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Abstract Number: 905

The Association Between Lower Body Mass Index and Increased Risk of Giant Cell Arteritis Is Not Explained by Differences in Physical Activity

Karin Jakobsson1, Lennart T.H. Jacobsson1, Kenneth J. Warrington2, Eric L. Matteson3, Kimberly P. Liang4, Olle Melander5 and Carl Turesson1, 1Section of Rheumatology, Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden, 2Division of Rheumatology, Mayo Clinic, Rochester, MN, 3Rheumatology, Mayo Clinic, Rochester, MN, 4Department of Medicine, Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA, 5Unit of Hypertension and Cardiovascular Disease, Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: body mass, giant cell arteritis and physical activity

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Session Information

Title: Epidemiology and Health Services Research: Epidemiology and Outcomes of Rheumatic Disease II

Session Type: Abstract Submissions (ACR)

Background/Purpose:

There is limited data on predictors of giant cell arteritis (GCA). Low body mass index (BMI), a history of smoking and several hormonal factors have been associated with GCA in a retrospective case-control study, and we have confirmed the association with low BMI in a prospective study. Potential explanations for the association between BMI and GCA, include a difference in the level of physical activity. To our knowledge, the impact of physical activity on the risk of GCA has not been studied previously.

Our purpose was to examine potential influence of physical activity as a risk factor of GCA in a nested case-control study based on a prospective health survey.

Methods:

Incident cases of GCA among participants in a population based health survey, in which 30447 subject (12121 men and 18326 women) were included between 1991 and 1996, were used for the present study. As part of the health survey, information on medical history and life style factors was obtained using standard physical examinations and self-administered questionnaires. Information on physical activity were obtained by asking participants to estimate the number of minutes per week, for each of the four seasons, they spent performing 17 different physical activities. The answer was multiplied by an intensity factor depending on the activity creating a physical activity score. This method was adapted from the Minnesota physical activity questionnaire, and has been validated against accelerometer-monitoring, an objective measure of physical activity, in a subset of the present health survey population.

Individuals who developed GCA after inclusion was identified by linking the health survey database to the local patient administrative register and the national hospital discharge register. A structured review of the medical records of all identified cases was performed. Four controls for each validated case, matched for sex, year of birth and year of screening, who were alive and free of GCA when the index person was diagnosed with GCA, were selected from the health survey. The impact of BMI and physical activity as predictors of GCA was examined in conditional logistic regression models.

Results:

Fifty-five cases [mean age 73.6 years; standard deviation (SD 5.21), 43 women (78 %), 31 temporal artery biopsy positive] had a confirmed diagnosis of GCA after inclusion. The median time from screening to GCA diagnosis was 9.4 years (range 0.4-16.6). BMI at screening was lower in GCA cases than in matched controls (mean 24.7 vs 26.1 kg/m2). There was no association found between level of physical activity and development of GCA (mean score in cases and controls: 8349 vs 8134; p=0.95).  The association between higher BMI and reduced risk of GCA was similar in bivariate analysis (OR 0.91 per kg/m2; 95 % CI 0.84-0.99) and in multivariate analysis adjusted for physical activity (OR 0.92 per kg/m2; 95 % CI 0.84-1.00).

Conclusion:

GCA was predicted by a lower BMI, and this could not be explained by the level of physical activity at baseline. Physical activity did not influence the risk of GCA. Other factors, such as diet, genetics or hormonal factors, may explain the association between low BMI and GCA.


Disclosure:

K. Jakobsson,
None;

L. T. H. Jacobsson,
None;

K. J. Warrington,
None;

E. L. Matteson,
None;

K. P. Liang,
None;

O. Melander,
None;

C. Turesson,
None.

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