title: BsmI vitamin D receptor's polymorphism and bone mineral density in men and premenopausal women on long-term antiepileptic therapy.
abstract: BACKGROUND
  utilization of antiepileptic drugs (AEDs) has long been associated with bone deleterious effects. Furthermore, the BsmI restriction fragment polymorphism of the vitamin D receptor (VDR) has been associated with reduced bone mineral density (BMD), mostly in postmenopausal women. This study evaluates the association between bone metabolism of patients with epilepsy and the BsmI VDR's polymorphism in chronic users of AEDs.
  
  
  METHODS
  this study evaluated 73 long-term users of antiepileptic drug monotherapy, in a cross-sectional design. Fasting blood samples were obtained to estimate the circulating serum levels of calcium, magnesium, phosphorus, parathormone, 25 hydroxyvitamin D as well as the VDR's genotype. Bone mineral density at the lumbar spine was measured with Dual Energy X-Ray Absorptiometry.
  
  
  RESULTS
  bone mineral density was significantly associated with the genotype of VDR (mean BMD: Bb genotype 1.056 ± 0.126 g/cm(2) ; BB genotype 1.059 ± 0.113 g/cm(2) ; bb genotype 1.179 ± 0.120 g/cm(2) ; P < 0.05). Additionally, the presence of at least one B allele was significantly associated with lower bone mineral density (B allele present: BMD = 1.057 ± 0.12 g/cm(2) , B allele absent: BMD = 1.179 ± 0.119 g/cm(2) ; P < 0.01). Patients with at least one B allele had lower serum levels of 25 hydroxyvitamin D when compared with bb patients (22.61 ng/ml vs. 33.27 ng/ml, P < 0.05), whilst they tended to have higher levels of parathyroid hormone.
  
  
  CONCLUSIONS
  vitamin D receptor polymorphism is associated with lower bone mass in patients with epilepsy. This effect might be mediated through the vitamin D-parathormone pathway.
authors.affiliation: 2nd Department of Obstetrics and Gynecology, University of Athens, Aretaion Hospital, Athens, Greece.
authors.forename: I
authors.initials: I
authors.lastname: Lambrinoudaki
authors.forename: G
authors.initials: G
authors.lastname: Kaparos
authors.forename: E
authors.initials: E
authors.lastname: Armeni
authors.forename: A
authors.initials: A
authors.lastname: Alexandrou
authors.forename: C
authors.initials: C
authors.lastname: Damaskos
authors.forename: E
authors.initials: E
authors.lastname: Logothetis
authors.forename: M
authors.initials: M
authors.lastname: Creatsa
authors.forename: A
authors.initials: A
authors.lastname: Antoniou
authors.forename: E
authors.initials: E
authors.lastname: Kouskouni
authors.forename: N
authors.initials: N
authors.lastname: Triantafyllou
mesh_terms: D015502:Absorptiometry, Photon; D000293:Adolescent; D000328:Adult; D000483:Alleles; D000927:Anticonvulsants / Q000627:therapeutic use*; D015519:Bone Density / Q000235:genetics*; D002136:Calcium, Dietary; D002220:Carbamazepine / Q000031:analogs & derivatives / Q000627:therapeutic use; D003430:Cross-Sectional Studies; D004827:Epilepsy / Q000188:drug therapy* / Q000235:genetics*; D005260:Female; D005838:Genotype; D006801:Humans; D000077287:Levetiracetam; D008297:Male; D008875:Middle Aged; D000078330:Oxcarbazepine; D010889:Piracetam / Q000031:analogs & derivatives / Q000627:therapeutic use; D011110:Polymorphism, Genetic; D017697:Premenopause / Q000235:genetics; D018167:Receptors, Calcitriol / Q000235:genetics*; D012044:Regression Analysis; D018709:Statistics, Nonparametric; D014635:Valproic Acid / Q000627:therapeutic use
chemical_list: D000927:Anticonvulsants; D002136:Calcium, Dietary; D018167:Receptors, Calcitriol; D002220:Carbamazepine; D000077287:Levetiracetam; D014635:Valproic Acid; D000078330:Oxcarbazepine; D010889:Piracetam