cholecalciferol and Bone-Diseases

Vitamin D deficiency occurs frequently in patients with cystic fibrosis (CF). Vitamin D is important for optimal mineralization of bone and may be important for other comorbidities commonly occurring in patients with CF. Vitamin D deficiency in patients with CF can arise from various causes including pancreatic exocrine insufficiency, lack of outdoor activity, and alterations of vitamin D metabolism. Due to fat malabsorption stemming from pancreatic insufficiency, higher oral doses of vitamin D are necessary to correct and maintain optimal vitamin D status in patients with CF. Recent studies have demonstrated that higher vitamin D status is associated with better lung function and that vitamin D therapy may help recovery from pulmonary exacerbations of CF. The mechanisms by which vitamin D may exert its beneficial actions in CF are unclear but likely related to the role vitamin D has in modulating the adaptive and innate immune response. Large randomized clinical studies to evaluate the potential role of vitamin D as adjunctive therapy in CF that goes beyond bone are necessary.

Topics: Bone Diseases; Cholecalciferol; Clinical Trials as Topic; Comorbidity; Cystic Fibrosis; Ergocalciferols; Humans; Inflammation; Lung; Randomized Controlled Trials as Topic; Respiratory Function Tests; Vitamin D; Vitamin D Deficiency

To summarize recommendations from the 2011 US Institute of Medicine report (on vitamin D) and the new guideline from the US Endocrine Society with emphasis on treating and preventing vitamin D deficiency, including patients with inflammatory bowel disease and prior gastric bypass.. The US Institute of Medicine Recommended Dietary Allowance of vitamin D is 400 IU per day for children younger than 1 year of age, 600 IU per day for children at least 1 year of age and adults up to 70 years, and 800 IU per day for older adults. The US Institute of Medicine concluded that serum 25-hydroxyvitamin D [25(OH)D] of 20 ng/ml or more will cover the requirements of 97.5% of the population. The US Endocrine Society's Clinical Practice Guideline suggested that 400-1000 IU per day may be needed for children aged less than 1 year, 600-1000 IU per day for children aged 1 year or more, and 1500-2000 IU per day for adults aged 19 years or more to maintain 25(OH)D above the optimal level of 30 ng/ml. Patients with inflammatory bowel disease even in a quiescent state and those with gastric bypass malabsorb vitamin D and need more vitamin D to sustain their vitamin D status.. Difference in the recommendations from the US Institute of Medicine and the US Endocrine Society's Practice Guideline reflects different goals and views on current evidence. Significant gaps remain in the literature, and studies of vitamin D treatment assessing changes in outcomes at different 25(OH)D levels are needed.

Topics: Asymptomatic Diseases; Bone Diseases; Cholecalciferol; Dietary Supplements; Ergocalciferols; Humans; Nutrition Policy; Practice Guidelines as Topic; Vitamin D; Vitamin D Deficiency; Vitamins

There is a recent renewed interest in vitamin D metabolism and pathophysiology, due to its recent description as a hormone with a positive impact on global health rather than a strictly bone hormone: vitamin D could be a protective factor against infection, autoimmunity, cardiovascular morbidity, and cancer. By contrast, vitamin D deficiency appears to be increasingly frequent worldwide. We propose a review of these new aspects of vitamin D metabolism, with a focus on vitamin D status in a local pediatric cohort. There is an urgent need for revisiting current guidelines on vitamin D supplementation and for closely monitoring serum vitamin D in children with chronic diseases, i.e., at greater risk of cardiovascular impairment, bone morbidity, infectious disease, and acute inflammation.

Topics: Autoimmune Diseases; Bacterial Infections; Bone and Bones; Bone Density Conservation Agents; Bone Diseases; Cardiovascular Diseases; Child; Cholecalciferol; Evidence-Based Medicine; France; Global Health; Humans; Inflammation; Meta-Analysis as Topic; Neoplasms; Prevalence; Risk Factors; Virus Diseases; Vitamin D; Vitamin D Deficiency

Vitamins D and K are lipid-phase nutrients that are pleiotropic - endowed with versatile homeostatic capacities at the organ, tissue, and cellular levels. Their metabolic and physiologic roles overlap considerably, as evidenced in the bone and cardiovascular systems. Vitamin D₃ (cholecalciferol, D₃) is the prehormone for the vitamin D endocrine system. Vitamin D₃ undergoes initial enzymatic conversion to 25-hydroxyvitamin D (25D, calcidiol), then to the seco-steroid hormone 1alpha, 25-dihydroxyvitamin D (1,25D, calcitriol). Beyond its endocrine roles in calcium homeostasis, 1,25D likely has autocrine, paracrine, and intracrine effects. At least 17 tissues likely synthesize 1,25D, and 35 carry the vitamin D receptor (VDR). Vitamin D functional deficiency is widespread in human populations. Vitamin K₁ (phylloquinone) is more abundant in foods but less bioactive than the vitamin K₂ menaquinones (especially MK-4, menatetrenone). Menadione (vitamin K₃) has minimal K activity. Vitamin K compounds undergo oxidation-reduction cycling within the endoplasmic reticulum membrane, donating electrons to activate specific proteins via enzymatic gamma-carboxylation of glutamate groups before being enzymatically re-reduced. Warfarin inhibits this vitamin K reduction, necessitating K supplementation during anticoagulation therapy. Along with coagulation factors (II, VII, IX, X, and prothrombin), protein C and protein S, osteocalcin (OC), matrix Gla protein (MGP), periostin, Gas6, and other vitamin K-dependent (VKD) proteins support calcium homeostasis, facilitate bone mineralization, inhibit vessel wall calcification, support endothelial integrity, are involved in cell growth control and tissue renewal, and have numerous other effects. This review updates vitamin D and K skeletal and cardiovascular benefits and evidence for their synergy of action.

