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铟肺病例中吸烟导致肺气肿的进展

Progression of Smoking-Induced Emphysema in a Case with Indium Lung.

机构信息

Department of Medicine, Nikko Memorial Hospital.

Department of Pulmonary Medicine, Graduate School of Comprehensive Human Science, University of Tsukuba.

出版信息

Tohoku J Exp Med. 2023 Feb 28;259(3):247-252. doi: 10.1620/tjem.2022.J115. Epub 2022 Dec 29.

DOI:10.1620/tjem.2022.J115
PMID:36596501
Abstract

Recently, it has become clear that inhaled indium-tin oxide causes emphysematous as well as interstitial changes in the lung. Here, we present a 59-year-old male ex-smoker, quitting smoking at the age of 55. He had been engaged in indium-tin oxide processing from 27 to 37 years of age, with 22 years having passed since the final exposure to indium. He was found to have a high serum indium concentration and Krebs von den Lungen-6 (KL-6). Furthermore, bilateral centrilobular emphysema was recognized in high-resolution computed tomography (HRCT). After transferring jobs to a non-indium-tin oxide section, KL-6 returned to a normal level within 4 years, whereas neither serum indium concentration nor emphysema had decreased to normal despite 22 years having passed since the exposure ended. At the age of 59, a thoracoscopic lung biopsy was performed to assess the contribution of smoking and that of indium to the lung destruction. The pathological findings demonstrated cholesterol granulomas with the accumulation of macrophages and multinucleated giant cells that had phagocytosed particles. Together with the typical findings of indium lung, fibrotic and emphysematous changes were observed. The elemental analysis of the biopsied specimens revealed excessive deposition of indium throughout the airways, interstitial spaces and alveoli. The pathological findings of this case may be the result of two kinds of pulmonary damage, i.e., smoking and indium. This report indicates that occupationally-inhaled indium could remain in the lung for as long as 22 years and continue to insult the lung tissue with inflammation caused by smoking.

摘要

最近,吸入氧化铟锡已明确会导致肺气肿以及肺间质变化。在这里,我们介绍一位 59 岁的男性,曾是吸烟者,在 55 岁时戒烟。他从 27 岁到 37 岁期间从事氧化铟锡加工工作,距离最后一次接触氧化铟已经过去了 22 年。他的血清铟浓度和 Krebs von den Lungen-6(KL-6)很高。此外,高分辨率计算机断层扫描(HRCT)显示双侧中心性肺气肿。在调离至非氧化铟锡加工岗位后,KL-6 在 4 年内恢复正常水平,而尽管暴露结束已经 22 年,血清铟浓度和肺气肿都没有恢复正常。在 59 岁时,进行了胸腔镜肺活检以评估吸烟和铟对肺部破坏的影响。病理发现显示有胆固醇肉芽肿,其中有巨噬细胞和多核巨细胞积聚,吞噬了颗粒。同时存在典型的铟肺表现,还观察到纤维化和肺气肿变化。活检标本的元素分析显示铟在整个气道、间质和肺泡中过度沉积。该病例的病理发现可能是两种类型的肺损伤的结果,即吸烟和铟。本报告表明,职业性吸入的铟在肺部可能会残留长达 22 年,并通过吸烟引起的炎症持续损害肺组织。

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