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Biomedical subjects

D Aarskog

Publications and source records attributed to D Aarskog.

At least 55 records · Page 3Linked to original sources
PubMed1985

Plasma concentrations of vitamin D metabolites during puberty of diabetic children.

Plasma concentrations of 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, 24,25-dihydroxyvitamin D and vitamin D binding protein were determined in 87 serum samples from 46 Type 1 (insulin-dependent) diabetic children and adolescents at the various stages of puberty. The results were compared with data similarly obtained from healthy pubertal children. The diabetic patients had lower mean 1,25-dihydroxyvitamin D concentrations (p less than 0.05) and higher molar ratios of 24,25-dihydroxyvitamin D to 25-hydroxyvitamin D (p less than 0.05) than their healthy counter parts. In contrast to the reference group, the diabetic patients failed to attain the increase in 1,25-dihydroxyvitamin D normally seen during the pubertal stages of maximal growth velocity. The mean plasma levels of vitamin-D binding protein did not differ between the two groups, and a calculated 'free' 1,25-dihydroxyvitamin D value followed a pattern similar to that of total 1,25-dihydroxyvitamin D throughout puberty for both groups. The results suggest that the regulatory mechanisms of the vitamin D endocrine system are altered in diabetic children at puberty, resulting in a relative decrease in 1,25-dihydroxyvitamin D plasma concentration and increased 24,25-dihydroxyvitamin D levels.

24,25-Dihydroxyvitamin D 3↗
PubMed1985

Rapid effect of prednisolone on serum 1,25-dihydroxycholecalciferol levels in hypercalcemic sarcoidosis.

We have studied a hypercalcemic patient with sarcoidosis and advanced renal failure. Bone biopsy and urinary cAMP excretion indicated suppression of parathyroid function. 1,25(OH)2D levels were moderately elevated and dropped to low normal levels during prednisolone treatment. Discontinuation of prednisolone treatment caused deterioration of renal function and hypercalcemia, 1,25(OH)2D serum levels being within the normal range. Our data demonstrate the rapid speed at which prednisolone causes a drop in serum 1,25(OH)2D level. Since hypercalcemia was observed both during periods of hypercalciuria and normal serum 1,25(OH)2D levels, increased sensitivity to active vitamin D seems likely. There was no significant correlation between 25(OH)D, 24,25(OH)2D or 25,26(OH)2D. Furthermore there was no correlation between any of these three metabolites and either 1,25(OH)2D or serum calcium.

Calcitriol↗
PubMed1984

Anticonvulsant drug therapy in human pregnancy: effects on serum concentrations of vitamin D metabolites in maternal and cord blood.

Serum concentrations of the main vitamin D metabolites and of calcium, phosphate, and alkaline phosphatase were determined in each of the three trimesters of pregnancy and in simultaneously obtained maternal and cord blood at delivery in 22 epileptic women treated with diphenylhydantoin or carbamazepine alone or with a combination with one other drug. The results were compared with similarly obtained data from 22 normal pregnancies. Women in both groups received supplements of 400 IU vitamin D3 per day. All the women had 25-hydroxyvitamin D levels within the normal range for healthy adults (greater than 12 ng/ml) throughout pregnancy. The epileptic women had, however, significantly (p less than 0.05) lower median 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels and higher median 25,26-dihydroxyvitamin D values than the reference group. The 24,25-dihydroxyvitamin D concentrations did not differ significantly, but the median ratio of 24,25-dihydroxyvitamin D to 25-hydroxyvitamin D was higher in the epileptic women at the end of pregnancy (p = 0.05). The respective differences in cord serum concentrations reflected those of the mothers at delivery. Serum calcium tended to be lower during epileptic pregnancy, but none were hypocalcemic. The alkaline phosphatase and phosphate values did not consistently differ from those of the reference women. The median alkaline phosphatase level of cord serum was slightly higher in the epileptic group, but the calcium and phosphate levels were similar to the reference values. The various biochemical parameters of the carbamazepine-treated women tended to be intermediate between those of the healthy and diphenylhydantoin-treated groups. Antiepileptic drug therapy appears to affect vitamin D metabolism and calcium homeostasis during pregnancy. The derangements may not be of major clinical significance, however, in vitamin D-supplemented and normally functioning women on long-term low-dose therapy.

24,25-Dihydroxyvitamin D 3↗
PubMed1984

25-Hydroxyvitamin D and 1,25-dihydroxyvitamin D of D2 and D3 origin in maternal and umbilical cord serum after vitamin D2 supplementation in human pregnancy.