Topics: Bone and Bones; Bone Density; Bone Diseases; Calcification, Physiologic; Cardiovascular Diseases; Cardiovascular System; Cholecalciferol; Fractures, Bone; Humans; Nutritional Physiological Phenomena; Osteoblasts; Osteocytes; Vitamin D Deficiency; Vitamin K; Vitamin K 1; Vitamin K 2; Vitamin K 3; Vitamin K Deficiency

Several excellent reviews regarding nutrition and skeletal disorders have appeared in the last 20 yr. This review will cover several areas of vitamin D research, the area of feed deprivation, and bone abnormalities, because there has been considerable interest in these areas during the past 10 yr. Studies indicate that the quantitative requirement for cholecalciferol (D3) for broiler chickens is much greater than previously thought. Ascorbic acid may play a role in stimulating 1-hydroxylation of 25-hydroxycholecalciferol [25-(OH)D3], but the evidence is not clear under exactly what conditions this relationship is important in practical prevention of tibial dyschondroplasia. Studies indicate that dietary supplementation with 1,25-dihydroxycholecalciferol [1,25(OH)2D3] will reduce the incidence of tibial dyschondroplasia in three different strains of broilers bred to develop a high incidence of the disease. But it did not prevent the disease totally in the strains, unless high enough levels of 1,25-(OH)2D3 were fed to reduce growth rate. These studies indicate that these high tibial dyschondroplasia strains have a defect(s) in vitamin D metabolism. Studies continue to elucidate the role of ultraviolet light in preventing leg abnormalities. Only a few studies have been conducted on the efficacy of various vitamin D3 derivatives to prevent tibial dyschondroplasia. Feed deprivation continues to be an intriguing method of preventing tibial dyschondroplasia, and examination of exactly how this prevents the bone abnormality could open avenues for explaining the disease.

Topics: Animal Nutritional Physiological Phenomena; Animals; Bone Diseases; Cholecalciferol; Food Deprivation; Nutritional Requirements; Osteochondrodysplasias; Poultry Diseases; Rickets; Tibia; Ultraviolet Rays

Topics: Bone Diseases; Cell Differentiation; Cholecalciferol; Gene Expression Regulation; Humans; Receptors, Calcitriol

Topics: Animal Nutritional Physiological Phenomena; Animals; Bone Diseases; Brassica; Calcium; Cholecalciferol; Diet; Iguanas; Phosphorus

It is well known that hyperparathyroidism begins early in renal failure and progresses, probably not linearly, throughout the natural course of renal diseases and dialysis therapy. Recent progress in basic medical science has improved our understanding of the mechanisms by which the classically known stimuli for parathyroid hormone synthesis and secretion may act, including hypocalcaemia, hyperphosphataemia and vitamin D3 metabolism disturbances. In the treatment of hyperparathyroidism, although some authors stress the benefit of treating one of these stimuli, it is probably more effective to combine the treatment of them all. There is conclusive recent work showing the efficacy of using both CaCO3 and vitamin D3, either in chronic renal failure or in dialysis patients at every stage of hyperparathyroidism. Therefore, the treatment of hyperparathyroidism should start early, long before dialysis, and it should aim to correct any of the causal factors. Both CaCO3 and vitamin D3 derivatives may be used in the prevention and treatment of renal bone disease. The limits of this association are the increasingly often reported adynamic bone disease, which in our experience has not yet given major clinical problems, and hyperphosphataemia. Uncontrolled serum phosphate levels would counterbalance the beneficial effect of vitamin D3 derivatives on hyperparathyroidism.

Topics: Administration, Oral; Animals; Bone Diseases; Calcium; Calcium Carbonate; Cholecalciferol; Humans; Hyperparathyroidism; Kidney Failure, Chronic; Phosphates; Renal Dialysis

Topics: Bone Density; Bone Diseases; Calcitriol; Cholecalciferol; Humans; Vitamin D

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.

