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PubMed1984

Extended treatment of primary osteoporosis by sodium fluoride combined with 25 hydroxycholecalciferol.

Nineteen patients suffering from primary osteoporosis, all having at least one vertebral collapse, initially received 50 mg of sodium fluoride alone per day for 6-18 months. Subsequently fluoride was associated with 25-50 micrograms of 25 OH cholecalciferol (calcifediol) per day for 6-18 months in 12 of these patients and 9 were treated for 31-58 months. As control group, 9 patients were given placebo for 6-18 months. The effect of the treatment was assessed by three methods: 1) the metacarpal index (MI) determined by radiogrammetry, 2) the calcium content of the hand bone (Ca) measured by local neutron activation, 3) the iliac bone histomorphometry. MI and (Ca) did not change significantly at any time in any group. In each group there was a significant increase in trabecular bone volume, osteoid volume, osteoid surfaces and a significant decrease in mineralization fronts. On the other hand, the changes in osteoblastic surfaces, osteoclastic surfaces, number of osteoclasts/mm2 were not significant in any group. No change was observed in the placebo group. These data suggest that the increase in the trabecular volume of fluorided bone is mainly due to the increase in osteoid which itself is due to a bone mineralization defect despite the association of calcifediol. This is probably one of the reasons why (Ca) does not change significantly.

Aged↗

PubMed1998

Vitamin D treatment in myelodysplastic syndromes.

Myelodysplastic syndromes (MDS) are a group of clonal disturbances with defective cellular differentiation. Vitamin D3 (VD) analogues can act on the differentiation and maturity of different cell lines. We studied the effects of VD on a series of patients with MDS in an open-design trial. Nineteen patients, 12 men and seven women, with MDS were included. Patients were 74.8 +/- 5.6 years (mean +/- SD), seven had refractory anaemia with ringed sideroblasts, five had refractory anaemia, one had refractory anaemia with excess of blasts and six had chronic myelomonocytic leukaemia. All the patients were in a low to intermediate risk group. Mean follow-up period was 26.21 months, range 9-75. Responders were defined as follows: granulocyte or platelet count increase by 50%, or haemoglobin increase of 1.5 g/dl or transfusion needs decrease by 50%. The first five patients received 266 microg of calcifediol three times a week and the other 14 received calcitriol (0.25-0.75 microg/d). Response was observed in 11 patients. In the calcifediol-treated group, one case responded, three were nonresponders, and one showed progression. In the calcitriol group, 10 were responders (two with major response), and four were non-responders. No correlation was observed between baseline levels of vitamin D metabolites and the presence of response. No hypercalcaemia was observed. Treatment with vitamin D3 metabolites could induce a long-standing response of the haematological disturbance in some low-intermediate risk MDS patients without inducing hypercalcaemia.

Aged↗

PubMed1990

[Intestinal calcium and vitamin D absorption in essential arterial hypertension].

The intestinal absorption of calcium and seric levels of calcifediol and calcitriol were studied in 27 patients with essential blood hypertension (BH) and 20 normal patients in a control group. The hypertensive patients were divided in three groups depending on the plasmatic renin activity (PRA), (high, normal, low). We found a significantly higher rate of intestinal calcium absorption in the group of patients with BH and low PRA than in the control group (22.73 +/- 19.05 and 10.7 +/- 17.13% respectively) (p less than 0.025). The seric levels of calcitriol (1,25 (OH) 2D3) were significantly higher in the group of patients with hypertension and low PRA than in the control group (48.16 +/- 5.25 and 33.13 +/- 2.9 pg/ml respectively) (p less than 0.025). The seric levels of calcifediol (25-OH-D3) were significantly lower in low PRA patients than those patients in the control group (12.37 +/- 2.44 and 21.94 +/- 2.82 ng/ml respectively) (p less than 0.025). We concluded that patients with essential blood hypertension and low PRA have significantly lower calcitriol levels than any other group, probably conditioning the greater intestinal calcium absorption shown in this group.

Calcifediol↗

PubMed1996

Corticosteroid-induced bone loss. Prevention and management.