Serum concentrations of 25-hydroxyvitamin D (25-OHD) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] of vitamin D2 and D3 origin were determined separately in 10 women before vitamin intake in early pregnancy, and repeated in maternal and cord serum obtained at delivery after 20 to 30 wk of vitamin D2 supplementation in a dose of 400 IU/day. Before supplementation 25-OHD2 and 1,25-(OH)D2D2 were present in just traceable or nondetectable concentrations, but the levels increased in all to a mean +/- 1 SD of 7.3 +/- 3.7 ng/ml and 37.2 +/- 18.1 pg/ml, respectively (p less than 0.0025), by the time of delivery. At delivery the total 25-OHD and 1,25-(OH)2D levels were always lower in the cord than in the maternal serum (30.7 +/- 14.2 versus 20.1 +/- 9.1 ng/ml, and 90.1 +/- 31.2 versus 37.3 +/- 11.6 pg/ml, p less than 0.0025). The paired concentrations of 25-OHD were closely related (r = 0.89, p less than 0.0005), while the association for 1,25-(OH)2D was not statistically significant (r = 0.53, p less than .01). The 25-OHD of D2 and D3 origin accounted for a similar proportion of the total 25-OHD in the maternal and cord serum (ratio of 25-OHD2 to 25-OHD3: 0.40 +/- 0.28 versus 0.45 +/- 0.29, p = NS), as did the respective 1,25-(OH)2D metabolites [ratio of 1,25-(OH)2D2 to 1,25-(OH)2D3: 0.73 +/- 0.35 versus 0.90 +/- 0.50, p = NS].(ABSTRACT TRUNCATED AT 250 WORDS)

25-Hydroxyvitamin D 2↗
PubMed1984

Plasma concentrations of vitamin D metabolites before and during treatment of vitamin D deficiency rickets in children.

Plasma concentrations of 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D (1,25-(OH)2D), and 24,25-dihydroxyvitamin D (24,25-(OH)2D) were determined in 17 children with vitamin D deficiency rickets before therapy was started. Thirteen of them also had these tests repeated during treatment. The median 25-OHD concentration was at the lower limit of the reference range before, but increased distinctly within one week of treatment with 1 700-4 000 IU vitamin D per day (17 vs. 37 nmol/l, p less than 0.01). 24,25-(OH)2D was undetectable in twelve of the patients before therapy. Detectable concentrations were in the range of 1.7 to 3.5% of the corresponding 25-OHD levels throughout the study, and the two metabolites were closely correlated (r = 0.84, p less than 0.0005). The median 1,25-(OH)2D concentration was near the average of the reference range before, but increased to well above the upper limit of normal within one week of treatment (121 vs. 368 pmol/l, p less than 0.01). The levels were largely normal after 10 weeks of therapy, as were the plasma concentrations of calcium, phosphate, and alkaline phosphatase. Parathyroid activity, as judged by serum parathyroid hormone or urinary cyclic AMP concentrations, was stimulated in 11 of 12 children studied prior to treatment. It is concluded that there may be no clear-cut differences between normal nad rachitic values of the different vitamin D metabolites under practical clinical conditions. A low 25-OHD level combined with evidence of a stimulated parathyroid activity, and a rise of 1,25-(OH)2D levels to supernormal values following a few days of vitamin D therapy may be diagnostic clues.

24,25-Dihydroxyvitamin D 3↗
PubMed1984

Plasma concentrations of vitamin D metabolites in premature infants.

The plasma concentrations of 25-hydroxyvitamin D (OHD), 1,25-(OH)2D and 24,25-(OH)2D were determined in 28 healthy premature infants (median gestational age 33, range 28-36 wk; and median birth weight 1880, range 900-2350 g) during the first 5-10 wk of life, and in a reference group of 17 young adults. The infants received a vitamin D supplement of 500 IU/d and a diet low in calcium (Ca) and phosphorus (P) compared with that of corresponding intrauterine accretion rates. The median 25-OHD concentration increased from 11 (range 6-30) ng/ml at 1 d to 27 (range, 15-41) ng/ml by 5-10 wk of age (P less than 0.01). 1,25-(OH)2D concentrations at age 1 d were similar to the adult levels (median 37, range 8-64 versus 35, range 18-58 pg/ml), but increased significantly within 1 wk to 48 (26-156) pg/ml (P = 0.01), and between 1 and 3-4 wk of age to 104 (58-203) pg/ml (P less than 0.01). The levels at 5-10 wk were similar to the 3-4 wk value. 24,25-(OH)2D concentrations were persistently low compared with the adult levels (medians 0.4-0.5, range less than 0.3-2.1 versus 1.7, range 0.4-2.0 ng/ml, P less than 0.01). The relative concentrations, expressed as the ratio of 24,25-(OH)2D to 25-OHD, were comparable to those of the adults at birth, but decreased significantly within 2 wk. The data demonstrate that healthy premature infants can produce high plasma levels of 1,25-(OH)2D.

