Pathophysiology behind anticonvulsant osteomalacia.
Anticonvulsant drug-induced disorders in mineral and bone metabolism are discussed. 'Anticonvulsant osteomalacia' includes hypocalcaemia, elevated serum alkaline phosphatase, decreased serum 25-hydroxycholecalciferol (25 OHD3), radiological and histological signs of osteomalacia and a lower bone mineral content (BMC) than normal. The pathophysiological mechanism behind anticonvulsant osteomalacia is thought be an induction of the microsomal enzyme system in the liver, leading to a disturbance in the metabolism of vitamin D and a resulting vitamin D deficiency. It has been shown that treatment with vitamin D2 increase BMC whereas serum calcium was unchanged. Treatment with vitamin D3 or 25 OHD3 increases serum calcium whereas BMC was unchanged. These findings suggest that vitamin D2 and D3 are metabolized differently in anticonvulsant treated patients. With the present knowledge, preventive treatment of this relative mild pathological condition is not generally indicated.
D000469:Alkaline Phosphatase / Q000097:blood; D000927:Anticonvulsants / Q000009:adverse effects*; D001842:Bone and Bones / Q000187:drug effects; D002112:Calcifediol / Q000097:blood; D004827:Epilepsy / Q000188:drug therapy / Q000201:enzymology; D006801:Humans; D006996:Hypocalcemia / Q000139:chemically induced / Q000201:enzymology; D008903:Minerals / Q000378:metabolism; D010018:Osteomalacia / Q000139:chemically induced* / Q000201:enzymology
D000927:Anticonvulsants; D008903:Minerals; D000469:Alkaline Phosphatase; D002112:Calcifediol