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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A randomized controlled study was performed to investigate the effect of 2 years' monitored diphenylhydantoin (DPH) therapy on plasma 25-hydroxyvitamin D (25-OHD) in non-epileptic, non-institutionalized subjects. Mean +/- SEM plasma 25-OHD of 18 DPH-treated subjects at the end of 2 years' drug treatment was 59 +/- 8 nmol/l (23.6 +/- 3.2 ng/ml), which was not decreased compared to that of eighteen control subjects (54 +/- 8 nmol/l, 21.6 +/- 3.2 ng/ml). In addition, mean plasma 25-OHD had not changed 1 month after ceasing DPH. The treated group had a higher mean serum alkaline phosphatase (SAP) during DPH treatment, attributable to hepatic enzyme induction. It is concluded that therapeutic doses of DPH without other anticonvulsants do not have a clinically significant effect on plasma 25-OHD.
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PMID:Chronic diphenylhydantoin therapy does not reduce plasma 25-hydroxy-vitamin D. 38 83

The mean +/- SEM of the cord, 48-hr, and 7-day values for serum calcium, magnesium, human calcitonin (HCT), parathyroid hormone (PTH), and 25-hydroxy-vitamin D (25-OHD) for premature and term infants can be seen in Table 1. Mean cord calcium concentrations were similar for term and premature infants. Serum calcium concentrations fell in both term and premature infants at 48 hr, but decreased more in the premature infants (from 10.23 +/- 0.30 to 8.74 +/- 0.19 mg/dl) than in the term infants (from 10.5 +/- 0.26 to 9.6 +/- 0.23 mg/dl). Serum calcium values increased from 48 hr to 7 days in both groups, and there was no significant difference between term and premature infants' serum calcium concentrations (10.6 +/- 0.28 and 10.12 +/- 0.3 mg/dl, respectively) at that time. There was no significant difference between term and premature cord serum magnesium concentrations. Serum magnesium concentrations increased similarly by 48 hr in both groups and remained at these concentrations at 7 days of life. Serum HCT concentrations were elevated above normal adult levels (71.9 +/- 6.6 pg/ml, 81% less than 100 pg/ml, n = 63) in both premature and term cord sera, but premature cord concentrations (146 +/- 24 pg/ml) were significantly higher than term cord concentration (91 +/- 21 pg/ml). Both term and premature infants displayed a 2-3-fold increase in serum HCT by 48 hr and a partial fall by 7 days to concentrations still above those seen in cord sera (Fig. 1). Nine of 10 premature and 9 of 10 term infants had undetectable PTH concentrations in cord sera. In two premature infants, PTH serum concenttration remained undetectable at 48 hr. However, the majority of both premature and term infants had elevated levels of PTH at 48 hr. The mean PTH concentrations were lower but still elevated at 7 days with the suggestion of higher concentrations in premature infants (Fig 2). There were no significant differences in serum 25-OHD concentrations between term and premature sera at birth or at 7 days. There was a weakly positive correlation between 25-OHD and cord calcium (r = 0.45, P less than 0.05), and a negative correlation between cord calcium and 48-hr PTH (r = -0.53, P less than 0.01). Calcium and magnesium were significantly positively correlated in 48-hr (r = 0.83) and 7-day (r = 0.84) sera in premature infants but not in term infants. Cord 25-OHD and cord HCT levels were significantly positively correlated (r = 0.80, P less than 0.01) in the term infants but not the premature infants.
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PMID:Serial measurements of serum calcium, magnesium, parathyroid hormone, calcitonin, and 25-hydroxy-vitamin D in premature and term infants during the first week of life. 86 19

Preterm infants (birth weight, 1,089 +/- 91 g; gestational age, 28.9 +/- 0.7 weeks; mean +/- SEM) with mixed medical and surgical indications for parenteral nutrition (PN) were observed to determine the adequacy of infusates with fixed, low-dose vitamin D (25 IU/dl) and two combinations of calcium and phosphorus. The duration of low-dose vitamin D PN ranged from 5 to 52 days, with a median of 27 days. Twelve infants were randomly assigned to low (standard) Ca and P doses (5 mM each; 20 mg/dl of Ca and 15.5 mg/dl of P) and 13 high Ca and P doses (15 mM each; 60 mg/dl of Ca and 46.5 mg/dl of P). The maximum daily vitamin D intake was similar for both groups (31 +/- 1.3 versus 33 +/- 1.2 IU/kg). Vitamin D status in either group, as indicated by serum 25-hydroxyvitamin D (25-OHD) concentrations, was normal. There was no significant difference in observed changes of serial measurements of serum calcium, magnesium, phosphorus, alkaline phosphatase, creatinine (Cr), 25-OHD, and vitamin D-binding protein concentrations or urinary Ca:Cr and Mg:Cr ratios. In the low-dose Ca and P group, the serum P level was consistently less than 4 mg/dl in five infants, serum 1,25-dihydroxyvitamin D concentrations were higher, and tubular reabsorption of phosphorus was consistently greater than 95% and significantly higher than in the high-dose Ca and P groups. Severe bone demineralization apparent on X-ray occurred in two infants, with a fractured distal left ulna in one of the two infants.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Minimal vitamin D and high calcium and phosphorus needs of preterm infants receiving parenteral nutrition. 249 13