24,25-Dihydroxyvitamin D 3↗
PubMed1984

Effect of exchange transfusions with citrated blood on plasma concentrations of vitamin D metabolites in neonates.

The plasma concentrations of 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D (1,25-(OH)2D), and 24,25-dihydroxyvitamin D (24,25-(OH)2D) were determined pre- and postexchange , and in donors' blood in 10 blood exchange transfusions with citrated blood for neonatal hyperbilirubinemia. The postexchange concentrations of 25-OHD and 24,25-(OH)2D were intermediate between the levels before exchange and in donors' blood. Before therapy, the 1,25-(OH)2D concentrations were higher in the infants' than in donors' blood, and the pre-exchange levels were re-established during the procedure. The results suggest that postexchange concentrations of 25-OHD and 24,25-(OH)2D could be explained on the basis of redistribution of the metabolites between plasma and extravascular pools, whereas de novo synthesis was the most likely cause for the restoration of 1,25-(OH)2D levels.

24,25-Dihydroxyvitamin D 3↗
PubMed1983

Autosomal dominant partial lipodystrophy associated with Rieger anomaly, short stature, and insulinopenic diabetes.

We describe the clinical findings and natural history of an autosomal dominant form of partial lipodystrophy found in four affected individuals from three generations in the same family. The lipodystrophy was present from infancy/early childhood, involved primarily the face and local areas on the buttocks, and was nonprogressive. Affected individuals also had the Rieger anomaly, midface hypoplasia, short stature, retarded bone age, and hypotrichosis. An affected woman developed insulinopenic diabetes mellitus at 39 yr and another had glucose intolerance at 55 yr.

Adult↗
PubMed1983

Vitamin D metabolism in normal and hypoparathyroid pregnancy and lactation. Case report.

Plasma concentrations of vitamin D metabolites in 17 non-pregnant women, 22 pregnant women at delivery, and in eight lactating women 3 and 16 days after delivery, were compared with those in a postpartum hypoparathyroid patient treated with 1 alpha-hydroxyvitamin D (1 alpha-OHD). The mean concentration of 1,25-dihydroxyvitamin D [1,25-(OH)2 D] was 203 (SD 61) pmol/l in the pregnant, and 86 (SD 27) pmol/l in the non-pregnant women (P less than 0.0005). The levels 3 and 16 days after delivery were similar [57 (11) compared with 62 (19) pmol/l], and lower than the non-pregnant value (P less than 0.01). The 25-hydroxyvitamin D (25-OHD) concentration remained unchanged between the 3rd and 16th days after delivery, whereas the 24,25-dihydroxyvitamin D [24,25-(OH)2D] level increased from 2.7 (SD 1.8) to 3.7 (SD 2.3) nmol/l (P less than 0.025). The patient temporarily required an increased supplement of l alpha-OHD during pregnancy, but a dose which was appropriate before pregnancy resulted in marked hypercalcaemia and a rise of 1,25-(OH)2D concentration within 16 days of delivery despite lactation. The results suggest that the metabolic need for the active vitamin D metabolite 1,25-(OH)2D is increased during pregnancy and rapidly reduced during early lactation in healthy and hypoparathyroid women.

Adult↗
PubMed1983

Vitamin D nutritional status of premature infants supplemented with 500 IU vitamin D2 per day.

The vitamin D nutritional status of premature infants was assessed by determining plasma 25-hydroxyvitamin D concentrations before and during supplementation with 500 IU vitamin D2 per day. Fifty-one samples were collected from 25 healthy infants fed breast milk and a vitamin D3 fortified formula. Gestational age was 32.2 +/- 2.4 weeks (mean +/- 1 SD). 25-hydroxyvitamin D levels before supplementation correlated well with maternal values (r = 0.81). The infants' mean plasma concentration increased from 30.6 +/- 13.7 nmol/l (mean +/- 1 SD) after birth to 46.3 +/- 10.5 nmol/l after 9 +/- 1 days (p less than 0.0025), and to 65.3 +/- 16.6 nmol/l after 37 +/- 10 days of vitamin D2 treatment (p less than 0.0005). 25-hydroxyvitamin D2 and 25-hydroxyvitamin D3 were determined separately, and it appeared that the rise was accounted for by the D2 fraction while 25-hydroxyvitamin D3 concentrations were unchanged. The results demonstrate that vitamin D2 is well absorbed and hydroxylated in the 25 position by premature infants free of associated disease, and that a supplementation of 500 IU per day in addition to breast milk and a regular vitamin D fortified formula is adequate to rapidly establish 25-hydroxyvitamin D levels within the normal adult range.

