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PubMed2005

Should older people in residential care receive vitamin D to prevent falls? Results of a randomized trial.

OBJECTIVES: To determine whether vitamin D supplementation can reduce the incidence of falls and fractures in older people in residential care who are not classically vitamin D deficient. DESIGN: Randomized, placebo-controlled double-blind, trial of 2 years' duration. SETTING: Multicenter study in 60 hostels (assisted living facilities) and 89 nursing homes across Australia. PARTICIPANTS: Six hundred twenty-five residents (mean age 83.4) with serum 25-hydroxyvitamin D levels between 25 and 90 nmol/L. INTERVENTION: Vitamin D supplementation (ergocalciferol, initially 10,000 IU given once weekly and then 1,000 IU daily) or placebo for 2 years. All subjects received 600 mg of elemental calcium daily as calcium carbonate. MEASUREMENTS: Falls and fractures recorded prospectively in study diaries by care staff. RESULTS: The vitamin D and placebo groups had similar baseline characteristics. In intention-to-treat analysis, the incident rate ratio for falling was 0.73 (95% confidence interval (CI)=0.57-0.95). The odds ratio for ever falling was 0.82 (95% CI=0.59-1.12) and for ever fracturing was 0.69 (95% CI=0.40-1.18). An a priori subgroup analysis of subjects who took at least half the prescribed capsules (n=540), demonstrated an incident rate ratio for falls of 0.63 (95% CI=0.48-0.82), an odds ratio (OR) for ever falling of 0.70 (95% CI=0.50-0.99), and an OR for ever fracturing of 0.68 (95% CI=0.38-1.22). CONCLUSION: Older people in residential care can reduce their incidence of falls if they take a vitamin D supplement for 2 years even if they are not initially classically vitamin D deficient.

Accidental Falls↗
PubMed1980

Vitamin D supplements in pregnant Asian women: effects on calcium status and fetal growth.

In a double-blind trial of vitamin D supplements in pregnant Asian women calciferol (ergocalciferol, 1000 IU/day) was administered to 59 women and placebo to 67 controls during the last trimester. The two groups had similar distributions of maternal age, height, parity, number of vegetarians, countries of origin, and sex and gestation of the infants. At entry to the trial maternal serum 25-hydroxy vitamin D (25-OHD) concentrations were low in both treatment and control groups and significantly lower in vegetarians than non-vegetarians. Mothers in the treatment group gained weight faster in the last trimester than those in the control group, and at term they and their infants all had adequate plasma 25-OHD concentrations, Mothers and infants in the control group, however, had low plasma concentrations of 25-OHD and calcium and raised plasma alkaline phosphatase (bone isoenzyme) activity. Five of these infants developed symptomatic hypocalcaemia. Almost twice as many infants in the control group were small for gestational age (29% v 15%), but there were no significant differences between the two groups of infants in antropometric measurements. Infants in the control group, however, had larger fontanelles, suggesting impaired ossification of the skull. Because of the benefits to mothers and infants in the treatment group and the absence of side effects, vitamin D supplements should be given to all pregnant Asian women in the United Kingdom.

Alkaline Phosphatase↗
PubMed2005

Low-dose vitamin D prevents muscular atrophy and reduces falls and hip fractures in women after stroke: a randomized controlled trial.

OBJECTIVE: Vitamin D supplementation is suggested to reduce the risk of falls among ambulatory or institutionalized elderly subjects. The present study was undertaken to address the reduced risk of falls and hip fractures in patients with long-standing stroke by vitamin D supplementation. METHODS: Ninety-six elderly women with poststroke hemiplegia were followed for two years. Patients were randomly assigned to one of the two groups, and 48 patients received 1,000 IU ergocalciferol daily, and the remaining 48 received placebo. The number of falls per person and incidence of hip fractures were compared between the two groups. Strength and tissue ATPase of skeletal muscles on the nonparetic side were assessed before and after the study. RESULTS: At baseline, serum 25-hydroxyvitamin D levels were in the deficient range (<10 ng/ml) in all patients; and vitamin D treatment enhanced serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels. Vitamin D treatment accounted for a 59% reduction in falls (95% CI, 28-81%; p = 0.003). There were increases in the relative number and size of type II muscle fibers and improved muscle strength in the vitamin D-treated group. Hip fractures occurred in 4 of 48 placebo group and 0 in 48 vitamin D2 group during the 2-year study period (log-rank, p = 0.049). CONCLUSION: Vitamin D may increase muscle strength by improving atrophy of type II muscle fibers, which may lead to decreased falls and hip fractures.

