Search Results
Search for other papers by Eliana Piantanida in
Google Scholar
PubMed
Search for other papers by Daniela Gallo in
Google Scholar
PubMed
Research Center in Epidemiology and Preventive Medicine (EPIMED), University of Insubria, Varese, Italy
Search for other papers by Giovanni Veronesi in
Google Scholar
PubMed
Search for other papers by Eugenia Dozio in
Google Scholar
PubMed
Search for other papers by Eugenia Trotti in
Google Scholar
PubMed
Search for other papers by Adriana Lai in
Google Scholar
PubMed
Search for other papers by Silvia Ippolito in
Google Scholar
PubMed
Search for other papers by Jessica Sabatino in
Google Scholar
PubMed
Search for other papers by Maria Laura Tanda in
Google Scholar
PubMed
Search for other papers by Antonio Toniolo in
Google Scholar
PubMed
Research Center in Epidemiology and Preventive Medicine (EPIMED), University of Insubria, Varese, Italy
Search for other papers by Marco Ferrario in
Google Scholar
PubMed
Search for other papers by Luigi Bartalena in
Google Scholar
PubMed
Objective
The aim of this observational study was to clarify the link between vitamin D status and metabolic syndrome (MetS) in people with visceral obesity.
Design and methods
One hundred ninety-six consecutive patients (152 women; mean age 51 ± 13 years) with visceral obesity (mean body weight 103 ± 20 kg, mean waist circumference (WC) 119 ± 13 cm) were enrolled at the Obesity Outpatient Clinic of the University of Insubria in Varese. Anthropometric measurements were recorded. Laboratory tests, including vitamin D (25(OH)D)), fasting blood glucose (FBG), lipid profile, liver and kidney function tests were assessed. Vitamin D status was defined according to the European Society of Endocrinology guidelines, MetS to the 2009 harmonized definition.
Results
An inverse association emerged among 25(OH)D, body mass index (BMI) (P = 0.001) and WC (all P = 0.003). Serum 25(OH)D levels were inversely related to FBG and systolic blood pressure (SBP) (respectively, P = 0.01 and 0.02). Median serum 25(OH)D levels were 13.3 ng/mL (CI 95% 12; 15) in MetS and 16 ng/mL (CI 95% 14; 18) (P = 0.01) in non-MetS patients. Among patients with MetS, lower 25(OH)D concentrations were related to higher risk of hypertension (HT) (odds ratio (OR) 1.7, CI 95%, 0.7;4) and hyperglycemia (IFG)/type 2 diabetes (OR 5.5, CI 95% 2; 14).
Conclusion
Vitamin D status and MetS are inversely correlated in visceral obesity, particularly with regard to glucose homeostasis and BP. More extensive studies are required to investigate the potential for causality.
Search for other papers by Giuseppe Grande in
Google Scholar
PubMed
Search for other papers by Andrea Graziani in
Google Scholar
PubMed
Search for other papers by Antonella Di Mambro in
Google Scholar
PubMed
Search for other papers by Riccardo Selice in
Google Scholar
PubMed
Department of Medicine, University of Padova, Padova, Italy
Search for other papers by Alberto Ferlin in
Google Scholar
PubMed
Low bone mass is common in men with Klinefelter syndrome (KS), with a prevalence of 6–15% of osteoporosis and of 25–48% of osteopenia. Reduced bone mass has been described since adolescence and it might be related to both reduced bone formation and higher bone resorption. Although reduced testosterone levels are clearly involved in the pathogenesis, this relation is not always evident. Importantly, fracture risk is increased independently from bone mineral density (BMD) and testosterone levels. Here we discuss the pathogenesis of osteoporosis in patients with KS, with a particular focus on the role of testosterone and testis function. In fact, other hormonal mechanisms, such as global Leydig cell dysfunction, causing reduced insulin-like factor 3 and 25-OH vitamin D levels, and high follicle-stimulating hormone and estradiol levels, might be involved. Furthermore, genetic aspects related to the supernumerary X chromosome might be involved, as well as androgen receptor expression and function. Notably, body composition, skeletal mass and strength, and age at diagnosis are other important aspects. Although dual-energy x-ray absorptiometry is recommended in the clinical workflow for patients with KS to measure BMD, recent evidence suggests that alterations in the microarchitecture of the bones and vertebral fractures might be present even in subjects with normal BMD. Therefore, analysis of trabecular bone score, high-resolution peripheral quantitative computed tomography and vertebral morphometry seem promising tools to better estimate the fracture risk of patients with KS. This review also summarizes the evidence on the best available treatments for osteoporosis in men with KS, with or without hypogonadism.
