cholecalciferol has been researched along with Osteitis-Fibrosa-Cystica* in 12 studies
3 review(s) available for cholecalciferol and Osteitis-Fibrosa-Cystica
Article | Year |
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The effects of calciferol and its metabolites on patients with chronic renal failure. I. Calciferol, dihydrotachysterol, and calcifediol.
The available data with regard to the use of calciferol, dihydrotachysterol, and calcifediol in the management of renal insufficiency are reviewed. Very limited data are available with regard to calciferol therapy; with the advent of more active metabolites, the use of calciferol is not warranted. Dihydrotachysterol seems to be effective in the treatment of renal patients with osteitis fibrosa; its low cost makes therapy with this compound a reasonable alternative, although it should not be used in the treatment of patients with liver disease. Calcifediol seems to be effective in patients with osteitis fibrosa; however, limited data on histologic characteristics of bone are available. Detailed prospective studies are necessary to establish the therapeutic benefit of calcifediol. Topics: Absorption; Calcifediol; Cholecalciferol; Dihydrotachysterol; Ergocalciferols; Humans; Kidney Failure, Chronic; Osteitis Fibrosa Cystica; Structure-Activity Relationship | 1983 |
Treatment of renal osteodystrophy with calciferol (vitamin D) and related steroids.
Topics: Aluminum; Bone Regeneration; Calcium; Calcium Carbonate; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydrotachysterol; Dihydroxycholecalciferols; Ergocalciferols; Humans; Hydroxycholecalciferols; Intestinal Absorption; Osteitis Fibrosa Cystica; Osteomalacia; Parathyroid Glands; Phosphorus; Secretory Rate; Vitamin D | 1973 |
[Treatment of parathyroid diseases].
Topics: Calcitonin; Calcium; Cholecalciferol; Humans; Hyperparathyroidism; Hypocalcemia; Kidney Failure, Chronic; Osteitis Fibrosa Cystica; Osteomalacia; Parathyroid Glands; Phosphorus | 1971 |
9 other study(ies) available for cholecalciferol and Osteitis-Fibrosa-Cystica
Article | Year |
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Case report: Osteomalacia due to bisphosphonate treatment in a patient on hemodialysis.
No publications have reported on osteomalacia in patients receiving intermittent cyclical therapy with etidronate (a bisphosphonate) and undergoing long-term hemodialysis (HD).. We report on a 46-year-old Japanese man admitted to our hospital for further examination of left forearm pain. Maintenance HD was started at age 24 years, and the man had been on HD since then. At age 38 years, surgical parathyroidectomy was performed for secondary hyperparathyroidism; iliac crest bone biopsy performed at the same time showed osteitis fibrosa. The active vitamin D. We believe that intermittent cyclical etidronate therapy without administration of active vitamin D Topics: Bone and Bones; Bone Density Conservation Agents; Calcitriol; Cholecalciferol; Etidronic Acid; Humans; Ilium; Male; Middle Aged; Osteitis Fibrosa Cystica; Osteomalacia; Renal Dialysis; Vitamin D Deficiency | 2021 |
A patient with a history of breast cancer and multiple bone lesions: a case report.
Long-term severe hyperparathyroidism leads to thinning of cortical bone and cystic bone defects referred to as osteitis fibrosa cystica. Cysts filled with hemosiderin deposits may appear colored as "brown tumors." Osteitis fibrosa cystica and brown tumors are occasionally visualized as multiple, potentially corticalis-disrupting bone lesions mimicking metastases by bone scintigraphy or. We report a case of a 72-year-old white woman who presented with malaise, weight loss, and hypercalcemia. She had a history of breast cancer 7 years before. The practitioner, suspecting bone metastases, initiated bone scintigraphy, which showed multiple bone lesions, and referred her to our hospital for further investigations. Laboratory investigations confirmed hypercalcemia but revealed a constellation of primary hyperparathyroidism and not hypercalcemia of malignancy; in the latter condition, a suppressed rather than an increased value of parathyroid hormone would have been expected. A parathyroid adenoma was found and surgically removed. The patient's postoperative course showed a hungry bone syndrome, and brown tumors were suspected. With the background of a previous breast cancer and lytic, partly corticalis-disrupting bone lesions, there was a great concern not to miss a concomitant malignant disease. Biopsies were not diagnostic for either malignancy or brown tumor. Six months after the patient's neck surgery, imaging showed healing of the bone lesions, and bone metastases could be excluded.. This case shows essential differential diagnosis in a patient with hypercalcemia and multiple bone lesions. Whenever multiple, fluorodeoxyglucose-avid bone lesions are found, malignancy and metabolic bone disease should both be included in the differential diagnosis. Fluorodeoxyglucose-avid and corticalis-disrupting lytic lesions also occur in benign bone disease. There may be very few similar cases with heterogeneous and widespread bone lesions reported in the literature, but we think our patient's case is particularly remarkable for its detailed imaging and the well-documented course. Topics: Aged; Bone Neoplasms; Breast Neoplasms; Calcium; Cholecalciferol; Diagnosis, Differential; Female; Humans; Hypercalcemia; Hyperparathyroidism, Primary; Osteitis Fibrosa Cystica; Parathyroid Neoplasms; Parathyroidectomy; Positron Emission Tomography Computed Tomography; Treatment Outcome; Vitamins | 2017 |
Brown tumours of the tibia and second metacarpal bone in a woman with severe vitamin D deficiency.
