Background: Rickets and vitamin D deficiency appeared to increase in Alaskan children starting in the 1990s. We evaluated the epidemiology of rickets and vitamin D deficiency in Alaska native (AN) children in 2001-2010.
Methods: We analyzed 2001-2010 visits with rickets or vitamin D deficiency diagnosis for AN and American Indian children and the general US population aged <10 years. We conducted a case-control study of AN rickets/vitamin D deficient cases and age- and region-matched controls.
Results: In AN children, annual rickets-associated hospitalization rate (2.23/100,000 children/year) was higher than the general US rate (1.23; 95% CI 1.08-1.39). Rickets incidence increased with latitude. Rickets/vitamin D deficiency cases were more likely to have malnutrition (OR 38.1; 95% CI 4.9-294), had similar breast-feeding prevalence, and were less likely to have received vitamin D supplementation (OR 0.23; 95% CI 0.1-0.87) than controls.
Conclusions: Our findings highlight the importance of latitude, malnutrition, and lack of vitamin D supplementation as risk factors for rickets.
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http://dx.doi.org/10.1515/jpem-2014-0446 | DOI Listing |
Cell Biochem Funct
January 2025
Department of Metabolism and Systems Science, School of Medical Sciences, University of Birmingham, Birmingham, UK.
Endometriosis is a prevalent chronic gynaecological disorder, but its cause is still unclear, and both genetic and environmental factors may contribute disease aetiology. Prominent amongst the latter is vitamin D which can be obtained either by the action of sunlight on skin or from dietary sources. Serum levels of the main circulating form of vitamin D, 25-hydroxvitamin D (25(OH)D), have been reported to be inversely correlated with endometriosis, suggesting that vitamin D-deficiency may be a risk factor for the disease.
View Article and Find Full Text PDFArch Pediatr
December 2024
General Pediatric Department, Versailles hospital, Le Chesnay, France.
Scurvy is now considered to be a rare disease in European countries, even among children, but it still exists. We report the case of an 18-month-old boy who was initially hospitalized for a walking disorder and ultimately diagnosed with scurvy. Radiographs were compatible with rickets, but biological analysis ruled out this diagnosis.
View Article and Find Full Text PDFClin Endocrinol (Oxf)
December 2024
Department of Medicine, University of Auckland, Auckland, New Zealand.
Objective: Vitamin D deficiency (VDD) in children can cause hypocalcaemia and rickets, but the prevalence of these complications and the 25-hydroxyvitamin D (25OHD) concentrations below which they arise is uncertain. We investigated this in children (< 18 years) with 25OHD measurements.
Design, Measurement And Patients: We obtained 25OHD results from the regional laboratory database, alongside albumin-adjusted serum calcium (aCa), parathyroid hormone (PTH) and alkaline phosphatase (ALP) within 6 months of the index 25OHD.
Pediatr Dermatol
December 2024
Paediatric Endocrinology Division, Department of Paediatrics, Christian Medical College Vellore, Vellore, Tamil Nadu, India.
Vitamin D-dependent rickets type 2A (VDDR2A) is a rare cause of infantile-onset alopecia, characterized by severe hypotrichosis, small cutaneous cysts, early-onset treatment-resistant rickets, and hypocalcemia. Alopecia, often starting a few weeks to months after birth, may be the presenting feature. We present three cases of VDDR2A with genetic variants in the vitamin D receptor (VDR) gene, their clinical features and biochemical parameters.
View Article and Find Full Text PDFJ Bone Miner Res
December 2024
Department of Pediatrics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA.
Duan X, et al, report that CYP4A22 loss-of-function causes a new form of vitamin D-dependent rickets. Here we describe the basis for our rejection of their proposal and provide evidence that the CYP4A22 variant that they have identified (c.901del, p.
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