Type II pneumocyte hyperplasia

Mild-to-moderate interstitial chronic inflammation Type II pneumocyte hyperplasia in areas of inflammation... 

Chronic exposure to as little as 0.5 ppm NOj or acute exposure to higher concentrations has been shown to cause hyperplasia of the type II pneumocytes (Kleinerman 1970, Yuen and Sherwin 1971). 

BCNU long-term therapy (total dose 2760 mg and 3210 mg, respectively) induced marked hyperplasia and hypertrophy of type II pneumocytes (Mitsudo et al. 1984). 

Alveolar septa may show some degree of expansion due to capillaritis, edema, and/or interstitial fibrosis (84,85). Capillaritis, characterized by neutrophils within the septa, is usually focal and of mild to moderate intensity. Diffuse or prominent capillaritis, or vasculitis of larger blood vessels is atypical, and if present, suggests another disease process. When interstitial fibrosis is present, it too is usually patchy and mild. Type II pneumocytes may show hyperplasia and reactive atypia in response to alveolar damage. In some cases, hyaline membranes are seen focally (85). Ultrastructural studies have shown fragmentation of alveolar septal basement membranes and wide gaps between endothelial cells (90). 

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