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Felix Haglund Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden
Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden

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Gustaf Rosin Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden
Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden
Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden

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Inga-Lena Nilsson Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden

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C Christofer Juhlin Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden
Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden

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Ylva Pernow Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden

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Sophie Norenstedt Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden

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Andrii Dinets Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden
Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden
Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden

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Catharina Larsson Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden
Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden

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Johan Hartman Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden
Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden

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Anders Höög Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden
Department of Oncology–Pathology, Cancer Centre Karolinska, Department of Biosciences and Nutrition, Department of Molecular Medicine and Surgery, Department of Surgery #4, Karolinska Institutet, Stockholm, Sweden

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Primary hyperparathyroidism (PHPT) is a common endocrinopathy, frequently caused by a parathyroid adenoma, rarely by a parathyroid carcinoma that lacks effective oncological treatment. As the majority of cases are present in postmenopausal women, oestrogen signalling has been implicated in the tumourigenesis. Oestrogen receptor beta 1 (ERB1) and ERB2 have been recently identified in parathyroid adenomas, the former inducing genes coupled to tumour apoptosis. We applied immunohistochemistry and slide digitalisation to quantify nuclear ERB1 and ERB2 in 172 parathyroid adenomas, atypical adenomas and carcinomas, and ten normal parathyroid glands. All the normal parathyroid glands expressed ERB1 and ERB2. The majority of tumours expressed ERB1 (70.6%) at varying intensities, and ERB2 (96.5%) at strong intensities. Parathyroid carcinomas expressed ERB1 in three out of six cases and ERB2 in five out of six cases. The intensity of tumour nuclear ERB1 staining significantly correlated inversely with tumour weight (P=0.011), and patients whose tumours were classified as ERB1-negative had significantly greater tumour weight as well as higher serum calcium (P=0.002) and parathyroid hormone levels (P=0.003). Additionally, tumour nuclear ERB1 was not expressed differentially with respect to sex or age of the patient. Levels of tumour nuclear ERB2 did not correlate with clinical characteristics. In conclusion, decreased ERB1 immunoreactivity is associated with increased tumour weight in parathyroid adenomas. Given the previously reported correlation with tumour-suppressive signalling, selective oestrogen receptor modulation (SERMs) may play a role in the treatment of parathyroid carcinomas. Future studies of SERMs and oestrogen treatment in PHPT should consider tumour weight as a potential factor in pharmacological responsiveness.

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Fernanda A Correa Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Ericka B Trarbach Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Cintia Tusset Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Ana Claudia Latronico Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Luciana R Montenegro Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Luciani R Carvalho Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Marcela M Franca Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Aline P Otto Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Everlayny F Costalonga Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Vinicius N Brito Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Ana Paula Abreu Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Mirian Y Nishi Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Alexander A L Jorge Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Ivo J P Arnhold Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Yisrael Sidis Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Nelly Pitteloud Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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Berenice B Mendonca Unidade de Endocrinologia do Desenvolvimento, Unidade de Endocrinologia Genética, Centre Hospitalier Universitaire Vaudois (CHUV), Division of Endocrinology, Laboratório de Hormônios e Genética Molecular LIM42

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The genetic aetiology of congenital hypopituitarism (CH) is not entirely elucidated. FGFR1 and PROKR2 loss-of-function mutations are classically involved in hypogonadotrophic hypogonadism (HH), however, due to the clinical and genetic overlap of HH and CH; these genes may also be involved in the pathogenesis of CH. Using a candidate gene approach, we screened 156 Brazilian patients with combined pituitary hormone deficiencies (CPHD) for loss-of-function mutations in FGFR1 and PROKR2. We identified three FGFR1 variants (p.Arg448Trp, p.Ser107Leu and p.Pro772Ser) in four unrelated patients (two males) and two PROKR2 variants (p.Arg85Cys and p.Arg248Glu) in two unrelated female patients. Five of the six patients harbouring the variants had a first-degree relative that was an unaffected carrier of it. Results of functional studies indicated that the new FGFR1 variant p.Arg448Trp is a loss-of-function variant, while p.Ser107Leu and p.Pro772Ser present signalling activity similar to the wild-type form. Regarding PROKR2 variants, results from previous functional studies indicated that p.Arg85Cys moderately compromises receptor signalling through both MAPK and Ca2 + pathways while p.Arg248Glu decreases calcium mobilization but has normal MAPK activity. The presence of loss-of-function variants of FGFR1 and PROKR2 in our patients with CPHD is indicative of an adjuvant and/or modifier effect of these rare variants on the phenotype. The presence of the same variants in unaffected relatives implies that they cannot solely cause the phenotype. Other associated genetic and/or environmental modifiers may play a role in the aetiology of this condition.

