Interferon-induced prolonged biochemical response reduces hepatocarcinogenesis i

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J Med Virol. 2007 Oct;79(10):1485-90.

Interferon-induced prolonged biochemical response reduces

hepatocarcinogenesis in hepatitis C virus infection.

Arase Y, Ikeda K, Suzuki F, Suzuki Y, Kobayashi M, Akuta N, Hosaka T, Sezaki

H, Yatsuji H, Kawamura Y, Kobayashi M, Kumada H.

Department of Hepatology, Toranomon Hospital, Toranomon, Minato-ku, Tokyo,

Japan.

The aim of this study was to elucidate indicator of interferon (IFN) therapy

for reducing hepatocellular carcinoma (HCC) in chronic hepatitis C patients

without eradicating hepatitis C virus (HCV) RNA during IFN therapy.

Inclusion criteria were biopsy-proven chronic hepatitis or liver cirrhosis,

IFN period for more than 1.5 years and persistently positive HCV-RNA during

IFN therapy. Two hundred thirty-six patients satisfied above criteria were

treated with IFN for 1.5-5 years (median 1.8 years, mean 2 years). Mean age

was 55.1 years and male was 145(61%). Eighty-one (34%) patients had severe

fibrosis of the liver. These patients were prospectively monitored about HCC

after the termination of IFN therapy. We regarded biochemical response (BR)

as normalization of serum aminotransferase and alpha-fetoprotein for more

than 1 year during IFN therapy. Cumulative rate of development of HCC after

the termination of IFN therapy was 9.1% at 5th year and 26.5% at 10th year.

proportional analysis showed that HCC development after the termination

of IFN therapy occurred when histological staging was advanced (P < 0.0001)

and BR was not achieved (P = 0.009), age was >60 years (P = 0.026). The

relative risk of HCC development in patients with BR was 0.36 compared with

patients without BR. The attainment of BR during IFN therapy is effective in

reducing hepatocarcinogenesis for patients with chronic HCV infection. J.

Med. Virol. 79:1485-1490, 2007. © Wiley-Liss, Inc.

PMID: 17705189 [PubMed - in process]

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[Guest guest]

J Med Virol. 2007 Oct;79(10):1485-90.

Interferon-induced prolonged biochemical response reduces

hepatocarcinogenesis in hepatitis C virus infection.

Arase Y, Ikeda K, Suzuki F, Suzuki Y, Kobayashi M, Akuta N, Hosaka T, Sezaki

H, Yatsuji H, Kawamura Y, Kobayashi M, Kumada H.

Department of Hepatology, Toranomon Hospital, Toranomon, Minato-ku, Tokyo,

Japan.

The aim of this study was to elucidate indicator of interferon (IFN) therapy

for reducing hepatocellular carcinoma (HCC) in chronic hepatitis C patients

without eradicating hepatitis C virus (HCV) RNA during IFN therapy.

Inclusion criteria were biopsy-proven chronic hepatitis or liver cirrhosis,

IFN period for more than 1.5 years and persistently positive HCV-RNA during

IFN therapy. Two hundred thirty-six patients satisfied above criteria were

treated with IFN for 1.5-5 years (median 1.8 years, mean 2 years). Mean age

was 55.1 years and male was 145(61%). Eighty-one (34%) patients had severe

fibrosis of the liver. These patients were prospectively monitored about HCC

after the termination of IFN therapy. We regarded biochemical response (BR)

as normalization of serum aminotransferase and alpha-fetoprotein for more

than 1 year during IFN therapy. Cumulative rate of development of HCC after

the termination of IFN therapy was 9.1% at 5th year and 26.5% at 10th year.

proportional analysis showed that HCC development after the termination

of IFN therapy occurred when histological staging was advanced (P < 0.0001)

and BR was not achieved (P = 0.009), age was >60 years (P = 0.026). The

relative risk of HCC development in patients with BR was 0.36 compared with

patients without BR. The attainment of BR during IFN therapy is effective in

reducing hepatocarcinogenesis for patients with chronic HCV infection. J.

Med. Virol. 79:1485-1490, 2007. © Wiley-Liss, Inc.

PMID: 17705189 [PubMed - in process]

_________________________________________________________________

Booking a flight? Know when to buy with airfare predictions on MSN Travel.

http://travel.msn.com/Articles/aboutfarecast.aspx & ocid=T001MSN25A07001