Thomas Arnason1, Kirsten E Fleming, Ian R Wanless. 1. Division of Anatomical Pathology, Queen Elizabeth II Health Sciences Centre and Dalhousie University, Halifax, NS, Canada.
Abstract
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.
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.
Authors: Caner Ercan; Mairene Coto-Llerena; John Gallon; Lana Fourie; Mattia Marinucci; Gabriel F Hess; Jürg Vosbeck; Stephanie Taha-Mehlitz; Tuyana Boldanova; Marie-Anne Meier; Alexandar Tzankov; Matthias S Matter; Martin H K Hoffmann; Luca Di Tommaso; Markus von Flüe; Charlotte K Y Ng; Markus H Heim; Savas D Soysal; Luigi M Terracciano; Otto Kollmar; Salvatore Piscuoglio Journal: Commun Med (Lond) Date: 2022-02-03