Search Results

You are looking at 1 - 10 of 207 items for

  • Abstract: Bone x
  • Abstract: Mineral x
  • Abstract: Hyperparathyroidism x
  • Abstract: Hypoparathyroidism x
  • Abstract: Osteo* x
  • Abstract: Vitamin D x
Clear All Modify Search
Stefan Pilz Division of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Search for other papers by Stefan Pilz in
Google Scholar
PubMed
Close
,
Armin Zittermann Clinic for Thoracic and Cardiovascular Surgery, Herz- und Diabeteszentrum NRW, Ruhr University Bochum, Bad Oeynhausen, Germany

Search for other papers by Armin Zittermann in
Google Scholar
PubMed
Close
,
Christian Trummer Division of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Search for other papers by Christian Trummer in
Google Scholar
PubMed
Close
,
Verena Theiler-Schwetz Division of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Search for other papers by Verena Theiler-Schwetz in
Google Scholar
PubMed
Close
,
Elisabeth Lerchbaum Division of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Search for other papers by Elisabeth Lerchbaum in
Google Scholar
PubMed
Close
,
Martin H Keppel University Institute for Medical and Chemical Laboratory Diagnostics, Paracelsus Medical University, Salzburg, Austria

Search for other papers by Martin H Keppel in
Google Scholar
PubMed
Close
,
Martin R Grübler Department of Cardiology, Swiss Cardiovascular Center Bern, Bern University Hospital, University of Bern, Bern, Switzerland

Search for other papers by Martin R Grübler in
Google Scholar
PubMed
Close
,
Winfried März Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Graz, Austria
Medical Clinic V (Nephrology, Hypertensiology, Rheumatology, Endocrinology, Diabetology), Medical Faculty Mannheim, Ruperto-Carola University of Heidelberg, Heidelberg, Germany
Synlab Medical Center of Human Genetics Mannheim, Mannheim, Germany

Search for other papers by Winfried März in
Google Scholar
PubMed
Close
, and
Marlene Pandis Division of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Search for other papers by Marlene Pandis in
Google Scholar
PubMed
Close

Vitamin D testing and treatment is a subject of controversial scientific discussions, and it is challenging to navigate through the expanding vitamin D literature with heterogeneous and partially opposed opinions and recommendations. In this narrative review, we aim to provide an update on vitamin D guidelines and the current evidence on the role of vitamin D for human health with its subsequent implications for patient care and public health issues. Vitamin D is critical for bone and mineral metabolism, and it is established that vitamin D deficiency can cause rickets and osteomalacia. While many guidelines recommend target serum 25-hydroxyvitamin D (25[OH]D) concentrations of ≥50 nmol/L (20 ng/mL), the minimum consensus in the scientific community is that serum 25(OH)D concentrations below 25–30 nmol/L (10–12 ng/mL) must be prevented and treated. Using this latter threshold of serum 25(OH)D concentrations, it has been documented that there is a high worldwide prevalence of vitamin D deficiency that may require public health actions such as vitamin D food fortification. On the other hand, there is also reason for concern that an exploding rate of vitamin D testing and supplementation increases costs and might potentially be harmful. In the scientific debate on vitamin D, we should consider that nutrient trials differ from drug trials and that apart from the opposed positions regarding indications for vitamin D treatment we still have to better characterize the precise role of vitamin D for human health.

Open access
Marcela Moraes Mendes Department of Nutrition, Faculty of Health Sciences, University of Brasília, Distrito Federal, Brazil
Department of Nutrition, Institute of Life Sciences, Federal University of Juiz de Fora, Governador Valadares, Minas Gerais, Brazil
Department of Nutrition, Faculty of Health and Medical Sciences, University of Surrey, University of Surrey, Guildford, UK

Search for other papers by Marcela Moraes Mendes in
Google Scholar
PubMed
Close
,
Patricia Borges Botelho Department of Nutrition, Faculty of Health Sciences, University of Brasília, Distrito Federal, Brazil

Search for other papers by Patricia Borges Botelho in
Google Scholar
PubMed
Close
, and
Helena Ribeiro Department of Environmental Health, Faculty of Public Health, University of São Paulo, São Paulo, Brazil