Topics: Bone Diseases; Cholecalciferol; Ergocalciferols; Humans; Hypoparathyroidism; Vitamin D

Topics: Androsterone; Animals; Bone Diseases; Calcium; Cholecalciferol; Dihydroxycholecalciferols; Enzyme Induction; Epilepsy; Estradiol; Humans; Hydroxycholecalciferols; Microsomes, Liver; Osteoporosis; Phosphates; Progesterone; Rickets; Testosterone; Vitamin D

Topics: Bone and Bones; Bone Diseases; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hydroxycholecalciferols; Hypoparathyroidism; Hypophosphatemia, Familial; Kidney; Liver Cirrhosis; Parathyroid Hormone; Phosphates; Protein Precursors; Pseudohypoparathyroidism; Vitamin D

Topics: Adolescent; Adult; Aged; Alkaline Phosphatase; Anticonvulsants; Bone Diseases; Child; Child, Preschool; Cholecalciferol; Diagnosis, Differential; Epilepsy; Female; Humans; Hypocalcemia; Infant; Male; Middle Aged; Osteomalacia; Phosphates; Rickets; Time Factors; Vitamin D; Vitamin D Deficiency

Topics: Bone Diseases; Calcium; Carcinoma; Cholecalciferol; Chromatin; Dihydroxycholecalciferols; Ergocalciferols; Homeostasis; Humans; Hydroxycholecalciferols; Intestinal Diseases; Intestinal Mucosa; Kidney; Kidney Diseases; Liver; Liver Diseases; Parathyroid Diseases; Receptors, Drug; Skin Diseases; Thyroid Neoplasms; Vitamin D Deficiency

Topics: Acute Kidney Injury; Animals; Bone Diseases; Calcium; Cholecalciferol; Deficiency Diseases; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Hypoparathyroidism; Kidney; Kidney Transplantation; Nephrectomy; Phosphorus; Rickets; Structure-Activity Relationship; Vitamin D

Topics: Biological Assay; Bone and Bones; Bone Diseases; Chemical Phenomena; Chemistry; Chemistry, Physical; Cholecalciferol; Chronic Disease; Humans; Kidney Diseases; Osteomalacia; Protein Binding; Radioimmunoassay; Research; Rickets; Vitamin D; Vitamin D Deficiency

Topics: Anticonvulsants; Bone and Bones; Bone Diseases; Calcium; Cell Membrane Permeability; Cholecalciferol; Cholesterol; Ergocalciferols; Gastrointestinal Diseases; Humans; Hypoparathyroidism; Hypophosphatemia, Familial; Intestinal Mucosa; Kidney; Kidney Failure, Chronic; Parathyroid Hormone; Sarcoidosis; Skin; Vitamin D

Topics: Animals; Anticonvulsants; Bone Diseases; Calcium; Calcium Metabolism Disorders; Cholecalciferol; Enzyme Induction; Epilepsy; Humans; Intestinal Absorption; Liver; Phenobarbital; Phenytoin; Rats; Swine

Topics: Adolescent; Animals; Anticonvulsants; Biliary Tract; Bone Diseases; Calcium; Child; Cholecalciferol; Enzyme Induction; Epilepsy; Humans; Intestinal Absorption; Kidney; Liver; Metabolic Diseases; Phenobarbital; Phenytoin; Tritium; Vitamin D; Vitamin D Deficiency

Topics: Bone and Bones; Bone Diseases; Calcium; Cholecalciferol; Dihydrotachysterol; Homeostasis; Intestinal Absorption; Kidney; Kidney Failure, Chronic; Uremia; Vitamin D

Topics: Animals; Biological Transport; Bone Development; Bone Diseases; Calcification, Physiologic; Calcium; Cholecalciferol; Fanconi Syndrome; Humans; Hypoparathyroidism; Intestinal Absorption; Kidney; Liver; Rats; Rickets; Uremia; Vitamin D; Vitamin D Deficiency

Large populations consume fluoride-contaminated water, especially in developing countries. The toxic effects of fluorosis take three forms: clinical, skeletal and dental. Research thus far indicates that the manifestations of fluorosis are irreversible. However, it has been observed that the ingestion of calcium, vitamin C or vitamin D, individually, is effective in protection from fluoride toxicity to a certain extent. Therefore, a double blind control trial was conducted to examine the effect of a combination of calcium, vitamin D3 and ascorbic acid supplementation in fluorosis-affected children. In the present study, 25 children were selected from an area consuming water containing 4.5 p.p.m. of fluoride, All the children were in the age group 6-12 years and weighed 18-30 kg. They were graded for clinical, radiological and dental fluorosis and relevant biochemical parameters. Grade I skeletal fluorosis and all grades of the manifestation of dental and clinical fluorosis were observed. The children were given ascorbic acid, calcium and vitamin D3 well below the toxic dosages in a double blind manner using lactose as a placebo. Follow up revealed a significant improvement in dental, clinical and skeletal fluorosis and relevant biochemical parameters in these children. Thus, the study indicated that fluorosis can be reversed, at least in children, by a therapeutic regimen that is fairly cheap, simple and easily available and without any side effects.

