Department of Family Medicine, Warsaw Medical University, Warsaw, Poland.
Eur J Med Res. 2009 Dec 7;14 Suppl 4(Suppl 4):259-64. doi: 10.1186/2047-783x-14-s4-259.
Clinical symptoms and radiological changes are useful in monitoring patients with interstitial lung diseases (ILD). Neovascularization participates in the pathogenesis of idiopathic pulmonary fibrosis and other ILD. The objective of the study was to examine the relationships between angiogenic activity of sera from ILD patients and clinical or radiological status.
Serum samples were obtained from 83 patients with sarcoidosis, 31 with idiopathic pulmonary fibrosis (IPF), 29 with hypersensitivity pneumonitis (HP), 16 with collagen diseases with pulmonary manifestation (CD), 13 with scleroderma (SCL), 14 with Wegener's granulomatosis (WG), 12 with pulmonary Langerhans cell histiocytosis (HIS), 12 with pneumoconiosis (PNC), 10 with drug-induced lung disease (DLD), 5 with cryptogenic organizing pneumonia (COP), and from 36 healthy volunteers. As an angiogenic test we used a cutaneous angiogenesis assay according to Sidky and Auerbach. Clinical status was evaluated using a special questionnaire. In all patients chest radiographs were performed.
The angiogenic properties of sera from ILD differed depending on the clinical diagnosis. The strongest proangiogenic effect was induced by sera from patients with HP (mean number of new vessels 16.8), CD (16.6), sarcoidosis (16.3), IPF (16.2), and PNC (15.7). In the case of DLD (13.2), the effect was comparable to healthy controls (13.5). In contrast, sera from SCL (mean number of the vessels 10.5) and HIS patients (10.8) significantly inhibited angiogenesis compared with controls. The angiogenic activity of sera from patients with hilar or mediastinal lymph nodes involvement was higher than that of sera from patients with lung fibrosis. There were also differences in the serum angiogenic activity in relation to the severity of dyspnea.
The data showed that sera from ILD patients constitute a source of mediators modulating angiogenesis, but the pattern of reaction is different in various diseases. Sera from HP, sarcoidosis, IPF, and CD patients demonstrated the strongest proangiogenic activity. However, sera from SCL and HIS inhibit angiogenesis. Angiogenic activity of examined sera was related to the clinical and radiological changes.
临床症状和影像学改变可用于监测间质性肺疾病（ILD）患者。血管新生参与特发性肺纤维化和其他ILD 的发病机制。本研究旨在探讨ILD 患者血清的血管生成活性与临床或影像学状态之间的关系。
从 83 例结节病患者、31 例特发性肺纤维化（IPF）患者、29 例过敏性肺炎（HP）患者、16 例伴有肺部表现的胶原血管病（CD）患者、13 例硬皮病（SCL）患者、14 例韦格纳肉芽肿（WG）患者、12 例肺朗格汉斯细胞组织细胞增生症（HIS）患者、12 例尘肺（PNC）患者、10 例药物性肺疾病（DLD）患者、5 例隐源性机化性肺炎（COP）患者和 36 名健康志愿者中采集血清样本。我们使用 Sidky 和 Auerbach 的皮肤血管生成测定法作为血管生成试验。使用专门的问卷评估临床状况。所有患者均进行了胸部 X 线检查。
ILD 患者血清的血管生成特性因临床诊断而异。HP（新生血管平均数 16.8）、CD（16.6）、结节病（16.3）、特发性肺纤维化（16.2）和尘肺（15.7）患者的血清诱导出最强的促血管生成作用。药物性肺疾病（13.2）患者的作用与健康对照组（13.5）相当。相比之下，硬皮病（血管平均数 10.5）和肺朗格汉斯细胞组织细胞增生症患者（血管平均数 10.8）的血清明显抑制了血管生成，与对照组相比差异有统计学意义。有肺门或纵隔淋巴结受累患者的血清血管生成活性高于有肺纤维化患者的血清血管生成活性。在呼吸困难严重程度方面，血清血管生成活性也存在差异。
数据表明，ILD 患者的血清构成了调节血管生成的介质来源，但在各种疾病中的反应模式不同。HP、结节病、特发性肺纤维化和 CD 患者的血清表现出最强的促血管生成活性。然而，硬皮病和肺朗格汉斯细胞组织细胞增生症患者的血清抑制血管生成。所检查的血清的血管生成活性与临床和影像学变化有关。