Search for other papers by Marc Blondon in
Google Scholar
PubMed
Search for other papers by Emmanuel Biver in
Google Scholar
PubMed
Search for other papers by Olivia Braillard in
Google Scholar
PubMed
Search for other papers by Marc Righini in
Google Scholar
PubMed
Search for other papers by Pierre Fontana in
Google Scholar
PubMed
Search for other papers by Alessandro Casini in
Google Scholar
PubMed
Objective
Vitamin D deficiency is associated with increased risks of arterial and venous cardiovascular events. Hypothetically, supplementation with vitamin D may lead to a less prothrombotic phenotype, as measured by global coagulation assays and fibrin clot structure.
Methods
In this prospective cohort study, we enrolled adult outpatients attending the Primary Care Division of the Geneva University Hospitals with a severe vitamin D deficiency (25-hydroxyvitamin-D3 (25-OHD) <25 nmol/L), excluding obese patients or with a recent acute medical event. We evaluated changes in coagulation times, thrombin generation assay, clot formation and clot lysis time, 25-OHD and parathormone before and 1–3 months after cholecalciferol oral supplementation with one-time 300,000 IU then 800 IU daily. Paired t-tests with a two-sided alpha of 0.05 compared absolute mean differences.
Results
The 48 participants had a mean age of 43.8 ± 13.8 years. After supplementation, 25-OHD levels increased from 17.9 ± 4.6 nmol/L to 62.5 ± 20.7 nmol/L 6.4 ± 3.0 weeks after inclusion. Endogenous thrombin potential and thrombin generation peak values both decreased significantly (−95.4 nM × min (95%CI −127.9 to −62.8), P < 0.001; −15.1 nM (−23.3 to −6.8), P < 0.001). The maximum absorbance by turbidimetry decreased significantly (P = 0.001) after supplementation. There was no change in clot lysis time, coagulation times or plasminogen activator inhibitor-1 and homocysteine levels.
Conclusions
In severe vitamin D deficiency, a high-dose cholecalciferol supplementation was associated with a reduction in thrombin generation and an average decreased number of fibrin protofibrils per fibers and fibrin fiber size measured by turbidimetry. This suggests that severe vitamin D deficiency may be associated with a potentially reversible prothrombotic profile.
Search for other papers by R Perchard in
Google Scholar
PubMed
Search for other papers by L Magee in
Google Scholar
PubMed
Search for other papers by A Whatmore in
Google Scholar
PubMed
Search for other papers by F Ivison in
Google Scholar
PubMed
Department of Paediatric Endocrinology, Royal Manchester Children’s Hospital, Central Manchester Foundation Hospitals NHS Trust, Manchester, UK
Search for other papers by P Murray in
Google Scholar
PubMed
Search for other papers by A Stevens in
Google Scholar
PubMed
Search for other papers by M Z Mughal in
Google Scholar
PubMed
Search for other papers by S Ehtisham in
Google Scholar
PubMed
Search for other papers by J Campbell in
Google Scholar
PubMed
Search for other papers by S Ainsworth in
Google Scholar
PubMed
Search for other papers by M Marshall in
Google Scholar
PubMed
Search for other papers by M Bone in
Google Scholar
PubMed
Search for other papers by I Doughty in
Google Scholar
PubMed
Department of Paediatric Endocrinology, Royal Manchester Children’s Hospital, Central Manchester Foundation Hospitals NHS Trust, Manchester, UK
Search for other papers by P E Clayton in
Google Scholar
PubMed
Background
Higher 25(OH)D3 levels are associated with lower HbA1c, but there are limited UK interventional trials assessing the effect of cholecalciferol on HbA1c.
