Evaluation of bone turnover in seronegative spondyloarthropathy (SSPA)‎ : relationship to disease activity

الملخص EN

The aim of this study was to provide insight into the biochemical markers of bone metabolism in patients with seronegative spondyloarthropathy (SSPA) and to determine their relationships with clinical and laboratory critera of disease activity.

Fifty-seven patients with SSPA were enrolled in this study, (33 patients with ankylosing spondylitis (AS), 16 patients with psoriatic arthritis (PsA) and 8 patients with reactive arthritis (ReA)).

Ten healthy volunteers were served as control.

Clinical and radiological status was assessed for each patient.

Serum calcium, alkaline phosphatase (ALP) and bone-specific alkaline phosphatase (B-ALP), urinary calcium and free D-pyridinoline cross links (f-Dpyr) were assayedfor patients and controls.

Urinary excretion of f-Dpyr was significantly increased in AS and ReA, and in AS was correlated with inflammatory measures (ESR and CRP), P-0.01 for each.

In PsA, patients with ESR>30 mm/hour had significantly higher levels of f-Dpyr than those with ESR<30 mm/hour (P=0.024) and those with CRP>6 mg/L than those with CRP<6 mg/L (P=0.046).

No significant difference in urinary calcium excretion was observed in the patients groups compared with controls.

As regard to bone formation, in AS, serum calcium was significantly decreased and ALP but not B-ALP level was elevated compared with controls, positive correlation was also found between ALP and inflammatory measures (ESR and CRP).

In PsA patients, a significant increase in serum ALP and B-ALP, but not serum calcium was noted compared with controls.

No variation was observed in patients with ReA.

Finally, f-Dpyr excretion did not correlate with age, disease duration and no clear difference was observed between men and women Conclusion: The urinary excretion of bone resorption markers (f-Dpyr) is increased in patients with SSpA, uncoupled by bone formation particularly in AS, leading to bone loss in those patients, and disease activity had a role in this bone turnove