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Biochemical markers of bone metabolism in mild ankylosing spondylitis and their relationship with bone mineral density and vertebral fractures.
Journal of Rheumatology 1999 October
OBJECTIVE: To determine the relationship of biochemical markers of bone metabolism in patients with mild ankylosing spondylitis (AS) with disease activity, bone mineral density (BMD), and vertebral fractures.
METHODS: A total of 56 male patients with mild AS were studied. All patients had BMD measured by dual x-ray absorptiometry of the lumbar spine and hip and radiographs of the thoracic and lumbar spines. Radiographs of patients with AS were evaluated morphometrically and vertebral fractures were defined using established criteria. Serum osteocalcin, total and bone alkaline phosphatase (ALP, BALP, respectively), 25-hydroxyvitamin D (25-OHD), parathyroid hormone (PTH), urinary deoxypyridinoline (Dpyr), and pyridinoline (Pyr) were measured in the patients with AS and compared with 52 age and sex matched controls. Thirty-nine healthy male subjects aged 50-60 years, recruited from primary care registers, had spinal radiographs and served as controls for vertebral fractures.
RESULTS: Patients with AS had reduced BMD of the lumbar spine, 0.98 (0.1) g/cm2 [T score = -1.14 (1.2) and Z score = -1.01 (1.2)], and femoral neck, 0.83 (0.1) g/cm2 [T score = -1.44 (1.2) and Z score = -0.73 (1.1)]. Of the 56 patients with AS, 11 (19.6%) had a vertebral fracture, whereas only one of 39 control subjects did (2.6%). Patients with AS had significantly lower mean serum osteocalcin compared with controls [9.03 (2.7) microg/l vs 11.05 (2.33) microg/l; p < 0.001], and significantly higher mean serum ALP [73.09 (19.5) U/l vs 53.02 (16.7) U/l; p < 0.001] and BALP [38.54 (9.9) U/l vs 30.35 (8.28) U/l; p < 0.001]. There was no significant difference in the excretion of Dpyr and Pyr between patients with AS and controls [4.90 (3.9) nmol/mmol vs 4.00 (3.6) nmol/mmol, and 15.66 (10.8) nmol/mmol vs 12.24 (10.3) nmol/mmol, respectively]. There were no significant differences in the mean 25-OHD and PTH levels in patients with AS compared to controls [20.03 (1.6) micromol/l vs 18.9 (2.9) micromol/l and 3.31 (1.5) pmol/l vs 2.63 (0.4) pmol/l, respectively]. The biochemical markers of bone formation and resorption correlated well with inflammatory indices of disease activity (acute phase reactants), but not with BMD of the lumbar spine or femoral neck. No significant difference was seen in any marker of bone turnover when AS patients with vertebral fractures were compared with those without.
CONCLUSION: Bone turnover in patients with mild AS is characterized by low serum osteocalcin and ALP in the presence of normal calciotropic hormones. Biochemical markers of bone metabolism do not correlate with BMD or vertebral fractures. The disparity between osteocalcin and alkaline phosphatase in patients with AS needs further evaluation.
METHODS: A total of 56 male patients with mild AS were studied. All patients had BMD measured by dual x-ray absorptiometry of the lumbar spine and hip and radiographs of the thoracic and lumbar spines. Radiographs of patients with AS were evaluated morphometrically and vertebral fractures were defined using established criteria. Serum osteocalcin, total and bone alkaline phosphatase (ALP, BALP, respectively), 25-hydroxyvitamin D (25-OHD), parathyroid hormone (PTH), urinary deoxypyridinoline (Dpyr), and pyridinoline (Pyr) were measured in the patients with AS and compared with 52 age and sex matched controls. Thirty-nine healthy male subjects aged 50-60 years, recruited from primary care registers, had spinal radiographs and served as controls for vertebral fractures.
RESULTS: Patients with AS had reduced BMD of the lumbar spine, 0.98 (0.1) g/cm2 [T score = -1.14 (1.2) and Z score = -1.01 (1.2)], and femoral neck, 0.83 (0.1) g/cm2 [T score = -1.44 (1.2) and Z score = -0.73 (1.1)]. Of the 56 patients with AS, 11 (19.6%) had a vertebral fracture, whereas only one of 39 control subjects did (2.6%). Patients with AS had significantly lower mean serum osteocalcin compared with controls [9.03 (2.7) microg/l vs 11.05 (2.33) microg/l; p < 0.001], and significantly higher mean serum ALP [73.09 (19.5) U/l vs 53.02 (16.7) U/l; p < 0.001] and BALP [38.54 (9.9) U/l vs 30.35 (8.28) U/l; p < 0.001]. There was no significant difference in the excretion of Dpyr and Pyr between patients with AS and controls [4.90 (3.9) nmol/mmol vs 4.00 (3.6) nmol/mmol, and 15.66 (10.8) nmol/mmol vs 12.24 (10.3) nmol/mmol, respectively]. There were no significant differences in the mean 25-OHD and PTH levels in patients with AS compared to controls [20.03 (1.6) micromol/l vs 18.9 (2.9) micromol/l and 3.31 (1.5) pmol/l vs 2.63 (0.4) pmol/l, respectively]. The biochemical markers of bone formation and resorption correlated well with inflammatory indices of disease activity (acute phase reactants), but not with BMD of the lumbar spine or femoral neck. No significant difference was seen in any marker of bone turnover when AS patients with vertebral fractures were compared with those without.
CONCLUSION: Bone turnover in patients with mild AS is characterized by low serum osteocalcin and ALP in the presence of normal calciotropic hormones. Biochemical markers of bone metabolism do not correlate with BMD or vertebral fractures. The disparity between osteocalcin and alkaline phosphatase in patients with AS needs further evaluation.
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