Background: Vitamin D deficiency is still prevalent worldwide, including the Middle East. A cohort of patients with nutritional rickets was treated with vitamin D(2) (ergocalciferol) alone. After this intervention, patients were followed to document changes in z scores for height after treatment. The secondary aim was to determine the proportion of affected children who had vitamin D deficiency or calcium deficiency.
Methods: Z score for height was calculated as the difference between the observed value and the median value, divided by the SD of the population. Z scores were compared in patients before and after treatment.
Results: The improvement in z score after treatment was 0.86 +/- 0.95. The 95% confidence interval for the mean difference was 1.32-0.40 (t = 3.95, P < 0.001). With a diagnostic cut-off for 25 hydroxyvitamin D(3) (25D) deficiency of <25 nmol/L, only half were diagnosed with severe vitamin D deficiency. The remaining patients had presumable calcium deficiency. The alkaline phosphatase (ALP) was negatively correlated to z scores, implying that higher ALP concentrations predicted severe bone disease (lower z scores). The variables 25D and age were moderately and positively correlated (Pearson's r = 0.59, 95%CI: 0.15-0.84; P = 0.01), indicating that younger infants had the lowest 25D levels.
Conclusion: Vitamin D alone was efficient in resolving radiological and biochemical disturbances as well as improving z scores for height in a cohort of children with nutritional rickets, which included patients with 25D deficiency as well as calcium deficiency. The results support the hypothesis of the interplay and continuum of 25D deficiency and calcium deficiency in the pathogenesis of rickets.
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http://dx.doi.org/10.1111/j.1442-200X.2008.02700.x | DOI Listing |
Pediatr Nephrol
January 2025
Pediatric Nephrology Services, Department of Pediatrics, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry, 605006, India.
Background: Limited research exists regarding the genetic profile, clinical characteristics, and outcomes of refractory rickets in children from India.
Methods: Patients with refractory rickets aged ≤ 18 years were enrolled. Data regarding clinical features, etiology, genotype-phenotype correlation, and estimated glomerular filtration rate (eGFR) were recorded.
Sci Rep
January 2025
The Rowett Institute, University of Aberdeen, Foresterhill, Aberdeen, UK.
Vitamin D is essential for healthy skeletal growth and is increasingly recognised for its role in chronic disease development, inflammation and immunity. 25-hydroxyvitamin D (25(OH)D) concentrations are an indicator of vitamin D status and are normally analysed in plasma or serum samples in clinical settings, while archaeological studies rely on the identification of skeletal markers of vitamin D deficiency, such as rickets. Here, we determined 25(OH)D concentrations in hair specimens ('locks') that had been sampled close to the root, aligned by cut end, and sliced into sequential segments from participants (n = 16), from Aberdeen, Scotland, using a modified protocol designed to minimise sample size.
View Article and Find Full Text PDFReprod Health
January 2025
Department of Public Health Nutrition, College of Medicine and Health Sciences, Wollo University, Dessie, Ethiopia.
Background: Exposure to sunlight aids in the body's production of vitamin D, guards against rickets, and treats newborn jaundice. In Ethiopia, the magnitude of sunlight exposure practice varies across studies. Thus, this study aimed to estimate the pooled practices and factors associated with sunlight exposure of infants among mothers in Ethiopia.
View Article and Find Full Text PDFMo Med
November 2024
Department of Pediatrics, Division of Endocrinology and Diabetes and the Division of Bone and Mineral Diseases; Washington University School of Medicine, St. Louis, Missouri.
Metabolic bone diseases are a heterogenous group of conditions that all result in aberrant bone mineral homeostasis with resulting skeletal disease. The underlying causes are variable, ranging from nutritional deficiencies to pathogenic variants in skeletal genes. To properly diagnose and treat these conditions, a clinician needs to understand bone metabolism as well as recognize the signs of disease in a patient.
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