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Huge focal nodular hyperplasia difficult to distinguish from well‐differentiated hepatocellular carcinoma
Author(s) -
Hanaoka Jun,
Shimada Mitsuo,
Utsunomiya Tohru,
Imura Satoru,
Morine Yuji,
Ikemoto Tetsuya,
Mori Hiroki
Publication year - 2012
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/j.1872-034x.2012.00974.x
Subject(s) - medicine , focal nodular hyperplasia , hepatocellular carcinoma , hepatectomy , inferior vena cava , pathology , hemangioma , radiology , surgery , resection
We present a 43‐year‐old man with huge focal nodular hyperplasia (FNH) that was difficult to distinguish from well‐differentiated hepatocellular carcinoma (HCC). He previously had abnormal portal vein circulation due to hypoplasia of the intrahepatic portal vein, which was treated with a superior mesenteric vein–inferior vena cava shunt. Laboratory findings included predominantly indirect hyperbilirubinemia with concomitant elevation in aspartate aminotransferase (AST), alanine aminotransferase (ALT), and ammonia. Serum α‐fetoprotein and des‐γ‐carboxy prothrombin were slightly elevated. Multidetector‐row computed tomography detected the primary tumor in the left liver lobe, which partially showed a central stellate scar. Gd ethoxybenzyl diethylenetriamine pentaacetic acid‐enhanced magnetic resonance imaging showed some low‐intensity areas in the tumor in the hepatocyte phase. 99mTc‐galactosyl human serum albumin scintigraphy showed normal intake of agent in the tumor. We could not rule out well‐differentiated HCC. Extended left hepatectomy was performed. Final histopathological findings showed that most of the tumor was FNH against a background of portal vein hypoplasia with moderate atypia and hemorrhage. And immunohistochemical analysis revealed high expression of organic anion transporter (OATP) 1B3 and low expression of multidrug resistance‐associated protein (MRP) 2 in a part of the tumor. The patient has remained alive with no hepatic lesion for 1 year after surgery. We describe a case of huge FNH that was difficult to distinguish from well‐differentiated HCC even by current fully preoperative imaging technology and demonstrate the effectiveness of curative surgical resection.