Schreuder Anton, Jacobs Colin, Scholten Ernst T, Prokop Mathias, van Ginneken Bram, Lynch David A, Schaefer-Prokop Cornelia M
Department of Radiology and Nuclear Medicine, Radboudumc, Nijmegen, The Netherlands.
Fraunhofer MEVIS, Bremen, Germany.
PeerJ. 2020 Jul 3;8:e9166. doi: 10.7717/peerj.9166. eCollection 2020.
One of the main pathophysiological mechanisms of chronic obstructive pulmonary disease is inflammation, which has been associated with lymphadenopathy. Intrapulmonary lymph nodes can be identified on CT as perifissural nodules (PFN). We investigated the association between the number and size of PFNs and measures of COPD severity.
CT images were obtained from COPDGene. 50 subjects were randomly selected per GOLD stage (0 to 4), GOLD-unclassified, and never-smoker groups and allocated to either "Healthy," "Mild," or "Moderate/severe" groups. 26/350 (7.4%) subjects had missing images and were excluded. Supported by computer-aided detection, a trained researcher prelocated non-calcified opacities larger than 3 mm in diameter. Included lung opacities were classified independently by two radiologists as either "PFN," "not a PFN," "calcified," or "not a nodule"; disagreements were arbitrated by a third radiologist. Ordinal logistic regression was performed as the main statistical test.
A total of 592 opacities were included in the observer study. A total of 163/592 classifications (27.5%) required arbitration. A total of 17/592 opacities (2.9%) were excluded from the analysis because they were not considered nodular, were calcified, or all three radiologists disagreed. A total of 366/575 accepted nodules (63.7%) were considered PFNs. A maximum of 10 PFNs were found in one image; 154/324 (47.5%) contained no PFNs. The number of PFNs per subject did not differ between COPD severity groups ( = 0.50). PFN short-axis diameter could significantly distinguish between the Mild and Moderate/severe groups, but not between the Healthy and Mild groups ( = 0.021).
There is no relationship between PFN count and COPD severity. There may be a weak trend of larger intrapulmonary lymph nodes among patients with more advanced stages of COPD.
慢性阻塞性肺疾病的主要病理生理机制之一是炎症,这与淋巴结病有关。肺内淋巴结在CT上可表现为肺裂旁结节(PFN)。我们研究了PFN的数量和大小与慢性阻塞性肺疾病严重程度指标之间的关联。
CT图像取自慢性阻塞性肺疾病基因研究(COPDGene)。根据全球慢性阻塞性肺疾病倡议(GOLD)分期(0至4期)、未分类的GOLD组和从不吸烟者组,每组随机选取50名受试者,并分为“健康”、“轻度”或“中度/重度”组。26/350(7.4%)名受试者有缺失图像,被排除在外。在计算机辅助检测的支持下,一名经过培训的研究人员预先定位直径大于3mm的非钙化不透明区。两名放射科医生将纳入的肺部不透明区独立分类为“PFN”、“非PFN”、“钙化”或“非结节”;分歧由第三名放射科医生裁决。采用有序逻辑回归作为主要统计检验。
观察者研究共纳入592个不透明区。共有163/592(27.5%)的分类需要裁决。共有17/592个不透明区(2.9%)被排除在分析之外,因为它们不被视为结节、已钙化或三名放射科医生均存在分歧。共有366/575个被接受的结节(63.7%)被视为PFN。一张图像中最多发现10个PFN;154/324(47.5%)的图像中没有PFN。不同慢性阻塞性肺疾病严重程度组之间,每位受试者的PFN数量无差异(P = 0.50)。PFN短轴直径可显著区分轻度组和中度/重度组,但不能区分健康组和轻度组(P = 0.021)。
PFN数量与慢性阻塞性肺疾病严重程度之间无关联。在慢性阻塞性肺疾病晚期患者中,肺内淋巴结可能存在稍大的趋势。