title: Effects of antiepileptic drug therapy on vitamin D status and biochemical markers of bone turnover in children with epilepsy.
abstract: Reports of decreased serum 25-hydroxyvitamin D (25-OHD) and altered bone metabolism associated with antiepileptic drug (AED) treatment are inconsistent and predominantly restricted to adults. In this cross-sectional observational study, the aim was to evaluate the influence of AED treatment on vitamin D status and markers of bone turnover in children with epilepsy. In 38 children taking AEDs and 44 healthy control subjects, blood samples were collected to determine the levels of serum 25-OHD, intact parathyroid hormone (iPTH), calcium (Ca), phosphate (P), bone alkaline phosphatase (BAP), osteocalcin (OC) and C terminal telopeptide of type I collagen (ICTP). More than 75% of the patients were vitamin D deficient (serum 25-OHD<20 ng/mL) and 21% of the patients had an insufficient vitamin D status (serum 25-OHD=20-30 ng/mL). In the patients, the serum levels of OC (p = 0.002) and BAP (p < 0.001) were significantly increased, but ICTP (p = 0.002) concentrations were significantly decreased compared with the control group. When patients where divided into two groups according to their medication (mono- or polytherapy), significantly lower 25-OHD (p = 0.038) and ICTP (p = 0.005) levels and elevated BAP (p = 0.023) concentrations were found in patients under polytherapy. An association between 25-OHD and the measured bone markers could not be determined. Our results indicate that the prevalence of vitamin D deficiency in epilepsy patients under AED treatment is high, especially under polytherapy, and alteration markers of bone formation and resorption suggests an accelerated skeletal turnover. The routine monitoring of serum 25-OHD and vitamin D supplementation on an individual basis should be considered.
authors.affiliation: Nutrition Physiology and Human Nutrition Unit, Institute of Food Science, Leibniz University of Hannover, Wunstorfer Str. 14, 30453, Hannover, Germany. sina.nettekoven@lw.uni-hannover.de
authors.forename: Sina
authors.initials: S
authors.lastname: Nettekoven
authors.forename: Alexander
authors.initials: A
authors.lastname: Ströhle
authors.forename: Birgit
authors.initials: B
authors.lastname: Trunz
authors.forename: Maike
authors.initials: M
authors.lastname: Wolters
authors.forename: Susanne
authors.initials: S
authors.lastname: Hoffmann
authors.forename: Rüdiger
authors.initials: R
authors.lastname: Horn
authors.forename: Martin
authors.initials: M
authors.lastname: Steinert
authors.forename: Georg
authors.initials: G
authors.lastname: Brabant
authors.forename: Ralf
authors.initials: R
authors.lastname: Lichtinghagen
authors.forename: Hans-Jürgen
authors.initials: HJ
authors.lastname: Welkoborsky
authors.forename: Ingrid
authors.initials: I
authors.lastname: Tuxhorn
authors.forename: Andreas
authors.initials: A
authors.lastname: Hahn
mesh_terms: D000469:Alkaline Phosphatase / Q000097:blood; D000927:Anticonvulsants / Q000008:administration & dosage / Q000009:adverse effects*; D015415:Biomarkers / Q000097:blood; D001862:Bone Resorption / Q000097:blood* / Q000139:chemically induced* / Q000517:prevention & control; D002118:Calcium / Q000097:blood; D002648:Child; D024042:Collagen Type I / Q000097:blood; D003430:Cross-Sectional Studies; D004827:Epilepsy / Q000097:blood / Q000188:drug therapy*; D005260:Female; D006801:Humans; D008297:Male; D015675:Osteocalcin / Q000097:blood; D010281:Parathyroid Hormone / Q000097:blood; D011795:Surveys and Questionnaires; D014807:Vitamin D / Q000031:analogs & derivatives / Q000097:blood*; D014808:Vitamin D Deficiency / Q000097:blood* / Q000139:chemically induced* / Q000378:metabolism / Q000517:prevention & control
chemical_list: D000927:Anticonvulsants; D015415:Biomarkers; D024042:Collagen Type I; D010281:Parathyroid Hormone; D015675:Osteocalcin; D014807:Vitamin D; C104450:25-hydroxyvitamin D; D000469:Alkaline Phosphatase; D002118:Calcium