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Malachi J McKenna Metabolism Laboratory, Department of Endocrinology, School of Medicine and Medical Sciences, St Vincent's University Hospital, Elm Park, Dublin 4, Ireland
Metabolism Laboratory, Department of Endocrinology, School of Medicine and Medical Sciences, St Vincent's University Hospital, Elm Park, Dublin 4, Ireland
Metabolism Laboratory, Department of Endocrinology, School of Medicine and Medical Sciences, St Vincent's University Hospital, Elm Park, Dublin 4, Ireland

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Barbara F Murray Metabolism Laboratory, Department of Endocrinology, School of Medicine and Medical Sciences, St Vincent's University Hospital, Elm Park, Dublin 4, Ireland

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Myra O'Keane Metabolism Laboratory, Department of Endocrinology, School of Medicine and Medical Sciences, St Vincent's University Hospital, Elm Park, Dublin 4, Ireland

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Mark T Kilbane Metabolism Laboratory, Department of Endocrinology, School of Medicine and Medical Sciences, St Vincent's University Hospital, Elm Park, Dublin 4, Ireland

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Background

The Institute of Medicine 2011 Report on Dietary Reference Intakes for Calcium and Vitamin D specified higher intakes for all age groups compared to the 1997 report, but also cautioned against spurious claims about an epidemic of vitamin D deficiency and against advocates of higher intake requirements. Over 40 years, we have noted marked improvement in vitamin D status but we are concerned about hypervitaminosis D.

Objective

We sought to evaluate the 25-hydroxyvitamin D (25OHD) trend over 20 years.

Design

We retrieved all results of serum 25OHD from 1993 to 2013 (n=69 012) that was trimmed to one sample per person (n=43 782). We conducted a time series analysis of the monthly averages for 25OHD using a simple sequence chart and a running median smoothing function. We modelled the data using univariate auto-regressive integrated moving average (ARIMA) and forecast 25OHD levels up to 2016.

Results

The time series sequence chart and smoother function demonstrated a steady upward trend with seasonality. The yearly average 25OHD increased from 36.1 nmol/l in 1993 to 57.3 nmol/l in 2013. The ARIMA model was a good fit for the 25OHD time series; it forecasted monthly average 25OHD up to the end of 2016 with a positive stationary R 2 of 0.377.

Conclusions

Vitamin D status improved over the past 40 years, but there remains a dual problem: there are groups at risk of vitamin D deficiency who need public health preventative measures; on the other hand, random members of the population are taking unnecessarily high vitamin D intakes for unsubstantiated claims.

Open access
Yuan Liu Department of Endocrinology, Qilu Hospital of Shandong University, Jinan, China
Institute of Endocrine and Metabolic Diseases of Shandong University, Jinan, China
Key Laboratory of Endocrine and Metabolic Diseases, Shandong Province Medicine & Health, Jinan, China

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Siyi Guo Department of Endocrinology, Qilu Hospital of Shandong University, Jinan, China
Institute of Endocrine and Metabolic Diseases of Shandong University, Jinan, China
Key Laboratory of Endocrine and Metabolic Diseases, Shandong Province Medicine & Health, Jinan, China

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Jinsong Wu Department of Endocrinology, Qilu Hospital of Shandong University, Jinan, China
Institute of Endocrine and Metabolic Diseases of Shandong University, Jinan, China
Key Laboratory of Endocrine and Metabolic Diseases, Shandong Province Medicine & Health, Jinan, China

