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Biomedical subjects

H F DeLuca

Publications and source records attributed to H F DeLuca.

At least 55 records · Page 3Linked to original sources
PubMed1979

Rickets with alopecia: an inborn error of vitamin D metabolism.

Rickets with alopecia, an inborn error of vitamin D metabolism, is described in two sisters. The rachitic disorder began during the first year of life and was refractory to 50,000 IU of vitamin D2/day. Surprisingly, both children had marked elevations in serum concentrations of 1,25-(OH)2D. Although the molecular basis for this disorder is not evident to date, intestinal end-organ unresponsiveness to exceedingly high levels of 1,25-(OH)2D was present, in addition to hyporesponsiveness of bone to these high levels of the hormone, since normocalcemia was maintained despite elevated serum levels of PTH. Therapy with oral 1,25-(OH)2D3 failed to reverse the disorder, but oral phosphorus supplements resulted in significant radiographic and clinical improvement.

Alopecia↗
PubMed1979

1,25-Dihydroxyvitamin D3 in childhood hepatic osteodystrophy.

Osteodystrophy frequently accompanies severe childhood hepatobiliary disease. Proposed causes include malabsorption of vitamin D and calcium, and diminished 25-hydroxylation of vitamin D. Two children, ages 23 and 35 months, with radiographic and biochemical evidence of rickets with extrahepatic biliary atresia, were treated with 1,25-dihydroxyvitamin D3. The minimal effective therapeutic dose and efficacy of 1,25-(OH)2D3 in the treatment of rickets associated with severe childhood hepatic disease were determined. Oral 1,25-(OH)2D3 was ineffective at doses of 0.10 microgram/kg/day. Parenteral doses of 0.20 microgram/kg/day effectively produced radiographic, bone mineral (photon absorptiometric), and biochemical evidence of healing. The need for four times the physiologic dose of 1,25-(OH)2D3 by the parenteral route suggested enhanced catabolism of, or end-organ resistance to, 1,25-(OH)2D3 in our patients with severe cholestatic liver disease treated with phenobarbital.

Bile Ducts↗
PubMed1979

In vitro production of 1,25-dihydroxyvitamin D3 by rat placental tissue.

Weanling female rats were fed a vitamin D-deficient diet for 4 months until they reached maturity. They were mated with normal, vitamin D-replete male rats and, at 20 days of pregnancy, the female rats were killed and their placentae were removed, homogenzied, and incubated with 25-hydroxyvitamin D3. The incubation mixtures were extracted and the extracts were subjected to Sephadex LH-20 column chromatography followed by high-pressure liquid chromatography. The 1,25-dihydroxyvitamin D3 region of the high-pressure liquid chromatogram was recycled to purity and the structure of the product was identified as 1,25-dihydroxyvitamin D3 by ultraviolet absorption spectrophotometry and by mass spectrometry. Thus it is now evident that placenta, in addition to renal tissue, is capable of converting 25-hydroxyvitamin D3 to the hormonal form of vitamin D, 1,25-dihydroxyvitamin D3.

Animals↗
PubMed1979

Vitamin D metabolism during pregnancy and lactation in the rat.

The plasma concentration of the major vitamin D metabolites; 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and 24,25-dihydroxyvitamin D were measured during pregnancy and lactation in the adult female rat. The concentrations of these metabolites were also measured in rat pups during lactation and after weaning. The plasma concentration of 1,25-dihydroxyvitamin D in the adult female increases from a control value of 26 pg/ml to 86 pg/ml during the latter stages of pregnancy, reaches a peak of 158 pg/ml during lactation, and then returns to control levels by 3 weeks postweaning. Plasma concentrations of 24,25-dihydroxyvitamin D fall dramatically during pregnancy from a control level of 3.9 ng/ml to 1.6 ng/ml remain low during lactation, and return to control levels by 3 weeks postweaning. In the neonatal rat pup at 14 days postpartum, 1,25-dihydroxyvitamin D plasma concentration is 25 pg/ml and 24,25-dihydroxyvitamin D concentration is 2.8 ng/ml. By day 25 postpartum, 1,25-dihydroxyvitamin D concentrations reached levels of 101 pg/ml, whereas 24,25-dihydroxyvitamin D concentrations fell to 1.9 ng/ml.

Age Factors↗
PubMed1979

On the physiological basis of vitamin A-stimulated growth.

The influence of vitamin A depletion on tissue composition was studied in rats that were marginally vitamin A deficient, i.e. at their weight plateau stage. The total number of cells (DNA) was decreased in most organs as a result of vitamin A depletion. In thymus, spleen and the sublingual glands there was also a dramatic reduction in the number of cells per gram of tissue and in thymus and sublingual glands there was an increase in the protein to DNA ratio as a result of absence of dietary.vitamin A. We present the hypothesis that vitamin A stimulates growth by a direct role in cell replication in addition to or instead of stimulating the differentiation of epithelial and bone cells.

Animals↗
PubMed1979

Evidence that increased circulating 1 alpha, 25-dihydroxyvitamin D is the probable cause for abnormal calcium metabolism in sarcoidosis.

