Abstract

To the Editor: A 65-year-old male patient was referred to King Faisal Hospital and Research Centre after he presented with jaundice, fever, abdominal discomfort and biochemical evidence of chronic hepatitis C virus (HCV) hepatitis with no clinical or histological evidence of cirrhosis. HCV polymerase chain reaction (PCR) was positive and HCV quantitation was 4682 copies/mL. Liver function test (LFT) results were ALT 225 IU/L (reference range, 5-60 IU/L), AST 104 IU/L (reference range, 5-43 IU/L), total bilirubin 20 μml/L (reference range, 5.1-17.0 μmol/L), INR 1.2 (reference range, 0.9-1.1), and albumin 38 g/L (reference range, 35-50 g/L). Liver biopsy showed chronic hepatitis grade II, stage II portal fibrosis and no evidence of cirrhosis. Alpha-fetoprotein was 6 μgm/L. The patient completed a full year of combination therapy of pegulated interferon 3 million units subcutaneously 3 times/week with ribavirin 1000 mg orally daily and achieved a negative viral PCR with normal LFTs. He had 3 years of follow-up with a sustained virological response (sustained loss of detectable virus in response to antiviral therapy) and was then discharged from our clinic and instructed to follow-up at his local hospital. A CT scan at discharge showed no evidence of cancer (image not available). Two years later he was referred back from his local hospital with a huge right hypochondrial mass associated with pain but no jaundice, fever or weight loss. The mass was about 10 cm in diameter, difficult to separate from the liver, ill-defined, lobulated and hard. Basic tests, including CBC and renal profile were normal. ALT 27 IU/L (reference range, 5-60 IU/L), AST 35 IU/L (reference range, 5-43 IU/L), ALP 75 IU/L (reference range, 30-120 IU/L), total bilirubin 14 μml/L (reference range, 5.1-17.0 μmol/L), INR 1.0 (reference range, 0.9-1.1), and albumin 42 g/L (reference range, 35-50 g/L). AFP was 2.3 μgm/L and carcinoembryonic antigen (CEA) was 2.1 μgm/L. Ultrasound of the abdomen showed a huge liver mass (8cm×11cm) and the right portal vein branch was not visualized distally. CT of the abdomen showed the same mass at segment 5 and 8 which was consistent with hepatocellullar carcinoma (HCC) showing the classical triphasic pattern, i.e., heterogenous enhancement in the arterial phase, but early rapid washout in the portal-venous phase leaving the HCC lesion hypo-dense compared to the surrounding normal tissue (Figure 1). The patient underwent surgical removal of both segments (5 and 8). Histopathology of the mass confirmed the diagnosis of HCC. H&E stain showed the HCC pseudoglandular and trabecular pattern (Figure 2) and extensive lymphovasculer invasion. Immunohistochemical stain for CD34 was positive and showed wrapping of the tumor cluster by endothelial cells. The rest of the non-neoplastic livers showed only mild steatosis and no cirrhosis at all (Trichrome stain) (Figure 3).

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