Accidental Falls↗
PubMed1976

Radioligand receptor assay for 25-hydroxyvitamin D2/D3 and 1 alpha, 25-dihydroxyvitamin D2/D3.

A competitive protein binding assay for measurement of the plasma concentration of 1 alpha, 25-dihydroxyvitamin D3 [1alpha, 25-(OH)2D3] has been extended to include the immediate precursor of this hormone, 25-hydroxyvitamin D3 (25-OHD3). In addition, the assay system is capable of measuring the two metabolic products of ergocalciferol, namely. 25-hydroxyvitamin D2 (25-OHD2) and 1alpha, 25-dihydroxyvitamin D2 [1alpha, 25-(OH)2D2]. The target tissue assay system consists of a high affinity cytosol receptor protein that binds the vitamin D metabolites and a limited number of acceptor sites on the nuclear chromatin. By utilizing a series of chromatographic purification steps, a single plasma sample can be assayed for any of the four vitamin D metabolites either individually or combined. Therefore, the assay procedure allows for both the quantitative and qualitative assessment of the total active vitamin D level in a given plasma sample. To show that the binding assay was capable of measuring 1alpha, 25-(OH)2D2 as well as 1alpha, 25 (OH)2D3, two groups of rats were raised. One group, supplemented with vitamin D3, produced assayable material that represented 1alpha, 25-(OH)2D3. The other group, fed only vitamin D2 in the diet, yielded plasma containing only 1alpha, 25-(OH)2D2 as the hormonal form of the vitamin. The circulating concentrations of the two active sterols were nearly identical (15 ng/100 ml) in both groups, indicating that the competitive binding assay can be used to measure both hormonal forms in plasma. In a separate experiment, 1alpha, 25-(OH)2D2 was generated in an in vitro kidney homogenate system using 25-OHD2 as substrate. Comparison of this sterol with 1alpha, 25-(OH)2D3 in the assay system showed very similar binding curves; the D2 form was slightly less efficient (77%). Comparison of the respective 25-hydroxy forms (25-OHD2 vs. 25-OHD3) at concentrations 500-fold that of 1alpha, 25-(OH)2D3, again suggested that the binding of the D2 metabolite was slightly less efficient (71%). Finally, the assay was employed to measure the total active vitamin D metabolite pools in the plasma of normal subjects and patients with varying degrees of hypervitaminosis D. The normal plasma levels of 25-OHD and 1alpha, 25-(OH)2D measured in Tucson adults were 25-40 ng/ml and 2.1-4.5 ng/100 ml, respectively. Both sterols were predominately (greater than 90%) in the form of vitamin D3 metabolites in this environment. Typical cases of hypervitaminosis D exhibited approximately a 15-fold increase in the plasma 25-OHD concentration, and a dramatic changeover to virtually all metabolites existing in the form of D2 vitamins. In contrast, the circulating concentration of 1alpha, 25-(OH)2D was not substantially enhanced in vitamin D-intoxicated patients. We therefore conclude that hypervitaminosis D is not a result of abnormal plasma levels of 1alpha, 25-(OH)2D but may be cuased by an excessive circulating concentration of 25-OHD.

Animals↗
PubMed1978

A familial syndrome of decrease in sensitivity to 1,25-dihydroxyvitamin D.

Typical features of hereditary vitamin D-dependent (pseudovitamin D-deficient) rickets were observed beginning at ages 20 and 5 months in a brother and sister. Both had calcium malabsorption correctable with high doses of 25-hydroxyvitamin D. During periods of hypocalcemia they both manifested secondary hyperparathyroidism with hypophosphatemia and high serum concentrations of endogenously produced 1,25-dihydroxyvitamin D. 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. Chemical features of vitamin D deficiency were corrected in the presence of high circulating concentrations of 1,25-dihydroxyvitamin D2, produced endogenously, or of 1,25-dihydroxyvitamin D3, administered by mouth. Serum concentrations of 25-hydroxyvitamin D2, 25-hydroxyvitamin D3, 24,25-dihydroxyvitamin D, and 1,25-dihydroxyvitamin D were normal in five first degree relatives. We conclude that in these five first degree relatives. We conclude that in these siblings, rickets and osteomalacia resulted from a hereditary decreased sensitivity to 1,25-dihydroxyvitamin D at the intestine and perhaps other vitamin D target tissues.

