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PubMed1977

High pressure liquid chromatographic separation and identification of vitamins D2 and D3 in the presence of fat-soluble vitamins in dosage forms.

A simple and rapid qualitative method is described for determining the presence of vitamin D2 (ergocalciferol) and/or vitamin D3 (cholecalciferol) in various preparations by reverse phase high pressure liquid chromatography (HPLC). When both D2 and D3 are present, this method effectively separates and identifies each vitamin D form by its respective retention time. A significant difference between vitamins D2 and D3 exists in their antirachitic activity in poultry. Preparations can be tested rapidly by this method to ascertain that the correct D vitamin form has been added. Fat-soluble vitamins such as vitamins A, E, K1, and K3 do not interfere. Vitamins D2 and D3 were separated at the baseline in model preparations. As little as 2 ng each of vitamin D2 and vitamin D3 can be separated and identified.

Cholecalciferol↗

PubMed1979

Naturally occurring vitamin D3 in fish products analysed by HPLC, using vitamin D2 as an international standard.

A chemical method for the analysis of naturally occurring vitamin D is proposed. The unsaponifiable matter of oils and tissues is prepared, cholesterol is partly removed by double precipitation at low temperature in methanol. The vitamin D fraction is collected on an adsorption column by high performance liquid chromatography. The fraction is further purified and the vitamins D2 and D3 are separated on a partition column (reverse phase) by HPLC. Recovery was 89 to 93%, standard deviation 3%. The only vitamin D analogue found in fish oils, livers and fillets, was cholecalciferol (D3). Hence, ergocalciferol (D2) could be used as an internal standard. The provitamins ergosterol and 7-dehydrocholesterol, as well as the previtamins, were separated from the vitamin D-fraction on the adsorption column. Results in the range 0.050 to 134 microgram D3 per gram (2 to 5360 I.U. per gram) are given. One cod liver oil was analysed in a rat bioassay, giving supporting results.

Adsorption↗

PubMedDate not supplied

[Comparative study of the hemolytic action of group D vitamins].

Hemolytic effects of the vitamins of the D group (ergocalciferol - D2, cholecalciferol - D3, and 1 alpha-hydroxycholecalciferol - 1 alpha-OH-D3) were compared using rat erythrocytes. The latent period of hemolysis, caused by 1 alpha-OH-D3 was approximately 3-fold shorter as compared with the hemolysis caused by D2 or D3. Apparent values for energy of activation of hemolysis, estimated at 30-45 degrees, constituted for D2 - 23.2 kcal/mol, D3 - 25.3 kcal/mol, 1 alpha-OH-D3 - 13.1 kcal/mol. Despite the higher hemolytic activity, the rate of 1 alpha-ON-D3 autooxidation was distinctly lower than that of D3.

Animals↗

PubMed1986

[Comparative studies of calcium resorption modified by vitamin D2 and D3 in patients with chronic renal failure and dialysis patients].

In 16 patients with a chronic renal insufficiency at the stage of the compensated retention and 13 test persons of the chronic haemodialysis programme determinations of the total calcium and of the ionized calcium fraction as well as investigation of the intestinal calcium absorption by means of the isotope 47Ca were performed. In these cases the influence of vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol) on these parameters of the calcium metabolism was compared. Under the treatment with vitamin D a normalization of the serum calcium levels concerning the total calcium concentration as well as with regard to the ionized calcium fraction was achieved; this effect took place parallel to the improvement of the intestinal calcium absorption. Vitamin D3, had a more favourable effect than vitamin D2. The necessary doses are below 40,000 U a day.

Blood Urea Nitrogen↗

PubMedDate not supplied

[Functional activity of mitochondria and intensity of nucleic acid and protein synthesis in rat liver and small intestine mucosa with different supplies of vitamin D].

Decrease in total content of mitochondrial protein in mucosa of small intestine, an alteration of distribution of the protein between the fractions of mitochondria, distinct decrease in the respiratory activity of mitochondria and in the activity of succinate- and NADH-dehydrogenases were observed in rats deficient in vitamin D. Deficiency in vitamin D was accompanied by decreased incorporation of labelled precursors into total, nuclear and mitochondrial DNA and RNA by 20-50% and into mitochondrial proteins--by 50% in mucosa of small intestine; these patterns were unaltered in liver tissue. Administration of ergocalciferol (at a dose 1000 IU) into rats normalized the impairments studied, whose alteration correlated with the increase of calcium concentration in blood serum.

Animals↗

PubMed1983

Acute vitamin D3 toxicosis in horses: case reports and experimental studies of the comparative toxicity of vitamins D2 and D3.

