Eskenasy A, Diaconită G
Morphol Embryol (Bucur). 1976 Jan-Mar;22(1):19-28.
Forty-eight cases of operated pseudotumoral chronic pneumonites were anatomoclinically and histogenetically studied. Two groups of cases can be established. The first one (21 cases), in which the histogenetic mechanism is related to previous bronchopulmonary infections, suppurations, and immune processes of the immediate type, is characterized by numerous granulocytic foci, granulomatous structure, Arthus type vasculites and fibrous evolution. The unefficient therapy could be one of the determining factors of this evolution, by maintenance of active germs and released antigens. The second group (27 cases) is characterized by hypertrophic bronchites reflecting the prolonged penetration of airborne antigens, by a step by step involvement of peribronchial and parenchymatous structures. A multiphasic development is comparatively demonstrated in the different cases, and dominated by various proportions of plasmocytes and fibroblasts interfering with a restorative granulomatous process involving the intra- and interlobular areas and evolving to a fibrogranulomatous state. Obstructive pneumonitic phenomena and reactive endoalveolitis obliterans interfere, too. Correlations between the dynamics of this picture and the experimental data assert an immune mechanism with repeated immediate and delayed hypersensitivity reactions and auto-aggressive phenomena, determined by released antigens and inductors of cell proliferation and differentiation, as the main processes conducing to the building up of the pseudotumoral chronic pneumonites.
对48例经手术治疗的假瘤性慢性肺炎进行了解剖临床和组织发生学研究。可将病例分为两组。第一组（21例），其组织发生机制与先前的支气管肺部感染、化脓以及速发型免疫过程有关，其特征为有大量粒细胞灶、肉芽肿结构、阿瑟斯型血管炎和纤维化演变。无效的治疗可能是这种演变的决定性因素之一，因为它使活跃的病菌和释放的抗原持续存在。第二组（27例）的特征是肥厚性支气管炎，反映了空气传播抗原的长期侵入，支气管周围和实质结构逐步受累。在不同病例中相对显示出多相发展，以不同比例的浆细胞和成纤维细胞为主，它们干扰了涉及小叶内和小叶间区域的修复性肉芽肿过程，并演变为纤维肉芽肿状态。阻塞性肺炎现象和反应性闭塞性肺泡炎也起干扰作用。这种情况的动态变化与实验数据之间的相关性表明，以释放的抗原以及细胞增殖和分化诱导剂所决定的反复速发型和迟发型超敏反应及自身攻击现象的免疫机制，是导致假瘤性慢性肺炎形成的主要过程。