Aims
(1) To assess the baseline 25(OH)D3 status in a Manchester cohort of children with type 1 diabetes (T1D). (2) To determine the effect of cholecalciferol administration on HbA1c.
Methods
Children with T1D attending routine clinic appointments over three months in late winter/early spring had blood samples taken with consent. Participants with a 25(OH)D3 level <50 nmol/L were treated with a one-off cholecalciferol dose of 100,000 (2–10 years) or 160,000 (>10 years) units. HbA1c levels before and after treatment were recorded.
Results
Vitamin D levels were obtained from 51 children. 35 were Caucasian, 11 South Asian and 5 from other ethnic groups. 42 were vitamin D deficient, but 2 were excluded from the analysis. All South Asian children were vitamin D deficient, with mean 25(OH)D3 of 28 nmol/L. In Caucasians, there was a negative relationship between baseline 25(OH)D3 level and HbA1c (r = −0.484, P < 0.01). In treated participants, there was no significant difference in mean HbA1c at 3 months (t = 1.010, P = 0.328) or at 1 year (t = −1.173, P = 0.248) before and after treatment. One-way ANCOVA, controlling for age, gender, ethnicity, BMI and diabetes duration showed no difference in Δ HbA1c level.
Conclusion
We report important findings at baseline, but in children treated with a stat dose of cholecalciferol, there was no effect on HbA1c. Further studies with larger sample sizes and using maintenance therapy are required.
Centre de Référence des Maladies Rares du Calcium et du Phosphore Filière de Santé Maladies Rares OSCAR, Paris, France
Centre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université de Paris, INSERM, UMRS1138, Paris, France
Search for other papers by Jean-Philippe Bertocchio in
Google Scholar
PubMed
Search for other papers by Natalie Grosset in
Google Scholar
PubMed
Search for other papers by Lionel Groussin in
Google Scholar
PubMed
Search for other papers by Peter Kamenický in
Google Scholar
PubMed
Search for other papers by Fabrice Larceneux in
Google Scholar
PubMed
Search for other papers by Anne Lienhardt-Roussie in
Google Scholar
PubMed
Université Paris-Saclay, Inserm U1185, Physiologie et Physiopathologie Endocriniennes, Assistance Publique-Hôpitaux de Paris, Service d’Endocrinologie et Diabète de l’Enfant, Centre de Référence des Maladies Rares du Calcium et du Phosphore et Filière de Santé Maladies Rares OSCAR, Hôpital Bicêtre Paris Saclay, Le Kremlin-Bicêtre, France
Search for other papers by Agnès Linglart in
Google Scholar
PubMed
Centre de Référence des Maladies Rares du Calcium et du Phosphore Filière de Santé Maladies Rares OSCAR, Paris, France
Assistance Publique-Hôpitaux de Paris, Institut Necker-Enfants Malades, INSERM U1151 – CNRS UMR 8253, Paris, France
Search for other papers by Gérard Maruani in
Google Scholar
PubMed
Association Francophone de Chirurgie Endocrinienne (AFCE), France
Search for other papers by Eric Mirallie in
Google Scholar
PubMed
Search for other papers by François Pattou in
Google Scholar
PubMed
Search for other papers by Riyad N H Seervai in
Google Scholar
PubMed
Search for other papers by Coralie Sido in
Google Scholar
PubMed
Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Biochimie et Génétique Moléculaires, Paris, France
INSERM, U1169, Université Paris Sud, Hôpital Bicêtre, Le Kremlin Bicêtre, France
Search for other papers by Caroline Silve in
Google Scholar
PubMed
INSERM, U1418, CIC-EC, Hôpital Européen Georges Pompidou, Paris, France
Search for other papers by Aurélie Vilfaillot in
Google Scholar
PubMed
Search for other papers by Antoine Tabarin in
Google Scholar
PubMed
Search for other papers by Marie-Christine Vantyghem in
Google Scholar
PubMed
Centre de Référence des Maladies Rares du Calcium et du Phosphore Filière de Santé Maladies Rares OSCAR, Paris, France
Centre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université de Paris, INSERM, UMRS1138, Paris, France
CNRS, ERL8228, Paris, France
Search for other papers by Pascal Houillier in
Google Scholar
PubMed
Search for other papers by the investigators of the Épi-Hypo study in
Google Scholar
PubMed
Context
Recent guidelines have provided recommendations for the care of patients with chronic hypoparathyroidism. Very little is known about actual physicians’ practices or their adherence to such guidelines.