Acute vitamin D toxicosis was diagnosed in 2 horses fed a grain ration containing 1,102,311 IU of cholecalciferol (vitamin D3)/kg (500,000 IU/lb) for about 30 days. Horse 1 died acutely with extensive mineralization of cardiovascular and other soft tissues. Horse 2, which had severe clinical signs and clinicopathologic changes of toxicosis, was treated with nonsteroidal antiinflammatory drugs and recovered in about 6 months. In an experimental study, the toxicity of ergocalciferol (vitamin D2) and cholecalciferol was compared in 2 horses (No. 3 and 4) given the respective vitamins at a daily dosage of 33,000 IU/kg of initial (day 0) body weight for 30 days. Except for slight loss in body weight (8%) during the 1st few days of treatment, horse 3 remained clinically normal. Horse 4 developed limb stiffness and tachycardia, became anorectic, weak, and recumbent, lost 29% of body weight, and had polydipsia and polyuria. Horses 2, 3, and 4 developed persistent hyperphosphatemia. Horse 2 remained normocalcemic whereas horses 3 and 4 became hypercalcemic by day 28. In horse 3, serum vitamin D2 metabolite concentrations on days 0, 1, 14, and 26 were: vitamin D2 (ng/ml) = less than 5.0, 5.7, 71.4, and 188.0; 25-hydroxy-vitamin D2 (ng/ml) = less than 5.0, less than 5.0, 43.1, and 117.5; and 1,25-dihydroxy-vitamin D (pg/ml) = 19.7, 23.2, 25.0, and 45.7, respectively. In horse 4, serum vitamin D3 metabolite concentrations on the same days were: vitamin D3 (ng/ml) = less than 5.0, 110.0, 1,049.0, and 887.0; 25-hydroxy-vitamin D3 (ng/ml) = less than 5.0, 18.9, 201.0 and 182.0; and 1,25-dihydroxy-vitamin D (pg/ml) = 21.5, 18.9, 25.2, and 21.6, respectively. Urine of horses 2 and 4 became acidic (pH 6). Horses 2, 3, and 4 became hyposthenuric, but the decrease in urine specific gravity (sp gr) in horse 3 occurred only after 3 weeks of treatment and was only moderate (sp gr, 1.018 to 1.021) and nonprogressive. Hyposthenuria was evident in horse 4 on day 4 (sp gr, 1.028), and was progressive and marked (sp gr, days 28 to 32: 1.006 to 1.009). Urine sp gr of horse 2 ranged from 1.002 to 1.007. Fractures were demonstrated radiographically and histologically in the costochondral junctions of horses 3 and 4. Mineralization of cardiovascular and other soft tissues developed in horses 3 and 4, with lesions being more severe and having a wider tissue distribution in horse 4.

Acute Disease↗

PubMed1982

Effect of vitamin D2 on the assay of 24,25-dihydroxyvitamin D3 in man.

Serum levels of the dihydroxylated metabolite of vitamin D3, 24,25-dihydroxycholecalciferol (24, 25(OH)2D3) were measured by competitive protein-binding assay in 2 anephric patients while undergoing therapy with 25-hydroxycholecalciferol (25(OH)D3) and, at a later date, vitamin D2, ergocalciferol. Whereas there was no increase in serum levels of 24, 25 (OH)2D3 when the patients were treated with 25 (OH)D3, a significant increase was apparently seen when vitamin D2 was given. These results suggest that a metabolite of vitamin D2, non-renal in origin, may be interfering in the assay for 24, 25 (OH)2D3. The different levels of serum 24, 25 (OH)2D3 in anephric man found by various groups of workers are explained by these results.

24,25-Dihydroxyvitamin D 3↗

PubMed1995

[Hypophosphatemic osteomalacia acquired after renal transplantation: a a cause of severe osteoporosis].

Renal osteodystrophy improves after renal transplantation but, after the procedure, other forms of bone disease emerge. We report a male patient that received a renal allograft four years before, who consulted for low back pain secondary to multiple vertebral compression fractures. The patient had good renal function, a parathormone independent hyperphosphaturia, normal 25-OH cholecalciferol, increased urinary hydroxyproline, decreased osteocalcin, reduced bone density and a bone biopsy revealing osteomalacia. The diagnosis of hypophosphatemic osteomalacia was reached and treatment with phosphates and ergocalciferol was started but, despite this, the patient suffered a new fracture two years later. Two mechanisms can produce hypophosphatemia after a renal transplantation: a parathormone excess due to the previous renal failure, that disappears during the first year after the transplantation or a derangement in renal phosphate transport that can be due to a generalized proximal tubule solute transport derangement (Fanconi syndrome), parathormone hypersensitivity or to an "idiopathic" hyperphosphaturia. Despite a good treatment, bone mass is not recovered and there is a high fracture risk. Mineral metabolism must be closely monitored after a renal allograft and its alterations must be quickly treated.

