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The vitamin D status in ankylosing spondylitis in relation to intestinal inflammation, disease activity, and bone
E Klingberg1, G Oleröd2, O Hammarsten2
1Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at the University of Gothenburg, Gröna stråket 14, SE-41345, Gothenburg, Sweden. eva.klingberg@vgregion.se.
Unlabelled:
We assessed the vitamin D status in ankylosing spondylitis (AS) patients and healthy controls in the late winter when no vitamin D is produced by the sunlight. The vitamin D status was often poor, but not lower in AS and not associated with disease activity or signs of gut inflammation.
Introduction:
The aims of the study were to investigate the vitamin D levels attained mainly by dietary intake in ankylosing spondylitis (AS) in comparison with healthy controls and in relation to gut inflammation, measured indirectly by fecal calprotectin, disease activity, osteoproliferation, bone mineral density (BMD), and vertebral fractures.
Methods:
Serum 25-hydroxy vitamin D (25(OH)D) was measured in 203 AS patients and 120 healthy controls at the end of "the vitamin D winter," when the out-door UVB irradiation is too low to allow synthesis of vitamin D3 in the skin at the latitude of Gothenburg, Sweden. Fecal calprotectin was measured in stool samples. Disease activity was assessed with CRP, ESR, ASDASCRP, BASDAI, BAS-G, BASFI, and BASMI. Lateral spine radiographs were scored for osteoproliferation and vertebral fractures using the mSASSS and Genant scores. BMD was measured in the lumbar spine and femoral neck.
Results:
Vitamin D insufficiency (a serum 25(OH)D <50 nmol/L) was found in approximately 50 % of the AS patients, but serum 25(OH)D was not different from healthy controls and not significantly correlated with fecal calprotectin, gastrointestinal symptoms, disease activity parameters, mSASSS, BMD, or vertebral fractures.
Conclusions:
The vitamin D status was often poor in the late winter in AS but not different from the healthy controls. No evidence for a connection between subclinical gut inflammation, malabsorption, and hypovitaminosis D was found. Serum 25(OH)D was not associated with disease activity, osteoproliferation, BMD, or vertebral fractures. We suggest that the lower vitamin D levels in AS, previously found by others, may be caused by reduced out-door UVB exposure.
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