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At least 343 records · Page 19Linked to original sources
PubMed1996

Successful treatment of secondary hyperparathyroidism in hemodialysis patients with oral pulse 1-alpha-hydroxy-cholecalciferol therapy.

We have used high-dose oral pulse therapy with 1 alpha-hydroxycholecalciferol (1 alpha-OH-D3) to treat 40 hemodialysis patients suffering form secondary hyperparathyroidism. Forty patients with intact parathyroid hormone (PTH) levels of > 150 pg/ml were treated with 4 micrograms oral 1 alpha-OH-D3 twice weekly for 1 year. The mean PTH level was 515 +/- 50 pg/ml prior to treatment, which fell to 191 +/- 42 pg/ml after 6 months of treatment (p < 0.00001), and to 164 +/- 39 pg/ml after 12 months of treatment. Patients with very high PTH levels (> 800 pg/ml) suppressed less well than patients with lower levels (150-300 pg/ml). The therapeutic end point of PTH < 100 pg/ml was achieved in 23 patients (58%). The main side effect of the treatment was hypercalcemia, but this was symptomatic in only 3 patients, all above the age of 70 years. In summary, oral high-dose pulse therapy with 1 alpha-OH-D3 was highly effective in suppressing PTH levels in hyperparathyroid hemodialysis patients, and side effects were relatively few.

Administration, Oral↗
PubMed1984

Marked suppression of secondary hyperparathyroidism by intravenous administration of 1,25-dihydroxy-cholecalciferol in uremic patients.

Current evidence suggests that administration of 1,25(OH)2D3 to patients with chronic renal insufficiency results in suppression of secondary hyperparathyroidism only if hypercalcemia occurs. However, since the parathyroid glands possess specific receptors for 1,25(OH)2D3 and a calcium binding protein, there is considerable interest in a possible direct effect of 1,25(OH)2D3 on parathyroid hormone (PTH) secretion independent of changes in serum calcium. Recent findings indicate substantial degradation of 1,25(OH)2D3 in the intestine, therefore, it is possible that while oral administration of the vitamin D metabolite increases intestinal calcium absorption, the delivery of 1,25(OH)2D3 to peripheral target organs may be limited. We therefore compared the effects of orally or intravenously administered 1,25(OH)2D3 on the plasma levels of 1,25(OH)2D3 and the effects of these two modes of treatment on PTH secretion. Whereas oral administration of 1,25(OH)2D3 in doses adequate to maintain serum calcium at the upper limits of normal did not alter PTH levels, a marked suppression (70.1 +/- 3.2%) of PTH levels was seen in all 20 patients given intravenous 1,25(OH)2D3. Temporal studies suggested a 20.1 +/- 5.2% decrease in PTH without a significant change in serum calcium with intravenous 1,25(OH)2D3. In five patients the serum calcium was increased by the oral administration of calcium carbonate, the decrement in serum i-PTH was only 25 +/- 6.65% when compared with 73.5 +/- 5.08% (P less than 0.001) obtained by the administration of intravenous 1,25(OH)2D3. Thus, a similar serum calcium achieved by intravenous 1,25(OH)2D3 rather than calcium carbonate has a greater suppressive effect in the release of PTH. These studies indicate that 1,25(OH)2D3 administered intravenously rather than orally may result in a greater delivery of the vitamin D metabolite to peripheral target tissues other than the intestine and allow a greater expression of biological effects of 1,25(OH)2D3 in peripheral tissues. The use of intravenous 1,25(OH)2D3 thus provides a simple and extremely effective way to suppress secondary hyperparathyroidism in dialysis patients.

Administration, Oral↗
PubMed1987

The effect of 1,25-dihydroxy-cholecalciferol on the TRH induced TSH release in rats.

