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Clinical features and etiology of hepatocellular carcinoma arising in patients with membranous obstruction of the inferior vena cava: In reference to hepatitis viral infection
Author(s) -
Matsui Shigeru,
Ichida Takafumi,
Watanabe Masashi,
Sugitani Soichi,
Suda Tsuyoshi,
Takahashi Toru,
Asakura Hitoshi
Publication year - 2000
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1046/j.1440-1746.2000.02303.x
Subject(s) - medicine , hepatocellular carcinoma , hbsag , hepatitis b virus , viral hepatitis , hepatitis b , hepatitis c virus , hepatitis , inferior vena cava , virology , virus , pathology , gastroenterology
Background and Aims: Budd–Chiari syndrome (BCS) comprises hepatic vein thrombosis and inferior vena cava (IVC) obstruction known as membranous obstruction of the IVC (MOVC). The latter is frequently complicated by hepatocellular carcinoma (HCC). The etiology of MOVC‐associated HCC in relation to hepatitis viral infection is not known. In this study, we investigated the clinical features and etiology of HCC in MOVC. Methods: Membranous obstruction of IVC and HCC were diagnosed and studied by using imaging techniques. Sera from patients with MOVC, complicated by HCC, were examined for hepatitis viral antigens and antibodies (hepatitis B surface antigen (HBsAg), antibody to HBsAg (anti‐HBs), antibody to hepatitis B core antigen (anti‐HBc) and third generation antibody to hepatitis C virus (anti‐HCV)) and for hepatitis viral nucleic acids (hepatitis B virus (HBV)‐DNA, hepatitis C virus (HCV)‐RNA, hepatitis G virus (HGV)‐RNA and TT virus DNA). Results: We studied 12 patients with BCS who were seen between April 1968 and February 1999. All of them had MOVC. Hepatocellular carcinoma developed in three (25%) of them. There were no obvious differences in the clinical features and imaging findings concerning MOVC between patients with and without HCC. Hepatocellular carcinoma in these three patients showed no clear trend in clinical features and imaging findings. Of the hepatitis viral markers examined, HBsAg, anti‐HBc and HBV‐DNA were positive in only one of three patients with HCC and all of the viral markers were negative in the other two patients. Conclusions: Chronic congestion in the liver, caused by an outflow block of hepatic veins and subsequent histopathologic change, must have led to HCC in two patients without any hepatitis viral markers. Patients with MOVC should be followed closely as a high‐risk group for HCC.