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Bone turnover markers, anterior pituitary and gonadal hormones, and bone mass evaluation using quantitative computed tomography in ankylosing spondylitis.

El Maghraoui A, Tellal S, Chaouir S, Lebbar K, Bezza A, Nouijai A, Achemlal L, Bouhssain S, Derouiche el M

Rheumatology and Rehabilitation Department, Military Hospital Mohammed V, Rabat, Morocco. abdellahe@menara.ma

The objective of this study was to determine bone mineral density (BMD) distribution in ankylosing spondylitis (AS) using quantitative computed tomography (QCT), to study bone turnover and anterior pituitary and gonadal hormonal axis in AS, and to look for correlations between BMD, bone remodeling markers and gonadal and anterior pituitary hormones. Forty-three male consecutive patients with AS were enrolled prospectively [mean (SD) age of 36.4 (11.3) years (range: 17-67) and mean disease duration of 6.8 (5.2) years (range: 0.4-19)]. Spine BMD was measured in all patients by QCT, and the results were compared to 29 male patients undergoing lumbar CT scan for sciatica. Bone turnover and anterior pituitary and gonadal axis were assessed in 29 patients, and the results were compared to 30 male healthy blood donors. The mean (SD) BMD was 127.7 mg/cm(3) (48.9) (range: 8.8-265.7) and 152.1 (25.3) (range: 34.2-190.4) in patients and controls, respectively (p = 0.018). Patients had lower serum levels of osteocalcin and higher levels of serum testosterone, luteinizing hormone (LH), and prolactin than controls with a significant statistical difference. There was a positive significant statistical correlation between BMD and chest expansion, Schober's test, C7-wall distance, and negative significant statistical correlation with age, disease duration, Bath Ankylosing Spondylitis Metrology Index (BASMI), Bath Ankylosing Spondylitis Radiology Index (BASRI), and serum prolactin. No correlation was observed between bone turnover parameters and AS symptomatic and structural severity indexes. BMD is lower with increasing age and late and severe disease. Decreased bone formation with normal resorption and increased levels of serum prolactin may be involved in its pathophysiology.

Published 21 July 2005 in Clin Rheumatol, 24(4): 346-51.
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