Absorption↗
PubMed1980

Vitamin D metabolism in hypoparathyroidism.

Only moderately reduced serum 1,25-dihydroxyvitamin D [1,25(OH)2D3] levels were found in 13 hypoparathyroid patients and in 1 pseudohypoparathyroid patient, indicating that factors other than parathyroid hormone are able to mediate the basal production of 1,25(OH)2D3. A significant correlation was found between the levels of circulating 25-hydroxyvitamin D (25OHD) and 1,25(OH)2D, suggesting that a high concentration of 25OHD was able to increase the renal production of 1,25(OH)2D, whereas hypocalcemia and changes in serum phosphate became less important in the present situation. The serum 25OHD and 1,25(OH)2D concentrations were followed during the change of treatment from ergocalciferol to 1 alpha-hydroxycholecalciferol (1 alpha-OHD3). A biological half-life of 3 weeks could be estimated for the plasma 25OHD. The increase in serum 1,25(OH)2D correlated with the dose of 1 alpha-OHD3 given, whereas no correlation was found between the serum calcium level and the 1,25(OH)2D concentration. Unexpected increases and decreases in serum calcium were observed at the same dose of 1 alpha-OHD3 in the same patient and at serum 1,25(OH)2D concentrations within the physiological range.

25-Hydroxyvitamin D 2↗
PubMed1992

Tertiary hyperparathyroidism during high phosphate therapy of familial hypophosphatemic rickets.

We report the development of severe tertiary hyperparathyroidism in three girls treated for familial hypophosphatemic rickets and characterize parathyroid function in vivo and in vitro. All patients had been previously treated with relatively large doses of inorganic phosphorus (125 mm/day) and ergocalciferol or calcitriol for several years and had radiographic evidence of long-standing hyperparathyroidism. Even in the presence of extremely elevated PTH levels, oral phosphate lowered serum calcium levels in vivo and further stimulated PTH secretion. Profound multiglandular parathyroid hyperplasia was found in each patient at surgery. Examination of the secretory characteristics of the excised parathyroid tissue revealed that either relatively high calcium concentrations were generally needed to suppress PTH secretion or PTH secretion was not suppressible. Caution is recommended when relatively large doses of phosphate are used to treat familial hypophosphatemic rickets.

Calcitriol↗
PubMed2006

Doxercalciferol treatment of secondary hyperparathyroidism.

OBJECTIVE: To review the pharmacology, pharmacokinetics, effectiveness, safety, and therapeutic considerations related to the use of doxercalciferol in the treatment of secondary hyperparathyroidism. DATA SOURCES: A MEDLINE search (1966-June 2006) was conducted using the key words vitamin D, ergocalciferols, and secondary hyperparathyroidism. Text word searches were also performed for the terms 1-alpha-hydroxy-vitamin D(2), 1-alpha-hydroxyergocalciferol, Hectorol, and doxercalciferol. Searches were limited to studies published in English and conducted in human subjects. STUDY SELECTION AND DATA EXTRACTION: All published clinical studies evaluating the safety and effectiveness of doxercalciferol in secondary hyperparathyroidism were reviewed, and anecdotal patient reports were also evaluated. Selected clinical studies involving the use of calcitriol and/or paricalcitol in the treatment of secondary hyperparathyroidism were also included. DATA SYNTHESIS: Doxercalciferol effectively reduces parathyroid hormone levels in patients with chronic kidney disease (CKD). Both oral and intravenous administration can significantly increase serum calcium and/or phosphorus levels as evidenced by placebo-controlled clinical trials. This agent has not been studied comparatively with calcitriol or paricalcitol to assess relative safety. CONCLUSIONS: Doxercalciferol is approved for and effective in the treatment of secondary hyperparathyroidism related to CKD, both before and during dialysis, but has not demonstrated a lower incidence of hypercalcemia and/or hyperphosphatemia in relation to other vitamin D therapies. The drug is available in both oral and intravenous dosage forms. Doxercalciferol should be maintained as a formulary alternative for patients unresponsive to or intolerant of other vitamin D therapies, but comparative randomized studies are needed to differentiate its place in therapy.

