Division of Epidemiology, Statistics and Prevention, Eunice Kennedy Shriver National Institute of Child Health and Human Development, 6100 Executive Blvd, Room 7B13A, MSC 7510, Rockville, MD 20852, USA.
To review the published literature on serum 25-hydroxyvitamin D concentrations in US children.
Articles were identified by searching MEDLINE using 25-hydroxyvitamin D, vitamin D, hypovitaminosis D, vitamin D insufficiency, vitamin D deficiency, children, and adolescents as key words and by screening references from original studies.
Studies were included if they fulfilled the following a priori criteria: contained a well-defined sample of children, included only healthy children, presented data on serum 25-hydroxyvitamin D concentrations, were published in the past 10 years, and were conducted in the United States.
Serum 25-hydroxyvitamin D concentrations and prevalence of low vitamin D status (hypovitaminosis D).
Fourteen articles fulfilled the criteria. There were no consistent definitions of hypovitaminosis D; values corresponding to vitamin D deficiency ranged from less than 5 ng/mL to less than 12 ng/mL, and those for vitamin D insufficiency ranged from less than 10 ng/mL to less than 32 ng/mL (to convert 25-hydroxyvitamin D concentrations to nanomoles per liter, multiply by 2.496). The following assays were used: radioimmunoassay (7 studies), competitive binding protein assay (3 studies), automated chemiluminescence protein-binding assay (3 studies), and enzyme-linked immunosorbent assay (1 study). Breastfed infants in winter who did not receive vitamin D supplementation were the most severely vitamin D deficient (78%). Estimates of the prevalence of hypovitaminosis D ranged from 1% to 78%. Older age, winter season, higher body mass index, black race/ethnicity, and elevated parathyroid hormone concentrations were associated with lower 25-hydroxyvitamin D concentrations.
Although overt vitamin D deficiency is no longer common in US children, lesser degrees of vitamin D insufficiency are widespread.
"Vitamin D deficiency may also be a risk factor for the development of autoimmune and other chronic diseases    , loss of muscle mass, and muscle weakness . Finally, a number of studies have also suggested that vitamin D may confer protection against diabetes mellitus Type 1, hypertension, multiple sclerosis, and cancer . Thus, vitamin D insufficiency may have important health consequences not only because of the vitamin's role in the maintenance of normal bone mass turnover but also because of its role as an immunoregulatory agent. "
[Show abstract][Hide abstract] ABSTRACT: Objective. This paper aims to assess 25(OH)D levels in Italian children and adolescents identifying risk factors for 25(OH)D deficiency and to evaluate whether a normal 25(OH)D value can be restored in 25(OH)D-deficient patients. Methods. We evaluated 25(OH)D levels in 679 Italian children and adolescents (≤10, 11-20, 21-30, and >30 ng/mL were defined as severe deficiency, deficiency, insufficiency, and sufficiency, resp.). Of these, 365 25(OH)D-deficient were followed up for 1 year; 205 were treated with cholecalciferol (Arm A: 400 I.U.) and 160 by improving the environmental variables influencing 25(OH)D levels (Arm B). Results. At cross-sectional evaluation, 11.3% showed sufficiency, 30.0% insufficiency, and 58.7% 25(OH)D deficiency. Mean 25(OH)D was 19.08 ± 8.44 ng/mL. At the enrollment time (T 0), no difference was found between Arms A and B with respect to distribution and 25(OH)D levels. At end time (T 1) 26.0% (29.7% in Arm A versus 20.6% in Arm B) showed sufficiency, 38.4% (42.0% versus 34.4%) insufficiency, and 35.6% (28.3% versus 45.0%) 25(OH)D deficiency. Mean 25(OH)D level was 23.71 ± 6.83 ng/mL. Conclusions. Neither changes of lifestyle nor 400 I.U. cholecalciferol supplementation alone appears to be sufficient to restore adequate 25(OH)D levels.
