Search Results
You are looking at 91 - 93 of 93 items for
- Abstract: Calcium x
- Abstract: Hyperparathyroidism x
- Abstract: Menopause x
School of Nursing, Institute of Clinical Sciences, University of Birmingham, Edgbaston, Birmingham, UK
Search for other papers by Jane Fletcher in
Google Scholar
PubMed
Search for other papers by Emma L Bishop in
Google Scholar
PubMed
Search for other papers by Stephanie R Harrison in
Google Scholar
PubMed
Search for other papers by Amelia Swift in
Google Scholar
PubMed
Search for other papers by Sheldon C Cooper in
Google Scholar
PubMed
Search for other papers by Sarah K Dimeloe in
Google Scholar
PubMed
Search for other papers by Karim Raza in
Google Scholar
PubMed
Search for other papers by Martin Hewison in
Google Scholar
PubMed
Vitamin D has well-documented effects on calcium homeostasis and bone metabolism but recent studies suggest a much broader role for this secosteroid in human health. Key components of the vitamin D system, notably the vitamin D receptor (VDR) and the vitamin D-activating enzyme (1α-hydroxylase), are present in a wide array of tissues, notably macrophages, dendritic cells and T lymphocytes (T cells) from the immune system. Thus, serum 25-hydroxyvitamin D (25D) can be converted to hormonal 1,25-dihydroxyvitamin D (1,25D) within immune cells, and then interact with VDR and promote transcriptional and epigenomic responses in the same or neighbouring cells. These intracrine and paracrine effects of 1,25D have been shown to drive antibacterial or antiviral innate responses, as well as to attenuate inflammatory T cell adaptive immunity. Beyond these mechanistic observations, association studies have reported the correlation between low serum 25D levels and the risk and severity of human immune disorders including autoimmune diseases such as inflammatory bowel disease, multiple sclerosis, type 1 diabetes and rheumatoid arthritis. The proposed explanation for this is that decreased availability of 25D compromises immune cell synthesis of 1,25D leading to impaired innate immunity and over-exuberant inflammatory adaptive immunity. The aim of the current review is to explore the mechanistic basis for immunomodulatory effects of 25D and 1,25D in greater detail with specific emphasis on how vitamin D-deficiency (low serum levels of 25D) may lead to dysregulation of macrophage, dendritic cell and T cell function and increase the risk of inflammatory autoimmune disease.
Search for other papers by Johanna Öberg in
Google Scholar
PubMed
Search for other papers by Rolf Jorde in
Google Scholar
PubMed
Diagnostic Clinic, University Hospital of North Norway, Tromso, Norway
Search for other papers by Yngve Figenschau in
Google Scholar
PubMed
Search for other papers by Per Medbøe Thorsby in
Google Scholar
PubMed
Search for other papers by Sandra Rinne Dahl in
Google Scholar
PubMed
Search for other papers by Anne Winther in
Google Scholar
PubMed
Division of Internal Medicine, University Hospital of North Norway, Tromso, Norway
Search for other papers by Guri Grimnes in
Google Scholar
PubMed
Objective
Combined hormonal contraceptive (CHC) use has been associated with higher total 25-hydroxyvitamin D (25(OH)D) levels. Here, we investigate the relation between CHC use and vitamin D metabolism to elucidate its clinical interpretation.
Methods
The cross-sectional Fit Futures 1 included 1038 adolescents. Here, a subgroup of 182 girls with available 25(OH)D, 1,25-dihydroxyvitamin D (1,25(OH)2D), 24,25-dihydroxyvitamin D (24,25(OH)2D), vitamin D-binding protein (DBP) and measured free 25(OH)D levels, in addition to parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23), was investigated. Vitamin D metabolites were compared between girls using (CHC+) and not using CHC (CHC−). Further, the predictability of CHC on 25(OH)D levels was assessed in a multiple regression model including lifestyle factors. The ratios 1,25(OH)2D/25(OH)D and 24,25(OH)2D/25(OH)D (vitamin D metabolite ratio (VMR)) in relation to 25(OH)D were presented in scatterplots.
Results
CHC+ (n = 64; 35% of the girls) had higher 25(OH)D levels (mean ± s.d., 60.3 ± 22.2) nmol/L) than CHC- (n = 118; 41.8 ± 19.3 nmol/L), P -values <0.01. The differences in 25(OH)D levels between CHC+ and CHC− were attenuated but remained significant after the adjustment of lifestyle factors. CHC+ also had higher levels of 1,25(OH)2D, 24,25(OH)2D, DBP and calcium than CHC−, whereas 1,25(OH)2D/25(OH)D, PTH, FGF23 and albumin were significantly lower. Free 25(OH)D and VMR did not statistically differ, and both ratios appeared similar in relation to 25(OH)D, irrespective of CHC status.
Conclusion
This confirms a clinical impact of CHC on vitamin D levels in adolescents. Our observations are likely due to an increased DBP-concentration, whereas the free 25(OH)D appears unaltered.
Search for other papers by Matteo Scopel in
Google Scholar
PubMed
Search for other papers by Eugenio De Carlo in
Google Scholar
PubMed
Search for other papers by Francesca Bergamo in
Google Scholar
PubMed
Search for other papers by Sabina Murgioni in
Google Scholar
PubMed
Search for other papers by Riccardo Carandina in
Google Scholar
PubMed
Search for other papers by Anna Rita Cervino in
Google Scholar
PubMed
Search for other papers by Marta Burei in
Google Scholar
PubMed
Search for other papers by Federica Vianello in
Google Scholar
PubMed
Search for other papers by Vittorina Zagonel in
Google Scholar
PubMed
Search for other papers by Matteo Fassan in
Google Scholar
PubMed
Search for other papers by Roberto Vettor in
Google Scholar
PubMed
We considered 351 patients affected by neuroendocrine tumors (NETs), followed at the University Hospital of Padua and at the Veneto Oncological Institute. Of these, 72 (20.5%) suffered from bone metastases. The sample was divided according to the timing of presentation of bone metastases into synchronous (within 6 months of diagnosis of primary tumor) and metachronous (after 6 months). We collected data on the type and grading of the primary tumor and on the features of bone metastases. Our analysis shows that the group of synchronous metastases generally presents primary tumors with a higher degree of malignancy rather than the ones of the metachronous group. This is supported by the finding of a Ki-67 level in GEP-NETs, at the diagnosis of bone metastases, significantly higher in the synchronous group. Moreover, in low-grade NETs, chromogranin A values are higher in the patients with synchronous metastases, indicating a more burden of disease. The parameters of phospho-calcium metabolism are within the normal range, and we do not find significant differences between the groups. Serious bone complications are not frequent and are not correlated with the site of origin of the primary tumor. From the analysis of the survival curves of the total sample, a cumulative survival rate of 33% at 10 years emerges. The average survival is 80 months, higher than what is reported in the literature, while the median is 84 months. In our observation period, synchronous patients tend to have a worse prognosis than metachronous ones with 52-months survival rates of 58 and 86%.
