153 Elastin in pulmonary pathology in well-differentiated adenocarcinomas, and found a normal pattern or an increase in the amount of elastin, but not a decrease in the latter. Overall, these finding indicate that normal lung and lepidic-pattern tumours either retained normal elastin or showed thick elastin, but that disruption/degradation of elastic fibers occurred in central fibrotic areas only, in association with invasion. Collapse In the pulmonary pathology literature, two different descriptions have been used for ‘collapse’. In 1985, the term ‘collapse’ was used in adenocarcinomas with a central ‘scar’, showing a recognisable collapsed alveolar framework within condensed elastic tissue on elastin staining. With haematoxylin and eosin staining, the condensed elastic tissue could be mistaken for fibrosis. In fact, elastin staining emphasised the preponderance of elastic over collagenous tissue275. This was also noted by Shimosato et al.276 10 and supported by Yamashiro et al. 277: the central part of the tumour shows collapsed alveolar spaces (absence of air) with condensation of elastin. However, these condensations of elastic fibers with some fibrosis are not infrequent. In this setting, fibrosis is defined as collagenous278, whereby elastosis is not an essential component of the fibrotic reaction. In the Japanese literature, the central part may be fibrotic as well as elastotic, whereas, in the above-mentioned 1985 study, this central area was characterized by elastin condensation without fibrosis. This meaning of collapse is a ‘biological’ collapse with loss of alveolar architecture. This alteration is present before the surgical procedure, and does not include the area outside the scar with peripheral lepidic growth and possible increased alveolar wall thickness. Another definition of collapse120 involves ‘iatrogenic collapse’—i.e. an artefact of deflation—whereby the alveolar air, vascular blood and lymph volumes are reduced during surgery. Owing to the lack of negative pressure between the pleural leaves, the natural recoiling of the elastic fibers places alveolar walls in close proximity to each other120. This effect can be seen as an ‘iatrogenic’ or ‘mechanical’ ‘collapse’; here, the alveolar architecture is maintained but is harder to evaluate morphologically. Examples of collapse involving areas with lepidic growth have recently been published279. The effect of iatrogenic collapse can be reduced during gross handling, e.g. by bronchial and/or transpleural perfusion with formalin. The distance between the alveolar walls will be enlarged by the perfusion process, but the effect of the iatrogenic collapse may not be fully mitigated. The enlarged formalin-containing spaces between the alveolar walls are, light-microscopically, the equivalent of air-filled (clear) spaces. Gross handling differs between laboratories throughout the world: Japanese laboratories280 273 281 and some laboratories outside Japan perform perfusion fixation198, whereas many pathology laboratories in the world will have the influence of prominently collapsed lung tissue in the diagnostic process. Perfusion fixation of the human lung has been performed for research282 283 284 285 286 and clinically287 in the past. For optimal preservation of the alveolar architecture, a perfusion fixation method may be chosen281 198. For an understanding of the published images of adenocarcinoma, it is useful if these studies 12
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