Section of Rheumatology, Department of Clinical Sciences, Lund University, Malmö, Department of Rheumatology & Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden, Division of Rheumatology, Mayo Clinic College of Medicine, Rochester, MN, Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA, USA and Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden.
Section of Rheumatology, Department of Clinical Sciences, Lund University, Malmö, Department of Rheumatology & Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden, Division of Rheumatology, Mayo Clinic College of Medicine, Rochester, MN, Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA, USA and Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden. Section of Rheumatology, Department of Clinical Sciences, Lund University, Malmö, Department of Rheumatology & Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden, Division of Rheumatology, Mayo Clinic College of Medicine, Rochester, MN, Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA, USA and Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden.
Rheumatology (Oxford). 2015 Mar;54(3):433-40. doi: 10.1093/rheumatology/keu331. Epub 2014 Sep 5.
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.
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.
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(2) (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).
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.
本研究旨在通过基于两项前瞻性健康调查的嵌套病例对照研究,探讨巨细胞动脉炎(GCA)的潜在危险因素。
我们使用了两项基于人群的健康调查,即马尔默预防医学计划(MPMP)和马尔默饮食癌症研究(MDCS)。通过将 MPMP 和 MDCS 数据库与多个患者管理登记处进行链接,确定纳入后发生 GCA 的个体。对所有确诊病例的病历进行了结构化审查。从相应的数据库中为每例确诊病例选择 4 名性别、出生年份和筛查年份匹配的对照。在条件逻辑回归模型中检查了 GCA 的潜在预测因素。
在 MPMP 或 MDCS 纳入后,83 例患者(70%为女性,64%活检阳性,诊断时的平均年龄为 71 岁)确诊为 GCA。较高的 BMI 与随后发生 GCA 的风险显著降低相关[比值比(OR)0.91/kg/m(2)(95%可信区间 0.84,0.98)]。吸烟总体上不是 GCA 的危险因素[OR 1.36(95%可信区间 0.77,2.57)],尽管女性吸烟者的风险呈上升趋势[OR 2.14(95%可信区间 0.97,4.68)]。在调整了吸烟和正规教育程度的多变量分析中,BMI 与 GCA 之间的负相关仍然显著(P = 0.027)。
在这项研究中,GCA 由基线时较低的 BMI 预测。潜在的解释包括脂肪组织减少对调节炎症的激素途径的影响。