International Journal of Endocrinology 11/2014; 2014:583039. DOI:10.1155/2014/583039 · 1.95 Impact Factor
"Studies in adults have demonstrated that parathyroid hormone concentrations are at their ideal physiologic concentrations when 25OHD concentrations are above 32 ng/mL [14,15]. Similar data in children are unavailable . According to Avery's disease of the newborn, iPTH levels are usually dependent on the serum calcium status. "
[Show abstract][Hide abstract] ABSTRACT: Neonatal late-onset hypocalcemia is defined as hypocalcemia developed after postnatal 3 days and associated with hypoparathyroidism, high phosphate diets and vitamin D deficiency. We experienced the increment of neonatal late onset hypocalcemia over 1 year. We tried to evaluate the relationship between late onset hypocalcemia and maternal hypovitaminosis D.
The medical records in the neonates with late-onset hypocalcemia during January 2007 to July 2008 were retrospectively reviewed. Among those patients, 17 paired sera of mothers and neonates had collected. The levels of 25-OH vitamin D (25OHD) and intact parathyroid hormone (iPTH) were measured and were compared with neonate and the mother.
The mean gestational age was 38(+1) weeks, and the mean body weight was 2,980 g. The onset time of hypocalcemia was 5.9 days of age. Most of them (88.2%) were feeding with formula and no one was only breast milk feeding. Of the 17 patients, 13 were born in spring or in winter. The median levels of calcium, phosphorus, alkaline phosphatase, iPTH and 25OHD were 7.0 mg/dL, 8.6 mg/dL, 191.0 U/L, 57.2 pg/mL and 24.0 ng/mL in neonates. The levels of 25OHD of 6 neonates were <20 ng/mL. A total of 16 mothers were considered vitamin D-deficient (<20 ng/mL), and vitamin D insufficient (20<25OHD<30 ng/mL).
Neonatal late-onset hypocalcemia in our study seems to be influenced by maternal vitamin D deficiency and insufficiency. Sun tanning and vitamin D supplements from winter to spring would be helpful to prevent maternal vitamin D deficiency, one of the causes of neonatal late-onset hypocalcemia.
"Vitamin D is an essential nutrient that maintains the homeostasis of calcium and phosphorous levels in the body. The importance of vitamin D was recently emphasized when it was reported to be involved in cell differentiation and proliferation, immune function, and the prevention and treatment of certain cancers.1,2 Research has shown that adult epilepsy patients can exhibit a deficiency of vitamin D.3,4 In particular, hepatic enzyme-inducing antiepileptic drugs, such as phenytoin and carbamazepine, induce cytochrome P450 enzymes in the liver, thereby promoting the catabolism of vitamin D and its derivatives. "
[Show abstract][Hide abstract] ABSTRACT: Purpose
This study was to evaluate the relationship of 25(OH)D3 levels with anticonvulsant use and other possible factors in epileptic children and adolescents.
Materials and Methods
We studied 143 patients with epilepsy (90 boys, 53 girls; 11.21±4.49 years), who had been treated with anticonvulsants for more than 1 year. Patients who had taken multiple vitamins before the blood test and those who have the limitation of physical activity (wheelchair-bound) were excluded from the study. We evaluated the difference in vitamin D status according to the type and number of anticonvulsants taken and other factors such as gender, age, intelligence and seizure variables.
For patients with mental retardation or developmental delay, 25(OH)D3 levels were lower than the levels in patients with normal intelligence quotient levels (p=0.03). 25(OH)D3 levels were lower in patients who had taken anticonvulsants for more than 2 years as compared to those who had taken them for less than 2 years (p=0.03). Those taking oxcarbazepine had significantly lower vitamin D levels than patients taking valproic acid (p=0.01). However, no effects of number of anticonvulsants taken were detectable. More than two-thirds of the patients were diagnosed with osteopenia or osteoporosis in patients showing either vitamin D insufficiency or deficiency.
The possibility of vitamin D deficiency can be considered in pediatric patients taking anticonvulsants if they have mental retardation or developmental delay or if they have been taking anticonvulsants for more than 2 years or taking hepatic enzyme inducing drugs.
Yonsei medical journal 03/2014; 55(2):417-21. DOI:10.3349/ymj.2014.55.2.417 · 1.29 Impact Factor
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