An unusual but unmissable link between summer-type hypersensitivity pneumonitis and asthma in an old house.

While hypersensitivity pneumonitis (HP) and asthma are usually recognized as different disease entities based on their different allergic mechanisms, they may have some connections. A previously healthy 54-year-old Japanese man with no history of allergic diseases was hospitalized due to fever and breathlessness. He had lived in an old musty wooden house. He was diagnosed with acute summer-type HP induced by Trichosporon asahii based on bilateral ground-glass opacities on chest computed tomography (CT), a high titer of serum anti-T. asahii antibody, an increased number of lymphocytes and a decreased CD4/CD8 ratio in bronchoalveolar lavage fluid (BALF) and lung pathology suggestive of HP. However, untypical increased eosinophils in BALF (25.2%) and infiltrative eosinophils around bronchial walls were observed. After systemic corticosteroid treatment was started, he recovered, and was discharged with oral prednisone. However, two weeks after returning to his former house, he had fever and severe cough, and was re-hospitalized. While chest CT showed no abnormal shadows indicating a worsening of HP, pulmonary function test revealed a typical obstructive defect and eosinophilic inflammation in his sputum. He spontaneously recovered after re-hospitalization without increasing any treatments. During this second hospitalization, he was diagnosed with asthma, although it remains to be determined whether both HP and asthma were caused by T. asahii. Clinicians should not miss the possible overlapping presentations between HP and asthma, caused by environmental antigens.

Elevated levels of periostin and TGF-ß1 in the bronchoalveolar lavage fluid of patients with idiopathic eosinophilic pneumonia.

BACKGROUND: Periostin is induced in bronchial epithelial cells and fibroblasts by various stimuli including interleukin (IL)13 and transforming growth factor (TGF)-ß1, and is involved in allergic diseases such as asthma and atopic dermatitis, playing an important role in tissue remodeling and fibrosis. The role of periostin in the pathogenesis of eosinophilic lung diseases, however, is unclear. OBJECTIVE: To examine the contribution of periostin to eosinophilic inflammation of the lung in humans, we evaluated periostin, IL-13, and TGF-ß1 levels in the bronchoalveolar lavage fluid (BALF) of patients with eosinophilic pneumonia (EP). METHODS: Periostin, IL-13, and TGF-ß1 concentrations in the BALF were measured by enzyme-linked immunosorbent assay in patients with acute EP, chronic EP, idiopathic pulmonary fibrosis (IPF), and sarcoidosis. Further, we analyzed the relationship between periostin, IL-13, and TGFß-1, levels and the number of inflammatory cells in the BALF. RESULTS: The absolute number of eosinophils, and the periostin, IL-13, and TGF-ß1 levels in the BALF were significantly higher in patients with EP than in patients with IPF and sarcoidosis. Concentrations of periostin significantly correlated with the concentrations of TGF-ß1, but not those of IL-13, in the BALF of patients with EP. Periostin levels also significantly correlated with the absolute number of eosinophils in the BALF of patients with IPF, but not EP. CONCLUSIONS: Our findings suggest that TGF-ß1 might increase the production of periostin in the lungs of patients with EP. Periostin might contribute the pathogenesis of not only EP, but also IPF.