Topics: Ascorbic Acid; Bone Diseases; Calcium; Child; Cholecalciferol; Double-Blind Method; Drug Monitoring; Drug Therapy, Combination; Fluoride Poisoning; Fluorosis, Dental; Humans; Radiography; Severity of Illness Index

With the aim of preventing postmenopausal bone loss, a placebo-controlled double-blind trial of 2 years duration was performed. We randomized 315 healthy volunteers in their early natural menopause to seven treatment and three placebo groups: 17 beta-oestradiol, oestriol and sequential norethisteron (hormones); bendroflumethiazide 5 mg/day (thiazide); hormones and thiazide; sodium fluoride 20 mg/day; vitamin D3 2000 IU/day (D3); fluoride and D3; and 1 alpha (OH) vitamin D3 0.25 microgram/day (1 alpha D3). All participants were given daily calcium supplement of 500 mg. Every 3 months we measured the bone mineral content (BMC) of both forearms by photon absorptiometry and chemical quantities in blood and 48 h urinary collections. The study was completed by 264 (84%). The combined placebo groups showed a linear fall in BMC reaching 3.3% after 2 years (P < 0.001). Hormones and hormones and thiazide led to a 2.5% gain in BMC (P < 0.01). Thiazide alone postponed the BMC fall for 6 months. After 2 years the thiazide group showed a BMC fall of 1.5% (P < 0.05), less than that of the placebo group (P < 0.05). BMC declined by 3.6%, 4.5%, 3.7% and 3.7% during the respective use of fluoride, D3, fluoride and D3 and 1 alpha D3. Nevertheless, the urinary calcium excretion during 1 alpha D3 and D3 treatment was 1--1.5 mmol/day higher than in the placebo groups. Apparently, there is no real alternative to oestrogen/gestagen in the prevention of postmenopausal osteoporosis.

Topics: Benzothiadiazines; Blood Pressure; Bone and Bones; Bone Diseases; Cholecalciferol; Clinical Trials as Topic; Diuretics; Double-Blind Method; Drug Combinations; Estrogens; Female; Fluorides; Humans; Menopause; Middle Aged; Minerals; Sodium Chloride Symporter Inhibitors

There is a lack of studies providing comprehensive data on the prevalence of mineral and bone disorders (MBD) laboratory abnormalities after kidney transplantation in Russia.. to obtain real-world data on the prevalence of the main mineral abnormalities among kidney transplant recipients and to revise their concomitant MBD therapy.. This cross-sectional study included 236 patients with successful kidney transplantation. Their serum intact parathyroid hormone (iPTH), total calcium (Ca), phosphorus (P), and alkaline phosphatase (ALP) levels were measured.. Only 6.2% of our cohort had all laboratory parameters within the target range, whereas persistent HPT along with hypercalcemia was noted in almost one third of the patients (31%). Normal iPTH levels were observed in 13% cases; 84% of the patients had hyperparathyroidism. The fraction of patients with target iPTH did not differ between the groups with normal and decreased estimated glomerular filtration rate (eGFR) (p=0.118). Hypercalcemia was observed in 29% cases. The serum P level varied significantly in groups with different eGFR (p<0.0001), increasing with declining graft function. Furthermore, 40.7% of patients had ALP above the target range. While 123 patients received active vitamin D (alfacalcidol), 33 received monotherapy with inactive vitamin D (cholecalciferol). The control group consisted of 57 medication-naïve patients. The serum total Ca level varied significantly between the groups (p=0.0006), being higher in patients supplemented with cholecalciferol. The fraction of patients with normocalcemia was lowest in the cholecalciferol group (chi-square, р=0.0018).. The prevalence of biochemical abnormalities after kidney transplantation is high. Alfacalcidol usage may be safer than using cholecalciferol to prevent hypercalcemia development.

Topics: Biomarkers; Bone Diseases; Cholecalciferol; Cross-Sectional Studies; Humans; Hypercalcemia; Kidney Transplantation; Minerals; Parathyroid Hormone; Vitamin D

Patients with sickle cell disease (SCD) are at risk for bone fragility from multiple factors including vitamin D deficiency. To date, no studies have evaluated the efficacy and safety of long-term vitamin D therapy for bone disease in children with SCD. We report a cohort of 4 children with SCD found to have severe vitamin D deficiency, secondary hyperparathyroidism, and abnormal bone mineral density treated with monthly high-dose oral cholecalciferol over 2 years. All patients exhibited a positive response to therapy without hypervitaminosis D or hypercalcemia. Further studies are needed to standardize guidelines for optimal vitamin D dosing and prevention of toxicity.