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Rongai Wang Department of Endocrinology, Qilu Hospital of Shandong University, Jinan, China
Health Management Center, The Second Affiliated Hospital of Zhejiang Chinese Medicine University, Zhejiang, China

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Jinbo Liu Department of Endocrinology, Qilu Hospital of Shandong University, Jinan, China
Institute of Endocrine and Metabolic Diseases of Shandong University, Jinan, China
Key Laboratory of Endocrine and Metabolic Diseases, Shandong Province Medicine & Health, Jinan, China

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Yan Liu Department of Endocrinology, Qilu Hospital of Shandong University, Jinan, China
Institute of Endocrine and Metabolic Diseases of Shandong University, Jinan, China
Key Laboratory of Endocrine and Metabolic Diseases, Shandong Province Medicine & Health, Jinan, China

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Bin Lv Department of Thyroid Surgery, General Surgery, Qilu Hospital of Shandong University, Jinan, China

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Nan Liu Department of Thyroid Surgery, General Surgery, Qilu Hospital of Shandong University, Jinan, China

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Ling Jiang Department of Endocrinology, Qilu Hospital of Shandong University, Jinan, China
Institute of Endocrine and Metabolic Diseases of Shandong University, Jinan, China
Key Laboratory of Endocrine and Metabolic Diseases, Shandong Province Medicine & Health, Jinan, China

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Xiaoli Zhang Department of Endocrinology, Qilu Hospital of Shandong University, Jinan, China
Institute of Endocrine and Metabolic Diseases of Shandong University, Jinan, China
Key Laboratory of Endocrine and Metabolic Diseases, Shandong Province Medicine & Health, Jinan, China

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The clinical presentation of primary hyperparathyroidism (PHPT) differs between patients from developed and developing countries. In China, the clinical pattern has changed over the past few decades. Our aim was to elucidate general changes in the clinical characteristics of PHPT from 2010 to 2021. We enrolled 343 patients with PHPT at the Qilu Hospital of Shandong University, Jinan, China, from January 2010 to May 2021, including both surgical and non-surgical patients. Patients were divided into two subgroups, 2010–2016 (group A, n  = 152) and 2017–2021 (group B, n  = 191), based on the time span. We compared clinical manifestations and laboratory result data between these two groups. The mean patient age was 52.59 ± 13.55 years, and the male-to-female ratio was 1:2.54. Of the 343 patients, 183 (53.35%) had symptomatic PHPT; bone pain, urolithiasis, and fatigue were the most common symptoms. Post-operative pathology showed that 96.20% of the patients had parathyroid adenoma, whereas 2.41% had parathyroid carcinoma. Great changes occurred between 2010 and 2021; the percentage of patients with asymptomatic PHPT (aPHPT) increased from 36.18% in group A to 54.97% in group B. Moreover, patients in group B showed significantly lower serum calcium, alkaline phosphatase, parathyroid hormone, and urinary phosphate levels but higher serum 25-hydroxyvitamin D levels than those in group A. Clinical presentations in group B were also milder. In conclusion, the clinical characteristics of Chinese PHPT patients changed dramatically from 2010 to 2021, with asymptomatic PHPT (aPHPT becoming the predominant type over the last 3 years.

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

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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

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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

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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

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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

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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

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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

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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
Adriana J van Ballegooijen Department of Health Sciences, Department of Epidemiology and Biostatistics, Department of Public Health, Department of General Practice, Department of Internal Medicine and Cardiovascular Research Institute Maastricht, Department of Internal Medicine, Faculty of Earth and Life Sciences, EMGO Institute for Health and Care Research, VU University Amsterdam, De Boelelaan 1085, 1081 HV Amsterdam, The Netherlands

