Smith P, Heath D
Thorax. 1974 Nov;29(6):643-53. doi: 10.1136/thx.29.6.643.
, , 643-653. The histopathology of the lungs from four human cases of paraquat poisoning is described. In two of them there was a dense mass of fibroblastic tissue which obliterated the lung architecture, and one of these showed an extensive deposit of collagen with honeycomb change. In a third case pulmonary fibrosis was less severe and could be demonstrated exclusively within the alveolar spaces. The fourth showed earlier lesions of capillary congestion, alveolar oedema, and hyaline membrane formation. We suggest that paraquat produces the same effect on the lung in man as in the rat, namely a diffuse, cellular, fibrosis. The intra-alveolar origin of this fibrosis is often obscured in the advanced stage of the disease and has been misinterpreted as fibrosing alveolitis. This fibrosis is associated with a pulmonary vascular disease. In assessing the histopathology of the lung in paraquat poisoning a history of oxygen therapy must be taken into account, for prolonged exposure to this gas may in itself induce pulmonary fibrosis.
描述了4例百草枯中毒患者肺部的组织病理学情况。其中2例有致密的成纤维组织团块,破坏了肺结构,其中1例显示有广泛的胶原沉积和蜂窝状改变。第3例肺纤维化较轻,仅在肺泡腔内可见。第4例显示有早期的毛细血管充血、肺泡水肿和透明膜形成。我们认为百草枯对人类肺部产生的作用与对大鼠的作用相同,即弥漫性、细胞性纤维化。这种纤维化的肺泡内起源在疾病晚期常被掩盖,并被误诊为纤维化肺泡炎。这种纤维化与肺血管疾病有关。在评估百草枯中毒时肺部的组织病理学情况时,必须考虑氧疗史,因为长时间接触这种气体本身可能会诱发肺纤维化。