title: Bone mineral density measured by dual-energy x-ray absorptiometry and novel markers of bone formation and resorption in patients on antiepileptic drugs.
abstract: In patients on antiepileptic drugs, bone loss has been mainly demonstrated at radial sites using old technology and has been ascribed to drug-induced vitamin D deficiency rather than to any direct effects of the treatment on bone cells. We examined 38 epileptic patients (24 women and 14 men) aged 20-49 years who were using either carbamazepine or phenytoin or both. Bone mineral density (BMD) at the lumbar spine and three femoral sites was measured by dual-energy x-ray absorptiometry (DXA) and serum and urine markers of bone and mineral metabolism were determined. The latter included the C-terminal extension peptide of type I procollagen (PICP), a putative serum marker of bone formation, and the cross-linked carboxyl-terminal telopeptide of human type I collagen (ICTP), a novel serum marker of bone matrix degradation. In female patients on phenytoin, weight- and height-adjusted BMD was reduced at the femoral neck and the Ward's triangle (p < 0.05) but was at the control level in the other patient groups at all four measurement sites. Compared with controls, the serum concentrations of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were reduced by 26% (p < 0.01) and by 27% (p < 0.001) in female patients. These changes were independent of the therapy used. They were not present in male patients. For both genders the serum levels of vitamin D binding protein were normal. Both female and male patients had hypocalcemia, but women only showed hypocalciuria.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Third Department of Medicine, University of Helsinki, Finland.
authors.forename: M J
authors.initials: MJ
authors.lastname: Välimäki
authors.forename: M
authors.initials: M
authors.lastname: Tiihonen
authors.forename: K
authors.initials: K
authors.lastname: Laitinen
authors.forename: R
authors.initials: R
authors.lastname: Tähtelä
authors.forename: M
authors.initials: M
authors.lastname: Kärkkäinen
authors.forename: C
authors.initials: C
authors.lastname: Lamberg-Allardt
authors.forename: P
authors.initials: P
authors.lastname: Mäkelä
authors.forename: R
authors.initials: R
authors.lastname: Tunninen
mesh_terms: D015502:Absorptiometry, Photon; D000328:Adult; D000469:Alkaline Phosphatase / Q000097:blood; D015519:Bone Density / Q000187:drug effects* / Q000502:physiology; D001846:Bone Development / Q000187:drug effects*; D001862:Bone Resorption / Q000139:chemically induced*; D002118:Calcium / Q000097:blood / Q000652:urine; D002220:Carbamazepine / Q000009:adverse effects* / Q000627:therapeutic use; D003094:Collagen / Q000097:blood; D024042:Collagen Type I; D004827:Epilepsy / Q000188:drug therapy*; D005260:Female; D005269:Femur; D006801:Humans; D006887:Hydroxycholecalciferols / Q000097:blood; D008159:Lumbar Vertebrae; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D010281:Parathyroid Hormone / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D010455:Peptides / Q000097:blood; D010672:Phenytoin / Q000009:adverse effects* / Q000627:therapeutic use; D011347:Procollagen / Q000097:blood
chemical_list: D024042:Collagen Type I; D006887:Hydroxycholecalciferols; D010281:Parathyroid Hormone; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; C052929:collagen type I trimeric cross-linked peptide; C042813:procollagen type I carboxy terminal peptide; D015675:Osteocalcin; D002220:Carbamazepine; D010672:Phenytoin; D003094:Collagen; D000469:Alkaline Phosphatase; D002118:Calcium