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PubMed1976

Occult osteomalacia amongst healthy and pregnant women in Pakistan.

A survey has been carried out on 206 healthy Pakistani women attending with their sick children at the paediatric outpatients department and 252 pregnant Pakistani women near term attending the antenatal clinic of the Karachi Prosgraduate Medical Centre. 12-6% of helathy women and 33% of pregnant women had biochemical abnormalities in serum calcium, phosphorus, and alkaline phosphatase which were corrected with subsequent administration of vitamin D. The absence of clinical disease has been ascribed to the supplementation received through the ultraviolet irradiation of the skin.

Alkaline Phosphatase↗
PubMed1976

Florid and subclinical rickets among immigrant children in Glasgow.

200 Asian 300 African, Chinese, or Scottish children were examined for clinical, biochemical, and radiological evidence of vitamin-D deficiency. Among the Asians there were 10 with florid rickets and 15 with subclinical rickets. Among the African, Chinese, and Scottish children there were no cases of florid rickets and only 7 cases of subclinical rickets (3 African, 3 Chinese, and 1 Scottish). Loss of metaphyseal definition is considered to be the radiological pattern of minimal active rickets and metaphyseal bands to represent the healing stage. Serum 25-hydroxycholecalciferol concentrations were low in clinical and subclinical minimal active rickets although there was some overlap with the wide range found in the "normal" group. Elevated serum-alkaline-phosphatase levels alone should not be regarded as indicating vitamin-D deficiency. The continuing prevalence of rickets in Asian children and in particular among schoolchildren warrants immediate action, which is long overdue.

Africa↗
PubMed1976

Prevention of vitamin-D deficiency in Asians.

Asian families living in Glasgow were studied between December, 1973, and June, 1974. One group of families served as a control; their mean serum-25-hydroxy-vitamin-D (25-hydroxy-cholecalciferol and 25-hydroxyergocalciferol) remained low, being 5-1 +/- 0-8 (S.E.M.) ng/ml at the end of the study. A second group was given 3000 units of vitamin D2 in a capsule weekly; this raised the mean concentration of 25-hydroxy-vitamin-D to 18-1 +/- 2-9 ng/ml. The variable effectiveness of this supplement was attributable to some subjects not taking the capsules regularly. The third group of families was provided with chupatty flour fortified with vitamin D(6000 units per kg). This increased mean serum-25-hydroxy-vitamin-D very uniformly to a mean value of 19-5 +/- 1-2 ng/ml. It is concluded that vitamin-D deficiency in Asian immigrants could be substantially reduced by fortification of chupatty flour with vitamin D.

Adolescent↗
PubMed1977

25-Hydroxylation of vitamin D in primary biliary cirrhosis.

The ability to 25-hydroxylate vitamin D was investigated in thirty-nine patients with symptomatic primary biliary cirrhosis (P.B.C.). In seven previously untreated patients serum-25-hydroxy-vitamin-D (25-OHD) concentration increased after regular monthly injections of vitamin D. After a single injection of vitamin D in eight P.B.C. patients serum-25-OHD did not change significantly over 12 days; in contrast there were significant increases in eight normal subjects and in seven patients with nutritional osteomalacia. Twenty-three of twenty-five P.B.C. patients on regular vitamin-D therapy had normal serum-25-OHD values. These results indicate that serum-25-OHD concentrations become normal in P.B.C. if adequate amounts of vitamin D are presented to the liver as substrate.

Adult↗
PubMed1977

Comparison of oral 25-hydroxycholecalciferol, vitamin D, and ultraviolet light as determinants of circulating 25-hydroxyvitamin D.

Circulating concentrations of 25-hydroxyvitamin D (25-OHD) were measured during short-term and long-term oral treatment with 25-hydroxycholecalciferol (25-OHD3), 25-H.C.C.) or with vitamin D in over 200 subjects over a period of 5 years. Ten times more vitamin D than 25-OHD3 was required to produce equivalent plasma-25-OHD concentrations. Plasma-25-OHD was a power function of dosage with both compounds. These data indirectly measure the superior therapeutic potency of 25-OHD3, show that dose-response relations with both compounds may be useful in diagnosis, and indicate that there are pronounced constraints on 25-hydroxylation of vitamin D. Together with the effects of ultraviolet light, now shown to be equivalent to oral vitamin D in doses of 8000-10 000 I.U. daily, these constraints may protect against vitamin-D deficiency in winter.

Administration, Oral↗
PubMed1978

Osteomalacia after small-intestinal resection.

