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At least 505 records · Page 28Linked to original sources
PubMed1997

1alpha-hydroxyvitamin D2 partially dissociates between preservation of cancellous bone mass and effects on calcium homeostasis in ovariectomized rats.

Vitamin D metabolites can prevent estrogen depletion-induced bone loss in ovariectomized (OVX) rats. Our aim was to compare the bone-protective effects of 1alpha,25-dihydroxyvitamin D3 (1, 25(OH)2D3), 1alpha,25-dihydroxyvitamin D2 (1,25(OH)2D2), 1alpha-hydroxyvitamin D3 (1alpha(OH)D3), and 1alpha-hydroxyvitamin D2 (1alpha(OH)D2) in OVX rats. 1alpha(OH)D3 and 1alpha(OH)D2 are thought to be activated in the liver to form 1,25(OH)2D3 and 1, 25(OH)2D2, respectively. Forty-four 12-week-old female Fischer-344 rats were either OVX or sham-operated (SHAM). Groups of OVX rats (n = 7 each) received vehicle alone, 1,25(OH)2D3, 1,25(OH)2D2, 1alpha(OH)D3, or 1alpha(OH)D2, starting 2 weeks after surgery. All vitamin D metabolites were administered orally at a dose of 15 ng/day/rat. Urine and blood samples were collected 6, 9, 12, and 16 weeks after surgery. Serum samples were analyzed for total calcium and phosphate. Calcium, phosphate, creatinine, and free collagen cross-links (ELISA) were determined in urine. After tetracycline double labeling, the rats were sacrificed 16 weeks postsurgery, and the proximal tibiae and the first lumbar vertebrae were processed undecalcified for static and dynamic bone histomorphometry. 1,25(OH)2D3 and, to a slightly lesser extent, 1,25(OH)2D2 elevated vertebral cancellous bone mass in OVX rats to a level beyond that observed in SHAM animals, and both compounds increased serum calcium and urinary calcium excretion to similar extents. 1alpha(OH)D3 and 1alpha(OH)D2 resulted in a 64% and 84%, respectively, inhibition of ovariectomy-induced vertebral cancellous bone loss. In the proximal tibial metaphysis, all vitamin D metabolites tested could only partially prevent post-OVX trabecular bone loss, with a tendency for 1alpha(OH)D3 to be the least active compound. The effects of 1alpha(OH)D3 and 1alpha(OH)D2 on calcium homeostasis differed markedly, however. The mean increase in urinary calcium excretion over the whole experiment was fivefold for 1alpha(OH)D3, whereas the corresponding increase for 1alpha(OH)D2 was only twofold. We conclude that, compared with 1alpha(OH)D3, 1alpha(OH)D2 combined at least equal or higher bone-protective activity in OVX rats with distinctly less pronounced effects on calcium homeostasis. This effect was not due to a differential action of the corresponding main activation products, 1,25(OH)2D3 and 1,25(OH)2D2.

Animals↗
PubMed2003

19-nor-1alpha,25-dihydroxyvitamin D(2) (paricalcitol): effects on clonal proliferation, differentiation, and apoptosis in human leukemic cell lines.