Osteoporosis is one of the most serious adverse effects experienced by patients receiving long term corticosteroid therapy. Bone loss occurs soon after corticosteroid therapy is initiated and results from a complex mechanism involving osteoblastic suppression and increased bone resorption. There are a number of factors that may increase the risk of corticosteroid-induced osteoporosis [smoking, excessive alcohol (ethanol) consumption, amenorrhoea, relative immobilisation, chronic obstructive pulmonary disease, inflammatory bowel disease, hypogonadism in men, organ transplantation]. The initial assessment of patients about to start taking corticosteroids should include measurement of spinal bone density, urinary calcium level and plasma calcifediol (25-hydroxycholecalciferol) level; serum testosterone levels should also be measured when hypogonadism is suspected. Many different drugs have been used to prevent osteoporosis in patients receiving long-term corticosteroid therapy, including thiazide diuretics, cholecalciferol (vitamin D) metabolites, bisphosphonates, calcitonin, fluoride, estrogens, anabolic steroids and progesterone. At present, however, published studies have failed to demonstrate a reduction in the rate of fracture using different preventive pharmacological therapies in patients being treated with corticosteroids on a continuous basis. Among the drugs studied, bisphosphonates (pamidronic acid and etidronic acid) and calcitonin appear to be effective in increasing bone density. Cholecalciferol preparations have been reported to be effective in some, but not all, studies. Limited data have shown positive results with thiazide diuretics, estrogen, progesterone and nandrolone. When treating patients with corticosteroids, the lowest effective dose should be used, with topical corticosteroids used whenever possible. Auranofin may be considered in patients with corticosteroid-dependent asthma. Patients should take as much physical activity as possible, maintain an adequate daily intake of calcium (1000 mg/day0 and cholecalciferol (400 to 800 U/day), stop smoking and avoid excessive alcohol intake. It is important to detect and treat hypogonadism in men, if present, and to replace gonadal hormones in postmenopausal women or amenorrhoeic premenopausal women, and to detect and correct cholecalciferol deficiency. A thiazide diuretic should be considered if hypercalciuria is present (urinary calcium excretion in excess of 4 mg/kg/day). High-risk patients and those with established osteoporosis should be treated with bisphosphonates (cyclical etidronic acid or intravenous pamidronic acid), nasal calcitonin, or calcifediol or calcitriol. Patients receiving cholecalciferol preparations should be carefully monitored for hypercalciuria and hypecalcaemia.

Adrenal Cortex Hormones↗

PubMed1985

Families of children with idiopathic hypercalciuria. Evidence for the hormonal basis of familial hypercalciuria.

Six children with idiopathic hypercalciuria and their families were examined with an oral calcium loading test. Family members were divided into two clinical categories: group 1 consisted of the six index children and their parents and siblings with urolithiasis or unexplained hematuria; group 2 comprised the remaining parents and siblings without signs or symptoms associated with hypercalciuria. The results revealed that fasting urinary excretion of calcium was similar in both groups, but group 1 displayed a greater calciuric response to an oral calcium load. Serum concentrations of calcitriol (1,25-dihydroxyvitamin D3) and calcium were higher in group 1 than in group 2, while parathyroid activity was lower in group 1 patients. Urinary excretion of sodium, phosphorus, and magnesium, urine pH, serum levels of calcifediol (25-hydroxyvitamin D3) and phosphorus, and the renal tubular threshold for phosphate were not significantly different in the two groups. These findings suggest that idiopathic hypercalciuria may arise from a disturbance in the regulation of vitamin D metabolism that mediates enhanced intestinal absorption of calcium.

Adult↗

PubMed1994

Increase of calcitriol during treatment with protein-reduced diet in patients with renal failure.

