Arai Toru, Hirose Masaki, Sugimoto Eiji, Takimoto Takayuki, Inoue Yoshikazu, Sumikawa Hiromitsu, Takemura Tamiko, Shimizu Shigeki
Clinical Research Center, NHO Kinki Chuo Chest Medical Center, Sakai City 591-8555, Osaka, Japan.
Department of Cancer, Infection and Immunology, Graduate School of Medicine/Faculty of Medicine, Osaka University, Suita City 565-0871, Osaka, Japan.
Pathophysiology. 2025 Sep 15;32(3):47. doi: 10.3390/pathophysiology32030047.
Autoimmune pulmonary alveolar proteinosis (aPAP) is characterized by the accumulation of phospholipids and surfactant proteins in the peripheral air spaces due to alveolar macrophage dysfunction caused by anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) autoantibodies (GMAb). Hypersensitivity pneumonitis (HP) is a granulomatous lung disease associated with GM-CSF. In this report, we evaluated serial changes in serum GMAb levels in a 67-year-old male current smoker with HP and aPAP and examined their correlation with HP disease activity. GMAb levels increased at HP onset and decreased after HP remission with oral prednisolone therapy. After the first remission, the patient experienced three relapses and remissions. Although GMAb levels were not evaluated for all HP relapses and remissions, GMAb levels increased at one relapse but decreased at two remissions induced by the oral prednisolone therapy. Pulmonary fibrosis progressed, and the patient died of pneumonia. GMAb was at its almost normal levels at 8 months before the onset of pneumonia. We hypothesized that GMAbs may have been induced to improve HP through neutralizing GM-CSF. Although the hypothesis needs to be confirmed in additional patients, serial measurement of GMAb may be useful for a better understanding of the pathophysiology and deciding the appropriate treatment for HP with aPAP.
自身免疫性肺泡蛋白沉积症(aPAP)的特征是由于抗粒细胞-巨噬细胞集落刺激因子(GM-CSF)自身抗体(GMAb)导致肺泡巨噬细胞功能障碍,磷脂和表面活性物质蛋白在肺外周气腔中蓄积。过敏性肺炎(HP)是一种与GM-CSF相关的肉芽肿性肺病。在本报告中,我们评估了一名67岁男性现吸烟者同时患有HP和aPAP时血清GMAb水平的系列变化,并研究了它们与HP疾病活动度的相关性。GMAb水平在HP发病时升高,口服泼尼松龙治疗后HP缓解时下降。首次缓解后,患者经历了三次复发和缓解。虽然并非对所有HP复发和缓解情况都评估了GMAb水平,但在一次复发时GMAb水平升高,而在口服泼尼松龙治疗诱导的两次缓解时GMAb水平下降。肺纤维化进展,患者死于肺炎。在肺炎发作前8个月,GMAb几乎处于正常水平。我们推测GMAb可能是通过中和GM-CSF而被诱导产生以改善HP。尽管这一假说需要在更多患者中得到证实,但连续测量GMAb可能有助于更好地理解病理生理学,并为HP合并aPAP患者确定合适的治疗方案。