Histological examination of bone from 25 patients with small-intestinal resection showed that 9 (36%) had osteomalacia, which was severe in 5 and mild in 4. The serum-alkaline-phosphatase concentration was raised in all patients with severe osteomalacia, but serum calcium, phosphate, and alkaline-phosphatase concentrations were normal in the 4 patients with mild disease, 2 of whom had symptoms. Osteomalacia was diagnosed radiologically in only 3 patients. Osteomalacia appears to be commoner in patients with small-intestinal resection than has previously been thought, and bone biopsy is essential if all cases are detected. Although high-dose parenteral vitamin-D therapy is usually effective in the treatment of osteomalacia after small-intestinal resection, our findings showed that oral vitamin-D metabolites and their analogues may also be effective. This has important practical advantages.

Administration, Oral↗
PubMed1978

The continuing risk of vitamin-D intoxication.

Eight cases of vitamin-D poisoning are described. In six patients this therapy was unnecessary and in the remaining two patients inadequate supervision of the treatment resulted in overdosage. In five cases the history of vitamin-D therapy was either unknown or not appreciated by the referring clinician so that three surgical procedures of dubious value were performed on two patients. Large doses of vitamin D should only be used when strictly indicated and on the understanding that close biochemical and clinical supervision is necessary.

Adolescent↗
PubMed1980

Vitamin-D poisoning: survey of causes in 21 patients with hypercalcaemia.

Hypercalcaemia developed in 21 patients due to vitamin-D poisoning; 2 were poisoned twice and 2 were poisoned three times. All patients had taken milligram doses of vitamin D, which for 5 patients was inappropriate. For the other 16 patients (mainly with hypoparathyroidism) milligram doses of vitamin D were appropriate; the patients were poisoned either early in therapy, trying to correct the plasma-calcium too quickly, or, later, because of failure to follow up patients properly. 2 patients died as a result of their intoxication. Constant vigilance is essential when patients are taking large doses of vitamin D.

Calcium↗
PubMed1980

End-organ resistance to 1,25-dihydroxycholecalciferol.

A 13-year-old girl with total alopecia who in infancy had rickets unresponsive to large doses of vitamin D2 is described. She had profound hypocalcaemia which was resistant to treatment with high doses of dihydrotachysterol, 1 alpha-hydroxycholecalciferol, and 1,25-dihydroxycholecalciferol. Serum concentrations of 25-hydroxyvitamin D were normal but those of 1,25-dihydroxycholecalciferol were markedly raised (674 and 745 pg/ml). In addition, 24,25-dihydroxyvitamin D was undetectable in serum. Administration of synthetic 24,25-dihydroxycholecalciferol was followed by normocalcaemia which persisted long after treatment was stopped. Her sister, who died at the age of 10 months, also had had total alopecia, rickets, and hypocalcaemia resistant to vitamin-D2 therapy. In this familial syndrome there seems to be end-organ resistance to the action of 1,25-dihydroxycholecalciferol, possibly as a result of changes at the receptor sites.

Adolescent↗
PubMed1983

Screening for subclinical osteomalacia in the elderly: normal ranges or pragmatism?

Although osteomalacia is known to be common in some sections of the elderly population, the disease is often subclinical and there is uncertainty about the point at which treatment is necessary. Identification and treatment of osteomalacia are inseparably bound; the response of varying degrees of subclinical disease to treatment with vitamin D or alfacalcidol is described here. The response is assessed in relation to a simply derived reference range based on standard biochemical measurements together with a Jamshidi needle biopsy of the iliac crest. Although this technique does not define a truly normal range it identifies a treatable abnormality which could form the basis of further study of the problem of subclinical osteomalacia in the elderly.

Aged↗
PubMed2002

Preparation of chitosan/ethylcellulose complex microcapsule and its application in controlled release of vitamin D2.

A system which consists of chitosan (CS) microcores entrapped within enteric polymer is investigated. Vitamin D2 (VD2) used as a model drug, was efficiently entrapped in CS microcores using spray drying and was microencapsulated by coating of ethylcellulose. The morphology and release properties of microcapsules were tested. The factors which influenced the preparation, including molecular weight of CS, concentration of CS solution, concentration of acetic acid and loading of VD2, were discussed. The results of release in vitro showed that the microcapsules could realize sustained release in intestine juice.

Acetic Acid↗
PubMed1999

Paricalcitol, a new agent for the management of secondary hyperparathyroidism in patients undergoing chronic renal dialysis.

