of pain and joint stiffness, through appropriated rehabilitation. Much attention should be given to the dental and periodontal manifestations of HR. Besides vitamin D analogs and phosphate supplements that improve tooth mineralization, rigorous oral hygiene, active endodontic treatment of root abscesses and preventive protection of teeth surfaces are recommended. Current outcomes of this therapy are still not optimal, and therapies targeting the pathophysiology of the disease, i.e. FGF23 excess, are desirable. In this review, medical, dental, surgical, and contributions of various expertises to the treatment of HR are described, with an effort to highlight the importance of coordinated care.
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Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
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Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts, USA
Harvard Medical School, Boston, Massachusetts, USA
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Glucocorticoid use is the most common cause of secondary osteoporosis. Poor skeletal health related to glucocorticoid use is thought to involve inhibition of the Wnt/β-catenin signaling pathway, a key pathway in osteoblastogenesis. Sclerostin, a peptide produced primarily by osteocytes, is an antagonist of the Wnt/β-catenin signaling pathway, raising the possibility that sclerostin is involved in glucocorticoids’ adverse effects on bone. The aim of this study was to determine whether an acute infusion of cosyntropin (i.e. ACTH(1–24)), which increases endogenous cortisol, increases serum sclerostin levels as compared to a placebo infusion. This study was performed using blood samples obtained from a previously published, double-blind, placebo-controlled, randomized, cross-over study among healthy men and women who received infusions of placebo or cosyntropin after being supine and fasted overnight (ClinicalTrials.gov NCT02339506). A total of 17 participants were analyzed. There was a strong correlation (R2 = 0.65, P < 0.0001) between the two baseline sclerostin measurements measured at the start of each visit, and men had a significantly higher average baseline sclerostin compared to women. As anticipated, cosyntropin significantly increased serum cortisol levels, whereas cortisol levels fell during placebo infusion, consistent with the diurnal variation in cortisol. There was no significant effect of cosyntropin as compared to placebo infusions on serum sclerostin over 6–24 h (P = 0.10). In conclusion, this randomized, placebo-controlled study was unable to detect a significant effect of a cosyntropin infusion on serum sclerostin levels in healthy men and women.
Department of Endocrinology, Fujian Provincial Hospital, Fujian, China
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Department of Endocrinology, Fujian Provincial Hospital, Fujian, China
Fujian Provincial Key Laboratory of Medical Analysis, Fujian Academy of Medical, Fujian, China
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Objective
To establish a rapid, cost-effective, accurate, and acceptable osteoporosis (OP) screening model for the Chinese male population (age ≥ 40 years) based on data mining technology.
Materials and methods
This was a 3-year retrospective cohort study, which belonged to the sub-cohort of the Chinese Reaction Study. The research period was from March 2011 to December 2014. A total of 1834 subjects who did not have OP at the baseline and completed a 3-year follow-up were included in this study. All subjects underwent quantitative ultrasound examinations for calcaneus at the baseline and follow-ups that lasted for 3 years. We utilized the least absolute shrinkage and selection operator (LASSO) regression model to select feature variables. The characteristic variables selected in the LASSO regression were analyzed by multivariable logistic regression (MLR) to construct the predictive model. This predictive model was displayed through a nomogram. We used the receiver operating characteristic (ROC) curve, C-index, calibration curve, and clinical decision curve analysis (DCA) to evaluate model performance and the bootstrapping validation to internally validate the model.
Results
The predictive factors included in the prediction model were age, neck circumference, waist-to-height ratio, BMI, triglyceride, impaired fasting glucose, dyslipidemia, osteopenia, smoking history, and strenuous exercise. The area under the ROC (AUC) curve of the risk nomogram was 0.882 (95% CI, 0.858–0.907), exhibiting good predictive ability and performance. The C-index for the risk nomogram was 0.882 in the prediction model, which presented good refinement. In addition, the nomogram calibration curve indicated that the prediction model was consistent. The DCA showed that when the threshold probability was between 1 and 100%, the nomogram had a good clinical application value. More importantly, the internally verified C-index of the nomogram was still very high, at 0.870.
Conclusions
This novel nomogram can effectively predict the 3-year incidence risk of OP in the male population. It also helps clinicians to identify groups at high risk of OP early and formulate personalized intervention measures.
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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.
Laboratory for Anthropology and Skeletal Biology, Institute of Anatomy, Faculty of Medicine, University of Belgrade, Belgrade, Serbia
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An increasing number of patients worldwide suffer from bone fractures that occur after low intensity trauma. Such fragility fractures are usually associated with advanced age and osteoporosis but also with long-term immobilization, corticosteroid therapy, diabetes mellitus, and other endocrine disorders. It is important to understand the skeletal origins of increased bone fragility in these conditions for preventive and therapeutic strategies to combat one of the most common health problems of the aged population. This review summarizes current knowledge pertaining to the phenomenon of micropetrosis (osteocyte lacunar mineralization). As an indicator of former osteocyte death, micropetrosis is more common in aged bone and osteoporotic bone. Considering that the number of mineralized osteocyte lacunae per bone area can distinguish healthy, untreated osteoporotic and bisphosphonate-treated osteoporotic patients, it could be regarded as a novel structural marker of impaired bone quality. Further research is needed to clarify the mechanism of lacunar mineralization and to explore whether it could be an additional target for preventing or treating bone fragility related to aging and various endocrine diseases.