Seventy-one very low birth weight (less than or equal to 1500 gm) infants were studied to determine the sequential changes in serum vitamin D metabolite concentrations between infants with and without radiographically documented rickets, fractures, or both (R/F). Usual intake of vitamin D included 20 IU/kg/day from parenteral nutrition or 400 IU/day supplementation with enteral feeding. Radiographs of both forearms and serum samples were obtained at 3, 6, 9, and 12 months. Twenty-two infants had R/F. At 3 months, significantly lower mean (+/- SEM) serum phosphorus levels (4.5 +/- 0.4 vs 6.1 +/- 0.2 mg/dl), higher 1,25-dihydroxyvitamin D (1,25-[OH]2D) concentrations (96 +/- 5 vs 77 +/- 4 pg/ml), and higher free 1,25-(OH)2D index (1,25-[OH]2D:vitamin D binding protein ratio; 5.2 +/- 0.3 x 10(5) vs 4.0 +/- 0.2 x 10(5] were found in the R/F group. These values returned to normal and were similar between groups on subsequent measurements. Serum calcium, magnesium, and 25-hydroxyvitamin D (25-OHD) concentrations were normal and similar between groups. In both groups, serum vitamin D binding concentrations increased initially but remained stable and normal beyond 6 months. We conclude that in very low birth weight infants with R/F, the vitamin D status (as indicated by serum 25-OHD concentrations) is normal, and that lowered serum phosphorus levels, higher serum 1,25-(OH)2D levels, and a higher free 1,25-(OH)2D index support the thesis that mineral deficiency (especially of phosphorus) may be important in the pathogenesis of R/F in small preterm infants.
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PMID:Serum vitamin D metabolites in very low birth weight infants with and without rickets and fractures. 224 79

The adequacy of low dose vitamin D (25 IU/dl) parenteral nutrition (PN) solution was studied in 18 infants. All infants had surgical indications for PN. The birth weights were 2810 +/- 135 g and gestational ages 37.4 +/- 0.5 wk (mean +/- SEM). Duration of study ranged from 5 to 175 days. Thirteen infants were studied for up to 6 weeks and five infants for 71 to 175 days. Results showed that studied infants maintained growth along normal percentiles for weight, length, and head circumference. Vitamin D status as indicated by serum 25 hydroxyvitamin D (25 OHD) rose from 15 +/- 1.9 ng/ml to 26 +/- 2.8 ng/ml, mean +/- SEM (p less than 0.001) after 9 days, and remained normal up to 6 months. Five infants with biochemical liver dysfunction also had normal serum 25 OHD concentrations, indicating the hepatic 25 hydroxylation process was not severely impaired. Serum total and ionized calcium, phosphorus, and vitamin D-binding protein concentrations were normal. Serum magnesium was mildly elevated in five infants (2.6 to 3 mg/dl) on one occasion and resolved spontaneously. Serum alkaline phosphatase (AP) concentrations rose above baseline values in 12 of 17 infants, but remained within normal range (less than 400 IU/liter at 30 degrees C). Another infant with markedly elevated AP values died from liver dysfunction. Radiographs of the forearms were normal except for marked demineralization in one infant in spite of normal 25 OHD concentrations. We conclude that 25 IU vitamin D/dl of nutrient infusate is adequate to maintain normal vitamin D status, as indicated by normal serum 25 OHD concentrations in infants receiving PN for as long as 6 months.
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PMID:Vitamin D requirement in infants receiving parenteral nutrition. 310 39

