Centre de Recherche, Institut Universitaire de Cardiologie et de Pneumologie de Québec-Université Laval, Québec, Canada.
Hypoxia Pathophysiology Laboratory INSERM U1042, Grenoble Alpes University Hospital, Grenoble, France.
Int J Chron Obstruct Pulmon Dis. 2019 Dec 31;14:3053-3061. doi: 10.2147/COPD.S233834. eCollection 2019.
Fatty liver disease is associated with cardiometabolic disorders and represents a potential key comorbidity in Chronic Obstructive Pulmonary Disease (COPD). Some intermediary mechanisms of fatty liver disease (including its histological component steatosis) include tissue hypoxia, low-grade inflammation and oxidative stress that are key features of COPD. Despite these shared physiological pathways, the effect of COPD on the prevalence of hepatic steatosis, and the association between hepatic steatosis and comorbidities in this population remain unclear. Liver density measured by computed tomography (CT)-scan is a non-invasive surrogate of fat infiltration, with lower liver densities reflecting more fat infiltration and a liver density of 40 Hounsfield Units (HU) corresponding to a severe 30% fat infiltration.
We took advantage of the international cohort ECLIPSE in which non-enhanced chest CT-scans were obtained in 1554 patients with COPD and 387 healthy controls to analyse the liver density at T12-L1.
The distribution of liver density was similar and the prevalence of severe steatosis (density<40 HU) was not different (4.7% vs 5.2%, p=0.7) between COPD and controls. In patients with COPD, the lowest liver density quartile was associated, after age and sex adjustment, with coronary artery disease (OR=1.59, 95% CI 1.12 to 2.24) and stroke (OR=2.20, 95% CI 1.07 to 4.50), in comparison with the highest liver density quartile.
The present data indicate that a low liver density emerged as a predictor of cardiovascular comorbidities in the COPD population. However, the distribution of liver density and the prevalence of severe steatosis were similar in patients with COPD and control subjects.
脂肪肝疾病与心脏代谢紊乱有关,是慢性阻塞性肺疾病(COPD)的潜在关键合并症。脂肪肝疾病的一些中间机制(包括其组织学成分脂肪变性)包括组织缺氧、低度炎症和氧化应激,这些都是 COPD 的关键特征。尽管存在这些共同的生理途径,但 COPD 对肝脂肪变性患病率的影响以及该人群中肝脂肪变性与合并症之间的关联仍不清楚。通过计算机断层扫描(CT)测量的肝脏密度是脂肪浸润的非侵入性替代物,较低的肝脏密度反映了更多的脂肪浸润,肝脏密度为 40 亨氏单位(HU)对应于严重的 30%脂肪浸润。
我们利用国际 ECLIPSE 队列,该队列中对 1554 例 COPD 患者和 387 例健康对照者进行了非增强性胸部 CT 扫描,以分析 T12-L1 处的肝脏密度。
肝脏密度的分布相似,严重脂肪变性(密度<40 HU)的患病率在 COPD 患者和对照组之间没有差异(4.7%对 5.2%,p=0.7)。在 COPD 患者中,在校正年龄和性别后,最低的肝脏密度四分位数与冠状动脉疾病(OR=1.59,95%CI 1.12-2.24)和中风(OR=2.20,95%CI 1.07-4.50)相关,与最高的肝脏密度四分位数相比。
目前的数据表明,在 COPD 人群中,低肝脏密度是心血管合并症的预测因素。然而,在 COPD 患者和对照组中,肝脏密度的分布和严重脂肪变性的患病率相似。