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Peritumoral hyperplasia of the liver: a response to portal vein invasion by hypervascular neoplasms
Author(s) -
Arnason Thomas,
Fleming Kirsten E,
Wanless Ian R
Publication year - 2013
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/his.12032
Subject(s) - pathology , focal nodular hyperplasia , hepatocellular carcinoma , medicine , stromal cell
Aims Several cases of focal nodular hyperplasia ( FNH ) or similar hyperplastic lesions have been reported adjacent to hepatic neoplasms, including hepatocellular carcinoma, epithelioid haemangioendothelioma and hepatoblastoma. We refer to this hyperplastic response as peritumoral hyperplasia ( PTH ). Here, we report eight cases of PTH adjacent to primary hepatocellular carcinomas (two) and metastatic neuroendocrine tumours (three), gastrointestinal stromal tumour (one) and colon carcinomas (two). Methods and results Sections were stained with H&E and trichrome, and for glutamine synthetase, CD 34 and cytokeratin 7. PTH was composed of a peritumoral rim of hyperplastic hepatocytes up to 7.0 mm wide, delimited by adjacent hepatocellular atrophy. PTH had altered plate architecture, strong glutamine synthetase expression and variable sinusoidal endothelial cell CD 34 expression. The central tumour deposit typically invaded portal veins and was markedly hypervascular with CD 34‐positive capillaries. Conclusions We suggest that PTH is a hyperplastic response to increased blood flow in the peritumoral parenchyma. The increased flow occurs when portal vein invasion by a hypervascular tumour causes arterio‐portal shunting. While PTH shares some morphological features with FNH , it lacks the defining nodular architecture, central scar and bile ductules. PTH may be related pathophysiologically to FNH , but should be classified as a separate entity because of its distinct morphology and peritumoral location.