Ergocalciferols↗
PubMed1997

Interleukin-1alpha and beta in growth plate cartilage are regulated by vitamin D metabolites in vivo.

Matrix remodeling plays a prominent role in growth plate calcification. Since interleukin-1 (IL-1) has been implicated in stimulating proteinase production and inhibiting matrix synthesis in articular cartilage, we examined whether IL-1 was present in growth plate and whether the vitamin D metabolites, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3; 1,25) and 24,25(OH)2D3 (24,25), regulate the level of IL-1 found in this tissue. Sprague-Dawley rats were placed on normal (Normal rats) or rachitogenic diet (-VDP rats). The -VDP rats were either left untreated, injected 24 h prior to euthanasia with 24,25 (-VDP+24,25 rats) or 1,25 (-VDP+1,25 rats), or were given ergocalciferol (Ergo rats) orally, 48 h prior to euthanasia. Growth plates were harvested and extracted in buffer containing 1 M guanidine. IL-1 activity was measured by adding authentic cytokine or growth plate extracts to cultures of lapine articular cartilage and assaying release of glycosaminoglycans (GAGs) and changes in collagenase and neutral metalloproteinase activity. Neutralization of activity in the extracts was performed using polyclonal antisera to IL-1alpha or IL-1beta. An ELISA was used to determine levels of IL-1alpha and beta in the extracts. All extracts contained IL-1alpha and beta, as determined by ELISA. Levels of IL-1beta, but not IL-1alpha, were affected by the vitamin D status of the animal. Extracts from -VDP+24,25 animals contained significantly more IL-1beta than any of the other treatment groups, with the level found in these animals being 3-fold higher than normal and 2-fold higher than -VDP. Extracts were also tested in the bioassay to determine the level of active cytokine present. All growth plate extracts contained activity which altered GAG and proteinase release by lapine articular cartilage. Extracts from -VDP-, -VDP+1,25-, and -VDP+Ergo-treated rats stimulated a 40% increase in glycosaminoglycan release compared with extracts from normal rats. In contrast, extracts from -VDP+24,25-treated rats stimulated a 300% increase in glycosaminoglycan release. Both collagenase and neutral metalloproteinase activity of lapine cartilage were increased after incubation with the growth plate extracts. Collagenase activity was significantly increased 8- to 13-fold by the addition of extracts from -VDP-, -VDP+24,25-, or -VDP+1,25-treated animals. Neutral metalloproteinase activity was similarly increased by 4- to 10-fold. To characterize this activity further, growth plate extracts were incubated with neutralizing antibody to IL-1alpha or beta prior to addition to the lapine articular cartilage cultures. When antibodies were used separately, only partial inhibition was observed; incubation with both antibodies blocked 25% of the glycosaminoglycan release observed without antibody and greater than 80% of the enzyme activity released by the articular cartilage cultures. The results of this study show that growth plate cartilage contains both IL-1alpha and beta and indicate that vitamin D regulates the level of IL-1 in this tissue.

24,25-Dihydroxyvitamin D 3↗
PubMed1981

The influence of vitamin D intake on serum calcium in tuberculosis.

We report the first prospective controlled study designed to determine the effect of vitamin D ingestion on serum calcium concentration in patients with tuberculosis. Every patient admitted to the tuberculosis ward over a 6 month period, who was free of any condition which might influence serum calcium concentration, was randomly assigned to one of two groups. The diet of the first group was substituted with ergocalciferol 5000 units daily. The diet of the second group was not supplemented. In addition, the second group was randomly subdivided into two subgroups. The first subgroup received a diet unrestricted in vitamin D. The second subgroup received a diet containing less than 50 units of vitamin D. Serum calcium was determined at weekly intervals. In contradistinction to the results of a previously reported retrospective study, there was no significant difference between the group receiving supplemental vitamin D and the control group at any time during the entire period of study. Furthermore, there was no significant difference between the subgroup of patients receiving normal dietary vitamin D and the subgroup maintained on the diet restricted in vitamin D.

