Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bone histology, bone mineral content, and calcium absorption were evaluated in 10 patients with primary biliary cirrhosis and osteopenia, before and after 1 yr of treatment with oral 25-hydroxycholecalciferol. Before treatment, quantitative histomorphometric analysis of full-thickness iliac crest bone biopsy specimens with double-tetracycline labeling demonstrated that 9 of 10 patients had osteoporosis. None had osteomalacia. Fasting intestinal calcium absorption correlated well with trabecular bone volume (r = 0.85). Bone mineral content measured by 125I-photon absorption was low in 6 of 10 patients, and it correlated poorly with iliac crest trabecular bone volume. After 1 yr of treatment with oral 25-hydroxyvitamin D3, bone mineral content fell in all 8 patients who were restudied. Iliac crest trabecular bone volume increased in 3 patients, 2 of whom had the greatest pretreatment impairment in calcium absorption, but fell in 5. Bone fractures continued to occur in 3 of 5 patients who were alive after 1 yr and developed for the first time in a sixth patient. We conclude that 25-hydroxyvitamin D3 is ineffective in reversing the bone thinning in the majority of primary biliary cirrhosis patients, but it may be helpful in a few selected patients.
 ...
PMID:Osteoporosis in primary biliary cirrhosis: effects of 25-hydroxyvitamin D3 treatment. 707 48

The left thoracic limb was immobilized in a plaster cast in 6 grade weanling ponies for 6 weeks. Two ponies were injected intramuscularly each day with 2.4 micrograms of 25-hydroxycholecalciferol [25(OH)D3] per kg bodyweight, two with 1.2 micrograms and two received no injections. Immobilization of 25(OH)D3 treatment had no significant effect on mineral metabolism. Immobilization resulted in significantly decreased weight and specific gravity of metacarpus III (MCIII). Histologic examination and triple fluorochrome incorporation showed that the osteopenia was caused by atrophy of osteoblasts with failure of bone apposition. Immobilization caused retardation or cessation of proliferation of cartilage in the epiphyseal plate with thinning or premature closure. Treatment with 25(OH)D3 further reduced apposition and enhanced significantly the osteopenia as shown by quantitative morphometry of microradiographs of the MCIII metaphyses. There was parathyroid gland atrophy and fibrosis in proportion to the level of 25(OH)D3 treatment, which, in absence of hypercalcemia in all ponies, was interpreted to be a direct result of vitamin D treatment. It was concluded that immobilization osteopenia under the present design and duration is caused by failure of bone apposition and that treatment with 25(OH)D3 at dose levels applied is contraindicated.
 ...
PMID:Mineral metabolism and immobilization osteopenia in ponies treated with 25-hydroxycholecalciferol. 714 Mar 1