Objective
To describe the physicians’ practice patterns and their compliance with international guidelines.
Design
The cohort studies included were Épi-Hypo (118 physicians and 107 patients, from September 2016 to December 2019) and ePatients (110 patients, November 2019).
Methods
Internet-based cohorts involving all settings at a nationwide level (France). Participants were (i) physicians treating patients with chronic hypoparathyroidism and patients with chronic hypoparathyroidism either participating in the (ii) Épi-Hypo study (Épi-Hypo 2019 patients), or (iii) Hypoparathyroidism France, the national representative association (ePatients).
Results
The physicians’ specialties were mainly endocrinology (61%), nephrology (28%), family medicine (2.5%), pediatrics (2.5%), rheumatology (2%), or miscellaneous (4%) and 45% were practicing in public universities. The median number of pharmaceutical drug classes prescribed was three per patient. The combination of active vitamin D and calcium salt was given to 59 and 58% of ePatients and Épi-Hypo 2019 patients, respectively. Eighty-five percent of ePatients and 87% of physicians reported monitoring plasma calcium concentrations at a steady state at least twice a year. In 32 and 26% of cases, respectively, ePatients and physicians reported being fully in accordance with international guidelines that recommend targeting symptoms, plasma calcium and phosphate values, and urine calcium excretion.
Conclusions
The care of patients with chronic hypoparathyroidism involves physicians with very different practices, so guidelines should include and target other specialists as well as endocrinologists. Full adherence to the guidelines is low in France.
Search for other papers by Sarah Bakhamis in
Google Scholar
PubMed
Search for other papers by Faiqa Imtiaz in
Google Scholar
PubMed
Search for other papers by Khushnooda Ramzan in
Google Scholar
PubMed
Search for other papers by Edward De Vol in
Google Scholar
PubMed
Search for other papers by Osamah Al-Sagheir in
Google Scholar
PubMed
Search for other papers by Abdulrahman Al-Rajhi in
Google Scholar
PubMed
Search for other papers by Abdullah Alashwal in
Google Scholar
PubMed
Search for other papers by Bassam Bin Abbas in
Google Scholar
PubMed
Search for other papers by Nadia Sakati in
Google Scholar
PubMed
Search for other papers by Afaf Al-Sagheir in
Google Scholar
PubMed
Vitamin D deficiency remains a major cause of rickets worldwide. Nutritional factors are the major cause and less commonly, inheritance causes. Recently, CYP2R1 has been reported as a major factor for 25-hydroxylation contributing to the inherited forms of vitamin D deficiency. We conducted a prospective cohort study at King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia, to review cases with 25-hydroxylase deficiency and describe their clinical, biochemical, and molecular genetic features. We analyzed 27 patients from nine different families who presented with low 25-OH vitamin D and not responding to usual treatment. Genetic testing identified two mutations: c.367+1G>A (12/27 patients) and c.768dupT (15/27 patients), where 18 patients were homozygous for their identified mutation and 9 patients were heterozygous. Both groups had similar clinical manifestations ranging in severity, but none of the patients with the heterozygous mutation had hypocalcemic manifestations. Thirteen out of 18 homozygous patients and all the heterozygous patients responded to high doses of vitamin D treatment, but they regressed after decreasing the dose, requiring lifelong therapy. Five out of 18 homozygous patients required calcitriol to improve their biochemical data, whereas none of the heterozygous patients and patients who carried the c.367+1G>A mutation required calcitriol treatment. To date, this is the largest cohort series analyzing CYP2R1-related 25-hydroxylase deficiency worldwide, supporting its major role in 25-hydroxylation of vitamin D. It is suggested that a higher percentage of CYP2R1 mutations might be found in the Saudi population. We believe that our study will help in the diagnosis, treatment, and prevention of similar cases in the future.
