Disease relevance of ergocalciferol

• Bone response to phosphate salts, ergocalciferol, and calcitriol in hypophosphatemic vitamin D-resistant rickets [1].
• We evaluated oral 1,25-vitamin D3 for as long as 26 months in six prepubescent children with renal osteodystrophy previously treated with vitamin D2 [2].
• Her sister, who died at the age of 10 months, also had had total alopecia, rickets, and hypocalcaemia resistant to vitamin-D2 therapy [3].
• Effective 25-hydroxylation of vitamin D2 in alcoholic cirrhosis [4].
• Osteoporosis is the usual form of bone disease in alcoholic cirrhosis and a response to either vitamin D2 or 25-OH-D treatment is suggested [5].

Psychiatry related information on ergocalciferol

• Menatetrenone and vitamin D2 with calcium supplements prevent nonvertebral fracture in elderly women with Alzheimer's disease [6].

High impact information on ergocalciferol

• Radiologic studies and bone histomorphometric analyses showed that phosphate (alone or with ergocalciferol) induced the mineralization of the growth plate but not of the endosteal bone surface [1].
• 3. In three volunteers who each ingested 1.25 mg of vitamin D2, the total plasma D2 increased to 90 +/- 32 ng/ml by 4 h, and the D2 was evenly distributed between the upper and lower layers at 4, 8, and 24 h after the dose, indicating a continuing association of the vitamin with chylomicrons and lipoproteins, as well as with hDBP [7].
• Administration of NO-1886 for as long as 90 d significantly decreased the degree of atherosclerotic changes in the coronary arteries of vitamin D2-treated, cholesterol-fed rats [8].
• Calcification was induced by dietary supplements of cholesterol, vitamin D2, and calcium [9].
• We evaluated baseline vitamin D (vitamin D2 and D3), 25-OH vitamin D2 and D3, 1,25(OH)2 vitamin D, vitamin D-binding protein, bone mineral content and dietary mineral content in six children (mean age: 12.1 years) with cholestasis since infancy [10].

Chemical compound and disease context of ergocalciferol

• Metabolic bone disease in alcoholic cirrhosis: a comparison of the effect of vitamin D2, 25-hydroxyvitamin D, or supportive treatment [5].
• These results reveal further dissimilarities between ergocalciferol and cholecalciferol metabolism in mammals and suggest a mechanism for the lesser tendency of ergocalciferol to cause hypercalcemia relative to cholecalciferol [11].
• The available data with regard to the use of calciferol, dihydrotachysterol, and calcifediol in the management of renal insufficiency are reviewed [12].
• In each, normalization of serum calcium concentration and resolution of osteomalacia were obtained with continuous administration of high doses of ergocalciferol or high doses of 1,25-dihydroxycholecalciferol [13].
• A long-term study on the comparative effects of vitamin D2 and 25-hydroxycholecalciferol [25-(OH)D3], in five patients with severe lesions of osteomalacia and/or osteitis fibrosa, demonstrated the efficiency of 25 to 200 mug/day of 25-(OH)D3 and the lack of therapeutic action of 345 to 685 mug/day of vitamin D2 [14].

Biological context of ergocalciferol

• Vitamin D2 and 25-OH-D were equally effective in increasing bone density measurements [5].
• Studies on the mode of action of calciferol. Effects of dietary calcium and phosphorus on the relationship between the 25-hydroxyvitamin D3-1alpha-hydroxylase and production of chick intestinal calcium binding protein [15].
• Vitamin D2 hydroxylation reactions in the chick are virtually identical with those observed with the vitamin D3 series [16].
• Expression of CYP2R1 in cells led to the transcriptional activation of the vitamin D receptor when either vitamin D2 or D3 was added to the medium [17].
• CONCLUSIONS: We showed for the first time that ergocalciferol was well absorbed from lyophilized and homogenized mushrooms in humans and that vitamin D bioavailability can be studied in humans with such an experimental protocol [18].

