24-25-dihydroxyvitamin-d-3 and Bone-Diseases

Topics: 24,25-Dihydroxyvitamin D 3; Animals; Bone and Bones; Bone Diseases; Calcitriol; Dihydroxycholecalciferols; Male; Physical Exertion; Rats; Rats, Inbred Strains; Swimming

Fibrogenesis imperfecta ossium is a rare, acquired disorder of bone mineralization characterized by a morphologic abnormality of bone collagen that presents with bone pain and tenderness and usually results in the patient becoming bedridden. Onset of symptoms in the six previously reported cases of this disorder occurred in patients over 50 years of age. We report a case of fibrogenesis imperfecta ossium with symptoms starting at age 39 where the diagnosis was not made even after three bone biopsies because of the failure to recognize the characteristic morphologic abnormality of collagen. Elevated serum alkaline phosphatase, increased urinary hydroxyproline, and numerous osteoclasts on a bone biopsy are compatible with increased bone turnover. There was no apparent abnormality of vitamin D metabolism contributing to this disorder. Treatment with sodium fluoride, synthetic salmon calcitonin, and 24,25-dihydroxyvitamin D did not result in any apparent benefit.

Topics: 24,25-Dihydroxyvitamin D 3; Adult; Alkaline Phosphatase; Biopsy; Bone Diseases; Calcitonin; Calcium; Collagen; Dihydroxycholecalciferols; Female; Humans; Middle Aged; Phosphorus; Sodium Fluoride

We studied the effects of vitamin D metabolites in 29 patients established on chronic hemodialysis. The patients were divided into four groups; one was treated with 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] 0.5 microgram/day, one with 24R,25-dihydroxyvitamin D3 [24,25-(OH)2D3] 10 micrograms/day, and one with both metabolites. The control group was not given vitamin D. Plasma levels of both metabolites were low before treatment. 1,25-(OH)2D3 levels became normal, and 24,25-(OH)2D3 increased to supranormal levels after administration of the corresponding metabolite. Combined treatment produced still higher plasma levels of 24,25-(OH)2D3, suggesting an interaction between the two metabolites. Patients receiving 1,25-(OH)2D3 alone had a greater increase in plasma calcium than those receiving both metabolites. In control patients, hyperparathyroid bone disease worsened over the 10-month observation period. 1,25-(OH)2D3 improved hyperparathyroid bone disease in most patients, as reflected by a reduction in osteoclast and osteoblast numbers, but had no demonstrable effect on mild osteomalacia. 24,25-(OH)2D3 had no significant effect on plasma biochemistry or bone histology, and the effect of combined treatment on histology was similar to that of 1,25-(OH)2D3 alone. Stainable bone aluminum increased slightly in patients given 1,25-(OH)2D3, but aluminum did not affect the response to treatment. We conclude that 1,25-(OH)2D3 is a useful agent in the treatment of renal bone disease, but no therapeutic role is apparent for 24,25-(OH)2D3.

Topics: 24,25-Dihydroxyvitamin D 3; Adult; Aged; Alkaline Phosphatase; Aluminum; Bone Diseases; Calcitriol; Calcium; Dihydroxycholecalciferols; Drug Therapy, Combination; Female; Humans; Hyperparathyroidism; Kidney Failure, Chronic; Male; Middle Aged; Osteomalacia; Parathyroid Hormone; Phosphorus; Renal Dialysis

The degree of diabetic osteopenia and serum vitamin D metabolite levels were measured in 14 type 1 (insulin-dependent) and 168 type 2 (non-insulin-dependent) diabetic patients. Based on six indices obtained by microdensitometry, we found the bone mass in 28.6% of type 1 and 26.2% of type 2 diabetic patients to be decreased and in 14.3% and 11.9%, respectively, the decrease was severe. Our method of analysis of bone mass has shown that diabetic osteopenia differs from typical osteoporosis in character. In addition, serum 24,25-dihydroxyvitamin D was significantly decreased both in type 1 and in type 2 diabetes (p less than 0.01), but 1,25-dihydroxyvitamin D was significantly decreased only in type 1 diabetes (p less than 0.01) compared to the controls, being lower than that in type 2 diabetes (p less than 0.05). On the other hand, 25-hydroxyvitamin D was similar to that of the controls, in both types of diabetes.

Topics: 24,25-Dihydroxyvitamin D 3; Adolescent; Adult; Aged; Bone and Bones; Bone Diseases; Calcifediol; Calcitriol; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Dihydroxycholecalciferols; Female; Humans; Male; Middle Aged; Vitamin D

Severe hypokinesia of rats given the diet with a ratio of Ca:P = 1:0.5-1:3 was accompanied by hypocalcemia, development of osteoporosis, and some intensification of renal calcinosis. The decrease of phosphorus consumption (Ca:P = 1:0.5-1:1) prevented a development of these changes in intact animals and increased bone mineralization in hypokinetic ones. Excessive phosphorus consumption (Ca:P = 1:3) produced hypocalcemia, hyperphosphatemia, and some osteoporotic changes in the bones of intact animals and intensified these changes with hypokinesia. Administration of 24,25-dihydroxycholecalciferol, an active metabolite of vitamin D3, at a dose of 1.25 micrograms/d prevented a development of bone disorders, thus effectively stimulating diaphyses and epiphyses mineralization and correcting hypocalcemia in hypokinetic rats. 24,25(OH)2D3 at the same dose did not intensify nephocalcinosis and produced no toxic symptoms with hypokinetic animals.

Topics: 24,25-Dihydroxyvitamin D 3; Alkaline Phosphatase; Animals; Bone and Bones; Bone Diseases; Calcinosis; Calcium; Diet; Dihydroxycholecalciferols; Hypocalcemia; Kidney; Male; Osteoporosis; Phosphorus; Rats; Rats, Inbred Strains; Restraint, Physical