In order to evaluate the role of calcium regulating hormones in the pathogenesis of mitral ring calcification, we have studied the serum levels of PTH and vitamin D metabolites in aged females both with and without mitral ring calcification (MRC). In the patients with MRC (n = 17), significantly lower levels of serum total protein (6.6 +/- 0.2 in the MRC group vs 7.1 +/- 0.1 g/dl in the control group, mean +/- SEM), BUN (15.7 +/- 0.9 vs 18.3 +/- 0.9 mg/dl), creatinine (0.7 +/- 0.02 vs 0.9 +/- 0.02 mg/dl) and calcium (8.4 +/- 0.1 vs 9.2 +/- 0.1 mg/ml) were observed as compared with those in the controls (n = 32). Significantly higher PTH levels (0.57 +/- 0.07 vs 0.38 +/- 0.04 ng/ml) were found in the MRC group. Levels of all three vitamin D metabolites in the MRC group were significantly lower than those in the control group (25-OHD; 11.2 +/- 1.4 vs 19.6 +/- 1.2 ng/ml, 24,25(OH)2D; 0.7 +/- 0.1 vs 1.3 +/- 0.1 ng/ml and 1,25(OH)2D; 12.5 +/- 2.4 vs 43.0 +/- 3.5 pg/ml). The correlation coefficient between PTH and 1,25(OH) 2D was -0.382(n = 49, p less than 0.01). Thus, the significantly higher PTH levels in the MRC group might result in hypovitaminosis D. In conclusion, evidence of hypovitaminosis D in the patients with mitral ring calcification was demonstrated.
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PMID:Evidence of hypovitaminosis D in patients with mitral ring calcification. 324 33

Serum concentrations of 25-hydroxyvitamin D (25-OHD), 24,25-dihydroxyvitamin D [24,25-(OH)2D], and 1 alpha, 25-dihydroxyvitamin D [1, 25-(OH)2D] were measured in 30 ambulatory adult epileptic patients during long-term anticonvulsant treatment with phenytoin, phenobarbital, or carbamazepine. For the entire group, serum 24,25-(OH)2D was decreased (p less than 0.0005) as compared to normal subjects to a mean value of 0.7 +/- 0.1 (SEM) ng/ml. However, serum 1, 25-(OH)2D was increased at 50 +/- 7 pg/ml (p less than 0.025). Serum 25-OHD declined insignificantly to 19 +/- 3 ng/ml. All three drugs caused a significant reduction of serum 24,25-(OH)2D concentrations. A significant decrease in serum 25-OHD was observed only for the phenobarbital-treated patients. Serum 1, 25-(OH)2D was high in patients receiving phenytoin or carbamazepine but not in those taking phenobarbital. The findings suggest that while various anticonvulsant drugs appear to exert different effects on vitamin D metabolism, a universal finding is diminished serum 24,25-(OH)2D. The results support the notion that 24,25-(OH)2D deficiency may play an important role in the pathogenesis of anticonvulsant-induced osteomalacia.
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PMID:Decreased serum 24,25-dihydroxyvitamin D concentration during long-term anticonvulsant therapy in adult epileptics. 698 22

Hypercalcemia in human granuloma-forming diseases like sarcoidosis results from the endogenous overproduction of 1,25-dihydroxyvitamin D [1,25-(OH)2D] by disease-activated tissue macrophages. The recent identification of an immortalized chick myelomonocytic cell line, HD-11, that constitutively expresses a 25-hydroxyvitamin D (25-OHD) 1-hydroxylation reaction has alleviated dependence on studying primary macrophage cultures with no replicative potential in vitro. In these experiments we established conditions for the maximal expression of the HD-11 cell 25-OHD3-1-hydroxylation reaction and localized this activity to the mitochondrial fraction. On a per cell basis, the activity of HD-11 cell 25-OHD3 1-hydroxylation reaction was comparable to that in primary cultures of chick renal tubular epithelial cells, which express the authentic renal 25-OHD3 1-hydroxylase. Maximal product yield was achieved after incubation of HD-11 cells with 200 nM 25-OHD3 for 3 h. Although adherent monolayers possessed 3- to 4-fold more capacity for hormone production than cells in suspension, suspended cells exhibited easily detectable 25-OHD3 catalytic activity (0.58 +/- 0.08 pmol per 10(6) cells per h; +/- SEM), 50% of which remained solubilized in a sonicate of suspended cells cleared of nuclei and plasma membrane. Subcellular localization disclosed 91% of the residual activity to be concentrated in the mitochondrial subfraction. A detergent-solubilized extract of this mitochondrial subfraction contained 1.9 +/- 0.3 pmol 1,25-(OH)2D3 synthetic capacity per mg protein. The catalytic activity (1-hydroxylase activity) was concentrated 20.2-fold after chromatography on octyl-amino agarose and was associated with 0.054 nmol cytochrome P450 per mg protein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Subcellular localization and partial purification of the 25-hydroxyvitamin D3 1-hydroxylation reaction in the chick myelomonocytic cell line HD-11. 838 98

