燃煤型砷中毒患者肺功能损害与病理改变的特征

Characteristics of lung functional lesion and pathological variation in patients undergoing coal-burning arsenic poisoning

目的探讨慢性燃煤型砷中毒患者肺功能损害的特征及导致其发生的病理学基础。方法采用日本MINATO公司Autospiropal型肺功能仪,对98例慢性燃煤型砷中毒患者进行肺功能检测,并对其中22例行肺活检术患者的肺组织病理结果进行分析。结果 98例受检患者中,肺功能异常率82.7%(81/98)。其中限制型通气功能障碍为86.4%(70/81),混合型通气功能障碍为8.6%(7/81),阻塞型通气功能障碍为4.9%(4/81)。光镜下突出表现为肺间质中纤维样组织增多,肺间质增厚,淋巴细胞、中性粒细胞浸润,肺泡壁轻-中度水肿,肺泡壁增厚明显。电镜发现肺泡Ⅱ型上皮细胞变性、坏死、脱落,数量减少;胶原纤维增生显著。结论限制型通气功能障碍是慢性燃煤型砷中毒患者肺功能改变的主要临床类型,与肺间质中纤维组织增生、肺间质增厚及肺泡壁水肿所导致肺组织弹性下降和肺泡Ⅱ型上皮细胞受损等病理改变密切相关。

Objective To discuss the characteristics of the lung functional lesion in patients undergoing coal-burning arsenic poisoning and its pathological foundation.Methods The lung function of 98 patients with chronic coal-burning arsenic poisoning was detected by Autospiro pal lung function tester from MINATO Company of Japan.The pathological results of pulmonary tissue in 22 ones receiving lung biopsy were analyzed.Results Among the 98 patients,the lung disfunction rate was 82.7%（81/98）,in which restrictive ventilation function disturbance accounted for 86.4%（70/81）;mixed ventilation function disturbance accounted for 8.6%（7/81）;obstructive ventilation function disturbance accounted for 4.9%（4/81）.Increasing of fibrous tissue in pulmonary interstitium,thickening of pulmonary interstitium,infiltration of leukomonocyte and neutrophilic granulocyte,light-middle degree of edema in alveolar wall and obvious thickening of alveolar wall could be observed under the optical microscope.Type Ⅱalveolar epithelial cell degeneration,necrosis,shedding and decreasing of number were observed under the electron microscope,and hyperplasia of collagen fiber was obvious.Conclusion Restrictive ventilation function disturbance is the main clinical type of lung functional changes in patients undergoing coal-burning arsenic poisoning,which has close correlation with the pathological changes such as fibroplasias in pulmonary interstitium,thickening of pulmonary interstitium,decreasing of elasticity in lung issue caused by edema of alveolar wall and damage in type Ⅱ alveolar epithelial cell.