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SAT0279 The Vitamin D Status in Ankylosing Spondylitis in Relation to Intestinal Inflammation, Disease Activity, Osteoproliferation, Bone Mineral Density and Vertebral Fractures
  1. E. Klingberg1,
  2. G. Oleröd2,
  3. O. Hammarsten2,
  4. H. Forsblad-d'Elia1
  1. 1Department of Rheumatology and Inflammation Research
  2. 2Department of Clinical Chemistry and Transfusion Medicine, Sahlgrenska Academy At University Of Gothenburg, Göteborg, Sweden

Abstract

Background Vitamin D insufficiency is common in many regions of the world and a poor vitamin D status has been associated with several chronic illnesses, including rheumatoid arthritis and ankylosing spondylitis (AS). Earlier studies on AS have mainly studied the vitamin D levels attained during the summer. At northern latitudes no vitamin D3 can be produced in the skin during “the vitamin D winter” due to insufficient out-door UVB irradiation and the populations here are then dependent of the dietary intake of vitamin D.

Objectives We aimed to study the vitamin D levels attained mainly by dietary intake in AS in comparison with healthy controls and in relation to gastrointestinal symptoms and gut inflammation, measured indirectly by fecal calprotectin. The vitamin D levels were also correlated with measures of disease activity, osteoproliferation, bone mineral density (BMD) and vertebral fractures.

Methods Serum 25-hydroxy vitamin D (25(OH)D) was measured in the late winter in 203 AS patients and 120 healthy controls resident in Gothenburg, Sweden (57°41'N, 11°59'E).

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 by Dual-energy X-ray Absorptiometry 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, vertebral fractures or BMD.

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, vertebral fractures or BMD during the winter months. We suggest that the lower vitamin D levels in AS, previously found by others, is caused by reduced out-door UVB exposure. It is however imperative to diagnose and treat vitamin D insufficiency in AS given the increased risk of osteoporotic fractures associated with the disease.

Disclosure of Interest None declared

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