PubMed HealthSearch

PubMed · 6979978

Skeletal changes in preterm infants.

Abstract

The skeletal changes in 19 very low birthweight infants (less than 1500 g) were observed from birth to 10 weeks, by means of clinical, biochemical, and radiological techniques. All infants were receiving a supplement of 800 IU vitamin D a day from age 2 weeks. None of the infants showed any specific physical sign of rickets during the period of study. Six infants showed radiological evidence of skeletal demineralisation; 1 of these had severe changes of rickets and 1 had both rickets and fractures. These 6 infants were of shorter gestational periods and lower birthweights than the infants not showing radiological changes. They tended to have more clinical problems and to reach a predetermined volume of feeds (160 ml/kg a day) later than the unaffected infants. Serum alkaline phosphatase values were significantly higher at 5 weeks in the infants with abnormal radiographs than in those without. There were no significant differences between the two groups in relation to serum calcium, inorganic phosphate, 25 hydroxyvitamin D, and immunoreactive parathyroid hormone. The pathogenesis of the skeletal lesions of very low birthweight infants remains unknown.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

W W Koo, J M Gupta, V V Nayanar, M Wilkinson, S Posen. 1982. Skeletal changes in preterm infants.. https://doi.org/10.1136/adc.57.6.447

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Skeletal response to recombinant human growth hormone (rhGH) in children treated with long-term corticosteroids.

Corticosteroid therapy causes osteopenia and growth retardation in children; such changes are associated with diminished rates of bone formation and turnover. Since growth hormone activates bone remodeling, the biochemical and skeletal responses to rhGH were evaluated in four pediatric patients, aged 12.8 +/- 3 years, with long-term corticosteroid use (5 +/- 2 years). Recombinant human growth hormone (rhGH), 0.125 mg/kg, was given 3 times/week by subcutaneous injection for 12 months. Iliac crest bone biopsies were obtained after double tetracycline labeling before and at the end of rhGH therapy; serum levels of calcium, phosphorus, alkaline phosphatase, parathyroid hormone (intact), 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D3, osteocalcin (BGP), and insulin-like growth factor-1 (IGF-1) were measured every 3 months during the treatment period. The average dose of prednisone was 0.24 +/- 0.05 mg/kg/day initially, and this did not change during the study. Serum calcium, phosphorus, alkaline phosphatase, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D3, and BGP were unchanged during the rhGH therapy, but the serum IGF-1 level increased by 71%, p < 0.01. Eroded bone perimeter and cancellous bone area did not change significantly during rhGH therapy. Bone formation rates rose from 423 +/- 475 to 781 +/- 407 microns2/mm2/day, p < 0.05, and the length of double tetracycline-labeled bone perimeter increased by 85%, p < 0.05. The bone formation rate in the growth hormone group exceeded the values of an age-matched reference group (14.3 +/- 3 years), 780 +/- 407 microns2/mm2/day versus 411 +/- 479 microns2/mm2/day, p < 0.05.(ABSTRACT TRUNCATED AT 250 WORDS)

25-Hydroxyvitamin D 2

Unique form of rickets with low serum 25-hydroxyvitamin D in two normally nourished children.

We present an unusual type of rickets involving two children: a 2 year old boy and a 15 month old boy, who presented with marked bowing of the lower extremities and bulging of costochondral junctions. Both children had normal growth, with their height and body weight greater than the 50th and 97th percentile for age. Roentgenograms of their extremities showed the typical changes of vitamin D refractory rickets. Serum alkaline phosphatase levels were elevated and serum levels of calcium and phosphate were both within the normal range. No primary cause for the rickets, including nutritional deficiencies, was found in the two patients. Characteristic findings were persistently low serum 25-hydroxyvitamin D (25-OH-D) and normal 1,25-dihydroxyvitamin D (1,25-(OH)2-D). Improvements in clinical and X-ray findings were observed after either oral administration of 1 alpha-(OH)-D3 (9-15 micrograms per day) or massive vitamin D2 therapy (600,000 IU single injection). The low serum levels of 25-OH-D did not increase unless massive vitamin D2 therapy was also given. These two cases represent a unique form of rickets that does not meet the criteria for any type of previously known rickets.

25-Hydroxyvitamin D 2

Subclinical health effects in a population exposed to excess vitamin D in milk.

To evaluate subclinical health effects of excess vitamin D, a cross-sectional study was conducted of persons consuming milk from a dairy that had overfortified milk for at least 4 years. Milk consumption, sunlight exposure, medical symptoms, serum 25-hydroxyvitamin D (25[OH]D), serum and urinary calcium, and indicators of renal function were measured. Increased milk consumption was associated with increased serum 25(OH)D and urinary calcium. However, the prevalences of elevated serum 25(OH)D and calcium were no greater than expected, and data indicated normal renal function. It was concluded that most persons exposed to excess vitamin D exhibited no measurable adverse subclinical effects.

25-Hydroxyvitamin D 2