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K S Halvorsen

Publications and source records attributed to K S Halvorsen.

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Plasma and red cell folate values and folate requirements in formula-fed premature infants.

Plasma and red cell folate concentrations (lactobacillus casei activity) and other pertinent blood values have been studied during the 1st year of life in 41 premature infants (mean gestational age 31.6, range 26-35 weeks). They were formula-fed, 48.5 nmol (21 micrograms) folate per 1, from 1 month of age. The infants were divided into two groups according to their birth weights (BW): group A, BW less than or equal to 1750 g and group B, BW greater than 1750 g, respectively. One-half of the infants in each group received an extra 113.5 nmol (50 micrograms) folic acid daily. The premature infants were compared with 35 breast-fed term infants considered to have an optimal folate status. The infants not receiving folic acid supplementation had low plasma and red cell folate concentrations during the first months of life, while those receiving supplementation had values comparable to the breast-fed infants. No significant differences in the gain in weight and increase in length were observed when the folic acid supplemented infants in group A were compared with the non-supplemented infants. However, in the case of group B a significant increase in length and a somewhat greater weight gain were observed for infants with folic acid supplementation in comparison with those not given extra folate. No significant differences were observed between the haemoglobin, RBC and VPRC values in the folic acid supplemented and non-supplemented infants. It is estimated that the optimal folate intake during the first months of life in formula-fed premature infants is about 150 nmol (65 micrograms) per day. This amount is higher than previously recommended. The infants from all groups had a folate intake similar to, or above, the minimal daily requirement needed for erythropoiesis.

Adult

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