Tadokoro Akira, Ishii Tomoya, Bandoh Shuji, Yokomise Hiroyasu, Haba Reiji, Ishida Toshihiko
Department of Internal Medicine Division of Endocrinology and Metabolism, Hematology, Rheumatology and Respiratory Medicine, Faculty of Medicine, Kagawa University.
Nihon Kokyuki Gakkai Zasshi. 2011 Mar;49(3):203-7.
A 44-year-old Japanese woman was admitted to our hospital because of dry cough and dyspnea on exertion. She had never smoked. She had been passively exposed to smoking by her husband and co-workers from the age of 21 (1984) to 33 (1996). She had previously developed pneumothorax twice, in 1985. On admission, computed tomography (CT) of the chest showed reticulonodular opacities predominant in bilateral upper lung fields, and pulmonary function tests revealed a decrease in vital capacity. The differential diagnoses were sarcoidosis, idiopathic pulmonary fibrosis and pulmonary Langerhans cell histiocytosis (PLCH). Video-assisted thoracic surgery was performed to make a definitive diagnosis. A histological specimen revealed the presence of CD1a-positive Langerhans cells in bronchiolocentric nodular lesions, leading to a diagnosis of PLCH. She was given 0.5 mg/kg bodyweight/ day oral prednisolone. Her symptoms disappeared with steroid maintenance therapy, and her vital capacity on pulmonary function testing was prevented from further deterioration. Based on the pathogenesis of PLCH, this case suggested that not only active smoking, but also passive smoking, played an important role in the development of PLCH.
一名44岁的日本女性因干咳和劳力性呼吸困难入院。她从不吸烟。从21岁（1984年）到33岁（1996年），她一直被动接触丈夫和同事的吸烟环境。她曾在1985年两次发生气胸。入院时，胸部计算机断层扫描（CT）显示双侧上肺野以网状结节状阴影为主，肺功能测试显示肺活量下降。鉴别诊断包括结节病、特发性肺纤维化和肺朗格汉斯细胞组织细胞增多症（PLCH）。为明确诊断进行了电视辅助胸腔镜手术。组织学标本显示在以细支气管为中心的结节性病变中存在CD1a阳性的朗格汉斯细胞，从而诊断为PLCH。给予她每天0.5mg/kg体重的口服泼尼松龙。她的症状通过类固醇维持治疗消失，肺功能测试中的肺活量也得以防止进一步恶化。基于PLCH的发病机制，该病例表明不仅主动吸烟，被动吸烟在PLCH的发生中也起重要作用。