Topics: Adolescent; Anemia, Sickle Cell; Bone Density; Bone Diseases; Child; Cholecalciferol; Female; Humans; Male; Time Factors; Vitamin D Deficiency

Parathyroidectomy is the only effective therapy for osteitis fibrosa cystica in hyperparathyroidism.. The objective of this study was to describe the changes of skeletal and nonskeletal manifestations in a patient with hyperparathyroidism and renal failure after oral vitamin D therapy.. This was a descriptive case report.. The patient was followed up in a referral center.. A 55-yr-old male patient with moderate renal failure was referred for expansile lytic lesions affecting several ribs and the spinous process of T12. His creatinine was 1.8 mg/dl; calcium, 8.9 mg/dl; PTH, 666 pg/ml; and 1,25 dihydroxy-vitamin D, 27 pg/ml. Bone mineral density (BMD) Z-scores by dual-energy x-ray absorptiometry were -4.1 at the spine, -1.7 at the hip, and -4.3 at the forearm.. The main outcome measures were the skeletal manifestations of hyperparathyroidism.. At 10 months of therapy, calcium level was 10 mg/d, PTH level declined to 71 pg/ml, and BMD increased by 12% at the spine and 18% at the hip. Computerized tomography (CT) cuts revealed marked regression in the lytic lesions. At 2 yr, BMD increased by an additional 6% at the spine, and there were no further changes in the lytic lesions by CT. The vitamin D receptor genotype using the restriction enzymes Bsm1, Taq1, and Apa1 was Bb, tt, and AA.. We showed regression of severe skeletal abnormalities of hyperparathyroidism documented by serial CT images in response to oral vitamin D therapy. It is possible that the vitamin D receptor genotype of the patient modulated this response.

Topics: Bone Density; Bone Diseases; Calcium; Cholecalciferol; Genotype; Humans; Hydroxycholecalciferols; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Osteitis Fibrosa Cystica; Osteoporosis; Receptors, Calcitriol; Thalassemia; Tomography, X-Ray Computed; Vitamin D

Topics: Bone Diseases; Calcium Gluconate; Cholecalciferol; Diagnosis, Differential; Female; Humans; Infant; Radiography; Rickets; Wrist Joint

To study possible correction of bone disorders (osteopenia, Ca/P-imbalance, bone pain, limited volume of indolent movements) which are still a serious complication associated with renal diseases and pathogenic therapy (steroids).. The bone disorders were treated in 10 uremic hemodialyzed patients (8 men, 2 women; group 1) with vitamin D3 (calcitriol made in Russia) + rhEPO (recormon; Boehringer Mannheim), in 15 patients (15 women, 0 men) with lupus-nephritis (group 2) with vitamin D3 (n = 5, group 2a) or miscalcic (Sandoz) (n = 10, group 2b), in 2 patients (2 men, 0 women) with glomerulonephritis (group 3) with vitamin D3 + miacalcic. Additionally all the patients received Ca salts. In groups 2 and 3 renal function was normal. The duration of the treatment was 3-6 months.. In all the groups we obtained an analgetic effect (attenuation of bone pain and more indolent movements), improvement of life quality, diminished need in analgetics, elevation of serum Ca level (p > 0.05).. Treatment of renal patients with bone affection with vitamin D3 and miacalcic has an analgetic effect, improves life quality.

Topics: Adult; Analgesics; Bone Diseases; Calcitonin; Calcium; Cholecalciferol; Drug Therapy, Combination; Erythropoietin; Female; Glomerulonephritis; Humans; Lupus Nephritis; Male; Middle Aged; Quality of Life; Recombinant Proteins; Renal Dialysis; Treatment Outcome; Uremia

The effects of the excessive administration of the vitamin AD3E(V-AD3E) premix, vitamin A (V-A) or vitamin D3 (V-D3) on experimental development of Hyena disease in the calves were examined. Hyena disease was recognized in 4 calves, both of the 2 calves administered a high dose of V-AD3E premix (V-A 3,000,000, V-D3 300,000, and V-E 1,200 IU/day, V-AD3E group), 1 of the 2 calves administered a half dose of the V-AD3E premix, and 1 of the 2 calves administered only V-A (V-A 3,000,000 IU/day, V-A group) when each vitamin was administered orally for 10 days from 1 week after birth. Both of 2 calves administered only V-D3 (V-D3 300,000 IU/day) did not developed. In the 4 calves with Hyena disease (Hyena calves), the plasma retinylpalmitate showed high values which was suggesting the hypervitaminosis A, and the epiphysial growth plate was narrow and destroyed structure of column. Compared with the Hyena calf in the V-A group, the Hyena calves in the V-AD3E group showed earlier appearance time of Hyena disease, lower growth rate and shorter lengths of fore and hind limb bones. In conclusion, the present findings suggested that excessive V-A administration to suckling calves might cause Hyena disease by V-A effects to the epiphysial growth plate, moreover such effects may be promoted by the V-D3.

