Abstract
Objective. The aim of this study was to examine potential risk factors for GCA in a nested case-control study based on two prospective health surveys. Methods. We used two population-based health surveys, the Malmö Preventive Medicine Program (MPMP) and the Malmö Diet Cancer Study (MDCS). Individuals who developed GCA after inclusion were identified by linking the MPMP and MDCS databases to several patient administrative registers. A structured review of the medical records of all identified cases was performed. Four controls for every confirmed case, matched for sex, year of birth and year of screening, were selected from the corresponding databases. Potential predictors of GCA were examined in conditional logistic regression models. Results. Eighty-three patients (70% women, 64% biopsy positive, mean age at diagnosis 71 years) had a confirmed diagnosis of GCA after inclusion in the MPMP or MDCS. A higher BMI was associated with a significantly reduced risk of subsequent development of GCA [odds ratio (OR) 0.91/kg/m<sup>2</sup> (95% CI 0.84, 0.98)]. Smoking was not a risk factor for GCA overall [OR 1.36 (95% CI 0.77, 2.57)], although there was a trend towards an increased risk in female smokers [OR 2.14 (95% CI 0.97, 4.68)]. In multivariate analysis, adjusted for smoking and level of formal education, the inverse association between BMI and GCA remained significant (P = 0.027). Conclusion. In this study, GCA was predicted by a lower BMI at baseline. Potential explanations include an effect of reduced adipose tissue on hormonal pathways regulating inflammation.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 433-440 |
| Number of pages | 8 |
| Journal | Rheumatology (United Kingdom) |
| Volume | 54 |
| Issue number | 3 |
| DOIs | |
| State | Published - 2015 |
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Keywords
- Body mass index
- Giant cell arteritis
- Predictors
- Vasculitis
ASJC Scopus subject areas
- Rheumatology
- Pharmacology (medical)
Cite this
Body mass index and the risk of giant cell arteritis-results from a prospective study. / Jakobsson, Karin; Jacobsson, Lennart; Warrington, Kenneth J; Matteson, Eric Lawrence; Liang, Kimberly; Melander, Olle; Turesson, Carl.
In: Rheumatology (United Kingdom), Vol. 54, No. 3, 2015, p. 433-440.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Body mass index and the risk of giant cell arteritis-results from a prospective study
AU - Jakobsson, Karin
AU - Jacobsson, Lennart
AU - Warrington, Kenneth J
AU - Matteson, Eric Lawrence
AU - Liang, Kimberly
AU - Melander, Olle
AU - Turesson, Carl
PY - 2015
Y1 - 2015
N2 - Objective. The aim of this study was to examine potential risk factors for GCA in a nested case-control study based on two prospective health surveys. Methods. We used two population-based health surveys, the Malmö Preventive Medicine Program (MPMP) and the Malmö Diet Cancer Study (MDCS). Individuals who developed GCA after inclusion were identified by linking the MPMP and MDCS databases to several patient administrative registers. A structured review of the medical records of all identified cases was performed. Four controls for every confirmed case, matched for sex, year of birth and year of screening, were selected from the corresponding databases. Potential predictors of GCA were examined in conditional logistic regression models. Results. Eighty-three patients (70% women, 64% biopsy positive, mean age at diagnosis 71 years) had a confirmed diagnosis of GCA after inclusion in the MPMP or MDCS. A higher BMI was associated with a significantly reduced risk of subsequent development of GCA [odds ratio (OR) 0.91/kg/m2 (95% CI 0.84, 0.98)]. Smoking was not a risk factor for GCA overall [OR 1.36 (95% CI 0.77, 2.57)], although there was a trend towards an increased risk in female smokers [OR 2.14 (95% CI 0.97, 4.68)]. In multivariate analysis, adjusted for smoking and level of formal education, the inverse association between BMI and GCA remained significant (P = 0.027). Conclusion. In this study, GCA was predicted by a lower BMI at baseline. Potential explanations include an effect of reduced adipose tissue on hormonal pathways regulating inflammation.
AB - Objective. The aim of this study was to examine potential risk factors for GCA in a nested case-control study based on two prospective health surveys. Methods. We used two population-based health surveys, the Malmö Preventive Medicine Program (MPMP) and the Malmö Diet Cancer Study (MDCS). Individuals who developed GCA after inclusion were identified by linking the MPMP and MDCS databases to several patient administrative registers. A structured review of the medical records of all identified cases was performed. Four controls for every confirmed case, matched for sex, year of birth and year of screening, were selected from the corresponding databases. Potential predictors of GCA were examined in conditional logistic regression models. Results. Eighty-three patients (70% women, 64% biopsy positive, mean age at diagnosis 71 years) had a confirmed diagnosis of GCA after inclusion in the MPMP or MDCS. A higher BMI was associated with a significantly reduced risk of subsequent development of GCA [odds ratio (OR) 0.91/kg/m2 (95% CI 0.84, 0.98)]. Smoking was not a risk factor for GCA overall [OR 1.36 (95% CI 0.77, 2.57)], although there was a trend towards an increased risk in female smokers [OR 2.14 (95% CI 0.97, 4.68)]. In multivariate analysis, adjusted for smoking and level of formal education, the inverse association between BMI and GCA remained significant (P = 0.027). Conclusion. In this study, GCA was predicted by a lower BMI at baseline. Potential explanations include an effect of reduced adipose tissue on hormonal pathways regulating inflammation.
KW - Body mass index
KW - Giant cell arteritis
KW - Predictors
KW - Vasculitis
UR - http://www.scopus.com/inward/record.url?scp=84941651453&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84941651453&partnerID=8YFLogxK
U2 - 10.1093/rheumatology/keu331
DO - 10.1093/rheumatology/keu331
M3 - Article
VL - 54
SP - 433
EP - 440
JO - Rheumatology (United Kingdom)
JF - Rheumatology (United Kingdom)
SN - 1462-0324
IS - 3
ER -