The effect of 1,25-dihydroxy-vitamin D3 (1,25-(OH)2-D3) on the TRH induced TSH release was investigated. Wistar rats were injected with 1,25-(OH)2-D3 (0.05 microgram/kg/day) for three days, and TRH was injected iv on the third day. Blood was drawn every 10 min during the following 40 min, and TSH was determined. The TSH release was significantly higher in rats treated with 1,25-(OH)2-D3 than in controls. The rats treated with 1,25-(OH)2-D3 were hypercalcaemic and thus, in order to find out if the effect was mediated through hypercalcaemia rats treated as above, were infused with EDTA (30 mg/kg/100 min) starting 60 min before the TRH test. This treatment made the rats normocalcaemic, and the significant increase in the TSH release was still seen in the 1,25-(OH)2-D3 treated rats as compared to controls. The results thus indicate that 1,25-(OH)2-D3 enhances the TRH induced TSH release and that the effect is not mediated through an increase in the serum calcium concentration at the time of the TRH test. In order to find out if the effect could be mediated by changes in intracellular calcium the rats were treated with the calcium antagonist verapamil (25 mg/kg/day) and the adrenergic blocker propranolol (5 mg/kg/day) alone or together with 1,25-(OH)2-D3. In rats treated with verapamil or propranolol alone or 1,25-(OH)2-D3 + propranolol, no effect was observed on the TRH induced TSH release. Verapamil + 1,25-(OH)2-D3 significantly increased the TSH release as compared to both controls and rats treated with 1,25-(OH)2-D3 alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Treatment of psoriasis by the topical application of the novel cholecalciferol analogue calcipotriol (MC 903)

Calcipotriol (the synthetic compound MC 903) is a structural analogue of naturally occurring, biologically active calcitriol. Calcipotriol and calcitriol (1,25-dihydroxy vitamin D3) show similar receptor binding and comparable effects on cell differentiation. However, calcipotriol seems to be at least 100 times less potent in its effects on calcium metabolism. In a double-masked study involving 50 patients with psoriasis vulgaris, the efficacy and tolerability of ointments containing various calcipotriol concentrations (25, 50, or 100 micrograms/g) or the vehicle alone were compared in a study involving a right-left, within-patient randomized design. Patients were treated twice daily for 8 weeks. Marked improvement was seen in 40% of the patients treated with the 25-micrograms/g concentration of calcipotriol in 63% of patients treated with the 50-micrograms/g concentration, and in 88% treated with the 100-micrograms/g concentration. No patient treated with placebo had more than slight improvement. Five patients developed facial dermatitis during the study. The serum levels of ionized calcium were unchanged. This study demonstrates that calcipotriol ointment provides an effective and well-tolerated treatment of psoriasis vulgaris.

Administration, Topical↗
PubMedDate not supplied

[Effects of alpha-calcidiol (1 alpha-hydroxy-cholecalciferol) on the serum levels of osteocalcin in involutional osteoporosis].

We have examined the effects of 1 alpha-hydroxycolecalciferol (1 alpha) (1.5 micrograms for 5 days) on serum osteocalcin (OC) and other parameters of bone and mineral metabolism in 20 osteoporotic women and 11 age-matched normal women. After 1 alpha administration, a statistically significant (p less than 0.01) increase of serum OC, calcium and phosphate and urinary calcium and hydroxyproline was observed. In contrast, alkaline phosphatase was unchanged. There was no significant difference between normal and osteoporotic women in the changes of any of the parameters we monitored. In particular, OC increased in a comparable way in both groups. Thus, by means of an index that reflects the global activity of the skeleton, we could not find any apparent defect of osteoblastic responsiveness to the drug in osteoporotic subjects.

Aged↗
PubMed1978

[The action of vitamin D2 and of 25-hydroxy-cholecalciferol on calcemia and urinary calcium excretion in the alcoholic cirrhotic (author's transl)].

