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ARTICLE

Declining Incidence of Hepatocellular Carcinoma in Osaka, Japan, from 1990 to 2003

right arrow Hideo Tanaka, MD; Yasuharu Imai, MD; Naoki Hiramatsu, MD; Yuri Ito, PhD; Kazuho Imanaka, MD; Masahide Oshita, MD; Taizo Hijioka, MD; Kazuhiro Katayama, MD; Iwao Yabuuchi, MD; Harumasa Yoshihara, MD; Atsuo Inoue, MD; Michio Kato, MD; Tetsuo Takehara, MD; Shinji Tamura, MD; Akinori Kasahara, MD; Norio Hayashi, MD; and Hideaki Tsukuma, MD

3 June 2008 | Volume 148 Issue 11 | Pages 820-826

Background: Japan has the highest incidence rate of primary liver cancer attributed to chronic hepatitis C virus (HCV) infection among developed countries. Molecular clock analysis of HCV sequences revealed that the spread of HCV took place earlier in Japan than in other countries. This might influence recent temporal trends in hepatocellular carcinoma (HCC) incidence.

Objective: To characterize the contribution of HCV-related hepatocellular carcinoma (HCC) to recent changes in HCC incidence in Osaka, Japan.

Design: Population-based survey.

Setting: Osaka Cancer Registry and 10 hospitals in Osaka.

Participants: 63 862 patients with HCC that was diagnosed between 1981 and 2003 in Osaka Prefecture, including 5253 HCV-seropositive patients with HCC that was diagnosed between 1990 and 2003 at 10 hospitals.

Measurements: Incidence of HCC and estimated incidence rate of HCV-related HCC, measured by multiplying the prevalence of anti-HCV by the corresponding HCC incidence rate.

Results: Between 1981 and 2003, peak incidence of HCC among men age 50 to 59 years, 60 to 69 years, and 70 to 79 years occurred in 1986, 1995, and 2000, respectively, with marked downward trends thereafter (average annual change, –7.9, –22.3, and –12.4 per 100 000 persons, respectively). Similar trends were observed in women. Estimated sex- and age-specific incidence of HCV-related HCC (per 100 000 persons) decreased from 255 to 92 cases at the maximum in men age 60 to 69 years and from 61 to 34 cases in women age 60 to 69 years, whereas estimated incidence of non-HCV–related HCC did not change between 1990 and 2003.

Limitation: Infection was determined only by HCV seropositivity.

Conclusion: The incidence of HCC in Osaka started to decrease by 2000, mainly because of decreased HCV-related HCC.


Editors' Notes
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Context

  • Hepatitis C virus (HCV) infection in Japan began to spread during the 1920s, increased after World War II with an explosion in parenteral amphetamine use and paid blood donation, and decreased in the 1950s to 1960s with voluntary blood donation and penalties against amphetamine use. Evidence linking the trends in HCV infection to hepatocellular carcinoma rates in Japan is limited.

Contribution

  • Data from the Osaka Cancer Registry and 10 Osaka hospitals suggest that hepatocellular carcinoma rates began to decrease in 2000, mainly because of a decrease in HCV-associated cancer.

Implication

  • Control of HCV transmission within a population seems to be followed by a decrease in hepatocellular carcinoma.

—The Editors

 

Author and Article Information
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From Osaka Medical Center for Cancer and Cardiovascular Diseases, Ikeda Municipal Hospital, Osaka University Graduate School of Medicine, Osaka Police Hospital, National Hospital Organization Osaka Minami Medical Center, Osaka Koseinenkin Hospital, Otemae Hospital, Osaka Rousai Hospital, Osaka General Medical Center, and National Hospital Organization Osaka National Hospital, Osaka, Japan.

Acknowledgment: The authors thank the Osaka Cancer Registry for allowing use of their data and Ms. Yasue Kotani for assistance with statistical analysis.

Grant Support: By the Osaka Prefectural Government (1999–2000) and Grants-in-Aid for Hepatitis Research of the Japanese Ministry of Health, Labor, and Welfare.

Potential Financial Conflicts of Interest: None disclosed.

Reproducible Research Statement: Study protocol: Available by contacting Dr. Tanaka (e-mail, hitanaka{at}aichi-cc.jp). The protocol is only available in Japanese. Statistical code and data set: Not available.

Requests for Single Reprints: Hideo Tanaka, MD, 1-1 Kanokoden, Chikusa-ku Nagoya-shi, Aichi, Japan 464-8681; e-mail, hitanaka{at}aichi-cc.jp.

Current Author Addresses: Drs. Tanaka, Ito, Imanaka, and Tsukuma: 1-3-3 Nakamichi, Higashinari-ku, Osaka 537-8511, Japan.

Dr. Imai: 3-1-18 Johnan, Ikeda, Osaka 563-0025, Japan.

Drs. Hiramatsu and Takehara: 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.

Dr. Oshita: 10-31 Kitayama-cho, Tennouji-ku, Osaka 543-0035, Japan.

Dr. Hijioka: 2-1 Kido-Higashi-cho, Kawashinagano, Osaka 586-0008, Japan.

Dr. Katayama: 4-2-78 Fukushima, Fukushima-ku, Osaka 553-0003, Japan.

Dr. Yabuuchi: 1-5-34 Otemae, Chuo-ku, Osaka 540-0008, Japan.

Dr. Yoshihara: 1179-3 Nagasone-cho, Kita-ku, Sakai, Osaka 591-8025, Japan.

Dr. Inoue: 3-1-56 Bandai-Higashi, Sumiyoshi-ku, Osaka 558-0056, Japan.

Dr. Kato: 2-1-14 Hoenzaka, Chuo-ku, Osaka 540-0006, Japan.

Dr. Tamura: 5-7-1 Kayano, Minoh, Osaka 562-0014, Japan.

Drs. Kasahara and Hayashi: 2-15 Yamadaoka, Suita, Osaka 565-0871, Japan.

Author Contributions: Concept and design: H. Tanaka, Y. Imai, N. Hiramatsu.

Analysis and interpretation of the data: Y. Imai, K. Imanaka, M. Oshita, T. Hijioka, K. Katayama, I. Yabuuchi, H. Yoshihara, A. Inoue, M. Kato, T. Takehara, S. Tamura, A. Kasahara, H. Tsukuma.

Drafting of the article: H. Tanaka.

Final approval of the article: H. Tanaka, Y. Imai, N. Hiramatsu, Y. Ito, K. Imanaka, M. Oshita, T. Hijioka, K. Katayama, I. Yabuuchi, H. Yoshihara, A. Inoue, M. Kato, T. Takehara, S. Tamura, A. Kasahara, N. Hayashi, H. Tsukuma.

Statistical expertise: Y. Ito.

 

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