Vitamin D metabolites 25-OH-D3 (calcifediol) and 1,25-(OH)2-D3 (calcitriol) were measured in plasma in 16 patients with advanced chronic renal failure during treatment with a protein-restricted diet for 6 months. The glomerular filtration rate (GFR) decreased only marginally, from 8.3 to 7.9 ml/min, during the study while there was a significant decrease of serum urea levels after the initiation of the protein-reduced diet. Calcitriol levels rose significantly (p < 0.05) after 3 months from 17.1 to 27.7 pg/ml but fell after another 3 months to nearly their initial values, 15.3 pg/ml. The serum phosphate levels changed during the same periods from 1.99 to 1.67 to 1.93 mmol/l. There were significant inverse correlations between the calcitriol and phosphate levels at the start and after 3 months but not after 6 months. There was also a significant correlation between the changes in calcitriol and initial GFR. A subgroup of patients with decreased or unchanged calcitriol concentrations during dietary treatment had significantly higher serum phosphate and creatinine and significantly lower standard bicarbonate concentrations. Multivariate regression analysis for the pooled set of data with calcitriol as the dependent variable showed significant values for GFR (p < 0.02), body mass index (p < 0.02), and serum phosphate concentrations (p < 0.04). These results show the importance of phosphate control and renal function for the regulation of calcitriol synthesis.

Adult↗

PubMed2002

Dramatic improvement of BMD following vitamin D therapy in a bone marrow transplant recipient.

Bone marrow transplantation is now an established successful treatment for several hematologic malignancies. Bone loss is among the long-term adverse effects of this procedure. The underlying pathophysiology is believed to be multifactorial. We report a case of osteoporosis in a young patient who underwent allogenic bone marrow transplantation for acute lymphoblastic leukemia that was complicated by intestinal graft-versus- host disease. Her bone density measurement showed T-scores of -3.46 and -2.47 in the lumbar spine and femoral neck respectively. On evaluation, she had low normal serum calcium, low urine calcium, low 25- hydroxyvitamin D, elevated total and bone specific alkaline phosphatases, and elevated parathyroid hormone. Following treatment with calcifediol, the biochemical markers normalized and the bone mineral density increased by 88% in the lumbar spine and almost 60% in the femoral neck, both of which were above the mean for her age group. We believe that the graft-versus-host disease caused a malabsorptive state that led to vitamin D deficiency and possible resistance and consequent osteomalacia.

Adolescent↗

PubMed1984

Vitamin D conversion by sarcoid lymph node homogenate.

Recent studies suggest that hypercalcemia of sarcoidosis is due to high blood concentrations of calcitriol and that this compound may be synthesized at an extra-renal site. We report that sarcoid lymph node homogenate metabolized calcifediol to a substance indistinguishable from calcitriol, whereas six nonsarcoid lymph nodes failed to produce this compound.

Calcifediol↗

PubMed1985

Bone disease in alcohol abuse.

We evaluated bone disease in eight white men between the ages of 49 and 61 years who had been abusing alcohol for at least 10 years. The mean density of vertebral cancellous bone was 58% of normal, whereas the mean density of appendicular cortical bone was 90% of normal. Marked reduction in active bone resorption and bone formation was seen without evidence of osteomalacia. Serum levels of calcium and magnesium were in the lower range of normal; serum levels of phosphorus, calcifediol, and calcitriol were normal; and serum levels of parathyroid hormone and nephrogenous cyclic adenosine monophosphate were in the higher range of normal. These data suggest that bone disease in these subjects is not due to inhibition of parathyroid hormone secretion or function, or abnormal vitamin D metabolism, but to an inhibition of bone remodeling by a mechanism independent of the calciotropic hormones.

Adult↗

PubMed1999

Rickets caused by excessive renal phosphate loss and apparent abnormal vitamin D metabolism in a cat.

Rickets was diagnosed in a 1-year-old cat with a history of weakness, osteopenia, and recurrent fractures. Processes causing rickets include vitamin D deficiency caused by inadequate, nutrition, lack of exposure to sunlight, defective metabolism of parent vitamin D to active metabolites, inherited vitamin D receptor defects, hypoparathyroidism, chronic renal failure, renal loss of phosphate, or malabsorptive states resulting from gastrointestinal or hepatic diseases. On the basis of analysis of serum 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D2 and D3 concentrations, serum biochemical analysis, and urinary fractional clearance of electrolytes, the causes of rickets in our cat, were most compatible with a combination of excessive loss of phosphorus via the kidneys and deficient or abnormal hepatic 25-hydroxylation of vitamin D. Calcifediol treatment and twice daily administration of phosphate salts resulted in clinical improvement and increases in mineralization of the skeleton, as evidenced on radiographic evaluation.