In 2 similar groups of alcoholic cirrhotics with definite hepatic failure, the results of the oral administration of 25-hydroxycholecalciferol and of vitamin d2 on calcemia and urinary calcium excretion were studied. 25-hydroxycholecalciferol definitely increases calcemia and urinary calcium excretion, this action being superior to that of vitamin D2. This action which occurs, at least in part, by an increase in intestinal calcium absorption, deomonstrated the true nature of the "hepatic block" of vitamin D2 in alcoholic cirrhosis and the value of the administration of 25-hydroxycholecalciferol.

Calcium↗
PubMed1986

The role of ultimobranchial bodies in the modulation of the response of chick embryos to 1,25-dihydroxy-cholecalciferol.

Ultimobranchial bodies (UBBs) were dissected from 17-day-old chick embryos and grafted onto the chorioallantoic membrane of 8-day-old embryos. The embryos with UBB grafts as well as sham-grafted controls were injected on the 10th day of incubation with 100 ng 1,25(OH)2D3 dissolved in ethyl alcohol or with an equal volume of ethyl alcohol alone; embryos were sacrificed on the 13th day. Grafted UBBs showed ultrastructural characteristics typical of actively secreting glands. A histological study of the tibiae from all embryos showed that while the grafted embryos responded to the injection of 1,25(OH)2D3 with a peripheral rim of undermineralized bone trabeculae, sham-grafted embryos never did so. These results confirm the original hypothesis that the presence of differentiated UBBs is a precondition for the production of undermineralized bone (osteoid) by 1,25(OH)2D3. In a second series of experiments, similarly treated embryos were sacrificed on the 10th, 11th, 12th and 13th day; the levels of calcium and inorganic phosphate were determined in their blood. The injection of 1,25(OH)2D3 produced in all embryos hypercalcaemia and hypophosphataemia. However, the hypophosphataemic response was more prolonged in the embryos with UBB grafts than in sham-grafted ones. These results suggest that the grafted UBBs prolonged the hypophosphataemic response, probably by secreting calcitonin and thus reducing the rate of bone resorption. It is also probable that the prolonged hypophosphataemia produced or contributed to the undermineralization of the peripheral (subperiosteal) trabeculae.

Animals↗
PubMed1977

[Synthetic and biological activity of 25R and 25S diastereoisomers of dihydroxy-25,26 cholecalciferol (25,25(OH)2D3)].

The separation of 5-cholestene-3 beta, 25 (RS), 25-triol 3,26-diacetate into the diastereoisomers 25R and 25S by means of high pressure liquid chromatography (HPLC) is described. Their absolute configuration cannot be yet established. The less polar diastereoisomer is arbitrarily called 25 zeta1 and the more polar one 25 zeta2. Bromination, dehydrobromination and ultraviolet irradiation conducted to 25 zeta1, 26(OH2D3 and 25 zeta2, 26(OH)2D3 respectively. Their biological activity is described.

Animals↗
PubMed1984

1-alpha-OH-cholecalciferol (1-alpha-OHD3) and low phosphate diet in predialysis chronic renal failure: effects on renal function and on secondary hyperparathyroidism.

The effect of 1-alpha-OHD3 on the rate of decline of renal function was studied in 18 patients with predialytic chronic renal failure. 9 patients with serum creatinine 4.19 +/- 1.63 mg/dl, were treated with 1-alpha-OHD3 0.4 +/- 0.11 micrograms/day and a low phosphate diet and 9 patients, with serum creatinine 3.69 +/- 1.24 mg/dl, received the low phosphate diet alone. In the first group retrospectively in 8 patients up to 3-44 months and prospectively in all patients reciprocal values of serum creatinine levels fell linearly with time. Comparison of the slopes of the regression lines before and following the start of treatment did not show statistical differences in 6 cases, in 1 case the decline of renal function improved significantly and in 1 case it became positive. Serum calcium increased significantly (p less than 0.025), alkaline phosphatase decreased (p less than 0.005) and serum iPTH decreased in 6 of 8 cases. In the low phosphate diet group, serum calcium, alkaline phosphatase did not change while iPTH increased in 8 of 9 cases. The rate of decline of renal function before treatment in 3 cases did not improve after the institution of the diet. In conclusion improvement or prevention of secondary hyperparathyroidism in predialytic chronic renal failure can be achieved with daily doses of less than or equal to 0.5 micrograms 1-alpha OHD and a low phosphate diet. The small increment in serum calcium levels induced by the treatment did not accelerate the deterioration of renal function while showing a better control of alkaline phosphatase and serum iPTH than the low phosphate diet alone.