Regenerative Medicine Institute at CÚRAM SFI Research Centre, School of Medicine, National University of Ireland Galway (NUIG), Galway, Ireland
Search for other papers by Tomás P Griffin in
Google Scholar
PubMed
Search for other papers by Caroline M Joyce in
Google Scholar
PubMed
Search for other papers by Sumaya Alkanderi in
Google Scholar
PubMed
Search for other papers by Liam M Blake in
Google Scholar
PubMed
Search for other papers by Derek T O’Keeffe in
Google Scholar
PubMed
Search for other papers by Delia Bogdanet in
Google Scholar
PubMed
Department of Clinical Biochemistry, SUHCG, GUH, Galway, Ireland
Search for other papers by Md Nahidul Islam in
Google Scholar
PubMed
Lambe Institute for Translational Research, School of Medicine, NUIG, Galway, Ireland
Search for other papers by Michael C Dennedy in
Google Scholar
PubMed
Search for other papers by John E Gillan in
Google Scholar
PubMed
Search for other papers by John J Morrison in
Google Scholar
PubMed
Regenerative Medicine Institute at CÚRAM SFI Research Centre, School of Medicine, National University of Ireland Galway (NUIG), Galway, Ireland
Search for other papers by Timothy O’Brien in
Google Scholar
PubMed
Newcastle upon Tyne NHS Hospitals Foundation Trust, Newcastle upon Tyne, UK
NIHR Newcastle Biomedical Research Centre, Newcastle upon Tyne, UK
Search for other papers by John A Sayer in
Google Scholar
PubMed
Search for other papers by Marcia Bell in
Google Scholar
PubMed
Search for other papers by Paula M O’Shea in
Google Scholar
PubMed
Introduction
Inactivating mutations in CYP24A1, encoding vitamin D-24-hydroxylase, can lead to an accumulation of active vitamin D metabolites and consequent hypercalcaemia. Patient (infantile and adult) presentation is varied and includes mild-severe hypercalcaemia, hypercalciuria, nephrocalcinosis and nephrolithiasis. This study aimed to characterize the clinical and biochemical phenotypes of a family with two CYP24A1 missense variants.
Methods
The proband and seven family members underwent detailed clinical and biochemical evaluation. Laboratory measurements included serum calcium, intact parathyroid hormone (iPTH), vitamin D metabolites and urine calcium and creatinine.
Results
The proband presented during the second trimester of a planned pregnancy with flu-like symptoms. Laboratory tests showed elevated adjusted calcium of 3.27 (upper reference limit (URL: 2.30) mmol/L), suppressed iPTH (<6 ng/L), elevated 25(OH)D (264 (URL: 55) nmol/L) and elevated 1,25(OH)D (293 (URL: <280) pmol/L). Ionized calcium was 1.55 (URL: 1.28) mmol/L. Sanger sequencing revealed two heterozygous missense variants in the CYP24A1: p.(Arg439Cys), R439C and p.(Trp275Arg), W275R. The proband’s brother and sister had the same genotype. The brother had intermittent hypercalcaemia and hypervitaminosis D. Only the sister had a history of nephrolithiasis. The proband’s daughter and two nephews were heterozygous for the R439C variant. The proband and her brother frequently had elevated 25(OH)D:24,25(OH)2D ratios (>50) during follow-up.
