Metabolic syndrome biomarkers in prediction of lung function impairment.
Metabolic syndrome biomarkers in prediction of lung function impairment.
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预测肺功能损伤的代谢综合征生物标志物。
DOI：
10.1164/ajrccm.186.6.567a
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发表时间：
2012
影响因子：
24.7
通讯作者：
Tkacova,Ruzena
中科院分区：
文献类型：
--
作者：
Joppa,Pavol;Pobeha,Pavol;Tkacova,Ruzena
我们饶有兴趣地阅读了Naveed及其同事的研究（1），该研究表明，2001年9月11日之后，FEV 1正常的纽约消防局人员中，甘油三酯和高密度脂蛋白胆固醇异常与肺功能受损的易感性增加之间存在独立关联。作者得出结论，代谢生物标志物可能有助于评估与颗粒物吸入相关的肺功能损害风险（1）。此前，在一项基于人群的大型横断面研究中，代谢综合征的组成部分（包括脂质）与肺功能受损相关（2）。相反，在慢性阻塞性肺疾病（COPD）患者中，肺功能严重受损的超重患者的全因死亡风险降低-这一现象被称为“肥胖悖论”（3）。此外，患有严重肺气肿的COPD患者接受肺减容手术后肺功能的改善不仅与体重增加有关，而且与总胆固醇和高密度脂蛋白胆固醇以及甘油三酯的增加有关（4）。这些数据加上目前的发现（1）促使我们检验以下假设，即与健康人相比，COPD患者的甘油三酯和胆固醇水平较高可能与FEV 1降低减弱有关（1）。我们分析了作为正在进行的COPD代谢后果研究的一部分检索到的数据（5），在基线测量后12-18（12.2 ± 3.9）（平均6 SD）个月内，我们对肺功能检查、身体成分和血脂进行了重复评估。招募的39名患者中有29名完成了随访评估（24名男性;年龄63.3 6 7.5岁; FEV 1 52.9 6 24.5%;体重指数[BMI] 25.4 6 5.5 kg $ m 22 [14名患者有BMI。25 kg $ m 22]，7例伴血脂异常[1]）。基线甘油三酯和总胆固醇水平与FEV 1下降呈负相关（分别为R= 20.429，P= 0.023; R= 20.440，P= 0.019）;即基线甘油三酯和总胆固醇水平较高的患者在随访期间FEV 1下降较低。在多变量分析中，基线甘油三酯和总胆固醇仍然是FEV 1下降的预测因子，与年龄、性别、基线FEV 1和BMI无关（R2= 0.238，P= 0.046; R2= 0.253，P= 0.035，我们的数据补充了与“肥胖悖论”相关的研究。并证明与健康个体相比，甘油三酯和胆固醇增加可能与此类患者肺功能恶化减少有关（1）。然而，由于样本量小，我们认为目前的结果是非常初步的和假设生成。代谢综合征及其组分对COPD患者肺功能影响的机制有待进一步研究。
We read with interest the study by Naveed and colleagues (1) that demonstrated an independent association between abnormal triglycerides and high-density lipoprotein cholesterol and greater susceptibility to lung function impairment after September 11, 2001 in Fire Department of New York personnel with normal FEV1. The authors concluded that metabolic biomarkers may be useful for the assessment of risk of lung function impairment related to particulate matter inhalation (1). Previously, components of metabolic syndrome including lipids were linked to lung function impairment in a large cross-sectional population-based study (2). In contrast, among patients with chronic obstructive pulmonary disease (COPD), the all-cause mortality risk was reduced in overweight patients with severely impaired pulmonary function—a phenomenon known as the “obesity paradox”(3). Also, improvements in lung function following lung volume reduction surgery in COPD patients with severe emphysema were associated not only with weight gain but also with increases in total and highdensity lipoprotein cholesterol, and triglycerides (4). These data coupled with current findings (1) prompted us to test the hypothesis that higher triglyceride and cholesterol levels might relate to attenuated reductions in FEV1 in patients with COPD, in contrast to healthy persons (1). We analyzed the data retrieved as a part of an ongoing study on the metabolic consequences of COPD (5) in which we performed repeated evaluation of pulmonary function tests, body composition, and serum lipids within 12–18 (12.2 6 3.9)(mean 6 SD) months after baseline measurements. Twenty-nine of 39 recruited patients completed the follow-up assessment (24 men; age 63.3 6 7.5 yr; FEV1 52.9 6 24.5%; body mass index [BMI] 25.4 6 5.5 kg $ m 22 [14 had BMI. 25 kg $ m 22], 7 with dyslipidemia [1]). Baseline triglyceride and total cholesterol levels were inversely related to the FEV1 decline (R= 20.429, P= 0.023; R= 20.440, P= 0.019; respectively); that is, patients with higher triglyceride and total cholesterol levels at baseline had lower FEV1 decline during the follow-up. In multivariate analyses, baseline triglycerides and total cholesterol remained predictors of FEV1 decline independently of age, gender, baseline FEV1, and BMI (R2= 0.238, P= 0.046; R2= 0.253, P= 0.035, respectively).Our data complement studies related to “obesity paradox” in COPD and demonstrate that increased triglycerides and cholesterol may relate to reduced deterioration of lung function in such patients, in contrast to healthy individuals (1). Nevertheless, due to small sample size we consider the present results as very preliminary and hypothesis-generating. Further studies are needed to shed more light on the mechanisms related to the effects of metabolic syndrome and its components on lung function in COPD.
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DOI：
10.1164/rccm.201203-0457ed
发表时间：
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影响因子：
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