Adult↗
PubMed1998

Rat adipose tissue rapidly accumulates and slowly releases an orally-administered high vitamin D dose.

We investigated the effect of oral high-dose cholecalciferol on plasma and adipose tissue cholecalciferol and its subsequent release, and on plasma 25-hydroxyvitamin D (25(OH)D). Female Wistar rats (n 126) received 37.5 micrograms cholecalciferol/d for 14 d and were subsequently studied for a further 88 d. Two subgroups of eighteen rats each were fasted for 3 d immediately after treatment (days 14-17) and at the end of the study (days 98-101). During treatment, plasma cholecalciferol increased rapidly to reach a steady-state. Plasma 25(OH)D and adipose tissue cholecalciferol increased linearly for 1-2 d after treatment. Serum Ca and inorganic phosphate also increased. Subsequently half-lives of plasma cholecalciferol and 25(OH)D, and perirenal and subcutaneous adipose tissue were: 1.4, 22.5, 97.5 and 80.9 d respectively. Fasting, as compared with ad libitum feeding, caused increased plasma free fatty acids, weight loss up to 14% and increased adipose tissue cholecalciferol (nmol/g wet weight). It did not affect plasma cholecalciferol immediately after cholecalciferol treatment, but raised plasma 25(OH)D. Fasting at the end of the study decreased plasma cholecalciferol and increased plasma 25(OH)D. We conclude that orally-administered cholecalciferol rapidly accumulates in adipose tissue and that it is very slowly released while there is energy balance. Fasting causes preferential loss of triacylglycerols from adipose tissue, as opposed to cholecalciferol, but nevertheless augments plasma 25(OH)D. Adipose tissue may act as a 'buffer to functional vitamin D status' by preventing, to a certain extent, unregulated production of 25(OH)D from dietary vitamin D, and by slowly releasing vitamin D under fasting conditions.

Adipose Tissue↗
PubMed1987

Low dietary calcium reduces 25-hydroxycholecalciferol in plasma of rats.

We investigated whether dietary factors that are known to increase 1,25-(OH)2-cholecalciferol production can deplete plasma 25-OH-cholecalciferol. Plasma concentration of 25-OH-cholecalciferol, its metabolism in vivo and activities of renal mitochondrial 25-OH-cholecalciferol 1-hydroxylase (1-OHase) and 25-OH-cholecalciferol 24-hydroxylase (24-OHase) were measured in rats fed various amounts of calcium (Ca) and phosphorus (P). All diets contained 5 micrograms (200 IU) cholecalciferol per 100 g. For rats fed the "normal" diet (0.7% Ca and 1.2% P) the mean plasma 25-OH-cholecalciferol level was 11.0 +/- 0.8 nmol/L, and the mean 1-OHase activity was 30 +/- 5 fmol/(mg X min). All rats fed the low Ca (0.014%) diet had 1-OHase activities above 200 fmol/(mg X min) and undetectable plasma 25-OH-cholecalciferol levels (less than 2.5 nmol/L). The chi-square test interrelating plasma 25-OH-cholecalciferol and dietary Ca showed statistical significance (P less than 0.001). The high activity of 1-OHase that resulted from dietary Ca restriction increased utilization of 25-OH-cholecalciferol to the point of causing depletion of this metabolite in the circulation.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