Adult↗

PubMed1984

Continuous nasogastric phosphorus infusion in hypophosphatemic rickets of prematurity.

Radiologic and biochemical abnormalities associated with nutritional hypophosphatemic rickets were discovered in a 945-g preterm infant despite daily supplementation with 800 to 1,600 IU of ergocalciferol (vitamin D2) and an elevated serum 25-hydroxyvitamin D concentration. Vitamin D supplementation was stopped, and the rickets was corrected by phosphorus supplement alone with the use of a unique technique of long-term, continuous nasogastric phosphorus infusion. Normophosphatemia was rapidly achieved and effectively maintained. Hypocalcemia did not occur at rates of infusion of 100 mg of elemental phosphorus per day. The data are consistent with specific phosphorus deficiency as the cause of rickets in this infant, rather than insufficient vitamin D intake or disturbed vitamin D metabolism. We speculated that continuous phosphorus infusion prevents the intermittent hyperphosphatemia of bolus phosphorus supplement and that continuous phosphorus infusion may be useful in the treatment of other hypophosphatemic states of infancy.

Female↗

PubMed1981

Tumor-induced osteomalacia. Evidence of a surgically correctable alteration in vitamin D metabolism.

A 15-year-old boy was treated for nonfamilial hypophosphatemic rickets. Treatment with ergocalciferol, 100,000 units/day, and phosphorus, 2 to 4 g/day, failed to alleviate the rickets. Levels of 1 alpha, 25-dihydroxyvitamin D were low while levels of 25-hydroxyvitamin D were elevated. After removal of a benign fibroma, the level of 1 alpha, 25-dihydroxyvitamin D increased, the serum phosphorus level became normal, and the osteomalacia was cured. The alteration of vitamin D metabolism and associated hypophosphatemia in oncogenic osteomalacia is a potentially reversible cause of bone disease mediated by the tumor.

Adolescent↗

PubMed2004

Effect of Vitamin D on falls: a meta-analysis.

CONTEXT: Falls among elderly individuals occur frequently, increase with age, and lead to substantial morbidity and mortality. The role of vitamin D in preventing falls among elderly people has not been well established. OBJECTIVE: To assess the effectiveness of vitamin D in preventing an older person from falling. DATA SOURCES: MEDLINE and the Cochrane Controlled Trials Register from January 1960 to February 2004, EMBASE from January 1991 to February 2004, clinical experts, bibliographies, and abstracts. Search terms included trial terms: randomized-controlled trial or controlled-clinical trial or random-allocation or double-blind method, or single-blind method or uncontrolled-trials with vitamin D terms: cholecalciferol or hydroxycholecalciferols or calcifediol or dihydroxycholecalciferols or calcitriol or vitamin D/aa[analogs & derivates] or ergocalciferol or vitamin D/bl[blood]; and with accidental falls or falls, and humans. STUDY SELECTION: We included only double-blind randomized, controlled trials (RCTs) of vitamin D in elderly populations (mean age, 60 years) that examined falls resulting from low trauma for which the method of fall ascertainment and definition of falls were defined explicitly. Studies including patients in unstable health states were excluded. Five of 38 identified studies were included in the primary analysis and 5 other studies were included in a sensitivity analysis. DATA EXTRACTION: Independent extraction by 3 authors using predefined data fields including study quality indicators. DATA SYNTHESIS: Based on 5 RCTs involving 1237 participants, vitamin D reduced the corrected odds ratio (OR) of falling by 22% (corrected OR, 0.78; 95% confidence interval [CI], 0.64-0.92) compared with patients receiving calcium or placebo. From the pooled risk difference, the number needed to treat (NNT) was 15 (95% CI, 8-53), or equivalently 15 patients would need to be treated with vitamin D to prevent 1 person from falling. The inclusion of 5 additional studies, involving 10 001 participants, in a sensitivity analysis resulted in a smaller but still significant effect size (corrected RR, 0.87; 95% CI, 0.80-0.96). Subgroup analyses suggested that the effect size was independent of calcium supplementation, type of vitamin D, duration of therapy, and sex, but reduced sample sizes made the results statistically nonsignificant for calcium supplementation, cholecalciferol, and among men. CONCLUSIONS: Vitamin D supplementation appears to reduce the risk of falls among ambulatory or institutionalized older individuals with stable health by more than 20%. Further studies examining the effect of alternative types of vitamin D and their doses, the role of calcium supplementation, and effects in men should be considered.