Search for other papers by Helena Ribeiro in
Google Scholar
PubMed
Close

Vitamin D enhances calcium absorption and bone mineralisation, promotes maintenance of muscle function, and is crucial for musculoskeletal health. Low vitamin D status triggers secondary hyperparathyroidism, increases bone loss, and leads to muscle weakness. The primary physiologic function of vitamin D and its metabolites is maintaining calcium homeostasis for metabolic functioning, signal transduction, and neuromuscular activity. A considerable amount of human evidence supports the well-recognised contribution of adequate serum 25-hydroxyvitamin D concentrations for bone homeostasis maintenance and prevention and treatment strategies for osteoporosis when combined with adequate calcium intake. This paper aimed to review the literature published, mainly in the last 20 years, on the effect of vitamin D and its supplementation for musculoskeletal health in order to identify the aspects that remain unclear or controversial and therefore require further investigation and debate. There is a clear need for consistent data to establish realistic and meaningful recommendations of vitamin D status that consider different population groups and locations. Moreover, there is still a lack of consensus on thresholds for vitamin D deficiency and optimal status as well as toxicity, optimal intake of vitamin D, vitamin D supplement alone as a strategy to prevent fractures and falls, recommended sun exposure at different latitudes and for different skin pigmentations, and the extra skeletal effects of vitamin D.

Open access
Glenville Jones Department of Biomedical and Molecular Sciences, Queen’s University, Kingston, Ontario, Canada

Search for other papers by Glenville Jones in
Google Scholar
PubMed
Close

Vitamin D has many physiological functions including upregulation of intestinal calcium and phosphate absorption, mobilization of bone resorption, renal reabsorption of calcium as well as actions on a variety of pleiotropic functions. It is believed that many of the hormonal effects of vitamin D involve a 1,25-dihydroxyvitamin D3-vitamin D receptor-mediated transcriptional mechanism involving binding to the cellular chromatin and regulating hundreds of genes in many tissues. This comprehensive historical review provides a unique perspective of the many steps of the discovery of vitamin D and its deficiency disease, rickets, stretching from 1650 until the present. The overview is divided into four distinct historical phases which cover the major developments in the field and in the process highlighting the: (a) first recognition of rickets or vitamin D deficiency; (b) discovery of the nutritional factor, vitamin D and its chemical structure; (c) elucidation of vitamin D metabolites including the hormonal form, 1,25-dihydroxyvitamin D3; (d) delineation of the vitamin D cellular machinery, functions and vitamin D-related diseases which focused on understanding the mechanism of action of vitamin D in its many target cells.

Open access
Barbara J Boucher Blizard Institute, Barts & The London school of Medicine & Dentistry, Queen Mary University of London, London, UK

Search for other papers by Barbara J Boucher in
Google Scholar
PubMed
Close

Our knowledge of vitamin D has come a long way since the 100 years it took for doctors to accept, between 1860 and 1890, that both sunlight and cod liver oil (a well-known folk remedy) cured and prevented rickets. Vitamins D2/D3 were discovered exactly a hundred years ago, and over the last 50 years vitamin D has been found to have many effects on virtually all human tissues and not just on bone health, while mechanisms affecting the actions of vitamin D at the cellular level are increasingly understood, but deficiency persists globally. Observational studies in humans have shown that better provision of vitamin D is strongly associated, dose-wise, with reductions in current and future health risks in line with the known actions of vitamin D. Randomised controlled trials, commonly accepted as providing a ‘gold standard’ for assessing the efficacy of new forms of treatment, have frequently failed to provide supportive evidence for the expected health benefits of supplementation. Such RCTs, however, have used designs evolved for testing drugs while vitamin D is a nutrient; the appreciation of this difference is critical to identifying health benefits from existing RCT data and for improving future RCT design. This report aims, therefore, to provide a brief overview of the evidence for a range of non-bony health benefits of vitamin D repletion; to discuss specific aspects of vitamin D biology that can confound RCT design and how to allow for them.

