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Biomedical subjects

T Markestad

Publications and source records attributed to T Markestad.

At least 109 records · Page 6Linked to original sources
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

Serum concentrations of vitamin D metabolites in exclusively breast-fed infants at 70 degrees north.

The effect of prolonged breast-feeding on the serum concentrations of vitamin D metabolites, calcium, phosphate, and alkaline phosphatase was studied longitudinally in 7 infants from Northern Norway. They were exclusively breast-fed for a median of 7 1/2 months. Three of the mothers were supplemented with vitamin D throughout lactation. All but one of the infants had 25-hydroxyvitamin D (25-OHD) levels in the rachitic range (less than 20 nmol/l) on at least one occasion. Vitamin D supplementation of the mother had no apparent effect on the infants' 25-OHD levels, but the values increased during summer. The infant who had the lowest 25-OHD levels also had decreased 1,25-dihydroxyvitamin D (1,25-(OH)2D) concentrations, while the others maintained 1,25-(OH)2D levels within normal limits. 24,25-(OH)2D concentrations were undetectable when the 25-OHD levels were below 35 nmol/l, but the two metabolites were closely correlated for higher values of 25-OHD. Low 25-OHD levels were associated with decreased phosphate concentrations at 6 months. The calcium levels were normal throughout the study period of one year, as were all but two of the alkaline phosphatase values. Although none of the infants had clinical or biochemical evidence of rickets, the results suggest that the vitamin D supply from human milk is inadequate, and that routine vitamin D supplementation is advisable for breast-fed infants who are deprived of sunlight exposure.

Alkaline Phosphatase↗
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↗
PubMed1984

Serum concentrations of vitamin D metabolites in maternal and umbilical cord blood of Libyan and Norwegian women.

The serum concentrations of the vitamin D metabolites 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D (1,25-(OH)2D) and 24,25-dihydroxyvitamin D (24,25-(OH)2D), and vitamin D binding protein, calcium, phosphate and alkaline phosphatase were determined in 19 grand multiparous Libyan women at delivery, and in the umbilical cord blood of 14 of their babies. The results were compared with similarly collected data from 22 vitamin D-supplemented Norwegian mother-infant pairs. The median 25-OHD and 24,25-(OH)2D concentrations were significantly lower for the Libyan group (maternal 25-OHD: 34 vs 112 nmol/l; cord 25-OHD: 20 vs 76 nmol/l; maternal 24,25-(OH)2D: 0.6 vs 4.1 nmol/l; cord 24,25-(OH)2D: 0.4 vs 2.7 nmol/l, P less than 0.001 for all differences). In both groups the 25-OHD and 24,25-(OH)2D levels in maternal as well as in cord blood were closely associated (P less than 0.001). The median 1,25-(OH)2D level was similar for the two maternal groups (198 vs 194 pmol/l), but slightly lower for the Libyan than for the Norwegian cord samples (80 vs 93 pmol/l, P = 0.04). A calculated free 1,25-(OH)2D concentration (not bound to vitamin D binding protein) did not differ between the two maternal or cord groups. Calcium and phosphate concentrations were similar for the respective maternal and cord samples, while the median alkaline phosphatase level of cord blood was slightly higher for the Libyan group (P = 0.04). The results suggest that calcium and phosphate homoeostasis of pregnant women and their fetuses can be maintained despite wide variations in vitamin D supply and numerous repeated pregnancies.(ABSTRACT TRUNCATED AT 250 WORDS)

25-Hydroxyvitamin D 2↗
PubMed1983

Plasma concentrations of vitamin D metabolites in unsupplemented breast-fed infants.

Plasma concentrations of the vitamin D metabolites 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, 24,25-dihydroxyvitamin D and 25,26-dihydroxyvitamin D were determined in 12 solely breast-fed infants 4 days and 6 weeks after birth. They were not exposed to sunlight, but the mothers received an average of 600 IU vitamin D2 per day during the study period. The mothers' 25-hydroxyvitamin D levels did not change significantly (medians 42 and 58 nmol/l), but the median level dropped from 26 to 15 nmol/l in the infants (P less than 0.001). There was a close correlation between maternal and infant levels at 4 days (r = 0.95). The babies with the highest initial levels showed the most marked decrease by 6 weeks. The median concentrations of 24,25-dihydroxyvitamin D and 25,26-dihydroxyvitamin D decreased similarly from 1.7 to 0.8 and 0.63 to 0.35 nmol/l respectively, (P less than 0.001). The 1,25-dihydroxyvitamin D levels were within normal limits as were plasma calcium, phosphorus, and alkaline phosphatase. The data suggest that fetal stores of vitamin D may be rapidly depleted, and that breast milk may be inadequate as the only source of vitamin D, even for breast-fed infants of vitamin D-supplemented mothers.

