Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0005940 (bone disease)
 7,459 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cholecalciferol must be regarded as a pro-hormone rather than a vitamin, since it is normally produced in skin under the influence of ultraviolet light. Cholecalciferol must be metabolized in liver to 25-hydroxycholecalciferol and subsequently to 1,25-dihydroxycholecalciferol before it can act on intestine, bone and kidney to provide calcium and phosphorus for bone mineralization and neuromuscular activity. 1,25-Dihydroxycholecalciferol is metabolized in liver and intestine to a C-23-carboxylic acid that is inactive, 25-Hydroxycholecalciferol is metabolized to a variety of metabolic products, including 23S,25-dihydroxycholecalciferol, 23S,25R-25-hydroxycholecalciferol-26,23-lactone, 24R,25-dihydroxycholecalciferol and 25,26-dihydroxycholecalciferol. These metabolites are not involved in the known actions of vitamin D. 1,25-Dihydroxycholecalciferol localizes in the nuclei of target organs through a receptor mechanism. It is believed to initiate transcription of DNA that codes for calcium and phosphorus transport proteins, the nature of which is undetermined. Production of 1,25-dihydroxycholecalciferol is stimulated by low plasma calcium through parathyrin and by low plasma phosphorus. During pregnancy and lactation, 1,25-dihydroxycholecalciferol levels are greatly increased to meet calcium demands. However, vitamin D is not absolutely essential for reproduction. It is likely that some other hormone, possibly prolactin, functions at these periods to mobilize calcium. The clinical application of the vitamin D hormone and its analogues to the treatment of bone disease is presented to illustrate the application of basic science to medical practice. Evidence for each of these points is presented.
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PMID:Metabolism and molecular mechanism of action of vitamin D: 1981. 704 88

(1) While a number of medications have been shown to induce bone loss, the actual incidence and prevalence of medication-induced osteoporosis has not been well quantified. (2) Oral corticosteroids contribute to an increased prevalence of osteoporosis and an increased incidence of fracture in a number of different populations. The increased incidence of fracture in patients receiving inhaled corticosteroids for respiratory disease may be attributed to disease pathogenesis rather than the effects of medication. (3) Other therapies that increase the incidence and/or prevalence of medication-induced osteoporosis and fracture include androgen-deprivation therapy, aromatase inhibitors, protease inhibitors, selective serotonin reuptake inhibitors and prolactin-raising antiepileptic agents. (4) It is difficult to make definitive conclusions on the actual increase in the prevalence and/or incidence of osteoporosis in patients receiving certain medications, as values are often reported differently and studies are mainly retrospective and are therefore open to inherent selection biases and other confounders. Furthermore, there is little available information as to whether specific medications within a class are associated with a higher rate of bone disease than others.
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PMID:Incidence and prevalence of medication-induced osteoporosis: evidence-based review. 1852 57