Peritumoral hyperplasia of the liver: a response to portal vein invasion by hypervascular neoplasms

• Published in: Histopathology 2013-02, Vol.62 (3), p.458-464
• Main Authors: Arnason, Thomas, Fleming, Kirsten E, Wanless, Ian R
• Format: Article
• Language: English
• Subjects: Aged; Antigens, CD34 - analysis; Antigens, CD34 - biosynthesis; Biological and medical sciences; Female; focal nodular hyperplasia; Glutamate-Ammonia Ligase - analysis; Glutamate-Ammonia Ligase - biosynthesis; glutamine synthetase; Humans; Hyperplasia; Immunohistochemistry; Investigative techniques, diagnostic techniques (general aspects); liver; Liver - blood supply; Liver - pathology; Liver Neoplasms - blood supply; Liver Neoplasms - complications; Liver Neoplasms - pathology; Male; Medical sciences; Middle Aged; neuroendocrine tumour; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques; peritumoral hyperplasia; Portal Vein - pathology; Young Adult
• ISSN: 0309-0167; 1365-2559
• DOI: 10.1111/his.12032

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, CD34 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 CD34 expression. The central tumour deposit typically invaded portal veins and was markedly hypervascular with CD34‐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.