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Marjolein Visser Department of Health Sciences, Department of Epidemiology and Biostatistics, Department of Public Health, Department of General Practice, Department of Internal Medicine and Cardiovascular Research Institute Maastricht, Department of Internal Medicine, Faculty of Earth and Life Sciences, EMGO Institute for Health and Care Research, VU University Amsterdam, De Boelelaan 1085, 1081 HV Amsterdam, The Netherlands
Department of Health Sciences, Department of Epidemiology and Biostatistics, Department of Public Health, Department of General Practice, Department of Internal Medicine and Cardiovascular Research Institute Maastricht, Department of Internal Medicine, Faculty of Earth and Life Sciences, EMGO Institute for Health and Care Research, VU University Amsterdam, De Boelelaan 1085, 1081 HV Amsterdam, The Netherlands

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Marieke B Snijder Department of Health Sciences, Department of Epidemiology and Biostatistics, Department of Public Health, Department of General Practice, Department of Internal Medicine and Cardiovascular Research Institute Maastricht, Department of Internal Medicine, Faculty of Earth and Life Sciences, EMGO Institute for Health and Care Research, VU University Amsterdam, De Boelelaan 1085, 1081 HV Amsterdam, The Netherlands

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Jacqueline M Dekker Department of Health Sciences, Department of Epidemiology and Biostatistics, Department of Public Health, Department of General Practice, Department of Internal Medicine and Cardiovascular Research Institute Maastricht, Department of Internal Medicine, Faculty of Earth and Life Sciences, EMGO Institute for Health and Care Research, VU University Amsterdam, De Boelelaan 1085, 1081 HV Amsterdam, The Netherlands

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Giel Nijpels Department of Health Sciences, Department of Epidemiology and Biostatistics, Department of Public Health, Department of General Practice, Department of Internal Medicine and Cardiovascular Research Institute Maastricht, Department of Internal Medicine, Faculty of Earth and Life Sciences, EMGO Institute for Health and Care Research, VU University Amsterdam, De Boelelaan 1085, 1081 HV Amsterdam, The Netherlands

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Coen D A Stehouwer Department of Health Sciences, Department of Epidemiology and Biostatistics, Department of Public Health, Department of General Practice, Department of Internal Medicine and Cardiovascular Research Institute Maastricht, Department of Internal Medicine, Faculty of Earth and Life Sciences, EMGO Institute for Health and Care Research, VU University Amsterdam, De Boelelaan 1085, 1081 HV Amsterdam, The Netherlands

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Michaela Diamant Department of Health Sciences, Department of Epidemiology and Biostatistics, Department of Public Health, Department of General Practice, Department of Internal Medicine and Cardiovascular Research Institute Maastricht, Department of Internal Medicine, Faculty of Earth and Life Sciences, EMGO Institute for Health and Care Research, VU University Amsterdam, De Boelelaan 1085, 1081 HV Amsterdam, The Netherlands

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Ingeborg A Brouwer Department of Health Sciences, Department of Epidemiology and Biostatistics, Department of Public Health, Department of General Practice, Department of Internal Medicine and Cardiovascular Research Institute Maastricht, Department of Internal Medicine, Faculty of Earth and Life Sciences, EMGO Institute for Health and Care Research, VU University Amsterdam, De Boelelaan 1085, 1081 HV Amsterdam, The Netherlands

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Objective

A disturbed vitamin D–parathyroid hormone (PTH)–calcium axis may play a role in the pathogenesis of heart failure. Therefore, we investigated whether lower 25-hydroxyvitamin D (25(OH)D) and higher PTH are cross sectionally and after 8 years of follow-up associated with higher B-type natriuretic peptide (BNP) levels in older men and women.

Design and methods

We measured baseline 25(OH)D, PTH, and BNP in 502 subjects in 2000–2001 in the Hoorn Study, a population-based cohort. Follow-up BNP was available in 2007–2009 in 278 subjects. Subjects were categorized according to season- and sex-specific quartiles of 25(OH)D and PTH at baseline. We studied the association of 25(OH)D and PTH quartiles with BNP using linear regression analyses adjusting for confounders. Analyses were stratified by kidney function estimated glomerular filtration rate (eGFR; ≤60 ml/min per 1.73 m2) because of significant interaction.