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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.
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Background:
Whether polymorphisms in VDR gene affect the risk of postmenopausal osteoporosis or not remain unclear. Thus, the authors performed a meta-analysis to more robustly assess associations between polymorphisms in VDR gene and the risk of postmenopausal osteoporosis by integrating the results of previous literature.
Methods:
Medline, Embase, Wanfang, VIP and CNKI were searched comprehensively for eligible literature, and 67 genetic association studies were finally selected to be included in this meta-analysis.
Results:
We found that ApaI rs7975232 (dominant comparison: OR = 0.77, P = 0.007; allele comparison: OR = 0.81, P = 0.04), BsmI rs1544410 (dominant comparison: OR = 0.69, P = 0.002; allele comparison: OR = 0.78, P = 0.008) and TaqI rs731236 (recessive comparison: OR = 1.32 , P = 0.01) polymorphisms were significantly associated with the risk of postmenopausal osteoporosis in Caucasians, whereas FokI rs10735810 polymorphism was significantly associated with the risk of postmenopausal osteoporosis in Asians (dominant comparison: OR = 0.61, P = 0.0001; recessive comparison: OR = 2.02, P = 0.001; allele comparison: OR = 0.68, P = 0.002).
Conclusions:
This meta-analysis shows that ApaI rs7975232, BsmI rs1544410 and TaqI rs731236 polymorphisms may affect the risk of postmenopausal osteoporosis in Caucasians, while BsmI rs1544410 polymorphism may affect the risk of postmenopausal osteoporosis in Asians.
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X-linked hypophosphataemia (XLH) is caused by a pathogenic variant in the PHEX gene, which leads to elevated circulating FGF23. High FGF23 causes hypophosphataemia, reduced active vitamin D concentration and clinically manifests as rickets in children and osteomalacia in children and adults. Conventional therapy for XLH includes oral phosphate and active vitamin D analogues but does not specifically treat the underlying pathophysiology of elevated FGF23-induced hypophosphataemia. In addition, adherence to conventional therapy is limited by frequent daily dosing and side effects such as gastrointestinal symptoms, secondary hyperparathyroidism and nephrocalcinosis. Burosumab, a recombinant human IgG1 MAB that binds to and inhibits the activity of FGF23, is administered subcutaneously every 2 weeks. In clinical trials (phase 2 and 3) burosumab was shown to improve phosphate homeostasis that consequently resolves the skeletal/non-skeletal manifestations of XLH. Burosumab was licensed in Europe (February 2018) with the National Institute for Health and Care Excellence, UK approving use within its marketing authorisation in October 2018. In this publication, the British Paediatric and Adolescent Bone Group (BPABG) reviewed current evidence and provide expert recommendations for care pathway and management of XLH with burosumab.
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Jan van Goyen Medical Center, Department of Internal Medicine, Amsterdam, the Netherlands
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Department of Epidemiology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands
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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.
Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany
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Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany
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Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany
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Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany
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DFG Research Center and Cluster of Excellence for Regenerative Therapies, Technical University, Dresden, Germany
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Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany
DFG Research Center and Cluster of Excellence for Regenerative Therapies, Technical University, Dresden, Germany
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Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany
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Glucocorticoids (GC) are used for the treatment of inflammatory diseases, including various forms of arthritis. However, their use is limited, amongst others, by adverse effects on bone. The Wnt and bone formation inhibitor sclerostin was recently implicated in the pathogenesis of GC-induced osteoporosis. However, data are ambiguous. The aim of this study was to assess the regulation of sclerostin by GC using several mouse models with high GC levels and two independent cohorts of patients treated with GC. Male 24-week-old C57BL/6 and 18-week-old DBA/1 mice exposed to GC and 12-week-old mice with endogenous hypercortisolism displayed reduced bone formation as indicated by reduced levels of P1NP and increased serum sclerostin levels. The expression of sclerostin in femoral bone tissue and GC-treated bone marrow stromal cells, however, was not consistently altered. In contrast, GC dose- and time-dependently suppressed sclerostin at mRNA and protein levels in human mesenchymal stromal cells, and this effect was GC receptor dependent. In line with the human cell culture data, patients with rheumatoid arthritis (RA, n = 101) and polymyalgia rheumatica (PMR, n = 21) who were exposed to GC had lower serum levels of sclerostin than healthy age- and sex-matched controls (−40%, P < 0.01 and −26.5%, P < 0.001, respectively). In summary, sclerostin appears to be differentially regulated by GC in mice and humans as it is suppressed by GCs in humans but is not consistently altered in mice. Further studies are required to delineate the differences between GC regulation of sclerostin in mice and humans and assess whether sclerostin mediates GC-induced osteoporosis in humans.
