Background: Coeliac disease (CD) causes deficiency of various micronutrients including vitamin D, and there are no specific guidelines for treatment.
Aims: To determine the prevalence of vitamin D deficiency in children newly diagnosed with CD and the role of oral high-dose vitamin D in its treatment.
Methods: Calcium intake, sun exposure and biochemical and radiological parameters related to vitamin D deficiency were compared between 60 children aged 0-18 years diagnosed with CD and 60 healthy age- and sex-matched controls. The cases with serum 25(OH)D (<20 ng/ml) were given oral vitamin D (60,000 IU/week) and calcium (500 mg/day) for 12 weeks, along with a gluten-free diet (GFD); they were re-evaluated within a week of completion. The primary outcome measure was the serum 25(OH)D level, and secondary measures included serum calcium, phosphorus, alkaline phosphatase, parathormone and clinical and/or radiological rickets.
Results: The prevalence of vitamin D deficiency (25(OH)D <20 ng/ml) was significantly greater in the cases (=38, 63.3%) than in the controls (=27, 45.0%). Upon treatment, all 38 cases with vitamin D deficiency showed a significant rise in 25(OH)D levels along with normalisation of other biochemical abnormalities. Two children had 25(OH)D levels >100 ng/ml with no other feature suggestive of vitamin D toxicity.
Conclusions: Vitamin D deficiency is more prevalent in children with CD. Administration of oral high-dose vitamin D for 12 weeks along with a GFD leads to a robust response, indicating rapid mucosal recovery. The vitamin D dosage recommended for malabsorption states may be excessive in CD. ALP: alkaline phosphatase; CaBP: calcium-binding proteins; CD: coeliac disease; GFD: gluten-free diet; PTH: parathormone; RU: reproducibility units; 25(OH)D: 25 hydroxy vitamin D.
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http://dx.doi.org/10.1080/20469047.2021.1996089 | DOI Listing |
J Steroid Biochem Mol Biol
January 2025
Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA; Department of Medicine, VA Medical Center, St. Louis, MO, USA; Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO, USA. Electronic address:
Targeting optimal glycemic control based on hemoglobin A1c (A1c) values reduces but does not abolish the onset of diabetic kidney disease and its progression to chronic kidney disease (CKD). This suggests that factors other than the average glucose contribute to the residual risk. Vitamin D deficiency and frequent episodes of acute hyperglycemia (AH) are associated with the onset of albuminuria and CKD progression in diabetes.
View Article and Find Full Text PDFAnn Endocrinol (Paris)
January 2025
Department of Endocrinology, Diabetes and Metabolic Diseases, Angers University Hospital, Reference Center for Rare Thyroid and Hormone Receptor Diseases, 49933 Angers cedex 09, France; Univ Angers, Inserm, CNRS, MITOVASC, Equipe CarMe, SFR ICAT, F-49000 Angers, France. Electronic address:
Primary hyperparathyroidism is treated surgically. Postoperatively, close monitoring of blood calcium levels is necessary to detect any hypocalcemia. Postoperative PTH assays can be performed within 24 hours to identify patients who will not develop permanent hypoparathyroidism.
View Article and Find Full Text PDFAnn Endocrinol (Paris)
January 2025
Service d'Endocrinologie, Diabétologie, Métabolisme, Nutrition; Hôpital Huriez, CHU Lille; Inserm U1190, Institut Génomique Européen pour le Diabète, Université de Lille, F-59000 Lille, France. Electronic address:
The differential diagnosis of primary hyperparathyroidism can be considered clinically, biologically and radiologically. Clinically, primary hyperparathyroidism should be suspected in case of diffuse pain, renal lithiasis, osteoporosis, repeated fracture, cognitive or psychiatric disorder, or disturbance of consciousness. Nevertheless, the differential diagnosis of primary hyperparathyroidism is mainly biological, particularly in atypical forms, which must be differentiated from hypercalcemia with hypocalciuria or non- elevated PTH on the one hand, and from normo-calcemia with elevated PTH, hypophosphatemia or hypercalciuria on the other.
View Article and Find Full Text PDFAnn Endocrinol (Paris)
January 2025
University of Brest, CHU Brest, UMR1304 GETBO, 29200 Brest, France; Endocrinology and Diabetology Department, CHU Brest, 29200 Brest, France.
Primary hyperparathyroidism is now predominantly an asymptomatic pathology, as blood calcium assay has become systematic. Diagnosis therefore requires screening for target organ damage when this is not already indicative of primary hyperparathyroidism.Classical clinical manifestations include bone, kidney and muscle signs, and are characterized by reversibility after parathyroid surgery.
View Article and Find Full Text PDFAnn Endocrinol (Paris)
January 2025
Université Paris-Saclay, Inserm, Physiologie et Physiopathologie Endocriniennes, AP-HP, Hôpital Bicêtre, Service d'Endocrinologie et des Maladies de la Reproduction, Centre de Référence des Maladies Rares du Métabolisme du Calcium et du Phosphate, 94 275 Le Kremlin Bicêtre, France. Electronic address:
Preoperative treatment of PHPT aims to 1) manage severe and/or symptomatic hypercalcemia and 2) prevent postoperative hypocalcemia. Severe hypercalcemia, defined as a blood calcium level ≥ 3.5 mmol/L, requires admission to hospital in a conventional or critical care unit, depending on clinical symptoms and comorbidities.
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