Open access
Rong Xu Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

Search for other papers by Rong Xu in
Google Scholar
PubMed
Close
,
Difei Lian Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

Search for other papers by Difei Lian in
Google Scholar
PubMed
Close
,
Yan Xie Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

Search for other papers by Yan Xie in
Google Scholar
PubMed
Close
,
Lin Mu Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

Search for other papers by Lin Mu in
Google Scholar
PubMed
Close
,
Yali Wu Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

Search for other papers by Yali Wu in
Google Scholar
PubMed
Close
,
Zhilei Chen Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

Search for other papers by Zhilei Chen in
Google Scholar
PubMed
Close
, and
Baoyu Zhang Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

Search for other papers by Baoyu Zhang in
Google Scholar
PubMed
Close

Osteoporosis (OP) is a systemic bone disease in which bone density and quality decrease and bone fragility increases due to a variety of causes, making it prone to fractures. The development of OP is closely related to oxidative stress. Uric acid (UA) is the end product of purine metabolism in the human body. Extracellular UA has antioxidant properties and is thought to have a protective effect on bone metabolism. However, the process of UA degradation can lead to intracellular oxidative stress, which together with UA-induced inflammatory factors, leads to increased bone destruction. In addition, UA can inhibit vitamin D production, resulting in secondary hyperparathyroidism and further exacerbating UA-associated bone loss. This review summarizes the relationship between serum UA levels and bone mineral density, bone turnover markers, and so on, in the hope of providing new insights into the pathogenesis and treatment of OP.

Open access
Gabriella Oliveira Lima Laboratory of Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará, Belém, Pará, Brazil

Search for other papers by Gabriella Oliveira Lima in
Google Scholar
PubMed
Close
,
Alex Luiz Menezes da Silva Laboratory of Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará, Belém, Pará, Brazil

Search for other papers by Alex Luiz Menezes da Silva in
Google Scholar
PubMed
Close
,
Julianne Elba Cunha Azevedo Laboratory of Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará, Belém, Pará, Brazil

Search for other papers by Julianne Elba Cunha Azevedo in
Google Scholar
PubMed
Close
,
Chirlene Pinheiro Nascimento Laboratory of Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará, Belém, Pará, Brazil

Search for other papers by Chirlene Pinheiro Nascimento in
Google Scholar
PubMed
Close
,
Luana Rodrigues Vieira Laboratory of Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará, Belém, Pará, Brazil

Search for other papers by Luana Rodrigues Vieira in
Google Scholar
PubMed
Close
,
Akira Otake Hamoy Laboratory of Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará, Belém, Pará, Brazil

Search for other papers by Akira Otake Hamoy in
Google Scholar
PubMed
Close
,
Luan Oliveira Ferreira Laboratory of Experimental Neuropathology, Institute of Biological Sciences, Federal University of Pará, Belém, Pará, Brazil

Search for other papers by Luan Oliveira Ferreira in
Google Scholar
PubMed
Close
,
Verônica Regina Lobato Oliveira Bahia Multidisciplinary Laboratory of Animal Morphology, Institute of Biological Sciences, Federal University of Pará, Belém, Pará, Brazil

Search for other papers by Verônica Regina Lobato Oliveira Bahia in
Google Scholar
PubMed
Close
,
Nilton Akio Muto Amazon Bioactive Compounds Valorization Center, Institute of Biological Sciences, Federal University of Pará, Belém, Pará, Brazil

Search for other papers by Nilton Akio Muto in
Google Scholar
PubMed
Close
,
Dielly Catrina Favacho Lopes Laboratory of Experimental Neuropathology, Institute of Biological Sciences, Federal University of Pará, Belém, Pará, Brazil

Search for other papers by Dielly Catrina Favacho Lopes in
Google Scholar
PubMed
Close
, and
Moisés Hamoy Laboratory of Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará, Belém, Pará, Brazil

