Case 488 -- Liver mess in a cirrhotic liver

Contributed by Ahmed Bedeir MD and Parmjeet S. Randhawa, MD
Published on line in December 2006


The patient is a 72-year-old female with a history of cirrhosis secondary to alcohol abuse and hepatitis C. She presented with hepatic encephalopathy and refractory ascites. The patient also has a history of diabetes mellitus, hypothyroidism. Radiology showed a cirrhotic liver morphology with hypervascular mass 2.6 x 2.2cm within the caudate lobe worrisome for a hepatocellular carcinoma.


Liver function test were all elevated with highest levels: AST: 1177; ALT: 542; ALP: 157; GGTP: 52; TBILI: 7.5.
AFP: 2 ng/ml (normal <20).


The external surface of liver showed macronodules, the largest measuring 1.2 cm. The capsule is adherent to the right lobe. On cut surface, the parenchyma shows a subcapsular solid, firm, white nodule, measuring 3.0 x 2.0 x 2.5 cm, situated between the medial aspect of the right lobe and the caudate lobe, adjacent to the hilum, abutting a branch of the portal vein, as well as the liver capsule. The rest of the parenchyma shows numerous macronodules, the largest measuring 1.2 cm. No other lesions are identified (Figs. 1 and 2)


The histologic sections show an infiltrating lesion that is predominantly formed of gland like structures in sclerotic stroma. The glands are lined with highly atypical cells with nuclear pleomorphism and high N/C ratio (Figs 4, 5, 6 and 7). Some of the glands show bile plugs. The neoplasm infiltrates in the surrounding liver tissue and comes within 1 high power filed form the capsule. Neither Perineural nor vascular infiltration was identified. The remaining of the liver parenchyma shows portal tracts expansion by fibrous tissue, with extensive bridging fibrosis and formation of regenerative nodules. Most of the portal tracts contain lymphoplasmacytic inflammation. Interface activity and bile ductular proliferation are noted. The hepatic lobules contain mild mononuclear inflammatory cells. No apoptotic bodies, Mallory' s hyaline, ballooned hepatocytes, viral inclusions, ground glass cells, granulomas, florid duct lesion, fibro-obliterative duct lesion, or cholestasis are identified. The PAS-D stain is negative for alpha 1 antitrypsin deficiency. Iron stain shows no significant hemosiderosis. The trichrome stain confirms the presence of fibrosis.


The tumor was focally positive for CK 7 (Fig. 8). Negative for CK20, CDX2 TTF, GCDFP, ER, PR


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