Topics: Aging; Animals; Body Height; Body Weight; Bone Diseases; Cattle; Cattle Diseases; Cholecalciferol; Food, Fortified; Growth Plate; Male; Radiography; Vitamin A

Because previous studies indicated that cimetidine (CIMET) and isoniazid (ISON) may inhibit vitamin D metabolism in both rats and humans, experiments were conducted to evaluate the influence of these drugs on growth and bone development in male broiler chicks. Chicks were fed a corn and soybean meal basal diet containing various levels of the drugs for 21 days. Body weight gain (BWG), feed consumption per bird (FB), tibia ash (TA), tibia breaking force (TBF), and plasma calcium levels were measured. In birds fed a diet supplemented with 1,100 ICU D3/kg, CIMET at up to 300 ppm resulted in a significant linear decrease in TA as the drug level increased. Birds fed ISON up to 405 ppm had inconsistent responses in TA and TBF. Body weight gain was only depressed with the highest level of ISON (405 ppm). The effects of feeding 0, 150, or 300 ppm CIMET were also investigated when chicks were fed 200 or 1,000 ICU per kg vitamin D3. The interaction between vitamin D3 and CIMET was significant for BWG, FCB, TA, and TBF. These were significantly reduced as the CIMET level increased for birds fed the low vitamin D3 diet but were not significantly affected when fed the high D3 diet. In another study in which chicks were fed a diet with 1,100 ICU vitamin D3, lowering the dietary Ca, or P, or both did not result in any effect of CIMET on the chicks. The results indicate that CIMET possibly interferes with normal bone formation in chicks by altering vitamin D3 metabolism.

Topics: Animals; Bone Development; Bone Diseases; Calcium; Chickens; Cholecalciferol; Cimetidine; Isoniazid; Male; Tensile Strength; Tibia; Time Factors; Weight Gain

Because the pathogenesis of osteosclerosis in hypervitaminosis D is still not well elucidated, the authors experimentally studied hypervitaminosis D3 in 66 rabbits by injecting different doses of vitamin D3. Contact radiographs of bone specimens showed various signs of osteosclerosis, including dense epiphyses and metaphyses, thickened bony articular surfaces, dense metaphyseal bands, modeling defects at the metaphysis, and dense and thickened cortical bone. The corresponding pathologic sections showed that conspicuous metastatic calcification coated the trabeculae and filled bone marrow cavity and caverns in the original but porotic cortical and periosteal new bone. Rather than being resorbed, the metastatic calcifications were embedded in a thick layer of newly formed bone 6 to 14 weeks after vitamin D3 withdrawal. This study suggests that in hypervitaminosis D3, the osteoblasts and bone marrow undergo degeneration, leading to necrosis and calcification. After vitamin D3 withdrawal, osteoblasts reappear and become overactive, leading to overossification.

Topics: Animals; Bone Diseases; Calcinosis; Cholecalciferol; Osteosclerosis; Rabbits; Radiography

Topics: Bone Diseases; Calcitriol; Cholecalciferol; Humans; Quality Control; Radioimmunoassay

Topics: Animals; Bile; Bone Development; Bone Diseases; Calcitriol; Cholecalciferol; Gallbladder; Humans; Intestinal Diseases; Liver; Liver Diseases; Vitamin D

Recognition over the last ten years of the fact that vitamin D does not act as such, but must be converted into a hormonal form, has filled in the picture physiological endocrine regulation of calcium and phosphate homeostasis. While vitamin D has thus lost the dietetic significance associated with it for over 50 years. Nevertheless, new interpretations of the aetiopathogenesis of many demineralizing bone diseases are of much greater utility. Nor is it futuristic to suppose that all the biochemical parameters establishing one of the metabolisms that are under strict homeostatic control in the body, such as that of calcium and that of phosphate, are understood.

Topics: Bone Diseases; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Glucocorticoids; Humans; Hypoparathyroidism; Iatrogenic Disease; Intestinal Absorption; Osteomalacia; Osteoporosis; Phosphates; Rickets; Vitamin D

Calcium and phosphate metabolism as well as those substances which are essential in regulating this metabolism (parathyroid hormone, thyrocalcitonin and cholecalciferol) are briefly discussed. Of three known forms of bone disease (nutritional secondary hyperparathyroidism, rickets and hypervitaminosis A), the clinical symptoms, radiological changes, (histo)pathological findings, therapeutic procedures as well as the aetiological, pathogenic and pathophysiological features will be reviewed.

Topics: Animal Nutritional Physiological Phenomena; Animals; Birds; Bone and Bones; Bone Diseases; Calcitonin; Cat Diseases; Cats; Cholecalciferol; Dog Diseases; Dogs; Hyperparathyroidism, Secondary; Minerals; Osteoporosis; Parathyroid Hormone; Rickets; Vitamin A

The process of chronic hypophosphatemic vitamin D-resistant rickets--observation of two cases. With the male patient--our first case--the disease was sporadic and had not been recognized for a long time. In his early adulthood it manifested itself as Umbauzonen (pseudofractures) in the larger context of active osteomalacia. It was possible to observe the pseudofractures before and while the patient was treated with drugs. High doses of vitamin D 3 and dosage of phosphate mitigated the complains although with respect to the radiological, scintigraphic, humoral and histological findings there was only slow improvement or no improvement at all.--The patient's daughter is affected by the disease as well. In her case the pathological signs of her bones became better when treated with vitamin D 3.