Mean plasma 1(alpha),25-dihydroxyvitamin D[1(alpha),25(OH)(2)D] was significantly increased and serum parathyroid hormone was suppressed in three patients with sarcoidosis and hypercalcemia. Prednisone lowered the mean plasma 1(alpha),25(OH)(2)D to normal range and corrected the hypercalcemia. To elucidate the mechanism for the increased sensitivity to vitamin D in this disorder, the effects of orally-administered vitamin D(2) were determined in seven normal subjects, four patients with sarcoidosis and normal calcium metabolism and three patients with sarcoidosis and a history of hypercalcemia who were normocalcemic when studied. Serum and urinary calcium, serum 25-hydroxyvitamin D (25-OHD), plasma 1(alpha),25(OH)(2)D and, in some studies, calcium balance were measured. Vitamin D(2), 250 mug a day for 12 d, produced little, if any, change in mean plasma 1(alpha),25(OH)(2)D and in urinary calcium in the normals and in the patients with normal calcium metabolism. In contrast, vitamin D(2) produced increases in plasma 1(alpha),25(OH)(2)D from concentrations which were within the normal range (20-55 pg/ml) to abnormal values and increased urinary calcium in two patients with abnormal calcium metabolism. In an abbreviated study in the third patient, vitamin D(2), 250 mug a day for 4 d, also increased plasma 1(alpha),25(OH)(2)D abnormally from a normal value. There was a highly significant correlation between plasma 1(alpha),25(OH)(2)D and urinary calcium. Serum 25-OHD and serum calcium remained within the normal range in all subjects and patients. These findings provide evidence that the defect in calcium metabolism in sarcoidosis probably results from impaired regulation of the production and(or) degradation of 1(alpha),25(OH)(2)D. Prednisone may act to correct the abnormal calcium metabolism by reducing circulating 1(alpha),25(OH)(2)D.

Adult↗
PubMed1979

Intestinal calcium absorption and serum vitamin D metabolites in normal subjects and osteoporotic patients: effect of age and dietary calcium.

Intestinal calcium absorption assessed by a double-isotope method, decreased significantly with aging in 94 normal subjects (r = -0.22, P < 0.025). In 52 untreated patients with postmenopausal osteoporosis, calcium absorption was significantly lower than normal when either age or habitual calcium intake was used as a covariable (P < 0.001). Serum 25-hydroxyvitamin D (25-OH-D) and 1,25-dihydroxyvitamin D (1,25(OH)(2)D) were measured in 44 normal subjects and 27 osteoporotic patients. For all normals, calcium absorption and serum 1,25(OH)(2)D were positively correlated (r = 0.50, P < 0.001). In nonelderly normal subjects (ages 30-65 yr), dietary calcium intake correlated inversely with both calcium absorption (r = -0.39, P < 0.01) and with serum 1,25(OH)(2)D (r = -0.50, P < 0.01). Both osteoporotic patients and elderly normal subjects (ages 65-90 yr) differed from nonelderly normals in that these correlations were not present. In addition although serum 25-OH-D was normal, serum 1,25(OH)(2)D was significantly decreased in both osteoporotic patients and elderly normals (P < 0.001). In osteoporotic patients, calcium absorption increased significantly (P < 0.001) after 7 d administration of a small dose (0.4 mug/d) of synthetic 1,25(OH)(2)D(3). In osteoporotics mean serum immunoreactive parathyroid hormone was either normal (COOH-terminal assay) or low (NH(2)-terminal assay) relative to age-matched controls, and mean serum phosphate was increased. The data suggest that inadequate metabolism of 25-OH-D to 1,25(OH)(2)D contributes significantly to decreased calcium absorption and adaptation in both osteoporotics and elderly normal subjects. In patients with osteoporosis this abnormality could result from a decrease in factors that normally stimulate 1,25(OH)(2)D production, such as the decreased parathyroid hormone secretion and increased serum phosphate demonstrated in this group. In elderly subjects a primary abnormality in metabolism of 25-OH-D to 1,25(OH)(2)D, analagous to that seen in aging rats, cannot be excluded.

Adult↗
PubMed1979

Production of 1,25-dihydroxyvitamin D3 and formation of medullary bone in the egg-laying hen.

Renal 25-hydroxyvitamin D-1-hydroxylase, the percentage of medullary bone in the femur, plasma calcium, and plasma phosphorus were measured in female chickens reaching maturity. These parameters and plasma 1,25-dihydroxyvitamin D levels were also measured during the daily egg-laying cycle in mature hens. The renal 25-hydroxyvitamin D3-l-hydroxylase becomes elevated in maturing hens before and at the time of ovulation. This elevation in the 1-hydroxylase correlates with the elevation in total plasma calcium concentration but lags and at the time of ovulation and is followed by a further elevation of plasma 1,25-dihydroxyvitamin D levels. The plasma 1,25-dihydroxyvitamin D level remains high until 12 h postovulation. At this time, it falls to the preovulation level. No relationship could be found between the plasma 1,25-dihydroxyvitamin D levels and the changes in medullary bone found during the egg-laying cycle. However, plasma 1,25-dihydroxyvitamin D levels are highest immediately before and during the egg shell calcification phase of the egg-laying cycle.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1979

Potential use of 1,25-dihydroxycholecalciferol for prevention of parturient paresis.

Twelve cows, at least third parity, were assigned randomly to either a control or treatment group. Treated cows received .4 mg of the vitamin D metabolite, 1,25-dihydroxycholecalciferol intramusculary in 5 ml corn oil. Intramuscular injections were started 5 days before predicted calving with reinjections every 5 days until calving. Incidence of parturient paresis was 0 and 33% (2 of 6) in the treated and control groups. Response to treatment was rapid with elevated calcium in serum approximately 12 h postinjection. Treatment maintained or elevated calcium and phosphorus concentrations in serum during the critical period, 24 h pre- to 48 h postpartum, when milk fever is most likely to occur. There was, however, no significant difference between treatments at 72 h postpartum. Based on these observations 1,25-dihydroxycholecalciferol holds promise as a preventative of parturient paresis; however, further studies are needed on application and safety.

Animals↗