Ohmichi M, Miyazaki M, Ohchi T, Morikawa Y, Tanaka S, Sasaki H, Hiraga Y
Department of Respiratory Disease, Sapporo Hospital of Hokkaido Railway Company.
Nihon Kokyuki Gakkai Zasshi. 1998 Apr;36(4):374-80.
A previously healthy 26-year-old woman presented with a fever and coughing on October 1, 1995. Despite treatment with beta-lactam antibiotics at another hospital, she had a high fever, coughing, and dyspnea. A chest roentgenogram showed diffuse infiltrates in both lung fields. On October 9, she was transferred to our hospital. On admission, a chest X-ray film showed marked diffusely infiltrates in both lung fields and a effusion in the left lung. Arterial blood gas analysis after inhalation of 4 liters per minute of oxygen via a nasal cannula revealed a PaO2 of 39.0 torr. Despite treatment with various antibiotics, including minocyclin and gamma-globulin, her respiratory condition rapidly deteriorated. She was mechanically ventilated by with intermittent mandatory ventilation and positive end-experiatory pressure, and received antibiotics and methylprednisolone pulse therapy. He chest X-ray and arterial blood gase findings, gradually improved. The passive hemagglutination titer for Mycoplasma rose from 1:4 on October 9, to 1:2,560 on the 14th hospital day. Acute respiratory failure due to Mycoplasma pneumoniae pneumonia was diagnosed. A chest X-ray film obtained 2 months after admission showed linear-reticular shadows in both lung fields and pulmonary-function tests revealed abnormally low vital capacity and diffusing capacity. Examination of a specimen obtained by transbronchial lung biopsy revealed focal intraalveolar exudate with fibrin and macrophages. Very mild interstitial thickening was also noted. The lymphocyte stimulation responses to PPD, PHA, and Con A were low early in the illness and became normal after recovery. Several reports have said that an enhanced pulmonary cellular immune response may be responsible for the development of severe Mycoplasma pneumoniae, resulting in a temporary decrease in the cell-mediated immune response. This case supports that hypothesis. We believe that in severe cases, steroid therapy including pulse therapy should be started as soon as possible.
一名既往健康的26岁女性于1995年10月1日出现发热和咳嗽症状。尽管在另一家医院接受了β-内酰胺类抗生素治疗,但她仍持续高热、咳嗽并伴有呼吸困难。胸部X线片显示双肺野弥漫性浸润。10月9日,她被转至我院。入院时,胸部X线片显示双肺野明显弥漫性浸润,左侧胸腔有积液。经鼻导管每分钟吸入4升氧气后进行动脉血气分析,结果显示动脉血氧分压(PaO2)为39.0托。尽管使用了包括米诺环素和γ-球蛋白在内的多种抗生素进行治疗,她的呼吸状况仍迅速恶化。她接受了间歇强制通气和呼气末正压通气的机械通气治疗,并接受了抗生素和甲泼尼龙冲击治疗。她的胸部X线和动脉血气结果逐渐改善。支原体被动血凝滴度从10月9日的1:4升至住院第14天的1:2560。诊断为肺炎支原体肺炎所致的急性呼吸衰竭。入院2个月后拍摄的胸部X线片显示双肺野有线性网状阴影,肺功能测试显示肺活量和弥散量异常降低。经支气管肺活检获取的标本检查显示肺泡内有局灶性渗出物,伴有纤维蛋白和巨噬细胞。还发现有非常轻微的间质增厚。疾病早期对结核菌素纯蛋白衍生物(PPD)、植物血凝素(PHA)和刀豆蛋白A(Con A)的淋巴细胞刺激反应较低,恢复后变为正常。有几份报告称,肺部细胞免疫反应增强可能是重症肺炎支原体肺炎发病的原因,导致细胞介导的免疫反应暂时降低。本病例支持这一假说。我们认为,在重症病例中,应尽早开始包括冲击治疗在内的类固醇治疗。