Anatomical context of ergocalciferol

• When calcium uptake was measured at the mucosal or brush border surface it was found to be a cation-oriented, saturable process in both the +D3 and minus D3 systems and was enhanced by calciferol supplementation [19].
• The sum of this and other evidence suggests that of uptake of calcium is a calciferol-mediated event which is not the rate-limiting step in the total transport of this ion across the intestinal epithelial cell [19].
• CONCLUSION: CYP3A4 is a vitamin D 25-hydroxylase for vitamin D2 in human hepatic microsomes and hydroxylates both 1alpha(OH)D2 and 1alpha(OH)D3 [20].
• Vitamin D3 was the most abundant vitamin D compound in human milk, followed by vitamin D2, 25OHD3, and, finally, 25OHD2 [21].
• The effect on cortical bone loss of treating elderly women with 15,000 IU vitamin D2 weekly was evaluated by sequential radiographic morphometry of the metacarpals [22].

Associations of ergocalciferol with other chemical compounds

• Studies on the mechanism of action of calciferol. VIII. The effects of dietary vitamin D and the polyene antibiotic, filipin, in vitro, on the intestinal cellular uptake of calcium [19].
• Experience with 1,25-dihydroxycholecalciferol therapy in undergoing hemodialysis patients with progressive vitamin D2-treated osteodystrophy [23].
• At the femoral neck, there was no significant difference in bone mineral density change between the treatments over 2 years: alendronate (+0.9%), ergocalciferol (-3.2%), and calcitriol (-2.2%) [24].
• 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 [25].
• Five hundred thousand units of oral vitamin D2 resulted in significant increases in 25OHD (+24.3+/-16.9 ng/mL; P < 0.001) and the fasting urinary calcium/creatinine excretion ratio (+0.06+/-0.004; P = 0.01) and significant decreases in the serum concentration of PTH (-32.9+/-36.9 pg/mL; P < 0.001) and osteocalcin (-4.9+/-2.4 ng/mL; P < 0.001) [26].

Gene context of ergocalciferol

• We demonstrate the vitamin D analog, 19-nor-1alpha,25-dihydroxy vitamin D2, is also an effective inducer of CYP3A4 in Caco-2 cells, but with half the potency of 1,25-D3 [27].
• Hypercalcemia evoked by vitamin D2 treatment, which is known to degranulate thyroid C cells, reduced the thyroid content of both CGRP and CT [28].
• Induction was investigated from human mononuclear leukocytes (MNL), THP-1 cells (with and without enhancement by vitamin D2 for CD14), and peritoneal macrophages from C3H/HeJ (LPS nonresponder) and C3H/HeN (LPS responder) mice [29].
• In order to localize the production site of activin A in the bone tissues, we tried to immunolocalize activin A in fetal mouse calvaria cultured in a medium containing fetal calf serum, 1 alpha-25(OH)2 vitamin D2 and parathyroid hormone [30].
• The major metabolite of vitamin D2 by CYP105A1 was 25(OH)D2, while the major metabolites by CYP27A1 were both 24(OH)D2 and 27(OH)D2 [31].

Analytical, diagnostic and therapeutic context of ergocalciferol

• Oral administration of 50,000 IU of vitamin D2 failed to relieve symptoms or raise serum 25-OHD levels to normal [32].
• The rise in 25-hydroxyvitamin D in response to vitamin D2 absorption was significantly lower over time in the CF group than in the control group (P = 0.0012) [33].
• This was also the increase observed in a longitudinal study of vitamin D2 supplements in 11 patients [34].
• We also did a cross-sectional study of 22 patients receiving casein and ergocalciferol (25 micrograms/d) compared with 46 patients receiving amino acids and ergocalciferol (5 micrograms/d) for 6-58 mo [35].
• In order to demonstrate the physiological significance of the two new trihydroxy metabolites of vitamin D2, we induced hypervitaminosis D2 in a rat using [3 alpha-3H]vitamin D2 and analyzed its plasma for the various [3 alpha-3H]vitamin D2 metabolites on two different high-pressure liquid chromatography systems.(ABSTRACT TRUNCATED AT 250 WORDS)[36]

References