Search for other papers by Moisés Hamoy in
Google Scholar
PubMed
Close

Low plasma levels of vitamin D causes bone mineral change that can precipitate osteopenia and osteoporosis and could aggravate autoimmune diseases, hypertension and diabetes. The demand for vitamin D supplementation becomes necessary; however, the consumption of vitamin D is not without risks, which its toxicity could have potentially serious consequences related to hypervitaminosis D, such as hypercalcemia and cerebral alterations. Thus, the present study describes the electroencephalographic changes caused by supraphysiological doses of vitamin D in the brain electrical dynamics and the electrocardiographic changes. After 4 days of treatment with vitamin D at a dose of 25,000 IU/kg, the serum calcium levels found were increased in comparison with the control group. The electrocorticogram analysis found a reduction in wave activity in the delta, theta, alpha and beta frequency bands. For ECG was observed changes with shortened QT follow-up, which could be related to serum calcium concentration. This study presented important evidence about the cerebral and cardiac alterations caused by high doses of vitamin D, indicating valuable parameters in the screening and decision-making process for diagnosing patients with symptoms suggestive of intoxication.

Open access
Shu-Meng Hu Department of Nephrology, West China Hospital, Sichuan University, Chengdu, Sichuan, China

Search for other papers by Shu-Meng Hu in
Google Scholar
PubMed
Close
,
Yang-Juan Bai Department of Laboratory Medicine/Research Centre of Clinical Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan, China

Search for other papers by Yang-Juan Bai in
Google Scholar
PubMed
Close
,
Ya-Mei Li Department of Laboratory Medicine/Research Centre of Clinical Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan, China

Search for other papers by Ya-Mei Li in
Google Scholar
PubMed
Close
,
Ye Tao Department of Nephrology, West China Hospital, Sichuan University, Chengdu, Sichuan, China

Search for other papers by Ye Tao in
Google Scholar
PubMed
Close
,
Xian-Ding Wang Department of Urology/Institute of Urology, West China Hospital, Sichuan University, Chengdu, Sichuan, China

Search for other papers by Xian-Ding Wang in
Google Scholar
PubMed
Close
,
Tao Lin Department of Urology/Institute of Urology, West China Hospital, Sichuan University, Chengdu, Sichuan, China

Search for other papers by Tao Lin in
Google Scholar
PubMed
Close
,
Lan-Lan Wang Department of Laboratory Medicine/Research Centre of Clinical Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan, China

Search for other papers by Lan-Lan Wang in
Google Scholar
PubMed
Close
, and
Yun-Ying Shi Department of Nephrology, West China Hospital, Sichuan University, Chengdu, Sichuan, China

Search for other papers by Yun-Ying Shi in
Google Scholar
PubMed
Close

Introduction

Tertiary hyperparathyroidism (THPT) and vitamin D deficiency are commonly seen in kidney transplant recipients, which may result in persistently elevated fibroblast growth factor 23 (FGF23) level after transplantation and decreased graft survival. The aim of this study is to evaluate the effect of vitamin D supplementation on THPT, FGF23-alpha Klotho (KLA) axis and cardiovascular complications after transplantation.

Materials and methods

Two hundred nine kidney transplant recipients were included and further divided into treated and untreated groups depending on whether they received vitamin D supplementation. We tracked the state of THPT, bone metabolism and FGF23–KLA axis within 12 months posttransplant and explored the predictors and risk factors for intact FGF23 levels, KLA levels, THPT and cardiovascular complications in recipients.

Results

Vitamin D supplementation significantly improved FGF23 resistance, THPT and high bone turnover status, preserved better graft function and prevented coronary calcification in the treated group compared to the untreated group at month 12. The absence of vitamin D supplementation was an independent risk factor for THPT and a predictor for intact FGF23 and KLA levels at month 12. Age and vitamin D deficiency were independent risk factors for coronary calcification in recipients at month 12.

Conclusion

Vitamin D supplementation effectively improved THPT, FGF23 resistance and bone metabolism, preserved graft function and prevented coronary calcification after transplantation.

