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本文引用的文献

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Swedish Society of Rheumatology 2018 guidelines for investigation, treatment, and follow-up of giant cell arteritis.瑞典风湿病学会 2018 年巨细胞动脉炎的调查、治疗和随访指南。
Scand J Rheumatol. 2019 Jul;48(4):259-265. doi: 10.1080/03009742.2019.1571223. Epub 2019 Mar 6.
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Cardiovascular risk factors and incident giant cell arteritis: a population-based cohort study.心血管危险因素与巨细胞动脉炎发病的相关性:一项基于人群的队列研究。
Scand J Rheumatol. 2019 May;48(3):213-217. doi: 10.1080/03009742.2018.1506821. Epub 2018 Nov 21.
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Glucose metabolism controls disease-specific signatures of macrophage effector functions.葡萄糖代谢控制巨噬细胞效应功能的疾病特异性特征。
JCI Insight. 2018 Oct 18;3(20):123047. doi: 10.1172/jci.insight.123047.
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Smoking as a risk factor for giant cell arteritis: A systematic review and meta-analysis.吸烟作为巨细胞动脉炎的一个风险因素:系统评价和荟萃分析。
Semin Arthritis Rheum. 2018 Dec;48(3):529-537. doi: 10.1016/j.semarthrit.2018.07.001. Epub 2018 Jul 11.
5
Incidence of giant cell arteritis in Western Norway 1972-2012: a retrospective cohort study.1972-2012 年挪威西部巨细胞动脉炎的发病率:一项回顾性队列研究。
Arthritis Res Ther. 2017 Dec 15;19(1):278. doi: 10.1186/s13075-017-1479-6.
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Pyruvate controls the checkpoint inhibitor PD-L1 and suppresses T cell immunity.丙酮酸控制检查点抑制剂程序性死亡受体配体1(PD-L1)并抑制T细胞免疫。
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Immunoinhibitory checkpoint deficiency in medium and large vessel vasculitis.中大型血管炎中的免疫抑制检查点缺陷
Proc Natl Acad Sci U S A. 2017 Feb 7;114(6):E970-E979. doi: 10.1073/pnas.1616848114. Epub 2017 Jan 23.
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The PD1:PD-L1/2 Pathway from Discovery to Clinical Implementation.从发现到临床应用的PD1:PD-L1/2通路
Front Immunol. 2016 Dec 12;7:550. doi: 10.3389/fimmu.2016.00550. eCollection 2016.
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Risk of Diabetes Mellitus among Patients Diagnosed with Giant Cell Arteritis or Granulomatosis with Polyangiitis: Comparison with the General Population.巨细胞动脉炎或肉芽肿性多血管炎患者患糖尿病的风险:与普通人群的比较。
J Rheumatol. 2017 Jan;44(1):78-83. doi: 10.3899/jrheum.160797. Epub 2016 Oct 15.
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The temporal relationship between poor lung function and the risk of diabetes.肺功能不佳与糖尿病风险之间的时间关系。
BMC Pulm Med. 2016 May 10;16(1):75. doi: 10.1186/s12890-016-0227-z.

空腹血糖、胆固醇和甘油三酯水平与巨细胞动脉炎发展呈负相关。

Negative associations for fasting blood glucose, cholesterol and triglyceride levels with the development of giant cell arteritis.

机构信息

Rheumatology, Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden.

Department of Rheumatology, Skåne University Hospital, Malmö and Lund, Sweden.

出版信息

Rheumatology (Oxford). 2020 Nov 1;59(11):3229-3236. doi: 10.1093/rheumatology/keaa080.

DOI:10.1093/rheumatology/keaa080
PMID:32240313
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7590417/
Abstract

OBJECTIVES

To investigate metabolic features that may predispose to GCA in a nested case-control study.

METHODS

Individuals who developed GCA after inclusion in a population-based health survey (the Malmö Preventive Medicine Project; N = 33 346) were identified and validated through a structured review of medical records. Four controls for every validated case were selected from the database.

RESULTS

A total of 76 cases with a confirmed incident diagnosis of GCA (61% female, 65% biopsy positive, mean age at diagnosis 70 years) were identified. The median time from screening to diagnosis was 20.7 years (range 3.0-32.1). Cases had significantly lower fasting blood glucose (FBG) at baseline screening compared with controls [mean 4.7 vs 5.1 mmol/l (S.d. overall 1.5), odds ratio (OR) 0.35 per mmol/l (95% CI 0.17, 0.71)] and the association remained significant when adjusted for smoking [OR 0.33 per mmol/l (95% CI 0.16, 0.68)]. Current smokers had a reduced risk of GCA [OR 0.35 (95% CI 0.18, 0.70)]. Both cholesterol [mean 5.6 vs 6.0 mmol/l (S.d. overall 1.0)] and triglyceride levels [median 1.0 vs 1.2 mmol/l (S.d. overall 0.8)] were lower among the cases at baseline screening, with significant negative associations with subsequent GCA in crude and smoking-adjusted models [OR 0.62 per mmol/l (95% CI 0.43, 0.90) for cholesterol; 0.46 per mmol/l (95% CI 0.27, 0.81) for triglycerides].

CONCLUSION

Development of GCA was associated with lower FBG and lower cholesterol and triglyceride levels at baseline, all adjusted for current smoking, suggesting that metabolic features predispose to GCA.

摘要

目的

在一项巢式病例对照研究中,探讨可能导致巨细胞动脉炎(GCA)的代谢特征。

方法

从基于人群的健康调查(马尔默预防医学项目;N=33346)中纳入的个体中确定并验证发生 GCA 的患者,并通过对病历进行结构化审查来验证。每例确诊的 GCA 患者选择 4 名对照。

结果

共确定了 76 例经证实的 GCA 新发病例(61%为女性,65%经活检证实,诊断时的平均年龄为 70 岁)。从筛查到诊断的中位时间为 20.7 年(范围 3.0-32.1)。与对照组相比,病例组在基线筛查时的空腹血糖(FBG)显著较低[平均 4.7 与 5.1mmol/l(总体标准差为 1.5),每 mmol/l 的比值比(OR)为 0.35(95%CI 0.17,0.71)],且在调整吸烟因素后,该关联仍然显著[每 mmol/l 的 OR 为 0.33(95%CI 0.16,0.68)]。当前吸烟者 GCA 风险降低[OR 为 0.35(95%CI 0.18,0.70)]。病例组在基线筛查时的胆固醇[平均 5.6 与 6.0mmol/l(总体标准差为 1.0)]和甘油三酯水平[中位数 1.0 与 1.2mmol/l(总体标准差为 0.8)]均较低,且在未经调整和调整吸烟因素的模型中,与随后发生的 GCA 均呈显著负相关[胆固醇每 mmol/l 的 OR 为 0.62(95%CI 0.43,0.90);甘油三酯每 mmol/l 的 OR 为 0.46(95%CI 0.27,0.81)]。

结论

GCA 的发生与基线时的 FBG 降低以及胆固醇和甘油三酯水平降低有关,所有这些均与当前吸烟情况有关,提示代谢特征可能导致 GCA 的发生。