Adult↗
PubMed1981

Pharmacology and therapeutic use of vitamin D and its analogues.

The term vitamin D is generally used to describe a number of chemically related compounds with common antirachitic properties, but which have differences in the rapidity of their action, the way they are produced in the body, and the conditions under which their results are optimal. Ergocalciferol, cholecalciferol, 25-hydroxycholecalciferol (calcifediol), dihydrotachysterol, 1 alpha-hydroxycholecalciferol (alfacalcidol), and 1,25-dihydroxycholecalciferol (calcitriol) are currently the most commonly used vitamin D metabolites. In man, cholecalciferol produced on the skin and the fraction obtained from the diet in the gastrointestinal tract are converted in the liver to 25-hydroxycholecalciferol and then in the kidney to 1,25-dihydroxycholecalciferol. The demonstration of these metabolic pathways has helped to elucidate the aetiology of such conditions a hepatobiliary osteodystrophy, drug-induced anticonvulsant osteomalacia, the hypocalcaemia of hypoparathyroidism and above all azotaemic osteodystrophy. In the therapy of azotaemic osteodystrophy, the period of 'vitamin D resistance' when large doses of vitamin D2 and D3 had to be used is now over, and these patients can be efficiently and successfully treated with almost physiological doses of 1 alpha-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol. Attention to diet, calcium supplements and oral phosphate binders are also important. During repetitive haemodialysis, the above principles still hold true, but in some of these patients an osteomalacic syndrome resistant to 1,25-dihydroxycholecalciferol has been recognised. These patients readily become hypercalcaemic when given 1,25-dihydroxycholecalciferol and their fractures and osteomalacia do not improve. Aluminium intoxication, possibly related to the use of impure dialysis fluid, is currently thought to be the most likely explanation of this dialysis osteomalacic syndrome.

Bone Diseases↗
PubMed2000

Comparison of commercially available (125)I-based RIA methods for the determination of circulating 25-hydroxyvitamin D.

BACKGROUND: Measurement of circulating 25-hydroxyvitamin D [25(OH)D] is important in the management of metabolic bone disease. The aim of this study was to compare two widely used methods for the quantification of circulating 25(OH)D with attention to their abilities to measure 25-hydroxylated ergocalciferol (vitamin D(2)) [25(OH)D(2)] and cholecalciferol (vitamin D(3)) [25(OH)D(3)]. METHODS: We used two commercially available, Food and Drug Administration-approved, radioiodine ((125)I)-based RIA kits for the detection of 25(OH)D (DiaSorin, Stillwater, MN and IDS Ltd, Tyne and Wear, United Kingdom). These methods were tested for general assay performance, including antibody specificity. Results were compared with those of an HPLC-based direct ultraviolet detection method. RESULTS: Within- and between-run CVs were </=10%. Both methods quantitatively recovered 25(OH)D(3) added to serum, but only the DiaSorin kit quantitatively recovered 25(OH)D(2). The primary antibody in the IDS kit had unequal reactivities with pure 25(OH)D(2) and 25(OH)D(3), whereas the DiaSorin primary antibody reacted with them equally. In 50 patient samples assayed by HPLC, the IDS method, but not the DiaSorin method, underestimated total circulating 25(OH)D when significant circulating 25(OH)D(2) was present in patient samples. CONCLUSIONS: Some immunoassays may underestimate total 25(OH)D when 25(OH)D(2) constitutes an appreciable part of the total.

Adolescent↗
PubMedDate not supplied

Vitamin d deficiency in breast-fed toddlers.

SUMMARY: The evaluation of genu varum and intoeing in young toddlers is a frequent problem seen by the primary care physician and the orthopaedic surgeon. This report describes six nonwhite breast-fed toddlers with extreme genu varum. Clinical and radiographic findings were consistent with vitamin D-deficiency rickets. Within 3 to 6 months of the initiation of ergocalciferol treatment, reparative processes were evident on both radiographic and clinical examinations. Laboratory studies also showed underlying correction. With the current emphasis on the benefits of breast-feeding and the limitation of sunlight, this diagnosis must remain on the differential in the evaluation of genu varum.