Results

At baseline, subjects had a mean age of 69.9±6.6 years, mean 25(OH)D level was 52.2±19.5 nmol/l and mean PTH 6.1±2.4 pmol/l. Cross sectionally, 25(OH)D was associated with BNP in subjects with impaired kidney function (eGFR ≤60 ml/min) only. The association attenuated after adjustment for PTH. PTH was cross sectionally associated with BNP, also in subjects with impaired kidney function only: regression coefficient of highest quartile 9.9 pmol/l (95% confidence interval 2.5, 17.4) with a significant trend across quartiles. Neither 25(OH)D nor PTH was associated with BNP in longitudinal analyses.

Conclusion

This study showed overall no strong association between 25(OH)D and BNP. However, PTH was associated with BNP in subjects with impaired kidney function and may point to a potential role in myocardial function.

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Lasse Oinonen Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland

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Antti Tikkakoski Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland
Department of Clinical Physiology, Tampere University Hospital, Tampere, Finland

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Jenni Koskela Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland
Department of Internal Medicine, Tampere University Hospital, Tampere, Finland

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Arttu Eräranta Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland

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Mika Kähönen Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland
Department of Clinical Physiology, Tampere University Hospital, Tampere, Finland

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Onni Niemelä Department of Laboratory Medicine and Medical Research Unit, Seinäjoki Central Hospital, Seinäjoki, Finland

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Jukka Mustonen Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland
Department of Internal Medicine, Tampere University Hospital, Tampere, Finland

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Ilkka Pörsti Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland
Department of Internal Medicine, Tampere University Hospital, Tampere, Finland

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Parathyroid hormone has been related with the risk of hypertension, but the matter remains controversial. We examined the association of parathyroid hormone with central blood pressure and its determinants in 622 normotensive or never-treated hypertensive subjects aged 19–72 years without diabetes, cardiovascular or renal disease, or cardiovascular medications. The methods were whole-body impedance cardiography and analyses of pulse wave and heart rate variability. Cardiovascular function was examined in sex-specific tertiles of plasma parathyroid hormone (mean concentrations 3.0, 4.3 and 6.5 pmol/L, respectively) during head-up tilt. Explanatory factors for haemodynamics were further investigated using linear regression analyses. Mean age was 45.0 (s.d. 11.7) years, BMI 26.8 (4.4) kg/m2, seated office blood pressure 141/90 (21/12) mmHg, and 309 subjects (49.7%) were male. Only five participants had elevated plasma parathyroid hormone and calcium concentrations. Highest tertile of parathyroid hormone presented with higher supine and upright aortic diastolic blood pressure (P < 0.01) and augmentation index (P < 0.01), and higher upright systemic vascular resistance (P < 0.05) than the lowest tertile. The tertiles did not present with differences in pulse wave velocity, cardiac output, or measures of heart rate variability. In linear regression analyses, parathyroid hormone was an independent explanatory factor for aortic systolic (P = 0.005) and diastolic (P = 0.002) blood pressure, augmentation index (P = 0.002), and systemic vascular resistance (P = 0.031). To conclude, parathyroid hormone was directly related to central blood pressure, wave reflection, and systemic vascular resistance in subjects without cardiovascular comorbidities and medications. Thus, parathyroid hormone may play a role in the pathophysiology of primary hypertension.

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Natércia Neves Marques de Queiroz University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Franciane Trindade Cunha de Melo University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Fabrício de Souza Resende University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Luísa Corrêa Janaú University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Norberto Jorge Kzan de Souza Neto University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Manuela Nascimento de Lemos University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Ana Carolina Lobato Virgolino University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Maria Clara Neres Iunes de Oliveira University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Angélica Leite de Alcântara University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Lorena Vilhena de Moraes University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Tiago Franco David University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Wanderson Maia da Silva University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Scarlatt Souza Reis University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Márcia Costa dos Santos University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Ana Carolina Contente Braga de Souza University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Pedro Paulo Freire Piani University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Neyla Arroyo Lara Mourão University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Karem Mileo Felício University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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João Felício Abrahão Neto University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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João Soares Felício University Hospital João de Barros Barreto, Federal University of Pará, Endocrinology Division, Belem, Pará, Brazil

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Objective:

Investigate the prevalence of vitamin D deficiency in an equatorial population through a large-sample study.

