Arthritis Research UK, Medical Research Council, Bupa Foundation, and National Institute for Health Research.
SummaryBackgroundVitamin D has a role in regulating immune function, and its deficiency is a suggested risk factor for childhood pneumonia. Our aim was to assess whether oral supplementation of vitamin D3 (cholecalciferol) will reduce the incidence and severity of pneumonia in a high-risk infant population.MethodsWe did a randomised placebo-controlled trial to compare oral 100 000 IU (2·5 mg) vitamin D3 with placebo given to children aged 1–11 months in Kabul, Afghanistan. Randomisation was by use of a computer-generated list. Vitamin D or placebo was given by fieldworkers once every 3 months for 18 months. Children presenting at the study hospital with signs of pneumonia had their diagnosis confirmed radiographically. Our primary outcome was the first or only episode of radiologically confirmed pneumonia. Our analysis was by intention to treat. This study is registered with ClinicalTrials.gov, number NCT00548379.Findings1524 children were assigned to receive vitamin D3 and 1522 placebo. There was no significant difference between the incidence of first or only pneumonia between the vitamin D (0·145 per child per year, 95% CI 0·129–0·164) and the placebo group (0.137, 0·121–0·155); the incidence rate ratio was 1·06 (95% CI 0·89–1·27). From 652 children during five separate periods of testing serum calcifediol, only one child in each of two testing periods had results greater than 375 nmol/L in the intervention group—a toxic level.InterpretationsQuarterly bolus doses of oral vitamin D3 supplementation to infants are not an effective intervention to reduce the incidence of pneumonia in infants in this setting.FundingWellcome Trust and British Council.
Aims:To compare the vitamin D status of 34 children, 9-24 months old, living in an area of Delhi renowned for high levels of atmospheric pollution (Mori Gate), with a comparable age matched group of children from a less polluted (Gurgaon) area of the city. Methods: Serum concentrations of calcium, alkaline phosphatase (ALP), parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH)D), and 1,25-dihydroxyvitamin D (1,25(OH) 2 D) were measured. Haze scores, regarded as a surrogate marker of solar UVB radiation reaching ground level, were measured in both areas. Results: Mean 25(OH)D of children in the Mori Gate area was 12.4 (7) ng/ml, compared with 27.1 (7) ng/ml in children living in the Gurgaon area (p < 0.001). The median ALP (p < 0.05) and mean PTH (p < 0.001) concentrations were higher in children living in the Mori Gate area than in the Gurgaon area. The mean haze score in the Mori Gate area (2.1 (0.5)) was significantly lower (p < 0.05) than in the Gurgaon area (2.7 (0.4)), indicating less solar UVB reaching the ground in Mori Gate. Conclusion: We suggest that children living in areas of high atmospheric pollution are at risk of developing vitamin D deficiency rickets and should be offered vitamin D supplements.I n humans the main source of vitamin D is that formed in the skin by conversion of 7-dehydrocholesterol to cholecalciferol (vitamin D 3 ) on exposure to the sun's ultraviolet B (UVB) radiation. The importance of sunlight in the prevention and cure of rickets was observed over a century ago, by Palm, 1 who found rickets to be most prevalent in cities where people were exposed to low levels of sunlight. Vitamin D is essential for skeletal health and its deficiency results in development of rickets in growing children and osteomalacia in adults. There is concern that increasing atmospheric pollution related haze from industrial and vehicular sources might lead to absorption of UVB photons, thereby reducing the cutaneous vitamin D synthesis. 2-4Delhi (latitude 28.35°N) is one of the most polluted cities in the world; the vehicle population, a major contributor to the atmospheric pollution burden, has grown by over 12% annually for the past two decades. 5 In this cross sectional study we assessed the vitamin D status of infants and toddlers living in a downtown area of Delhi, renowned for high levels of atmospheric pollution, with a comparable group of children from a relatively less polluted area on the outskirts of the metropolitan boundary of the city. We hypothesised that serum total 25-hydroxycholecalciferol (25(OH)D), a reliable measure of an individual's vitamin D status, of children living in the area with high levels of atmospheric pollution would be lower than in those living in the less polluted area of the city.
Metabolic bone disease of prematurity (MBDP) is characterised by skeletal demineralisation, and in severe cases it can result in fragility fractures of long bones and ribs during routine handling. MBDP arises from prenatal and postnatal factors. Infants who are born preterm are deprived of fetal mineral accumulation, 80% of which occurs in the third trimester. Postnatally, it is difficult to maintain a comparable intake of minerals, and medications, such as corticosteroids and diuretic therapy, lead to bone resorption. With improvements in neonatal care and nutrition, the incidence of MBDP in preterm infants appears to have decreased, although the recent practice of administering phosphate supplements alone will result in secondary hyperparathyroidism and associated bone loss, worsening MBDP. Postnatal immobilisation and loss of placental supply of oestrogen also contribute to skeletal demineralisation. There is no single diagnostic or screening test for MBDP, with pitfalls existing for most radiological and biochemical investigations. By reviewing the pathophysiology of calcium and phosphate homeostasis, one can establish that plasma parathyroid hormone is important in determining the aetiology of MBDP – primarily calcipaenia or phosphopaenia. This will then direct treatment with the appropriate supplements while considering optimal physiological calcium to phosphate ratios.
Despite improvements in 25(OH)D status, treatment with vitamin D(2) was not shown to increase mineral accretion, bone geometry or strength, muscle force, or power. There were greater increases in jump velocity in girls with the lowest baseline 25(OH)D concentrations. Lack of effect of intervention after the period of peak mineral and muscle mass accretion suggests that earlier action is required.
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