PURPOSE: 19-Nor-1alpha,25-dihydroxyvitamin D(2) (paricalcitol) is an analogue of 1,25(OH)(2)D(3) with reduced calcemic effects that is approved for the suppression of parathyroid hormone in chronic renal failure. Paricalcitol has recently been reported to have anticancer activity in prostate cancer. In order to explore paricalcitol as a potential agent against leukemia, we tested its effects on HL-60 and U937 leukemia cell lines. METHODS: We studied cellular differentiation via expression of CD11b and CD14 surface antigens using flow cytometry, and via the nitroblue tetrazolium (NBT) assay. Cell cycle was analyzed using propidium iodide staining. Apoptosis was assessed with the annexin V assay. Cellular proliferation was determined via colony inhibition on semisolid medium. RESULTS: Paricalcitol induced the maturation of HL-60 and U937 cells, as shown by increased expression of CD11b differentiation surface antigen. CD14 showed increased expression in HL-60 but not in U937 cells. After exposure to paricalcitol at 10(-8) M for 72 h, the ability of HL-60 cells to reduce NBT was markedly increased. Conversely, U937 cells were unchanged. Paricalcitol inhibited colony formation of both HL-60 and U937 cell lines in semisolid medium after a 10-day incubation (estimated IC(50) of 3x10(-8) M in HL-60 cells and 4x10(-8) M in U937 cells). Paricalcitol at 10(-8) M and 10(-7) M caused a significant dose- and time-dependent increase of apoptosis in HL-60 cells ( P<0.05). In both HL-60 and U937 cells, exposure to 10(-7) M paricalcitol for 72 h increased the number of cells in G(0)/G(1) phase, and decreased the number of cells in S phase. CONCLUSIONS: Paricalcitol inhibits colony formation, induces maturation and causes cell cycle arrest in HL-60 and U937 cells. Additionally, paricalcitol induces apoptosis in HL-60 cells. These findings support the further evaluation of paricalcitol as an antileukemia agent.

Antineoplastic Agents↗
PubMed2005

Are new vitamin D analogues in renal bone disease superior to calcitriol?

Progression of chronic kidney disease is associated with an early reduction in serum calcitriol levels; thus, therapy with calcitriol should be initiated early in the course of chronic kidney disease to prevent the development of secondary hyperparathyroidism. Initial studies demonstrated a potential role of calcitriol in the prevention of growth retardation in children with chronic kidney disease prior to dialysis. But the optimal parathyroid hormone (PTH) levels that will maximize growth response during calcitriol treatment remain to be defined. Therapy with calcitriol has been shown to control the biochemical and skeletal manifestations of secondary hyperparathyroidism, but patients developed hypercalcemia, hyperphosphatemia and adynamic osteodystrophy. Thus, new vitamin D analogues with a lower hypercalcemic response have been developed. Although comparative studies are lacking, current evidence indicates that these new active vitamin D sterols (19-nor-paracalcitol and doxercalciferol) adequately control secondary hyperparathyroidism with minimal changes in serum calcium and phosphorus levels during treatment with calcium-containing binders. The long-term effect of such therapies on the skeleton and the process of vascular calcifications remain to be evaluated.

Calcitriol↗
PubMed2006

Paricalcitol versus calcitriol treatment for hyperparathyroidism in pediatric hemodialysis patients.

Secondary hyperparathyroidism (SHPT) remains a treatment dilemma in pediatric dialysis patients. Recent experience with paricalcitol (P), a vitamin D analogue, in adults with SHPT has shown equal efficacy and improved survival compared to traditional treatment with calcitriol (C). We present our experience with (C) compared to (P) treatment in our pediatric dialysis patients with SHPT. Twenty-one patients (mean age 11.5+/-5 years) with SHPT (intact parathyroid hormone (iPTH) averaging 1,228+/-496 pg/ml) were studied. Seventeen received (C) followed by (P); while an additional four were treated with either (C=1) or (P=3) alone. After 26+/-8 weeks, average percent (%) decrease in iPTH was similar with (C) and (P) (-60.4+/-34% versus -65.4+/-28%, respectively; p=0.6). In the (P) group, the effective dose in children was greater than in adult trials based on kilogram weight. Episodes of hypercalcemia between the treatment groups were not different. However, episodes of elevated calcium x phosphorus product (CaxP)> or =70 mg(2)/dl(2) occurred more frequently in the (C) group (odds ratio=1.5; p=0.01). Paricalcitol appears to be safe and effective in pediatric patients. Data suggest that dosing should be gauged according to degree of SHPT. This should serve as impetus for future pharmacokinetic studies in pediatric dialysis patients.

Adolescent↗
PubMed2001

Effects of vitamins on hepatic nuclear binding of L-tryptophan.

