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.
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.