Accidental Falls↗

PubMed1976

Specific colorimetric determination of niacinamide in dosage forms.

A chemical method for determining the amount of niacinamide in multicomponent preparations was developed. Neither niacin resulting from the degradation of niacinamide nor vitamin A, thiamine hydrochloride, riboflavin, ascorbic acid, ergocalciferol, or calcium pantothenate interferes. The method is based on the reaction of niacinamide with 1-chloro-2,4-dinitrobenzene, followed by the spectrophotometric measurement of the colored solution obtained after treatment with sodium hydroxide. The proposed method is at least as accurate as the methods currently in use. A structure is proposed for the colored product, and its route of formation is outlined.

Colorimetry↗

PubMed1993

Long-term total parenteral nutrition and osteoporosis: report of a case.

A patient who had been supported with total parenteral nutrition (TPN) for over 8 years is herein presented, with emphasis on the changes observed in calcium metabolism. The patient was a 31-year-old female, who had undergone a subtotal jejunal and ileal resection for superior mesenteric artery occlusion. TPN was started soon after the surgery. She had been on TPN support for 105 months. Back pain developed at 97 months after the initiation of TPN. During her course, the serum calcium levels were judged to be within the normal ranges, while the 1 alpha, 25(OH)2Vit.D declined. Intermittent hypercalciuria was occasionally observed. Both the serum level of calcium and urinary calcium loss correlated closely to the amount of calcium infused, but they were not influenced by the amount of vitamin D (ergocalciferol) received. The serum level of parathormone and calcitonin were also within the normal ranges. The patient's vertebral bone, which was obtained at autopsy, revealed histopathological changes characteristic of osteoporosis. Based on the above, we conclude that a careful monitoring of the amount of calcium infused is called for to prevent bone disease in patients on long-term parenteral nutrition.

Adult↗

PubMed1990

Hypercalcemic hyperparathyroidism and hypophosphatemic osteomalacia complicating neurofibromatosis.

Neurofibromatosis is sometimes complicated by impaired renal tubular reabsorption of phosphate, hypophosphatemia, and osteomalacia. Hyperparathyroidism has also been reported in patients with neurofibromatosis. When hypercalcemia and elevated levels of parathyroid hormone are found in osteomalacia, however, it may be difficult to determine if the hyperparathyroidism was primary or tertiary. We describe a patient with neurofibromatosis, hypercalcemic hyperparathyroidism, hypophosphatemic osteomalacia, vitamin D deficiency, and clear-cell hyperplasia of all four parathyroid glands. Serial biomechanical, bone biopsy, and densitometric studies confirmed that treatment with ergocalciferol, calcium, and phosphate supplements significantly improved the osteomalacia but caused increased parathyroid overactivity. After subtotal parathyroidectomy, the parathyroid hormone concentration became normal and the bone mineral content increased at the spine and hip, but inappropriate phosphaturia persisted. The findings indicate that hyperparathyroidism, osteomalacia, and vitamin D deficiency adversely affect each other.

Bone and Bones↗

PubMed2005

Limited availability of nutritional vitamin D causing inappropriate treatment of vitamin D deficiency rickets with a response resembling pseudohypoparathyroidism type II in a Japanese patient.

Vitamin D deficiency rickets occasionally resembles pseudohypoparathyroidism type II (PHP type II) with respect to the response to exogenous PTH in the presence of hypocalcemia. We encountered a Japanese patient with stage 2 vitamin D deficiency rickets, who had increased urinary cAMP excretion and no response of urinary phosphate or N-acetyl-beta-D-glucosaminidase excretion to exogenous PTH under normocalcemic and normophosphatemic conditions, after treatment with 1,25(OH)2 vitamin D3. This case shows that it is possible for a response mimicking that of PHP type II to occur when the serum calcidiol level is low due to causes other than hypocalcemia and secondary hyperparathyroidism. When the serum calcidiol level is low, the appropriate treatment should be cholecalciferol or ergocalciferol. However, because neither is commercially available as a useful formulation in Japan, physicians are forced to inappropriately use calcitriol or analogs.

Calcifediol↗

PubMed2002

A randomized trial of sodium fluoride (60 mg) +/- estrogen in postmenopausal osteoporotic vertebral fractures: increased vertebral fractures and peripheral bone loss with sodium fluoride; concurrent estrogen prevents peripheral loss, but not vertebral fractures.