Topics: Adult; Bone and Bones; Bone Diseases; Child, Preschool; Cholecalciferol; Chronic Disease; Extremities; Female; Humans; Male; Osteomalacia; Phosphates; Radiography; Thorax

Renal bone disease was assessed for an average of 5.5 years in 9 patients on maintenance haemodialysis. The investigative methods included serial biochemical estimations, radiographic skeletal surveys and quantitative bone histology. Repeated bone mineral analyses and neutron activation analyses of a hand were also performed in order to monitor changes in skeletal calcium content. Before treatment, progressive osteodystrophy was demonstrated by all techniques. Following therapy with the vitamin D analogues, all patients noted symptomatic improvement; serum alkaline phosphatase reverted to normal and serum parathyroid hormone concentrations decreased. Radiographically, subperiosteal erosions healed while the histological features of osteomalacia and osteitis fibrosa were abolished. Both bone mineral and neutron activation analyses indicated that progressive skeletal demineralisation had been halted. However, a sustained increase in the overall mineral content of bone was not demonstrated. Thus, vitamin D therapy although improving the biochemical, radiological, and histological features of renal osteodystrophy may not restore bone mass to osteopenic bone.

Topics: Adult; Alkaline Phosphatase; Bone and Bones; Bone Diseases; Cholecalciferol; Female; Humans; Long-Term Care; Male; Minerals; Osteomalacia; Parathyroid Hormone; Periosteum; Radiography; Vitamin D

Twelve children with chronic renal failure (CRF) and sixteen children receiving regular dialysis therapy (RDT) were treated with between 10,000 and 50,000 IU of vitamin D daily. This was associated with an increase in serum calcium levels and reduction in PTH levels. In the children with CRF, secondary hyperparathyroidism was improved with treatment but its development was not completely prevented nor was healing complete. In the patients receiving RDT, treatment with vitamin D improved the changes associated with secondary hyperparathyroidism in 50% of cases but these features sometimes reappeared despite continuing treatment. Hypercalcaemia or metastatic calcification was not seen. Subsequently, 1,25(OH)2D3 was administered to 14 children receiving RDT. This was associated with the return of serum calcium levels to normal, inhibition of PTH synthesis and an improvement in intestinal calcium absorption. Fibro-osteoclasia was cured and there was improvement in actual bone resorption. There was also improvement in osteoidosis in those children who showed disturbances of mineralisation. Calcification in the limbus area of the eyes may occur and hypercalcaemia was seen commonly. Treatment with 1,25(OH)2D3 should only be offered to children with severe renal bone disease. Neither vitamin D3 nor 1,25(OH)2D3 can guarantee complete recovery of osteodystrophy and of growth arrest in uraemic children.

Topics: Adolescent; Alkaline Phosphatase; Bone and Bones; Bone Diseases; Calcium; Child; Cholecalciferol; Humans; Kidney Failure, Chronic; Phosphates; Renal Dialysis

Topics: Bone Diseases; Cholecalciferol; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols

25-Hydroxyvitamin D (25-OHD) levels were measured in 39 patients with metabolic bone disease or hypoparathyroidism who had been treated with a constant high dose of vitamin D2 or D3 for at least 12 weeks. Plasma 25-OHD levels rose with increasing dosage, the relationship between dose and plasma level being approximately linear whether or not the dose was expressed on a weight-corrected basis. A therapeutic range of 25-OHD to be expected when patients with these conditions are treated with vitamin D has been established. There may be certain exceptions in which plasma 25-OHD levels within the range are associated with either an inadequate response to treatment or, conversely, the hypercalcaemia of vitamin D toxicity. There was no correlation between plasma calcium level and 25-OHD concentration in the group of patients studied. There was also no difference between the dose/25-OHD relationship of patients treated with vitamin D2 and that of patients receiving vitamin D3. Ten patients were started on treatment with large doses of vitamin D during the period of the study. The rate of rise of plasma 25-OHD was followed during treatment. The incremental rise in 25-OHD was calculated at the end of the first week of treatment in terms of dose per unit body weight. The rate of rise of plasma 25-OHD level was highly correlated with the dose used. Plasma 25-OHD levels after one weeks' treatment were only 15-20% of the expected steady-state level on the same dosage. The importance of a high priming dose when a rapid response is needed is thus emphasised.