Open access
Mohammed S Razzaque Department of Pathology, Lake Erie College of Osteopathic Medicine, Erie, Pennsylvania, USA

Search for other papers by Mohammed S Razzaque in
Google Scholar
PubMed
Close

Fibroblast growth factor‐23 (FGF23) controls the homeostasis of both phosphate and vitamin D. Bone-derived FGF23 can suppress the transcription of 1α‐hydroxylase (1α(OH)ase) to reduce renal activation of vitamin D (1,25(OH)2D3). FGF23 can also activate the transcription of 24‐hydroxylase to enhance the renal degradation process of vitamin D. There is a counter-regulation for FGF23 and vitamin D; 1,25(OH)2D3 induces the skeletal synthesis and the release of FGF23, while FGF23 can suppress the production of 1,25(OH)2D3 by inhibiting 1α(OH)ase synthesis. Genetically ablating FGF23 activities in mice resulted in higher levels of renal 1α(OH)ase, which is also reflected in an increased level of serum 1,25(OH)2D3, while genetically ablating 1α(OH)ase activities in mice reduced the serum levels of FGF23. Similar feedback control of FGF23 and vitamin D is also detected in various human diseases. Further studies are required to understand the subcellular molecular regulation of FGF23 and vitamin D in health and disease.

Open access
Shatha Alharazy Department of Physiology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia

Search for other papers by Shatha Alharazy in
Google Scholar
PubMed
Close
,
M Denise Robertson Department of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey, Guildford, UK

Search for other papers by M Denise Robertson in
Google Scholar
PubMed
Close
,
Susan Lanham-New Department of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey, Guildford, UK

Search for other papers by Susan Lanham-New in
Google Scholar
PubMed
Close
,
Muhammad Imran Naseer Centre of Excellence in Genomic Medicine Research, King Abdulaziz University, Jeddah, Saudi Arabia
Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia

Search for other papers by Muhammad Imran Naseer in
Google Scholar
PubMed
Close
,
Adeel G Chaudhary Centre of Excellence in Genomic Medicine Research, King Abdulaziz University, Jeddah, Saudi Arabia
Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia
Centre for Innovation in Personalized Medicine, King Abdulaziz University, Jeddah, Saudi Arabia

Search for other papers by Adeel G Chaudhary in
Google Scholar
PubMed
Close
, and
Eman Alissa Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia

Search for other papers by Eman Alissa in
Google Scholar
PubMed
Close

Background

Measurement of free 25-hydroyvitamin D (25(OH)D) status has been suggested as a more representative marker of vitamin D status than that of total 25(OH)D. Previously, free 25(OH)D could only be calculated indirectly; however, a newly developed direct assay for the measurement of free 25(OH)D is now available. The aim of this study therefore was to investigate directly measured total and free vitamin D levels association with metabolic health in postmenopausal healthy women living in Saudi Arabia.

Methods

A sample of 302 postmenopausal women aged ≥50 years (n  = 302) living in Saudi Arabia were recruited in a cross-sectional study design. Blood samples were collected from subjects for measurement of serum levels of total 25(OH)D, directly measured free 25(OH)D, metabolic bone parameters, lipid profile, and other biochemical tests.

Results

A positive correlation was found between directly measured free and total 25(OH)D (r = 0.64, P< 0.0001). Total but not free 25(OH)D showed significant association with serum intact parathyroid hormone (P = 0.004), whilst free 25(OH)D but not total 25(OH)D showed a significant association with total cholesterol and LDL-C (P = 0.032 and P = 0.045, respectively).

Conclusions

Free 25(OH)D and total 25(OH)D were found to be consistently correlated but with different associations to metabolic health parameters. Further research is needed to determine which marker of vitamin D status would be the most appropriate in population studies.

Open access
Ranganathan R Rao Warwickshire Institute for the Study of Diabetes, Warwick Medical School, Department of Endocrinology, Institute of Head and Neck Studies and Education (InHANSE), Endocrinology and Metabolism, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK

Search for other papers by Ranganathan R Rao in
Google Scholar
PubMed
Close
,
Harpal S Randeva Warwickshire Institute for the Study of Diabetes, Warwick Medical School, Department of Endocrinology, Institute of Head and Neck Studies and Education (InHANSE), Endocrinology and Metabolism, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK
Warwickshire Institute for the Study of Diabetes, Warwick Medical School, Department of Endocrinology, Institute of Head and Neck Studies and Education (InHANSE), Endocrinology and Metabolism, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK

Search for other papers by Harpal S Randeva in
Google Scholar
PubMed
Close
,
Sailesh Sankaranarayanan Warwickshire Institute for the Study of Diabetes, Warwick Medical School, Department of Endocrinology, Institute of Head and Neck Studies and Education (InHANSE), Endocrinology and Metabolism, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK
Warwickshire Institute for the Study of Diabetes, Warwick Medical School, Department of Endocrinology, Institute of Head and Neck Studies and Education (InHANSE), Endocrinology and Metabolism, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK

Search for other papers by Sailesh Sankaranarayanan in
Google Scholar
PubMed
Close
,
Murthy Narashima Warwickshire Institute for the Study of Diabetes, Warwick Medical School, Department of Endocrinology, Institute of Head and Neck Studies and Education (InHANSE), Endocrinology and Metabolism, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK
Warwickshire Institute for the Study of Diabetes, Warwick Medical School, Department of Endocrinology, Institute of Head and Neck Studies and Education (InHANSE), Endocrinology and Metabolism, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK

Search for other papers by Murthy Narashima in
Google Scholar
PubMed
Close
,
Matthias Möhlig Warwickshire Institute for the Study of Diabetes, Warwick Medical School, Department of Endocrinology, Institute of Head and Neck Studies and Education (InHANSE), Endocrinology and Metabolism, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK

Search for other papers by Matthias Möhlig in
Google Scholar
PubMed
Close
,
Hisham Mehanna Warwickshire Institute for the Study of Diabetes, Warwick Medical School, Department of Endocrinology, Institute of Head and Neck Studies and Education (InHANSE), Endocrinology and Metabolism, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK

Search for other papers by Hisham Mehanna in
Google Scholar
PubMed
Close
, and
Martin O Weickert Warwickshire Institute for the Study of Diabetes, Warwick Medical School, Department of Endocrinology, Institute of Head and Neck Studies and Education (InHANSE), Endocrinology and Metabolism, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK
Warwickshire Institute for the Study of Diabetes, Warwick Medical School, Department of Endocrinology, Institute of Head and Neck Studies and Education (InHANSE), Endocrinology and Metabolism, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK

Search for other papers by Martin O Weickert in
Google Scholar
PubMed
Close

Introduction/background

Vitamin D deficiency further increases circulating parathyroid hormone (PTH) levels in patients with primary hyperparathyroidism (pHPT), with potential detrimental effects on bone mass.

Methods

This was an observational clinical study in consecutive conservatively treated postmenopausal women (n=40) with pHPT and coexistent 25-hydroxyvitamin D deficiency (25OHD ≤50 nmol/l (≤20 ng/ml)). Patients who showed an increase in serum 25OHD above the threshold of vitamin D deficiency (>50 nmol/l; n=28) using treatment with various commonly prescribed vitamin D preparations were, for the purposes of statistical analyses, allocated to the treatment group. Patients who were retrospectively identified as having received no treatment with vitamin D and/or remained vitamin D deficient were considered as non-responders/controls (n=12). Adjusted calcium (adjCa), PTH and 25OHD concentrations were monitored in all subjects up to 54 months (mean observation period of 18±2 months).

Results

Prolonged increased vitamin D intake, regardless of the source (serum 25OHD, increase from 32.2±1.7 nmol/l at baseline to 136.4±11.6 nmol/l, P<0.0001), significantly reduced serum PTH (13.3±1.1 vs 10.5±1.0 pmol/l, P=0.0001), with no adverse effects on adjCa levels (2.60±0.03 vs 2.60±0.02 mmol/l, P=0.77) and renal function tests (P>0.73). In contrast, serum PTH remained unchanged (15.8±2.6 vs 16.3±1.9 pmol/l, P=0.64) in patients who remained vitamin D deficient, with a significant difference between groups in changes of PTH (P=0.0003). Intrapartial correlation analyses showed an independent negative correlation of changes in 25OHD with PTH levels (r ic=−0.41, P=0.014).

Conclusions

Prolonged treatment with vitamin D in various commonly prescribed preparations appeared to be safe and significantly reduced PTH levels by 21%.

Open access