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Progressive bone deficit in epilepsy

From the Departments of Neurology (R.D.S., B.P.H.) and Medicine (Endocrinology) (N.B.), University of Wisconsin–Madison.

Address correspondence and reprint requests to Dr. Raj D. Sheth, Department of Neurology, 600 Highland Ave-H6/574 CSC, Madison, WI 53792-5132 sheth{at}neurology.wisc.edu

Objective: Chronic treatment with antiepileptic medication is associated with reduced bone mineral density (BMD), which may underlie the two- to sixfold increase in fracture rates observed in patients with epilepsy. The objective was to determine the timing of the BMD deficit in ambulatory children with epilepsy.

Methods: A cross-sectional evaluation was conducted in 82 ambulatory children aged 6 to 18 years (12.4 ± 3.3 years) with epilepsy for <1 year (n = 18), 1 to 5 years (n = 37), and 6 or more years (n = 27). Controls were 32 healthy children aged 12.8 ± 2.6 years. Age- and sex-corrected total body BMD Z-score was measured.

Results: Total BMD Z-score was lower in children with epilepsy (0.10 ± 0.96; CI = –0.08, 0.34) compared to controls (0.57 ± 0.74; CI = 0.3, 0.84; p = 0.03). Increasing duration of epilepsy was associated with a progressive reduction in BMD compared to controls (Spearman r = –0.197; p = 0.03). Compared to controls, those with epilepsy for 1 to 5 years had a mean BMD Z-score of 0.13 ± 0.78 (CI = –0.13, 0.39; p = 0.04) and in those treated for 6 or more years BMD was 0.06 ± 1.11 (CI = –0.38, 0.5; p = 0.04). For those with epilepsy for <1 year BMD was 0.23 ± 1.1 (CI = –0.31, 0.77; p = 0.21).

Conclusions: Children treated for epilepsy sustain significant bone mineral density (BMD) deficit compared to controls during the initial 1 to 5 years of treatment which progressively worsens thereafter. This progressive BMD deficit may be a contributing factor to the increased fracture risk observed in patients with epilepsy and may accelerate aging-related osteoporosis.

Abbreviations: BMD = bone mineral density; DXA = dual energy x-ray.

Editorial, page 166

e-Pub ahead of print on December 5, 2007, at www.neurology.org.

Supported by the University of Wisconsin General Clinical Research Center.

Disclosure: Funded in part by an investigator initiated grant from GlaxoSmithKline.

Received November 2, 2006. Accepted in final form February 2, 2007.

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