Conclusions
W275R is a new pathogenic CYP24A1 mutation in compound heterozygotic form with R439C in this family.
Search for other papers by Maxime Duval in
Google Scholar
PubMed
Search for other papers by Kalyane Bach-Ngohou in
Google Scholar
PubMed
Search for other papers by Damien Masson in
Google Scholar
PubMed
Search for other papers by Camille Guimard in
Google Scholar
PubMed
Search for other papers by Philippe Le Conte in
Google Scholar
PubMed
Department of Emergency Medicine, CHU Nantes, Nantes, France
Search for other papers by David Trewick in
Google Scholar
PubMed
Objective
Severe hypocalcemia (Ca <1.9 mmol/L) is often considered an emergency because of a potential risk of cardiac arrest or seizures. However, there is little evidence to support this. The aim of our study was to assess whether severe hypocalcemia was associated with immediately life-threatening cardiac arrhythmias or neurological complications.
Methods
A retrospective observational study was carried out over a 2-year period in the Adult Emergency Department (ED) of Nantes University Hospital. All patients who had a protein-corrected calcium concentration measure were eligible for inclusion. Patients with multiple myeloma were excluded. The primary outcome was the number of life-threatening cardiac arrhythmias and/or neurological complications during the stay in the ED.
Results
A total of 41,823 patients had protein-corrected calcium (pcCa) concentrations measured, 155 had severe hypocalcemia, 22 were excluded because of myeloma leaving 133 for analysis. Median pcCa concentration was 1.73 mmol/L (1.57–1.84). Seventeen (12.8%) patients presented a life-threatening condition, 14 (10.5%) neurological and 3 (2.2%) cardiac during ED stay. However, these complications could be explained by the presence of underlying co-morbidities and or electrolyte disturbances other than hypocalcemia. Overall, 24 (18%) patients died in hospital. Vitamin D deficiency, chronic kidney disease and hypoparathyroidism were the most frequently found causes of hypocalcemia.
Conclusion
Thirteen percent of patients with severe hypocalcemia presented a life-threatening cardiac or neurological complication on the ED. However, a perfectly valid alternative cause could account for these complications. Further research is warranted to define the precise role of hypocalcemia.
Search for other papers by Kristin Godang in
Google Scholar
PubMed
Search for other papers by Karolina Lundstam in
Google Scholar
PubMed
Search for other papers by Charlotte Mollerup in
Google Scholar
PubMed
Search for other papers by Stine Lyngvi Fougner in
Google Scholar
PubMed
Search for other papers by Ylva Pernow in
Google Scholar
PubMed
Search for other papers by Jörgen Nordenström in
Google Scholar
PubMed
Search for other papers by Thord Rosén in
Google Scholar
PubMed
Search for other papers by Svante Jansson in
Google Scholar
PubMed
Search for other papers by Mikael Hellström in
Google Scholar
PubMed
Faculty of Medicine, University of Oslo, Oslo, Norway
Search for other papers by Jens Bollerslev in
Google Scholar
PubMed
Faculty of Medicine, University of Oslo, Oslo, Norway
Search for other papers by Ansgar Heck in
Google Scholar
PubMed
Search for other papers by the SIPH Study Group in
Google Scholar
PubMed
Context
Mild primary hyperparathyroidism has been associated with increased body fat mass and unfavorable cardiovascular risk factors.
Objective
To assess the effect of parathyroidectomy on fat mass, glucose and lipid metabolism.
Design, patients, interventions, main outcome measures
119 patients previously randomized to observation (OBS; n = 58) or parathyroidectomy (PTX; n = 61) within the Scandinavian Investigation of Primary Hyperparathyroidism (SIPH) trial, an open randomized multicenter study, were included. Main outcome measures for this study were the differences in fat mass, markers for lipid and glucose metabolism between OBS and PTX 5 years after randomization.
