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Airway-centered fibroelastosis is a distinct entity characterized by prominent airway-centered elastosis of the upper lobe with little or no pleural involvement. Little is known regarding its etiology; however, it was reported to have an idiopathic or asthma-associated etiology. We document, for the first time, 2 women (19 and 60 years old) who developed pleuroparenchymal fibroelastosis with a predominantly airway-centered distribution as a late complication (6 and 9 years later, respectively) of chemotherapy. The disease rapidly progressed following the manifestation of symptoms, and they subsequently died (3 and 2 years later, respectively). Therefore, post-chemotherapy long-term monitoring for this disease is warranted.

Autoimmune pulmonary alveolar proteinosis (APAP) is caused by macrophage dysfunction due to anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) autoantibody. We experienced 2 cases of APAP complicated with sarcoidosis in a 42-year-old woman and a 51-year-old man (age at the sarcoidosis diagnosis). APAP preceded sarcoidosis in the woman, and both diseases were diagnosed simultaneously in the man. Sarcoidosis lesions were observed in the lung, skin, and eyes, and the pathological findings of APAP were not marked at the diagnosis of sarcoidosis in either case. Low-grade positive serum anti-GM-CSF autoantibody was suspected to be correlated with the occurrence of sarcoidosis and resolution of APAP.

A 26-year-old man with a history of bronchial asthma was found to have high-density shadows along the bronchovascular bundle and in the subpleural area on computed tomography of the chest. Surgical lung biopsy specimens from the right S5 showed fibroelastosis in the subpleural and central airway area with alveolar destruction. He was diagnosed with airway-centered fibroelastosis of unknown cause after multidisciplinary discussions. The patient developed pulmonary hypertension and died 6 years later. The patient was younger in comparison to patients in earlier reports and had more obvious subpleural fibroelastic lesions in the upper lobes than in previously described cases.

Pulmonary veno-occlusive disease (PVOD) is a rare disease in the subgroup of conditions known as pulmonary arterial hypertension. Although a histological examination is needed for a definitive diagnosis, a non-invasive diagnosis is required for patients with pulmonary hypertension because a lung biopsy is deemed risky. We herein report a 32-year-old woman diagnosed with PVOD via a surgical lung biopsy and autopsy whose disease showed radiological findings mimicking those of hypersensitivity pneumonitis (pneumonia) at the time of the transbronchial lung biopsy, without obvious pulmonary hypertension on admission. When clinicians encounter patients with interstitial lung disease, they should not forget the possibility of PVOD and should be alert for emerging pulmonary hypertension.

A case of pulmonary hyalinizing granuloma (PHG) with Castleman's disease in a 43-year-old man is presented. He was asymptomatic, but the disease was recognized due to a routine chest roentgenographic study. Anemia, multiple lymphadenopathy, hypoalbuminemia and polyclonal hypergamma-globulinemia were observed. Histological examination of cervical lymph nodes revealed the plasma cell type of Castleman's disease. The diagnosis of PHG was confirmed by video-assisted thoracoscopical lung biopsy, and the immuno-histochemical staining of lamellar fibrosis for types I and III collagen was positive.