Patients with end-stage renal disease commonly develop secondary hyperparathyroidism. Calcitriol may be administered to such patients to decrease the synthesis and secretion of parathyroid hormone (PTH) and to help maintain calcium and phosphorus homeostasis. However, the doses of calcitriol required to suppress serum PTH concentrations can lead to hypercalcemia or hyperphosphatemia in many patients undergoing hemodialysis. Paricalcitol is a new vitamin D analogue that is safe and effective in suppressing elevated concentrations of PTH in patients with established hyperparathyroidism who are maintained on chronic hemodialysis. As with vitamin D, the biologic action of paricalcitol is mediated through activation of the vitamin D receptor (VDR). The VDR functions as a ligand-induced transcription factor regulating the rate of expression of genes that are involved in controlling not only calcium homeostasis and bone remodeling but also hormone secretion, inhibition of cell growth, and induction of cell differentiation. In vitro studies have shown that paricalcitol inhibits PTH secretion from bovine parathyroid cells in a dose-dependent manner. Studies in renally insufficient rats demonstrated that paricalcitol caused approximately 10 times less elevation of serum calcium concentrations than calcitriol. In clinical studies, paricalcitol effectively decreased PTH by about 60% over a 12-week period. Mean serum concentrations of calcium were significantly increased but remained within the normal range. There were occasional (5/414 determinations) transient elevations in serum calcium above the upper limit of normal in some (5/401) patients. Serum phosphorus values did not change significantly compared with baseline, although they tended to be slightly higher in the paricalcitol-treated group than in the group receiving placebo. Elevations of the calcium-times-phosphorus product were relatively few but occurred more often in the paricalcitol than in the placebo group. The terminal half-life of paricalcitol was 5 to 7 hours in healthy subjects; in patients undergoing hemodialysis, it was 14 hours. Adverse events associated with paricalcitol use included, among others, chills, feeling unwell, fever, sepsis, palpitations, dry mouth, gastrointestinal bleeding, nausea, vomiting, edema, light-headedness, and pneumonia. Paricalcitol should be considered as an alternative to calcitriol in the treatment of patients who are undergoing maintenance hemodialysis for end-stage renal disease, as it has a decreased potential to induce hypercalcemia and hyperphosphatemia. Additional studies are required to determine the long-term effects of therapy.

Animals↗
PubMed2003

Toxicity and dose-response studies of 1-alpha hydroxyvitamin D2 in LH-beta-tag transgenic mice.

PURPOSE: To determine the effectiveness of a vitamin D analog, 1alpha-hydroxyvitamin D(2) (1alpha-OH-D(2)), in inhibiting retinoblastoma in a transgenic retinoblastoma model (LHbeta-Tag mouse) and to evaluate its toxicity. DESIGN: Experimental study using an animal (LHbeta-Tag transgenic mouse) randomized (controlled) trial. PARTICIPANTS AND CONTROLS: Two hundred seventeen LHbeta-Tag transgene-positive 8- to 10-week-old mice total; 179 drug-treated animals, 38 control animals. METHODS: Mice were fed a vitamin D- and calcium-restricted diet and were randomized to treatment groups receiving control (vehicle), or 0.1, 0.3, 0.5, or 1.0 micro g/day of 1alpha-OH-D(2) via oral gavage 5 times weekly for 5 weeks. Body weight was measured at the start of treatment and twice weekly during treatment. Animals were euthanized on the last day of treatment. The eyes were enucleated, processed histologically, and serially sectioned. Representative sections from the superior, middle, and inferior regions of each globe were examined microscopically and tumor areas were measured using Optimas software. Serum was collected for serum calcium levels. Kidneys were removed for histologic processing and were analyzed microscopically for kidney calcification. MAIN OUTCOME MEASURES: Mean tumor area was measured to determine drug effectiveness. Toxicity was assessed by survival, weight loss over the treatment period, serum calcium, and kidney calcification. RESULTS: The mean tumor size in each 1alpha-OH-D(2) group was smaller than controls (all P values < 0.02): control, 90,248 micro m(2); 0.1 micro g, 31,545 micro m(2); 0.3 micro g, 16,750 micro m(2); 0.5 micro g, 30,245 micro m(2); and 1.0 micro g, 16,049 micro m(2). No dose-dependent response curve was evident. The survival percentage for each group was as follows: control, 97%; 0.1 micro g, 91%; 0.3 micro g, 88%; 0.5 micro g, 70%; and 1.0 micro g, 63%. Mortality was higher in the 0.5- micro g and 1.0- micro g doses (P values < 0.01) compared with other treatment groups and with the control group. Serum calcium levels were significant in all treatment groups compared with controls (all P values < 0.0001). CONCLUSIONS: In the LHbeta-Tag mouse, 1alpha-OH-D(2) inhibits retinoblastoma with no significant increase in mortality in lower doses (0.1-0.3 micro g). 1alpha-OH-D(2) has approval by the Food and Drug Administration as an investigative drug for cancer treatment, and has shown efficacy with low toxicity in adult cancer trials. 1alpha-OH-D(2) meets the criteria for human clinical trials.