Alkaline Phosphatase↗
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 season and vitamin D supplementation on plasma concentrations of 25-hydroxyvitamin D in Norwegian infants.

Plasma concentrations of 25-hydroxyvitamin D (25OHD) were determined in 81 vitamin D supplemented or unsupplemented infants at the end of winter. The values were compared with maternal levels and with concentrations found in 22 unsupplemented infants at the end of summer. The 25OHD levels of the neonates were lower, but closely related to maternal values (r = 0.95, p less than 0.0005). Unsupplemented breast-fed infants had lower 25OHD levels at 6 weeks than at 4 days (16 +/- 7 vs. 32 +/- 15 nmol/l, mean +/- 1 SD, p less than 0.0005). The mean 25OHD level of vitamin D supplemented 6-12 months old infants was intermediate between those of the unsupplemented nursed groups and the unsupplemented children studied during summer (53 +/- 28 vs. 85 +/- 28 nmol/l, p less than 0.0005). Six weeks old infants who had received a milk formula containing 400 IU vitamin D3 per liter had levels similar to the latter group (92 +/- 21 nmol/l). The data suggest that the vitamin D stores acquired during fetal life, or from ultraviolet light exposure during the summer, may be inadequate to maintain safe levels of 25OHD throughout the winter, but that a daily supplement of 400 IU is adequate to establish concentrations in the summer range.

Breast Feeding↗
PubMed1983

Plasma concentrations of 1,25-dihydroxyvitamin D, 24,25-dihydroxyvitamin D, and 25,26-dihydroxyvitamin D in the first year of life.

Plasma concentrations of 1,25-dihydroxyvitamin D [1,25-(OH)2D], 24,25-dihydroxyvitamin D [24,25-(OH)2D], and 25,26-dihydroxyvitamin D [25,26-(OH)2D] were determined in 80 healthy infants of 4 days, 6 weeks, 6 months, and 12 months of age. The 4-day-old babies received breast milk, while the 6-week-old infants were either exclusively breast or formula fed. The older infants were on mixed diets and received daily vitamin D supplements. The levels were analyzed with regard to age and the concentrations of 25-hydroxyvitamin D (25OHD), calcium, phosphate, magnesium, and alkaline phosphatase and were compared with adult levels of vitamin D metabolites. The median 1,25-(OH)2D concentration was highest at 4 days of age and lowest at 6 weeks, but, except for the 6-week-old group, all had higher levels than the adults (6 weeks, P less than 0.1; others, P less than 0.01). 1,25-(OH)2D and 25OHD levels showed significant correlation only at 4 days (r = 0.74; P less than 0.0005), and there were no consistent relationships between 1,25-(OH)2D and the other variables. The median concentration of 24,25-(OH)2D was lower (P less than 0.01), while the 25,26-(OH)2D value was similar to that in the adults. Both were, however, positively related to the 25OHD level [24,25-(OH)2D, r = 0.82; 25,26-(OH)2D, r = 0.65; P less than 0.0005], as in the adults. The ratio of 24,25-(OH)2D to 25OHD was lower beyond 4 days of life than in the adults (medians, 3.4% vs. 5.1%; P less than 0.02). The data suggest that 1,25-(OH)2D synthesis has relative priority over 24,25-(OH)2D production during infancy compared with that in adulthood.

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↗
PubMed1981

Vitamin D metabolism in idiopathic infantile hypercalcemia.

A 9-month-old boy who had the mild form of idiopathic infantile hypercalcemia was observed for 18 months. During the initial hypercalcemic stage, the serum concentration of 25-hydroxyvitamin D was normal. Urinary levels of cyclic adenosine monophosphate (cAMP) were low, and the serum concentrations of the dihydroxyl metabolites of vitamin D were appropriate to the high serum calcium concentration, with low 1,25-dihydroxyvitamin D and relatively high 24,25- and 25,26-dihydroxyvitamin D levels. Throughout the study period, there was a close positive correlation between the magnitude of the urinary cAMP excretion and the serum level of 1,25-dihydroxyvitamin D. The results indicate that excessive vitamin D intake leading to high serum levels of 25-hydroxyvitamin D are not decisive factors in the pathogenesis of idiopathic infantile hypercalcemia.

24,25-Dihydroxyvitamin D 3↗