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. 2012:2012:915128.
doi: 10.1155/2012/915128. Epub 2012 Sep 4.

Resection of nonalcoholic steatohepatitis-associated hepatocellular carcinoma: a Western experience

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Resection of nonalcoholic steatohepatitis-associated hepatocellular carcinoma: a Western experience

Brian Shrager et al. Int J Surg Oncol. 2012.

Abstract

Introduction. Hepatocellular carcinoma is now known to arise in association with nonalcoholic steatohepatitis. The aim of this study is to examine the clinicopathological features of this entity using liver resection cases at a large Western center. Methods. We retrospectively reviewed all cases of partial liver resection for hepatocellular carcinoma over a 10-year period. We included for the purpose of this study patients with histological evidence of nonalcoholic steatohepatitis and excluded patients with other chronic liver diseases such as viral hepatitis and alcoholic liver disease. Results. We identified 9 cases in which malignancy developed against a parenchymal background of histologically-active nonalcoholic steatohepatitis. The median age at diagnosis was 58 (52-82) years, and 8 of the patients were male. Median body mass index was 30.2 (22.7-39.4) kg/m(2). Hypertension was present in 77.8% of the patients and diabetes mellitus, obesity, and hyperlipidemia in 66.7%, respectively. The background liver parenchyma was noncirrhotic in 44% of the cases. Average tumor diameter was 7.0 ± 4.8 cm. Three-fourths of the patients developed recurrence within two years of resection, and 5-year survival was 44%. Conclusion. Hepatocellular carcinoma may arise in the context of nonalcoholic steatohepatitis, often before cirrhosis has developed. Locally advanced tumors are typical, and long-term failure rate following resection is high.

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Figures

Figure 1
Figure 1
Contrast-enhanced CT scan of NASH-associated HCC. (a) This arterial-phase image shows an enhancing lesion (arrow) in the left lobe of a steatotic liver. No gross radiographic evidence of cirrhosis is present. (b) The same tumor shows hypoenhancement or “washout” in the delayed portal venous-phase image.
Figure 2
Figure 2
Histopathological features of noncirrhotic NASH-associated HCC. (a) The nonneoplastic liver shows macrovesicular steatosis involving the perivenular zone (∗) with sparing of the periportal zones (arrowheads) (patient 8, H&E stain, 40x). (b) and (c) show at greater magnification the steatotic hepatocytes (arrows) and ballooning degeneration of hepatocytes (arrowheads) evident in the perivenular zone of the nonneoplastic parenchyma (patients 4 and 7, H&E stain, 100x and 200x). (d) Specialized collagen staining shows the central venule (∗) to be invested with a band of perivenular fibrosis; bridging fibrosis and cirrhotic nodules are notably absent (patient 7, Masson's trichrome stain, 200x). (e) and (f) show two examples of HCC arising within noncirrhotic NASH showing pseudoglandular (arrowheads) and trabecular (arrows) features and fat within tumor cells (right frame) (patients 7 and 8, H&E stain, 100x).

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