Clinical features of hepatitis C virus-related hepatocellular carcinoma and their association with α-fetoprotein and protein induced by vitamin K absence or antagonist-II

: Purpose: We investigated the differences in clinical features between α‐fetoprotein (AFP)‐predominant hepatocellular carcinoma (HCC) and protein induced by vitamin K absence or antagonist‐II (PIVKA‐II)‐predominant HCC, especially regarding host factors thought to contribute to hepatocarcinogenesis...

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Veröffentlicht in:Liver international 2006-09, Vol.26 (7), p.789-795
Hauptverfasser: Yano, Yoichi, Yamashita, Fumihiko, Kuwaki, Kotaro, Fukumori, Kazuta, Kato, Osamu, Yamamoto, Hiroshi, Ando, Eiji, Tanaka, Masatoshi, Sata, Michio
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Sprache:eng
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Zusammenfassung:: Purpose: We investigated the differences in clinical features between α‐fetoprotein (AFP)‐predominant hepatocellular carcinoma (HCC) and protein induced by vitamin K absence or antagonist‐II (PIVKA‐II)‐predominant HCC, especially regarding host factors thought to contribute to hepatocarcinogenesis in chronic hepatitis C virus (HCV) infection. Methods: HCV‐related HCC patients (n=306) were divided into four groups according to median AFP (48.1 ng/ml) and PIVKA‐II (60 mAU/ml). Host factors, tumor factors, survival, and risk factors affecting survival were compared. Results: Aspartate aminotransferase (AST; IU/L), alanine aminotransferase (ALT; IU/L), and platelet count (× 104/ml) were, respectively, 81, 67, and 8.2 in AFP‐predominant HCC (group A; n=66) vs. 50, 42, and 11.4 in PIVKA‐II‐predominant HCC (group P; n=52). Tumor sizes (mm) in groups A and P were 20 and 37, respectively. Significant differences were evident. Survival was identical between the two groups. Factors affecting survival were total bilirubin, portal tumor thrombus and number of nodule in group A, and albumin and tumor distribution in group P. Conclusions: PIVKA‐II‐predominant HCC had a milder hepatitis and a better‐preserved platelet count compared with AFP‐predominant HCC. Considering the strong relation between hepatocarcinogenesis and hepatic inflammation with chronic HCV infection, these differences indicate that hepatocarcinogenic mechanisms in PIVKA‐II‐predominant HCC may differ from those in AFP‐predominant HCC.
ISSN:1478-3223
1478-3231
DOI:10.1111/j.1478-3231.2006.01310.x