The major transporter of vitamin D metabolites in the circulation is the multifunctional plasma protein Gc, also known as group-specific component, Gc globulin, vitamin D-binding protein, or DBP. There are several phenotypes of Gc, and we examined the influence of Gc phenotype and Gc concentration on vitamin D status. By using isoelectric focusing we identified the Gc phenotype of 595 caucasian recent postmenopausal women enrolled into the Danish Osteoporosis Prevention Study (DOPS). We measured plasma concentration of Gc by immunonephelometry (coefficient of variation [CV] < 5%), 25-hydroxy vitamin D (25OHD) by a competitive protein-binding assay (CV 10%), and 1,25-dihydroxy-vitamin D (1,25(OH)(2)D) by a radioimmunoassay (CV 6--14%), and calculated index as the molar ratio of vitamin concentration divided by Gc concentration. Plasma levels of Gc, 25OHD, 25OHD index, and 1,25(OH)(2)D, but not 1,25(OH)(2)D index, differed significantly between women with different Gc phenotype, being highest in Gc1-1, intermediate in Gc1-2, and lowest in Gc2-2. In multiple regression analysis, Gc concentration was an independent predictor of 1,25(OH)(2)D, whereas Gc phenotype was a significant predictor of 25OHD concentration, even after adjustment for the effects of season, sunbathing habits, skin thickness, use of vitamin supplements, smoking, and body mass index (BMI). Plasma parathyroid hormone (PTH) level did not differ between Gc phenotypes. Despite the fact that more than 60% of the women with Gc phenotype Gc2-2 had plasma 25OHD levels of less than 50 nmol/L none of them had plasma PTH higher than reference limits. Bone mineral content (BMC), Bone mineral density (BMD), and bone markers did not differ between Gc phenotypes. In conclusion, plasma 1,25(OH)(2)D, 25OHD, and 25OHD index are related to Gc phenotype, and we speculate that the thresholds for vitamin D sufficiency differ between Gc phenotypes.

We conducted this study to assess the prevalence of vitamin D insufficiency in a population of normal perimenopausal women, to examine the influence of sun exposure and vitamin D intake on the concentration of 25-hydroxyvitamin D (25OHD) and to examine the association between parathyroid hormone (PTH) and 25OHD. A total of 2016 healthy women aged 45±58, who had recently undergone a natural menopause, were enrolled over a 2´5-year period in the Danish Osteoporosis Prevention Study. A marked seasonal fluctuation of 25OHD was seen, with an abrupt rise in June and high values until October. The fluctuation could be related to number of hours of sunshine per month with a two months time lag. Dietary vitamin D intake, vitamin supplementation, sunlight exposure, and use of sun-bed were all significantly related to 25OHD concentrations. Sun exposure seemed to contribute the most. The overall prevalence of vitamin D deficiency (defined as serum 25OHD , 25 nmolal) was 7 %. However, in the subgroup avoiding direct sunshine and abstaining from vitamin D supplementation 32´8 % were vitamin D deficient in the winter±spring period. Although mean PTH was increased in the group with low serum 25OHD, PTH was not a sensitive marker of hypovitaminosis D in the individual, as only 16 % of those with vitamin D deficiency had PTH levels above normal range. Thus, we have shown, that healthy middle-aged Danish women are prone to vitamin D insufficiency in the winter±spring period, if they avoid sun exposure in the summer period and abstain from vitamin D supplementation.

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A huge number of risk assessment tools have been developed. Far from all have been validated in external studies, more of them have absence of methodological and transparent evidence, and few are integrated in national guidelines. Therefore, we performed a systematic review to provide an overview of existing valid and reliable risk assessment tools for prediction of osteoporotic fractures. Additionally, we aimed to determine if the performance of each tool was sufficient for practical use, and last, to examine whether the complexity of the tools influenced their discriminative power. We searched PubMed, Embase, and Cochrane databases for papers and evaluated these with respect to methodological quality using the Quality Assessment Tool for Diagnostic Accuracy Studies (QUADAS) checklist. A total of 48 tools were identified; 20 had been externally validated, however, only six tools had been tested more than once in a population-based setting with acceptable methodological quality. None of the tools performed consistently better than the others and simple tools (i.e., the Osteoporosis Self-assessment

The primary goal of this cross-sectional in vivo study was to assess peripheral bone microarchitecture, bone strength, and bone remodeling in adult type 1 diabetes (T1D) patients with and without diabetic microvascular disease (MVDþ and MVD-, respectively) and to compare them with age-, gender-, and height-matched healthy control subjects (CoMVDþ and CoMVD-, respectively). The secondary goal was to assess differences in MVD-and MVDþ patients. Fifty-five patients with T1DM (MVDþ group: n ¼ 29) were recruited from the Funen Diabetes Database. Dual-energy X-ray absorptiometry (DXA), high-resolution peripheral quantitative computed tomography (HRpQCT) of the ultradistal radius and tibia, and biochemical markers of bone turnover were performed in all participants. There were no significant differences in HR-pQCT parameters between MVD-and CoMVD-subjects. In contrast, MVDþ patients had larger total and trabecular bone areas (p ¼ 0.04 and p ¼ 0.02, respectively), lower total, trabecular, and cortical volumetric bone mineral density (vBMD) (p < 0.01, p < 0.04, and p < 0.02, respectively), and thinner cortex (p ¼ 0.03) at the radius, and lower total and trabecular vBMD (p ¼ 0.01 and p ¼ 0.02, respectively) at the tibia in comparison to CoMVDþ. MVDþ patients also exhibited lower total and trabecular vBMD (radius p ¼ 0.01, tibia p < 0.01), trabecular thickness (radius p ¼ 0.01), estimated bone strength, and greater trabecular separation (radius p ¼ 0.01, tibia p < 0.01) and network inhomogeneity (radius p ¼ 0.01, tibia p < 0.01) in comparison to MVD-patients. These differences remained significant after adjustment for age, body mass index, gender, disease duration, and glycemic control (average glycated hemoglobin over the previous 3 years). Although biochemical markers of bone turnover were significantly lower in MVDþ and MVD-groups in comparison to controls, they were similar between the MVDþ and MVD-groups. The results of our study suggest that the presence of MVD was associated with deficits in cortical and trabecular bone vBMD and microarchitecture that could partly explain the excess skeletal fragility observed in these patients.