PMC:4156421 / 9985-12197 JSONTXT

{"project":"2_test","denotations":[{"id":"25192356-9843306-90446716","span":{"begin":1133,"end":1135},"obj":"9843306"},{"id":"25192356-15579729-90446717","span":{"begin":1139,"end":1141},"obj":"15579729"},{"id":"25192356-17965079-90446718","span":{"begin":1374,"end":1376},"obj":"17965079"}],"text":"Microscopic findings\nHistologic examination of lung tissue revealed diffuse fibrous thickening of alveolar septae (Figure 1, Figure S1). Changes were relatively uniform throughout the lung. Dense bundles of collagen and scant mononuclear inflammatory cell infiltrates existed within thickened septae. Focally, apical subpleural regions exhibited increased fibrosis and remodeling, with associated airspace enlargement. To further characterize the histologic changes and classify this patient's pulmonary fibrosis, we processed an additional 10 blocks of tissue from representative sections of all lobes of the right and left lung. The pattern of injury was uniform throughout the lungs, showing diffuse fibrocellular thickening of the vast majority of alveolar septae. One section from the right middle lobe contained changes of microscopic honeycombing in an area of subpleural fibrosis, where small cysts lined by respiratory epithelium are present and contain mucous and neutrophils (Figure S1). Microscopic honeycombing has been reported in NSIP and other lung diseases, and to our knowledge this entity is not specific for UIP [23], [24]. The temporal uniformity of the process, and clinical presentation are most compatible with a pathologic diagnosis of the fibrosing variant of nonspecific interstitial pneumonia (NSIP), in contrast to the initial diagnosis of IPF [25]. Some of the pulmonary arteries demonstrated fibrous intimal thickening, and the myocardium showed myocyte hypertrophy. Alveolar hemosiderin-laden macrophages were present within lung sections and most likely reflect pulmonary hemorrhage secondary to pulmonary hypertension. Finally, pathological sections revealed an acute bronchopneumonia, consistent with terminal bronchopneumonia most likely due to aspiration. Lymph nodes showed only nonspecific reactive changes.\nFigure 1 Histological demonstration of the NSIP pattern of IPF in the patient's lungs. Microscopic examination of the lungs.\n(A) 40×; (B) 400×. Note uniform fibrotic thickening of the alveolar septae and type II pneumocyte hypertrophy. There was no histologic evidence of sarcoidosis, hypersensitivity pneumonitis, organizing pneumonia, or diffuse alveolar damage."}