Abstract
Ninety five cases of hypersensitivity pneumonitis were studied and almost 70% of them were classified as summer-type hypersensitivity pneumonitis which has not been reported in countries other than Japan. Cases of summer-type hypersensitivity pneumonitis reveal the following unique characteristics; 1) occurrence in the summer season. 2) reccurrent episodes in the same summer season for several years (35.9% of cases). 3) provocation of symptoms when returning home (27.5% of cases). 4) familial occurrence (26.2% in this study). 5) a triad of clinical symptoms consisting of coughs, dyspnea and fever. 6) diffuse scattered nodular shadows on chest X-ray. 7) elevation of erythrocyte sedimentation rate and leukocytosis with neutrophilia. 8) decreased %VC, DLCO and PaO2 in pulmonary functions. 9) negative inversion of skin reactivity to PPD. 10) granulomata in the lung (found in 63% of biopsied cases).
Although biological air pollution such as ubiquitous fungus spores has been suggested as the offending antigen of summer-type hypersensitivity pneumonitis, but the causative antigen has not been defined yet.
Bronchoalveolar lavage of a case of summer-type hypersensitivity pneumonitis resulted in 25% alveolar macrophages and 75% lymphocytes, all of which were T-cells. Accumulation of T-cells to the inflammatory lesions in the lung, which means participation of cellular immunity in this disease process, may explain the negative conversion of PPD skin reactivity.
