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Poster Abstract Presentations
Session Title: Poster Session 1

Abstract 197: Active (1,25 OH), but not Inactive (25-OH) Vitamin D levels are inversely associated with aortic Vascular Inflammation, Non-calcified Coronary Plaque Burden and Visceral Adiposity in Psoriasis

Originally publishedhttps://doi.org/10.1161/atvb.38.suppl_1.197Arteriosclerosis, Thrombosis, and Vascular Biology. 2018;38:A197

    Introduction: Psoriasis (PSO), a chronic inflammatory disease associated with increased Cardiovascular (CV) risk provides an ideal model to study the role of vitamin D, a known anti-inflammatory molecule in PSO associated CV disease. Vitamin D exists as inactive 25-hydroxyvitamin D (25(OH)D) in the bloodstream which is converted to active 1,25-dihydroxyvitaminD (1,25(OH)2D) in target tissues. Cohort studies reporting CV disease among individuals with low vitamin D are inconsistent and solely measure 25(OH)D. While serum 25(OH)D is routinely measured , we propose that measurement of 1,25(OH)2D may perform better than 25(OH)D as a surrogate for CV disease.

    Methods: Consecutive PSO patients (N=122) and healthy controls (N=35) underwent FDG PET/CT and CCTA scans to measure vascular inflammation/ abdominal adiposity volume and coronary plaque burden respectively. Blood levels of both 1,25(OH)2D and 25(OH)D were measured by chemiluminescence (LIASON XL DIaSorin, Stillwater, MN).

    Results: PSO patients were middle-aged, mostly male, had moderate PSO severity and were at low CV risk by 10-year Framingham risk. PSO patients had lower serum 1,25(OH)2D compared to healthy controls (mean±SEM: 52.4±1.4 pg/ml versus 57.5±2.0, p<0.037) but 25(OH)D was not significantly different (28.7±1.3 versus 27.3±2.2, p=0.30). 1,25(OH)2D, but not 25(OH)D was negatively associated with PASI score beyond adjustment for CV risk factors and systemic/ biological therapy (B=-0.20, p=0.043 vs. B=0.12, p=0.25). Furthermore, serum 1,25(OH)2D but not 25(OH)D was inversely associated with non-calcified coronary burden (B=-0.16, p<0.001 versus B=0.01, p=0.84), vascular inflammation (B=-0.24, p=0.007 versus B=-0.13, p=0.16) and visceral adiposity (B=-0.43, p=0.026 versus B=-0.26, p=0.13) independent of traditional risk factors and statin/PSO therapy.

    Conclusion: Our data support that active 1,25(OH)2D may more accurately capture cardiometabolic disturbance compared to inactive 25(OH)D in humans.

    Footnotes

    Author Disclosures: M. Playford: None. A. Dey: None. C. Zierold: None. F. Blocki: None. F. Bonelli: None. A. Joshi: None. H. Teague: None. Y. Baumer: None. N.N. Mehta: Research Grant; Modest; Dr. Mehta is a full-time US Government Employee and has received research grants to the NIH from Abbvie, Janssen, Novartis and Celgene..