Brown tumours caused by vitamin D deficiency are rare. Most cases are caused by primary hyperparathyroidism, and are rarely caused by secondary hyperparathyroidism in cases of renal failure. We present a case of Brown tumours of the tibia and second metacarpal bone in a 50-year-old woman who had a low dietary intake of vitamin D and had worn a veil for most of her adult life. The Brown tumours were caused by vitamin D deficiency and secondary hyperparathyroidism. The patient improved on treatment with vitamin D3 and calcium supplements. This is a rare case and the first, to our knowledge, with a Brown tumour of the tibia caused by vitamin D deficiency due to decreased dietary intake and decreased exposure to sunlight. The course of treatment and investigations of the patient are described. Topics: Bone Neoplasms; Calcium, Dietary; Cholecalciferol; Clothing; Diet; Female; Hand; Humans; Hyperparathyroidism, Secondary; Leg; Metacarpal Bones; Middle Aged; Osteitis Fibrosa Cystica; Sunlight; Tibia; Vitamin D Deficiency | 2015 |
Regression of skeletal manifestations of hyperparathyroidism with oral vitamin D.
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 | 2006 |
Limitation by hyperphosphataemia of the "prophylactic" use of vitamin D metabolites in the treatment of osteitis fibrosa in patients on chronic haemodialysis.
Topics: Alkaline Phosphatase; Cholecalciferol; Humans; Osteitis Fibrosa Cystica; Parathyroid Hormone; Phosphates; Renal Dialysis; Vitamin D | 1979 |
Vitamin D metabolism and parathyroid function in man.
1. The metabolism of an intravenous pulse dose of double-isotope-labelled cholecalciferol has been studied in control subjects with widely differing states of vitamin D nutrition and in patients with primary disorders of parathyroid function. 2. The formation of labelled 1,25-dihydroxy-cholecalciferol [1,25-(OH)2D3] and labelled 24,25-dihydroxycholecalciferol [24,25-(OH)2D3] has been related to the prevailing concentrations in serum of 25-hydroxycholecalciferol [25-(OH)D3], immunoreactive parathyroid hormonel, calcium and orthophosphate (Pi). 3. In control subjects with relative vitamin D deficiency [serum 25-(OH)2D3 was related inversely to the serum 25-(OH)D3 and serum calcium, and directly to serum immunoreactive parathyroid hormone. No formation of 1,25-(OH)2D3 was detectable to form labelled 24,25(OH)2D3 preferentially. 4. No control subject produced significant amounts of both labelled 1,25-(OH)2D3 and labelled 24,25-(OH)2D3 simultaneously. 5. All subjects with primary hyperparathyroidism produced significant amounts of labelled 1,25-(OH)2D3 and labelled 24,25-(OH)2D3 simultaneously; the renal turnover of 25-(OH)D3 was apparently greater than in nutritionally matched controls. Serum labelled 1,25-(OH)2D3 in this disease was not correlated with serum 25-(OH)D3, immunoreactive parathyroid hormone, calcium or Pi. Production of labelled 24,25-(OH)2D3 was inappropriately high for the prevailing nutritional state. 6. The indirectly estimated their concentration of 1,25-(OH)2D3 showed only a fourfold variation in control subjects (45-180 pmol/l), compatible with its having a regulated hormonal function. 7. The data suggest that the production of 1,25-(OH)2D3 from a pulse dose of cholecalciferol is normally regulated, directly or indirectly, by the parathyroid hormone. Topics: Adult; Aged; Alkaline Phosphatase; Biopsy; Bone and Bones; Calcium; Cholecalciferol; Creatinine; Dihydroxycholecalciferols; Female; Humans; Male; Middle Aged; Osteitis Fibrosa Cystica; Parathyroid Glands; Parathyroid Hormone; Radioimmunoassay; Radioligand Assay | 1975 |
[Treatment of uremic osteopathy. Effects of vitamin D metabolites and vitamin D analogs in chronic uremia and experimental renal insufficiency].
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 | 1974 |
Calcium and the nervous system.
Topics: Adenylyl Cyclases; Anticonvulsants; Calcitonin; Calcium; Cholecalciferol; Cyclic AMP; Diagnosis, Differential; Humans; Hydroxycholecalciferols; Hypercalcemia; Hyperparathyroidism; Osteitis Deformans; Osteitis Fibrosa Cystica; Osteomalacia; Parathyroid Hormone; Pseudohypoparathyroidism; Radioimmunoassay; Thyroid Neoplasms | 1972 |
A comparison of vitamin D2 and D3 in New World primates. I. Production and regression of osteodystrophia fibrosa.
Topics: Alkaline Phosphatase; Animals; Calcium; Cholecalciferol; Diet; Ergocalciferols; Female; Male; Monkey Diseases; Osteitis Fibrosa Cystica; Phosphorus | 1967 |