Animals↗

PubMedDate not supplied

[Osteomalacia and anticonvulsant treatment in bedridden patients. Apropos of 2 cases].

This article sets two bedridden mental retarded clinical cases, under a long run anticonvulsive treatment, who suffered from an osteomalacia syndrome, concealed until spontaneous fractures occurred and cured by a calcifediol treatment. Through these two cases, we remind you that in a psychiatric hospital, and in particular among mental retarded patients, anticonvulsive therapy can easily coincide with feeding problems and lack of period of sunshine. The osteomalacia risk is no longer exceptional and is to be considered since its detection and treatment are simple and results are convincing.

Adult↗

PubMed1982

Metabolites and analogues of vitamin D. Which for what?

The discovery and chemical synthesis of several biologically active derivatives of vitamin D have increased the number of compounds available for the treatment of disorders of bone and mineral metabolism. Calcitriol is the most active natural metabolite of vitamin D, but analogues like dihydrotachysterol and calcifediol also are safe and effective therapeutic agents. These vitamin D congeners have been useful in the treatment of renal osteodystrophy, hypoparathyroidism, and other disorders refractory to vitamin D therapy. Certain analogues may offer distinct advantages over vitamin D, depending on the nature of the defect. All vitamin D derivatives should be used cautiously, with frequent monitoring of serum calcium levels to prevent toxic reactions.

Bone Diseases, Metabolic↗

PubMed1982

Calcitriol deficiency in idiopathic juvenile osteoporosis.

Low plasma calcitriol (1,25-dihydroxycholecalciferol) and normal serum calcifediol (25-hydroxycholecalciferol) levels were noted during the evaluation of an 11-year-old girl with diffuse osteoporosis and pathologic fractures. The onset of osteoporosis prior to puberty and the characteristic metaphyseal location of the fractures supported the diagnosis of idiopathic juvenile osteoporosis (IJO). Treatment with calcitriol, 1.0 microgram daily, was associated with bone mineral accretion and a diminished incidence of fractures. Plasma calcitriol levels returned to normal when the disease resolved following puberty. This experience suggests a relationship between calcitriol deficiency and the pathogenesis of IJO.

Bone and Bones↗

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↗

PubMed1994

Passive uptake in the small intestine and active uptake in the hindgut contribute to the highly efficient mineral metabolism of the common mole-rat, Cryptomys hottentotus.

Cryptomys hottentotus has no access to dietary or endogenous sources of cholecalciferol (D3). Serum concentrations of calcifediol (25(OH)D3) were undetectable (< 5 ng/ml) and calcitriol (1,25(OH)2D3), although detectable in plasma, was at a low concentration (31.40 (SEM 3.06 pg/ml). Despite their naturally impoverished vitamin D status, these animals exhibited highly efficient mineral absorption processes (Ca apparent fractional absorption efficiency, AFA (%) 95.33 (SEM 1.36); inorganic P (P(i)) AFA (%) 93.49 (SEM 0.81)). Furthermore, plasma mineral content was tightly regulated (Ca 2.57 (SEM 0.08) mmol/l; Mg 1.23 (SEM 0.05) mmol/l; P(i) 2.12 (SEM 0.15) mmol/l). Mode of uptake in C. hottentotus was unlike that in other D3-replete mammals. First, passive (rather than active) uptake occurred in the traditional site of active Ca absorption (with serosal:mucosal (S:M) ratios in the duodenum of 1.32 (SEM 0.13)), and the only site of active Ca uptake was the hindgut (caecum S:M 3.35 (SEM 0.46); proximal colon S:M 2.13 (SEM 0.30)). Despite the presence of active uptake in these hindgut regions, their overall contribution to the daily rate of mineral absorption was small (9.53 (SEM 1.27)%). These underground inhabitants rely upon highly efficient, passive mineral uptake. This is adequate to meet their mineral requirements and maintain mineral homeostasis in the absence of vitamin D.