Osteoporosis and fractures are increasingly recognized in children and adults with cystic fibrosis. To investigate the prevalence and pathogenesis of osteoporosis and low bone mass in adults with advanced pulmonary disease due to cystic fibrosis, we examined the relationships between bone mineral density (BMD), anthropomorphic variables, pulmonary status, glucocorticoid therapy, and vitamin D concentrations. BMD of the lumbar spine, hip, and proximal radius was measured by dual energy X-ray absorptiometry in 30 white adults (16 women), age 30 +/- 2 yr (mean +/- SEM). Compared with a normal control population, the patients had significantly reduced BMD at the lumbar spine (17 +/- 3%), total hip and femoral neck (24 +/- 3% and 20 +/- 4%, respectively). The radius was significantly less demineralized (4 +/- 2%; p <= 0.003) than the other sites. Moreover, only 21% of patients with cystic fibrosis had normal BMD (T score > -1.0) at the lumbar spine, 23% at the hip sites, and 39% at the radius. Age, weight, and body mass index (BMI) were most strongly correlated with bone mass, whereas glucocorticoid therapy and pulmonary function were not predictive. Despite oral vitamin D (400 to 800 IU daily), the mean serum 25-hydroxyvitamin D (25-OHD) concentration was at the low end of the normal range (16 +/- 2 ng/ml; normal 10 to 52 ng/ml); 8 of 20 patients (40%) had frankly low (<= 10 ng/ml) levels. BMD was significantly lower in patients with low 25-OHD concentrations at the lumbar spine (0.774 +/- 0.02 versus 0.913 +/- 0.04 g/cm2; p = 0.01) and total hip (0.648 +/- 0.04 versus 0.811 +/- 0.04 g/cm2; p = 0.01). Vertebral fractures were present in 19% of subjects and 41% had a confirmed history of previous fracture. In summary, osteoporosis, low bone mass, and fractures are common in adults with advanced cystic fibrosis lung disease. Despite oral supplements, vitamin D deficiency is also common and is associated with more severe demineralization at the lumbar spine and hip. We conclude that the widespread practice of oral supplementation with 400 to 800 units of vitamin D is ineffective in maintaining normal vitamin D stores in many patients with cystic fibrosis. To ensure adequacy of vitamin D stores, measurement of serum 25-OHD should be included in the routine management of patients with cystic fibrosis.
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PMID:Bone mass and vitamin D deficiency in adults with advanced cystic fibrosis lung disease. 962 Sep 24

Changes in plasma 25-hydroxyvitamin D (25-OHD) were used as an index of vitamin D status of cats. Plasma 25-OHD concentration of kittens given a purified vitamin D-free diet and exposed to direct summer sun for 15 h/wk declined at a similar rate as kittens given the same diet kept indoors. Similarly, plasma 25-OHD of kittens exposed to ultraviolet (UV) lamps declined at a similar rate as kittens not exposed, and these kittens developed clinical signs of vitamin D deficiency. Eight weaned kittens were given the vitamin D-free purified diet until their plasma concentrations of 25-OHD were < 5 nmol/L. They then had the hair on their backs clipped at weekly intervals and were paired on the basis of skin color and exposed to UV light for 2 h/d. One member of each pair was given an inhibitor of 7-dehydrocholesterol (5, 7-cholestradien-3beta-ol)-delta7-reductase (EC 1.3.1.21) in the diet. Cats receiving the inhibitor had a progressive increase in 25-OHD concentration of plasma with time to 91 +/- 22 nmol/L (mean +/- SEM), whereas cats not receiving the inhibitor had plasma 25-OHD concentrations that were not detectable (P < 0.001). Biopsy samples of skin from cats receiving the inhibitor had more than five times the concentration of 7-dehydrocholesterol (P < 0.001) than the skin of control cats. Low concentration of 7-dehydrocholesterol (presumably due to high activity of the reductase) in the skin of cats is the major impediment to effective vitamin D synthesis. Analysis of wild caught potential prey of cats indicated that these animals could supply adequate vitamin D to meet the requirement of growing kittens.
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PMID:Ineffective vitamin D synthesis in cats is reversed by an inhibitor of 7-dehydrocholestrol-delta7-reductase. 1020 68


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