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Abstract Number: 1394

Low Vitamin D Level Is Not Associated with Increased Risk of Cardiovascular Disease in Rheumatoid Arthritis Patients

Tarun S. Sharma1, Xiaoqin Tang2, Deepak Vedamurthy3, Jonida Cote4 and Androniki Bili4, 1Rheumatology, Geisinger Medical Center, Danville, PA, 2Biostatistics, Geisinger Center for Health Research, Danville, PA, 3Hospital Medicine, Geisinger Medical Center, Danville, PA, 4Rheumatology, Geisinger Health System, Danville, PA

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: Cardiovascular disease and rheumatoid arthritis (RA), Vitamin D

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Session Information

Title: Rheumatoid Arthritis - Clinical Aspects (ACR): Comorbidities, Treatment Outcomes and Mortality

Session Type: Abstract Submissions (ACR)

Background/Purpose:  Cardiovascular disease (CVD) is the leading cause of death in patients with Rheumatoid Arthritis (RA).  Vitamin D deficiency is prevalent in RA and it has also been shown to be related to disease activity in some studies which is attributed to its immunomodulatory properties. There have been increasing reports of an inverse relationship between vitamin D levels and CVD risk in the general population but no studies in the RA population. The aim of this study was to evaluate the association between Vitamin D levels and CVD risk in RA.

Methods:  A retrospective cohort of adult patients with RA (defined as ICD-9 714.0 twice by a rheumatologist) within a tertiary health system and with primary care physician within the health system from 1/1/2001 to 10/31/2013 was constructed (n=1459). Patients with prevalent diagnosis of CVD at the time of RA diagnosis (n=127) or those without available vitamin D levels (n=410) were excluded. Vitamin D level was analyzed as both a continuous and dichotomous variable with level <20 ng/ml defined as “deficient” and ≥20 ng/ml “sufficient” vitamin D level groups. Primary outcome was independent physician adjudicated incident CVD defined as a composite of CAD, stroke, transient ischemic attack or peripheral vascular disease. Data was censored for death or end of the study period and vitamin D levels closest to the censoring point were captured. Poisson regression models were used to calculate the relative risk (RR) for CVD between the deficient and sufficient vitamin D level groups. Cox regression models were used to calculate the hazard ratios (HR) for CVD between the two vitamin D groups. The models were adjusted for age, gender, BMI, smoking, RF and ACPA positivity, LDL, NSAID, corticosteroid, DMARD, statin and TNF inhibitor use. The study was designed to have an 80% power to detect a minimum HR for incident CVD of 2.5 between the two groups.

Results: 921 RA patients were included. Patients were 80.5% women, 96.9% Caucasian, with mean age of 58 years and BMI 30.4 kg/m2. Median time from vitamin D level measurement to CVD events was 2.7 years. There were 128 patients in the deficient and 793 patients in the sufficient vitamin D level groups with mean vitamin D levels of 14.3 ng/ml and 36.8 ng/ml respectively. There were 88 incident CVD events with an Incidence Rate (IR) of 14.8/1000 patent years; of these events, 19 were in the deficient and 69 in the sufficient vitamin D groups with Incidence Rate Ratio (IRR) of 1.43 (0.84-2.43, p=0.19) for CVD between the groups. In the multivariate fully adjusted Cox model, the HR for incident CVD events was 1.30 (95% CI 0.78-2.15 p=0.32) between the two groups. When treating vitamin D as a continuous variable, the HR for incident CVD was 0.99 (95% CI 0.97-1.004, p=0.14) between the deficient and sufficient vitamin D level groups.

Conclusion:  In this study, vitamin D level <20 vs. ≥20 ng/ml was not associated with increased risk of incident CVD in patients with RA. However, the study was powered to detect a minimum of double the risk between the vitamin D groups and may have missed an association of smaller magnitude.


Disclosure:

T. S. Sharma,
None;

X. Tang,
None;

D. Vedamurthy,
None;

J. Cote,
None;

A. Bili,
None.

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