Animals↗
PubMed1981

Reduced 2,25-dihydroxyvitamin D and 24,25-dihydroxyvitamin D in epileptic patients receiving chronic combined anticonvulsant therapy.

Thirty-one adult epileptic outpatients on chronic combined anticonvulsant therapy were investigated. Eleven patients took vitamin D2 supplementation 400-1200 IU/day as multivitamin tablets. Mean serum calcium and renal calcium excretion were reduced. Serum alkaline phosphatase and urinary hydroxyproline excretion were increased. Forearm bone mineral content was reduced. Serum concentrations of 25-hydroxyvitamin D (25-OHD), 24-25-dihydroxyvitamin D (24,25-(OH)2D) and 1,25-dihydroxyvitamin D (1,25-(OH)2D) were reduced (p less than 0.001). A positive correlation was found between the serum 25-OHD and 24,25-(OH)2D concentrations (p less than 0.05) with the highest levels in those receiving vitamin D2 supplementation (p less than 0.01). Serum 1,25-(OH)2D correlated positively with renal calcium excretion (r = 0.65, p less than 0.001) suggesting that the intestinal calcium absorption in epileptic patients depends on 1,25-(OH)2D levels.

24,25-Dihydroxyvitamin D 3↗
PubMed1997

A new analog of 1,25-(OH)2D3, 19-NOR-1,25-(OH)2D2, suppresses serum PTH and parathyroid gland growth in uremic rats without elevation of intestinal vitamin D receptor content.

We have previously reported that 19-nor-1,25-(OH)2D2, a new analog of 1,25-(OH)2D3, suppresses parathyroid hormone (PTH) secretion in uremic rats in the absence of hypercalcemia or hyperphosphatemia. In the current study, we examined the effect of 19-nor-1,25-(OH)2D2 on parathyroid gland growth and intestinal vitamin D receptor (VDR) content. After induction of uremia by 5/6 nephrectomy, rats were divided into five experimental groups and received intraperitoneal injections of vehicle, 1,25-(OH)2D3 (2 or 6 ng/rat), or 19-nor-1,25-(OH)2D2 (25 or 100 ng/rat) three times a week for 8 weeks. Twelve normal rats received vehicle and served as the normal control group. During the course of the study, rats were maintained on a 1.0% calcium and 0.8% phosphorus diet. The higher dose of 1,25-(OH)2D3, 6 ng, significantly decreased PTH from 52.7 +/- 10.2 pg/mL in the uremic control group to 25.7 +/- 6.7 pg/mL (P < 0.01). This dose of 1,25-(OH)2D3, however, increased serum levels of both ionized calcium (4.71 +/- 0.05 to 4.85 +/- 0.06 mg/dL; P < 0.05) and phosphorus (4.34 +/- 0.30 to 6.67 +/- 0.63 mg/dL; P < 0.01). Both doses of 19-nor-1,25-(OH)2D2 decreased serum PTH as effectively as 1,25-(OH)2D3 without changes in serum calcium or phosphorus. The 100-ng dose of 19-nor-1,25-(OH)2D2 decreased PTH to 20.7 +/- 3.1 pg/mL (P < 0.01) and suppressed parathyroid gland growth by more than 50%. Both doses of 19-nor-1,25-(OH)2D2 also decreased endogenous 1,25-(OH)2D3 levels compared with uremic control rats (25 ng:30.4 +/- 2.0, P < 0.05, and 100 ng:27.9 +/- 3.2, P < 0.01, v 48.4 +/- 6.6 pg/mL). The 6-ng dose of 1,25-(OH)2D3 elevated intestinal VDR content (138.5 +/- 20.0 fmol/mg protein) compared with animals receiving both doses of 19-nor-1,25-(OH)2D2 (25 ng:84.0 +/- 11.9, P < 0.05, and 100 ng:78.4 +/- 10.9, P < 0.01). This was probably attributable to the marked decrease in endogenous 1,25-(OH)2D3 levels caused by both doses of 19-nor-1,25-(OH)2D2 because intestinal VDR correlated directly with serum 1,25-(OH)2D3 (r = 0.963; P = 0.008). Thus, 19-nor-1,25-(OH)2D2 appears to exert a selective action on the parathyroid glands compared with the intestine. Its low calcemic and phosphatemic properties may result from the decreased endogenous 1,25-(OH)2D3 levels that lead to a reduction in intestinal VDR. This selectivity makes this analog ideal for the treatment of secondary hyperparathyroidism.

Animals↗