25-Hydroxyvitamin D 2↗
PubMed1983

Plasma concentrations of vitamin D metabolites in a case of rickets of prematurity.

Rickets was diagnosed in an extremely low-birthweight infant 16 weeks after birth. She had a normal plasma concentration of 25-hydroxyvitamin D, a relatively low level of 24,25-dihydroxyvitamin D, and a markedly elevated 1,25-dihydroxyvitamin D level compared with adult standards. The plasma concentrations of the vitamin D metabolites were, however, indistinguishable from those of healthy preterm infants who received a similar diet of human milk and vitamins. The results indicate that rickets was not caused by vitamin D deficiency or by abnormal vitamin D metabolism, but by calcium and/or phosphate deficiency, and that the calcium and phosphorous content of human milk may be inappropriately low for very low-birthweight infants.

24,25-Dihydroxyvitamin D 3↗
PubMed1983

Effect of estrogen on vitamin D metabolism in tall girls.

To determine the effect of estrogen on vitamin D metabolism in pubertal girls, we studied 16 tall girls treated with a daily dose of 4-8 mg estradiol valerate to curtail excessive adult height. In all but one girl the plasma concentration of 1,25-dihydroxyvitamin D (1,25-(OH)2D) increased to values significantly higher than the corresponding pretreatment value (P less than 0.0005). The ratio of 24,25-dihydroxyvitamin D (24,25-(OH)2D) to 25-hydroxyvitamin D decreased in all girls (P less than 0.0005). The vitamin D binding protein (DBP) also increased significantly after estrogen (P less than 0.025), and there was a significant positive correlation between the plasma concentration of 1,25-(OH)2D and DBP (r = 0.66; P less than 0.0005). The free fraction of 1,25-(OH)2D remained unchanged after estrogen. It appears that estrogen treatment increases the plasma concentration of 1,25-(OH)2D. The effect might be explained by the concomitant increase in DBP and/or by estrogen stimulation of renal 1 alpha-hydroxylase.

24,25-Dihydroxyvitamin D 3↗
PubMed1983

Effect of parathyroid hormone on cAMP and 1,25-dihydroxyvitamin D formation and renal handling of phosphate in vitamin D-dependent rickets.

Studies were carried out to compare the effects of parathyroid extract (PTE) on the serum concentration of 1,25-dihydroxyvitamin D (1,25[OH]2D), 24,25-dihydroxyvitamin D (24,25[OH]2D), 25,26-dihydroxy vitamin D (25,26[OH]2D) and cAMP, and the urinary excretion of calcium, phosphorus, and cAMP in two normal adult subjects, and in a girl with vitamin D-dependent rickets. The concentration of 1,25[OH]2D was markedly decreased even when she was receiving a daily dose of 25,000 IU of ergocalciferol. PTE infusion resulted in a prompt and distinct increase in the serum levels and the urinary excretion of cAMP in the patient and control subjects. In the control subjects the serum concentration of 1,25[OH]2D increased after the PTE infusion, whereas there was no response in the patient with vitamin D-dependent rickets. The two other dihydroxylated metabolites of vitamin D showed no consistent response to the PTE infusion in the control subjects or the patient. The patient showed no phosphaturic response to PTE while she was receiving high-dosage ergocalciferol treatment. By contrast, when the patient was re-studied after therapy with 1 alpha-hydroxyvitamin D, PTE infusion resulted in an increase in urinary phosphate excretion. These findings might lend support for the notion that 1,25[OH]2D has an effect on tubular phosphate resorption and has a permissive role in the phosphaturic effect of parathyroid hormone. The present findings also confirm that the formation of 1,25[OH]2D is impaired in vitamin D-dependent rickets and indicate that the renal 25-hydroxyvitamin D-1 alpha-hydroxylase is unresponsive to the stimulatory effect of parathyroid hormone in this condition.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