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Vitamin D Deficiency-Induced Vertebral Fractures May Cause Stooped Posture in Parkinson Disease

Sato, Yoshihiro MD; Iwamoto, Jun MD; Honda, Yoshiaki MD

American Journal of Physical Medicine & Rehabilitation: April 2011 - Volume 90 - Issue 4 - p 281-286
doi: 10.1097/PHM.0b013e3182063a42
Original Research Articles: Osteoporosis

Objective: To determine the pathogenesis of the stooped posture in Parkinson disease (PD), we prospectively studied fractures in a cohort of patients with Parkinson disease for 5 yrs.

Design: At baseline, we recorded the dietary intake of vitamin D and serum concentrations of parathyroid hormone and 25-hydroxyvitamin D. Bone mineral density and lateral thoracic and lumbar spine radiographs were obtained at baseline and every year for 5 yrs.

Results: During the 5-yr study period, stooped posture developed in 34 patients; the rest of the 58 patients did not show stooped posture. At baseline, mean serum 25-hydroxyvitamin D and parathyroid hormone levels were 10.9 ng/ml and 73.1 pg/ml, respectively, in the stooped group and 18.6 ng/ml and 56.4 pg/ml, respectively, in the nonstooped group. Bone mineral density in the stooped group was significantly lower than in the nonstooped group. Dietary intake of vitamin D in the stooped group was significantly lower than in the nonstooped group. During the study period, 19 (22%) patients in the nonstooped group developed new vertebral fracture, compared with 23 (100%) patients in the stooped group. The mean ± SD percentage changes in bone mineral density were −6.5 ± 0.6 in the stooped group and −3.8 ± 0.8 in the nonstooped group. Mean serum levels of 25-hydroxyvitamin D after 5 yrs were 7.0 ng/ml in the stooped group and 14.1 ng/ml in the nonstooped group.

Conclusions: Stooped posture in Parkinson disease may be caused by vertebral fractures resulting from vitamin D deficiency with compensatory hyperparathyroidism. Vitamin D supplementation may reduce stooped posture in patients with Parkinson disease.

From the Department of Neurology, Mitate Hospital, Tagawa (YS, YH); and Institute for Integrated Sports Medicine, Keio University School of Medicine, Tokyo, Japan (JI).

All correspondence and requests for reprints should be addressed to: Yoshihiro Sato, MD, Department of Neurology, Mitate Hospital, 3237 Yugeta, Tagawa 826-0041, Japan.

Financial disclosure statements have been obtained, and no conflicts of interest have been reported by the authors or by any individuals in control of the content of this article.

© 2011 Lippincott Williams & Wilkins, Inc.