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Biomedical subjects

R S Lorenc

Publications and source records attributed to R S Lorenc.

At least 55 records · Page 3Linked to original sources
PubMed1989

Endogenous, cutaneous vitamin D synthesis stimulation as an effective way of improving the vitamin D status in children with hepatobiliary malfunctions.

Repetitive (5 days) ultraviolet treatment was used to improve vitamin D status of 26 pediatric patients suffering from different hepatobiliary disorders. The treatment resulted in a significant improvement of patients' vitamin D and 25-hydroxyvitamin D levels regardless of their disease and other factors such as increased blood bilirubin content or jaundice. Presence of a dependence between the increase in 25-hydroxyvitamin D concentrations after treatment and its original levels was confirmed.

Adolescent↗
PubMed1989

[Changes in vitamin D metabolism in children following partial intestinal resection].

Six children (five after partial intestinal resection, one after colectomy) were studied with respect to absorption and metabolism of vitamin D. The results showed decreased 25-OH-D3 serum concentrations below 20 ng/ml (in two patients even below 10 ng/ml), possibly due to disturbed enterohepatic circulation of vitamin D metabolites.

Adolescent↗
PubMed1985

Rapid method for measuring physiological concentrations of 25-hydroxyvitamin D levels in blood serum.

A new single-step Extrelut column procedure for obtaining the 25-hydroxyvitamin D extract, suitable for a direct radiocompetitive test, is described. Separation of 0.1 ml of serum, on a small Extrelut column and radioassay allows a rapid, sensitive and accurate determination of 25-hydroxyvitamin D concentration. The detection limit of the determination was 2 nmol/l (0.8 microgram/l) of serum. The recovery of 250HD3 added to serum was 99-108%. Intra-assay and interassay CV values were 10 and 14%, respectively. Although the method does not permit separation of dihydroxylated metabolites of vitamin D from 25-hydroxyvitamin D, it is useful in clinical practice.

Binding, Competitive↗
PubMed1981

25-Hydroxyvitamin D3 metabolism in the pregnant rat: maternal-fetal relationship.

Metabolism of 3H-25OHD3 was studied in pregnant, D-deprived rats and their fetuses at 21 days' gestation. Significant changes in the circulating levels of 3H-24,25(OH)2D3 and 3H-1,25(OH)2D3 in maternal and fetal plasma occurred from 4 to 12 h after the administration of 233 ng of 3H-25OHD3. 3H-1,25(OH)2D3 appeared before 3H-24,25(OH)2D3 in both the mother and fetuses. Maternal plasma contained more 3H-1,25(OH)2D3 than fetal plasma and, contrariwise, fetal plasma contained more 3H-24,25(OH)2D3 than maternal plasma. Maternal nephrectomy studies showed that the in vivo synthesis of 3H-24,25(OH)2D3 at 6 h was dependent on circulating levels of 3H-1,25(OH)2D3. These results revealed aspects of maternal-fetal metabolism of 25OHD3 similar to those in the non-pregnant state as well as others unique to pregnancy.

Animals↗
PubMed1979

Evidence for extra-renal 1 alpha-hydroxylation of 25-hydroxyvitamin D3 in pregnancy.

The kidneys are thought to be the only organs capable of 1 alpha-hydroxylation of vitamin D and its metabolites. We have examined the in vivo conversion of 3H-(25,26)-25-hydroxyvitamin D3(25OHD3) to 3H-(25,26)-1 alpha,25-dihydroxyvitamin D3 [1 alpha,25(OH)2D3] in vitamin D-deficient, pregnant and nonpregnant rats. As expected, nephrectomy of nonpregnant, vitamin D-deficient rats prevented the conversion of 25OHD3 to 1 alpha,25(OH)2D3. In contrast, nephrectomy of pregnant, vitamin D-deficient rats reduced but did not abolish the formation of 1 alpha,25(OH)2D3 from its precursor. The identity of the radioactive metabolite formed from 3H-25OHD3 which circulated in nephrectomized, pregnant rats was established as 1 alpha,25(OH)2D3 by comigration with synthetic 1 alpha,25(OH)2D3 on high-pressure liquid chromatography. The simultaneous absence of 1 alpha,25(OH)2D3 in the fetal kidneys indicated that the site of 1 alpha-hydroxylation after nephrectomy of the pregnant rat was probably extra-renal in origin. Two sites of 1 alpha-hydroxylation of 25OHD3, one renal and the other extra-renal, either fetoplacental or maternal, may exist in the pregnant, vitamin D-deficient rat.

Animals↗
PubMed1978

The intestinal phosphate transport under condition of experimental hypercalcemia.

The analysis of the serum calcium and phosphate level changes in intact Vitamin D--dosed animals showed the increasing serum calcium values without any concomitant change in serum phosphate concentration. The observed discrepancy of intestinal phosphate transport in vitro and in vivo studies together with the effect of Vitamin D towards normalizing serum phosphate level in TPTX Vitamin D--dosed animals suggest the presence of Vitamin D as some phosphate regulatory factor. The participation of the possible role of 25 OH D3 in the observed phenomenon is under current investigations. In PTH supressed hypercalcemic conditions we did not reproduce, with the usage of 1alpha--OH D3, the regulatory effect of 1,25 (OH) 2D3 described by Garabedian et al. /1/.

Animals↗
PubMed1975

Phosphatemic action of 1,25-dihydroxyvitamin D3.

The action of a single intraperitoneal injection of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) was investigated in thyroparathyroidectomized (TPTX) vitamin D-deficient phosphate-depleted rats. After 14 h, plasma inorganic phosphorus (Pi) was significantly greater in animals receiving 1,25(OH)2D3 than in D-deficient controls, but urinary Pi excretion was very low in both groups and not significantly different in the rats given 1,25(OH)2D3. Clearance studies indicated that the D-deficient controls reabsorbed more than 99% of their filtered Pi. Avid Pi reabsorption continued even after the infusion of sufficient phosphate to raise the plasma and filtered Pi to approximately 3 times normal. Fractional calcium excretion (FECa) exceeded fractional sodium excretion (FENa) by severalfold, but FECa decreased strikingly during phosphate infusion. In animals that manifested a substantial elevation of plasma Pi after 1,25(OH)2D3, FECa was significantly less than in D-deficient controls. Therefore, the increase in plasma Pi following 1,25(OH)2D3 administration occurs independently of any effect on renal Pi reabsorption and may be responsible, at least in part, for the amelioration of hypercalciuria after 1,25(OH)2D3 treatment.

Animals↗