Results
In the OBS group, total cholesterol (Total-C) decreased from mean 5.9 (±1.1) to 5.6 (±1.0) mmol/L (P = 0.037) and LDL cholesterol (LDL-C) decreased from 3.7 (±1.0) to 3.3 (±0.9) mmol/L (P = 0.010). In the PTX group, the Total-C and LDL-C remained unchanged resulting in a significant between-group difference over time (P = 0.013 and P = 0.026, respectively). This difference was driven by patients who started with lipid-lowering medication during the study period (OBS: 5; PTX: 1). There was an increase in trunk fat mass in the OBS group, but no between-group differences over time. Mean 25(OH) vitamin D increased in the PTX group (P < 0.001), but did not change in the OBS group. No difference in parameters of glucose metabolism was detected.
Conclusion
In mild PHPT, the measured metabolic and cardiovascular risk factors were not modified by PTX. Observation seems safe and cardiovascular risk reduction should not be regarded as a separate indication for parathyroidectomy based on the results from this study.
Search for other papers by Rasmus Reinke in
Google Scholar
PubMed
Search for other papers by Stefano Christian Londero in
Google Scholar
PubMed
Search for other papers by Martin Almquist in
Google Scholar
PubMed
Search for other papers by Lars Rejnmark in
Google Scholar
PubMed
Search for other papers by Lars Rolighed in
Google Scholar
PubMed
Objective
Total thyroidectomy is associated with a high risk of postoperative hypoparathyroidism, mainly due to the unintended surgical damage to the parathyroid glands or their blood supply. It is possible that surgeons who also perform parathyroid surgery see lower rates of postoperative hypoparathyroidism. In a single institution, we investigated the effects of restricting total thyroidectomy operations for Graves’ disease to two surgeons who performed both thyroid and parathyroid surgeries. We aimed to evaluate the rates of postoperative hypoparathyroidism in a 10-year period with primary attention toward patients with Graves’ disease.
Design
Retrospective cohort study from a single institution.
Methods
We defined the rate of permanent hypoparathyroidism after total thyroidectomy as the need for active vitamin D 6 months postoperatively. Between 2012 and 2016, seven surgeons performed all thyroidectomies. From January 2017, only surgeons also performing parathyroid surgery carried out thyroidectomies for Graves’ disease.
Results
We performed total thyroidectomy in 543 patients. The rate of permanent hypoparathyroidism decreased from 28% in 2012–2014 to 6% in 2020–2021. For patients with Graves’ disease, the rate of permanent hypoparathyroidism decreased from 36% (13 out of 36) in 2015–2016 to 2% (1 out of 56) in 2020–2021. In cancer patients, the rate of permanent hypoparathyroidism decreased from 30% (14 out of 46) in 2012–2014 to 10% (10 out of 51) in 2020–2021.
Conclusion
Restricting thyroidectomy to surgeons who also performed parathyroid operations reduced postoperative hypoparathyroidism markedly. Accordingly, we recommend centralisation of the most difficult thyroid operations to centres and surgeons with extensive experience in parathyroid surgery.
Significance statement
Thyroid surgery is performed by many different surgeons with marked differences in outcome. Indeed, the risk of postoperative permanent hypoparathyroidism may be very high in low-volume centres. This serious condition affects the quality of life and increases long-term morbidity and the patients develop a life-long dependency of medical treatments. We encountered a high risk of hypoparathyroidism after the operation for Graves’ disease and restricted the number of surgeons to two for these operations. Further, these surgeons were experienced in both thyroid and parathyroid surgeries. We show a dramatic reduction in postoperative hypoparathyroidism after this change. Accordingly, we recommend centralisation of total thyroidectomy to surgeons with experience in both thyroid and parathyroid procedures.