Topics: Adolescent; Adult; Aged; Body Weight; Bone Diseases; Child; Child, Preschool; Cholecalciferol; Dose-Response Relationship, Drug; Ergocalciferols; Female; Humans; Hydroxycholecalciferols; Hypercalcemia; Hypoparathyroidism; Infant; Male; Middle Aged; Vitamin D

Five groups of 4 weanling pigs were fed a diet with 1.2% calcium and 1.0% phosphorus for 8 weeks with vitamin D3 at 1, 5, 25, 125 and 625 times the recommended levels, respectively. Hypercalcemia and hypophosphatasemia developed rapidly and persisted in Group 5 and developed more slowly but steadily in Group 4. Increasing levels of vitamin D3 influenced progressively and negatively the activity of resorbing osteocytes with osteopetrosis in Groups 2 and 3 and with osteonecrosis in Group 5. Atrophy of osteoblasts further contributed to the osteopenia in Group 5. Cartilage growth activity was arrested in Group 5. The negative effect on the resorbing osteocytes, which finally lead to death of the cells, was ascribed directly to vitamin D3 toxicosis since hypoparathyroidism and hypercalcitonism, both resulting from hypercalcemia, are not known to induce osteonecrosis. Since hypercalemia was finally as severe in Group 4 as in Group 5 and since there was soft tissue calcinosis only in Group 5, the calcinosis was always considered dystrophic, an interpretation supported by the observation that degenerative histologic changes preceded soft tissue calcinosis.

Topics: Animals; Bone Diseases; Bone Resorption; Calcinosis; Calcium; Cartilage; Cholecalciferol; Female; Humerus; Male; Parathyroid Glands; Swine; Swine Diseases; Thyroid Gland

Topics: Animals; Bone Diseases; Calcium; Chemical Phenomena; Chemistry; Cholecalciferol; Dihydrotachysterol; Dihydroxycholecalciferols; Disease Models, Animal; Humans; Hydroxycholecalciferols; Isomerism; Kidney Failure, Chronic; Microradiography; Osteitis Fibrosa Cystica; Osteomalacia; Phosphates; Rats; Renal Dialysis; Uremia; Vitamin D

Topics: Adult; Aged; Bone Diseases; Calcitonin; Child; Cholecalciferol; Ergocalciferols; Humans; Hypercalcemia; Metabolic Diseases; New Zealand; Organophosphonates; Osteitis Deformans; Osteomalacia; Osteoporosis; Parathyroid Hormone; Sarcoidosis; Vitamin D; Vitamin D Deficiency

Topics: Bone and Bones; Bone Diseases; Cholecalciferol; Humans; Osteomalacia; Rickets; Ultraviolet Rays; Ultraviolet Therapy; Vitamin D Deficiency

Topics: Animals; Biological Transport; Blood Urea Nitrogen; Bone Diseases; Calcium; Chickens; Cholecalciferol; Intestinal Absorption; Intestine, Small; Kidney; Kidney Failure, Chronic; Ligation; Male; Nephrectomy; Rats; Uremia; Ureter; Vitamin D

Topics: Administration, Oral; Animals; Bone Diseases; Cholecalciferol; Diet; Ergocalciferols; Gout; Haplorhini; Hypercalcemia; Kidney; Macaca; Nephrocalcinosis; Uric Acid; Vitamin A Deficiency

Topics: Alkaline Phosphatase; Animal Nutritional Physiological Phenomena; Animals; Arthritis; Bone Development; Bone Diseases; Bone Resorption; Calcium; Cholecalciferol; Diet; Hypocalcemia; Male; Phosphorus; Rhinitis, Atrophic; Swine; Zinc

Topics: Absorptiometry, Photon; Adrenal Cortex Hormones; Bone and Bones; Bone Diseases; Child; Cholecalciferol; Cobalt Isotopes; Humans; Iodine Radioisotopes; Lead; Methods; Microradiography; Minerals; Nephrotic Syndrome; Osteoporosis; Radioisotopes; Rickets

Topics: Animals; Bone and Bones; Bone Diseases; Bone Resorption; Carbon Isotopes; Cholecalciferol; Collagen; Hydroxyproline; Kidney Failure, Chronic; Male; Parathyroid Hormone; Proline; Rats; Skin; Tibia; Uremia

Topics: Animals; Bone and Bones; Bone Development; Bone Diseases; Bone Resorption; Calcitonin; Calcium Isotopes; Cholecalciferol; Culture Techniques; Dactinomycin; Hydroxyproline; Kidney Failure, Chronic; Parathyroid Hormone; Phosphates; Rats; RNA; Uremia

Topics: Animals; Bone and Bones; Bone Diseases; Calcium; Cholecalciferol; Humans; Kidney; Kidney Failure, Chronic; Liver; Rats; Uremia; Vitamin D

Topics: Animals; Biological Transport, Active; Bone Diseases; Calcium; Cholecalciferol; Duodenum; Intestinal Absorption; Intestinal Mucosa; Kidney Failure, Chronic; Male; Protein Binding; Rats; Tritium; Uremia; Vitamin D

Topics: Bone Diseases; Cholecalciferol; Humans; Kidney Failure, Chronic; Uremia

Topics: Adolescent; Body Height; Bone Diseases; Calcium; Child; Cholecalciferol; Diagnosis, Differential; Female; Humans; Hyperparathyroidism; Hypocalcemia; Hypoparathyroidism; Phosphorus Metabolism Disorders; Tetany

Topics: Animals; Bone Diseases; Cholecalciferol; Deficiency Diseases; Hypocalcemia; Osteoporosis; Rats; Rickets