Methods:

Cross-sectional study with 30,224 healthy individuals from the North Region, in Brazil (Amazônia – state of Pará), who had 25-hydroxy-vitamin D (25(OH)D) and intact parathyroid hormone (PTH) serum levels measured by immunoassay method. Those with history of acute or chronic diseases were excluded. Abnormal levels of calcium, creatinine, glycemia and albumin were also exclusion criteria.

Results:

25(OH)D levels were 29.1 ± 8.2 ng/mL and values <12.7 ng/mL were equal to < −2 s.d. below average. Hypovitaminosis D was present in 10% of subjects according to the Institute of Medicine (values <20 ng/mL) and in 59%, in consonance with Endocrine Society (values 20–30 ng/mL as insufficiency and <20 ng/mL as deficiency) criteria. Individuals were divided according to four age brackets: children, adolescents, adults and elderly, and their 25(OH)D levels were: 33 ± 9; 28.5 ± 7.4; 28.3 ± 7.7; 29.3 ± 8.5 ng/mL, respectively. All groups differed in 25(OH)D, except adolescents vs adults. Regression model showed BMI, sex, living zone (urban or rural) and age as independent variables to 25(OH)D levels. Comparing subjects with vitamin D deficiency (<20 ng/mL) to those with vitamin D insufficiency (20–30 ng/mL), a difference between PTH levels in these two groups was observed (95.9 ± 24.7 pg/mL vs 44.2 ± 64.5 pg/mL; P < 0.01). Additionally, the most accurate predictive vitamin D level for subclinical hyperparathyroidism in ROC curve was 26 ng/mL.

Conclusion:

Our equatorial population showed low prevalence of vitamin D hypovitaminosis ranging with age bracket. The insufficient category by Endocrine Society was corroborated by our PTH data.

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Jane Fletcher Nutrition Nurses, University Hospitals Birmingham NHS Trust, Queen Elizabeth Hospital Birmingham, Mindelsohn Way, Edgbaston, Birmingham, UK
School of Nursing, Institute of Clinical Sciences, University of Birmingham, Edgbaston, Birmingham, UK

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Emma L Bishop Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK

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Stephanie R Harrison Leeds Institute of Rheumatic and Musculoskeletal Medicine, Chapel Allerton Hospital, Leeds, UK

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Amelia Swift School of Nursing, Institute of Clinical Sciences, University of Birmingham, Edgbaston, Birmingham, UK

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Sheldon C Cooper Gastroenterology Department, University Hospitals Birmingham NHS Trust, Queen Elizabeth Hospital Birmingham, Mindelsohn Way, Edgbaston, Birmingham, UK

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Sarah K Dimeloe Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK

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Karim Raza Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK

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Martin Hewison Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK

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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.

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Johanna Öberg Tromso Endocrine Research Group, Department of Clinical Medicine, UiT The Arctic University of Norway, Tromso, Norway

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Rolf Jorde Tromso Endocrine Research Group, Department of Clinical Medicine, UiT The Arctic University of Norway, Tromso, Norway

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Yngve Figenschau Tromso Endocrine Research Group, Department of Clinical Medicine, UiT The Arctic University of Norway, Tromso, Norway
Diagnostic Clinic, University Hospital of North Norway, Tromso, Norway

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Per Medbøe Thorsby Hormone Laboratory, Department of Medical Biochemistry and Biochemical Endocrinology and Metabolism Research Group, Oslo University Hospital, Aker, Oslo, Norway

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Sandra Rinne Dahl Hormone Laboratory, Department of Medical Biochemistry and Biochemical Endocrinology and Metabolism Research Group, Oslo University Hospital, Aker, Oslo, Norway

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Anne Winther Division of Neurosciences, Orthopedics and Rehabilitation Services, University Hospital of North Norway, Tromso, Norway

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Guri Grimnes Tromso Endocrine Research Group, Department of Clinical Medicine, UiT The Arctic University of Norway, Tromso, Norway
Division of Internal Medicine, University Hospital of North Norway, Tromso, Norway

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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.

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