This study investigated the in vitro effects of selected vitamins on nuclear L-tryptophan receptor binding of rat liver. Our results revealed that some fat-soluble vitamins, beta-carotene, retinyl acetate, calciferol, alpha-tocopherol, and Trolox, as well as some water-soluble vitamins, thiamine and riboflavin, acted to inhibit in vitro 3H-tryptophan binding to hepatic nuclei. On the other hand, pyridoxine had little or no effect. The addition of dithiothreitol, a protective agent for sulfhydryl groups, along with each vitamin decreased the vitamin's inhibitory effect on in vitro 3H-tryptophan binding to nuclei, with the exception of riboflavin and calciferol. The addition of L-leucine, which alone had no inhibitory effect on in vitro 3H-tryptophan binding to hepatic nuclei but when added with unlabeled L-tryptophan negated the effect of unlabeled L-tryptophan, caused a markedly diminished inhibitory binding effect due to each of the following vitamins, thiamine, beta-carotene, retinyl acetate, and alpha-tocopherol and Trolox, but no effect on riboflavin and calciferol.

Animals↗
PubMed1978

Distinction between the common symptoms of the phosphate-depletion syndrome and glucocorticoid-induced disease.

A phosphate depletion syndrome developed in a steroid-dependent asthmatic patient. Initially, the clinical picture was confused with steroid-associated myopathy rather than the phosphate depletion syndrome which has similar symptoms. The classic biochemical findings led to the correct diagnosis. Cessation of phosphate-binding antacids and phosphorus repletion rapidly corrected the biochemical findings and led to the patient's clinical improvement. Platelet phosphate metabolism was evaluated; it was found to correlate with the phosphorus-depleted state and clinical recovery with phosphate repletion. Attention is drawn to the clinical entity of phosphate depletion which may mimic steroid-induced side effects, both of which may occur in patients receiving steroids and antacids.

Antacids↗
PubMed1984

Hypercalcemia in coccidioidomycosis.

Two patients with disseminated coccidioidomycosis and hypercalcemia are presented. One patient studied showed normal levels of 25-hydroxyvitamin D with depressed levels of 1 alpha,25-dihydroxyvitamin D. The serum calcitonin level was appropriate for the level of serum calcium, and the serum parathyroid hormone level was suppressed with elevation of the nephrogenous cAMP level. Intestinal absorption of calcium was elevated at 63 percent. Hypercalcemia and hypercalciuria persisted despite a 300 mg calcium diet. An osteotropic substance similar to the humoral hypercalcemia of malignancy is postulated.

25-Hydroxyvitamin D 2↗
PubMed1987

Hypercalcemic hyperparathyroidism complicating oncogenic osteomalacia. Effect of successful tumor resection on mineral homeostasis.

Described herein is a case of oncogenic osteomalacia that ran a course of at least 16 years before curative resection of a mixed mesenchymal tumor. Hypercalcemic hyperparathyroidism developed in the patient, and review of the literature indicated that this occurs in about 10 percent of reported cases. Changes in serum parathyroid hormone levels with and without phosphate supplement therapy and before and after tumor resection suggested that both the high intake of phosphate and the effect of the neoplasm on vitamin D bioactivation engendered the parathyroid overactivity. Despite marked hyperparathyroidism, serum 1,25-dihydroxyvitamin D levels were subnormal preoperatively but showed a sevenfold increase within 48 hours of tumor resection. Thereafter, a gradual increase in the maximal tubular reabsorption of phosphate occurred during several months. Biopsy of the iliac crest confirmed that tumor removal was followed by resolution of osteomalacia, but there was no accompanying increase in vertebral mineral density as assessed by quantitative computed tomography or in total-body bone mineral as measured with dual-photon absorptiometry. The findings presented are consistent with secretion by the tumor of a factor with a short half-life that is potent enough to inhibit renal 25-hydroxyvitamin D-1 alpha-hydroxylase despite hyperparathyroidism. The resulting subnormal circulating 1,25-dihydroxyvitamin D levels may have secondarily contributed to decreased renal tubular reabsorption of phosphate.

Chronic Disease↗