Animals↗

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↗

PubMed2006

Minimizing bone abnormalities in children with renal failure.

Renal osteodystrophy (ROD), a metabolic bone disease accompanying chronic renal failure (CRF), is a major clinical problem in pediatric nephrology. Growing and rapidly remodeling skeletal systems are particularly susceptible to the metabolic and endocrine disturbances in CRF. The pathogenesis of ROD is complex and multifactorial. Hypocalcemia, phosphate retention, and low levels of 1,25 dihydroxyvitamin D(3) related to CRF result in disturbances of bone metabolism and ROD. Delayed diagnosis and treatment of bone lesions might result in severe disability. Based on microscopic findings, renal bone disease is classified into two main categories: high- and low-turnover bone disease. High-turnover bone disease is associated with moderate and severe hyperparathyroidism. Low-turnover bone disease includes osteomalacia and adynamic bone disease. The treatment of ROD involves controlling serum calcium and phosphate levels, and preventing parathyroid gland hyperplasia and extraskeletal calcifications. Serum calcium and phosphorus levels should be kept within the normal range. The calcium-phosphorus product has to be <5 mmol(2)/L(2) (60 mg(2)/dL(2)). Parathyroid hormone (PTH) levels in children with CRF should be within the normal range, but in children with end-stage renal disease PTH levels should be two to three times the upper limit of the normal range. Drug treatment includes intestinal phosphate binding agents and active vitamin D metabolites. Phosphate binders should be administered with each meal. Calcium carbonate is the most widely used intestinal phosphate binder. In children with hypercalcemic episodes, sevelamer, a synthetic phosphate binder, should be introduced. In children with CRF, ergocalciferol (vitamin D(2)), colecalciferol (vitamin D(3)), and calcifediol (25-hydroxyvitamin D(3)) should be used as vitamin D analogs. In children undergoing dialysis, active vitamin D metabolites alfacalcidol (1alpha-hydroxy-vitamin D(3)) and calcitriol (1,25 dihydroxyvitamin D(3)) are applied. In recent years, a number of new drugs have emerged that hold promise for a more effective treatment of bone lesions in CRF. This review describes the current approach to the diagnosis and treament of ROD.

Bone Diseases↗

PubMed1992

Effects of long-term cholestyramine administration on vitamin D and parathormone levels in middle-aged men with hypercholesterolemia.

The objective of this study was to evaluate possible adverse effects of long-term bile acid-binding resin (cholestyramine) treatment on vitamin D, parathyroid hormone, and calcium levels in middle-aged men. A double-blind randomized clinical trial was carried out over a period of 7 to 10 years at the University of Minnesota's Lipid Research Clinic as part of the Lipid Research Clinic's Coronary Primary Prevention Trial. Two hundred and sixty-eight men aged 42 to 68 years who had been previously randomized in the CPPT to cholestyramine or placebo and who had taken at least 75% of the prescribed study medication (6 packets or 24 gm/day) as determined by packet counts for the duration of the Coronary Primary Prevention Trial including the last 4 months of the trial were studied: one group (n = 124) received cholestyramine and the other group (n = 144) received a corresponding dose of placebo. Serum samples were obtained at the time of the final study visit in cholestyramine and placebo groups. (Results are reported as mean +/- SD in SI units). There were no differences in plasma levels of calcium (2.3 +/- 0.1 mmol/L vs 2.3 +/- 0.1 mmol/L), phosphorus (0.99 +/- 0.14 mmol/L vs 0.98 +/- 0.12 mmol/L), albumin (45 +/- 3 gm/L vs 46 +/- 0.6 gm/L), calcifediol (62.6 +/- 29.2 nmol/L vs 63.4 +/- 28.4), 25(OH)D2 (14 +/- 11 nmol/L vs 12 +/- 10 nmol/L) or calcitriol (99 +/- 190 pmol/L vs 91 +/- 56 pmol/L).(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