Postmenopausal Caucasian women aged less than 80 years (n = 99) with one or more atraumatic vertebral fracture and no hip fractures, were treated by cyclical administration of enteric coated sodium fluoride (NaF) or no NaF for 27 months, with precautions to prevent excessive stimulation of bone turnover. In the first study 65 women, unexposed to estrogen (-E study), age 70.8 +/- 0.8 years (mean +/- SEM) were all treated with calcium (Ca) 1.0-1.2 g daily and ergocalciferol (D) 0.25 mg per 25 kg once weekly and were randomly assigned to cyclical NaF (6 months on, 3 months off, initial dose 60 mg/day; group F CaD, n = 34) or no NaF (group CaD, n = 31). In the second study 34 patients, age 65.5 +/- 1.2 years, on hormone replacement therapy (E) at baseline, had this standardized, and were all treated with Ca and D and similarly randomized (FE CaD, n = 17; E CaD, n = 17) (+E study). The patients were stratified according to E status and subsequently assigned randomly to +/- NaF. Seventy-five patients completed the trial. Both groups treated with NaF showed an increase in lumbar spinal density (by DXA) above baseline by 27 months: FE CaD + 16.2% and F CaD +9.3% (both p = 0.0001). In neither group CaD nor E CaD did lumbar spinal density increase. Peripheral bone loss occurred at most sites in the F CaD group at 27 months: tibia/fibula shaft -7.3% (p = 0.005); femoral shaft -7.1% (p = 0.004); distal forearm -4.0% (p=0.004); total hip -4.1% (p = 0.003); and femoral neck -3.5% (p = 0.006). No significant loss occurred in group FE CaD. Differences between the two NaF groups were greatest at the total hip at 27 months but were not significant [p < 0.05; in view of the multiple bone mineral density (BMD) sites, an alpha of 0.01 was employed to denote significance in BMD changes throughout this paper]. Using Cox's proportional hazards model, in the -E study there were significantly more patients with first fresh vertebral fractures in those treated with NaF than in those not so treated (RR = 24.2, p = 0.008, 95% CI 2.3-255). Patients developing first fresh fractures in the first 9 months were markedly different between groups: -23% of F CaD, 0 of CaD, 29% of FE CaD and 0 of E CaD. The incidence of incomplete (stress) fractures was similar in the two NaF-treated groups. Complete nonvertebral fractures did not occur in the two +E groups; there were no differences between groups F CaD and CaD. Baseline BMD (spine and femoral neck) was related to incident vertebral fractures in the control groups (no NaF), but not in the two NaF groups. Our results and a literature review indicate that fluoride salts, if used, should be at low dosage, with pretreatment and co-treatment with a bone resorption inhibitor.

Adult↗

PubMed1976

Studies on a 3beta-hydroxysteroid sulphotransferase from rat liver.

A steroid sulphotransferase (EC 2.8.2.2) was partially purified from female rat liver. The enzyme was active towards the substrates, dehydroepiandrosterone, epiandrosterone and pregnenolone but was inactive towards oestrogens, cholesterol and ergocalciferol. A pH optimum of 5.0 was recorded but the enzyme was unstable at low pH. The enzyme was stimulated slightly by the addition of reducing agents and inhibited by p-chloromercuribenzoate and HgCl2. Crude enzyme activity was markedly stimulated by divalent cations but this effect was not observed with purified enzyme. A Km of 13 muM was calculated for the donor substrate 3'-phosphoadenylyl sulphate and the acceptor substrate, dehydroepiandrosterone had a Km value of 6 muM. The enzyme appeared to be highly susceptible to product inhibition by adenosine 3', 5'-diphosphate.

Animals↗

PubMed1984

Effect of vitamin D and its metabolites on developing myogenic cultures.

Growth, protein synthesis and expression of creatine kinase (CK) by embryonic chick myogenic cells are inhibited by vitamin D and certain of its metabolites. 25-OH cholecalciferol was most active in concentrations of 10(-5) - 10(-6) M, with cholecalciferol and ergocalciferol less active in that order. Ergosterol had no activity of this sort. Inhibition of CK was most marked on the 4th and 5th day of culture and was due to suppression of the appearance of CK-NM and MB. CK-BB was not affected and CK-MB was more affected than CK-BB. Skin fibroblasts by comparison were slightly stimulated in growth at 10(-6) M and much less affected at 10(-5) M than the myogenic cells. It is suggested that vitamin D has a direct effect upon the muscle cell, to cause a selective diminution in the production of certain polypeptides.

Animals↗