Black or African American↗
PubMed2001

[Hypovitaminosis D: a veiled diagnosis].

Four cases of hypovitaminosis D were seen in a general practitioner's population in the Netherlands: a Somalian veiled woman aged 53 and her 11-year-old daughter, a dark-skinned Surinam woman aged 31, and a veiled Moroccan woman aged 56 years. This cause of myopathy has only been recently recognised and is more prevalent than often thought, especially in high-risk groups such as veiled and dark-skinned immigrants who lack sunlight in the Netherlands. Symptoms are muscle pain and mainly proximal muscle weakness resulting in difficulties in ascending a staircase or getting up out of a chair. The diagnosis is made on the basis of a detailed history and measurement of serum 25-hydroxyvitamin D. Calcium and serum alkaline phosphatase activity may be normal. Treatment with ergocalciferol is effective and cheap. As diagnosis and treatment are relatively simple, finding and treating hypovitaminosis D is a rewarding challenge to primary health care practitioners in the Netherlands.

25-Hydroxyvitamin D 2↗
PubMed2004

[Vitamin D deficiency/insufficiency in patients with chronic kidney disease stage 3 and 4 -- current concept and its therapeutic strategy].

Vitamin D deficiency/insufficiency, which is clinically represented by low 25(OH)D concentration, is frequently seen in patients with CKD stage 3 and 4. Although its cause is unknown, hypovitaminosis D is partly associated with low 1,25(OH)2D in these patients, possibly leading to advancement of renal osteodystrophy. Recently, in United States, K/DOQI (Kidney disease outcomes quality initiative) guideline indicated that vitamin D deficiency/insufficiency of 25(OH)D concentration less than 30 ng/mL should be treated by supplementation of ergocalciferol. A Japanese guideline to treat vitamin D deficiency/insufficiency should be urgently established.

Biomarkers↗
PubMed2004

[Vitamin D supplementation for chronic kidney disease according to the guideline issued by DOQI].

Supplementation of vitamin D in food is available in Japan, therefore, vitamin D deficiency is not likely to occur in our country. But, in the case of nephrotic syndrome and strict dietary protein restriction, low serum 25(OH)D level might develop in chronic kidney disease (CKD)patients. Guideline issued by National Kidney Foundation as DOQI recommend the use of vitamin D2 (ergocalciferol) when serum 25(OH)D level in CKD patients become less than 30 ng/mL. In addition, for the CKD patients with stage 5, the use of active vitamin D3 is recommended because a conversion to 1,25(OH)2D3, which is the most potent vitamin D, might be impossible in these patients. However, vitamin D2 product as a supplementary medicine is not available in Japan unfortunately. In this context, I try to explain the background of the recommendation of vitamin D2 for CKD patients.

Biomarkers↗
PubMed1991

Can vitamin D deficiency produce an unusual pain syndrome?

An unusual pain occurred in five patients in the presence of compromised vitamin D status and resolved 5 to 7 days after supplementation with vitamin D in the form of ergocalciferol. The pain had a hyperesthetic quality and did not respond to the use of analgesics, including opiate derivatives. Treatment with therapeutic levels of a tricyclic antidepressant did not bring relief of symptoms. In one case, months after treatment and subsequent improvement of vitamin D status and pain, the vitamin D status again declined and the pain recurred. The pain again resolved with vitamin D replacement and improvement of levels. There may be a pain syndrome associated with vitamin D depletion that appears as hyperesthesia worsened by light, superficial pressure or even small increments of movement. This pain restricts mobility and function and may lead to further complications, such as pressure sores.

Adult↗
PubMedDate not supplied

[Possible role of free radicals in the transformations and mechanism of physiological action of vitamin D].

Deficiency of vitamine D is accompanied with a decrease of ESR signal intensity from g = 2.003, as well as of the signals with g = 1.94 and gav. = 2.25 in the liver and kidneys of young rats. Injection of 2.5 g ergocalciferole (vitamine D2) to these animals results in a complete or partial normalization of the intensity of these signals during 6--16 hrs and an increase of the ESR signal intensity from g = 2.003 in small intestine mucosa.

Animals↗