Association of 1.25 vitamin D3 deficiency, disease activity and low bone mass in ankylosing spondylitis.
Vertebral fractures due to osteoporosis are a common but frequently unrecognized complication in established ankylosing spondylitis (AS). It is known that inflammatory activity in rheumatic diseases (i.e., proinflammatory cytokines) itself plays a possible role in the pathophysiology of bone loss. The aim of this study was to analyze whether inflammatory activity and an alteration of the vitamin D metabolism play a substantial role in the loss of bone mass in AS. In this cross-sectional study, 58 patients with established AS and an age- and sex-matched control group were examined. The vitamin D status was investigated, as was, in parallel, the relationship to disease activity (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP], Bath Ankylosing Spondylitis Disease Activity Index [BASDAI]), markers of bone metabolism (parathyroid hormone [PTH], 1.25 vitamin D3, 25 vitamin D3), calcium, bone alkaline phosphatase (bone-AP), urine cross-links, and plasma tumor necrosis factor alpha (TNFalpha). Bone mineral density was measured by quantitative computed tomography (QCT) of the lumbar spine. Osteoporosis was diagnosed in early as well as in progressive stages of AS (23/58=39.6%). Furthermore, serum levels of 1.25 vitamin D3 and PTH were negatively correlated with disease activity and TNFalpha. The excretion of cross-links showed a positive correlation with disease activity and TNFalpha, and 1.25 vitamin D3 and PTH were positively correlated with bone-AP. TNFalpha also positively correlated with disease activity. AS patients with osteoporosis showed significantly increased CRP, ESR, cross-links and PTH and a significantly decreased 1.25 D3. Osteoporosis is frequent in AS and high disease activity is associated with an alteration in vitamin D metabolites and increased levels of bone resorption in active AS. Our findings propose a close association of BMD, bone metabolism and inflammatory activity, possibly related to vitamin D inflammation interactions.
Lange
U
U
Kerckhoff-Clinic and Foundation, Department of Rheumatology, Clinical Immunology and Osteology, University Giessen, Sprudelhoff 11, 61231, Bad Nauheim, Germany. U.Lange@kerckhoff-klinik.de
Teichmann
J
J
Strunk
J
J
Müller-Ladner
U
U
Schmidt
K L
KL
D000293:Adolescent; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000032:analysis; D015519:Bone Density / Q000502:physiology; D001842:Bone and Bones / Q000378:metabolism*; D002762:Cholecalciferol / Q000097:blood / Q000172:deficiency*; D003430:Cross-Sectional Studies; D018450:Disease Progression; D005260:Female; D006801:Humans; D008159:Lumbar Vertebrae; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000150:complications / Q000378:metabolism; D010281:Parathyroid Hormone / Q000097:blood; D013167:Spondylitis, Ankylosing / Q000150:complications / Q000378:metabolism*; D014057:Tomography, X-Ray Computed / Q000379:methods; D014808:Vitamin D Deficiency / Q000097:blood / Q000150:complications / Q000503:physiopathology*
D015415:Biomarkers; D010281:Parathyroid Hormone; D002762:Cholecalciferol