: TP6.3 g dl, Alb4.3 g dl, GOT17 IU l, GPT26 IU l,

Transcription

1 5 Vol. 34, pp. 5 23, 2006 C IFN 0 2 : C 993 S7 C A F2 IFN IFNa2a 9MIU 24W HCV-RNA F HCV-RNA IFN S8 20 mm CT SPIO-MRI 6 TP6.3 g dl, Alb4.3 g dl, GOT7 IU l, GPT26 IU l, g-gtp40 IU l, ICG5R5, HCV-Ab, HCV-RNA, AFP 3.5 ng ml L3 40, PIVKAII37 mau mg CTA CTAP : IFN 0 IFN 0 C C IFN HCC IFN 0 HCC 57

2 6 Table Fig. Ultrasonography showed hypoechoic lesion in S8 of the liver in size 20 mm. In enhanced ultrasonography, there was no vascular spot in early arterial phase and an avascular area was noted in late parenchymal phase. : 63 : : HCV C IFN IFNa-2a Sustained Virological Response: SVR

3 C SVR 7 Fig. 2 Abdominal CT scan showed low density area in S8 of the liver arrow, and no enhancement on arterial and portal phase S8 5 mm 5 : 53 : : : 75 cm 85 kg BMI C mmhg 70 Table : AFP L3 : S8 20 mm Fig. CT S8 Fig. 2 MRI T T2 SPIO Super paramagnetic iron oxide MRI T2 Fig. 3 CT CTA S8 CT CTAP Fig. 4 HCC 6 8 RFA 4 CT Fig. 5 RFA Fig. 6 Fig IFN 59

4 8 A F IFN A0 F Fig AFP 6ng ml L RFA Fig. 3 In SPIO Super paramagnetic iron oxide MRI the lesion showed high intensity on T2 weighted image arrow. C IFN SVR: sustained virological responder 3 BR: biochemical responder 4 5 IFN 2 3 IFN IFN 5 Toyoda Schwartz IFN mm 9 20 IFN IFN 5 8 NASH Fig. 4 CT arteriography CTA showed tumor lesion with amorphous enhancement in S8. In enhanced CT arterial portography CTAP, the tumor lesion showed a filling defect. 60

5 C SVR 9 C Takase C IFN 2 F AST ALT NASH B C HBV HBc HBs HBV-DNA HBV-DNA HBV C HBc HCV HBV 22 HBc HBV-DNA HBV-DNA HBV Fig. 5 After 4 days of RFA treatment, only a low density area is seen in the area of the tumor. Fig. 6 Histology of tumor lesion ; high cellularity and high ratio of N C were observed with scattered fatty droplets. These findings strongly suggested a well di#erentiated adenocarcinoma. HE 0 Fig. 7 Clinical course 6

6 20 Fig. 8 Before IFN treatment, biopsy showed only mild inflammatory cell infiltration in portal area and moderate fibrosis A F2 a After.2 year of IFN treatment, inflammation had disappeared and revealed only mild fibrosis A0 F b HCC HCC CT MRI T2 CTA CTAP HCC C 5 Shiratori IFN 83 F F2 F F3 F0 IFN 0 IFN IFN IFN 0 IFN 0 Sobesky R, Mathurin P, Charlotte F et al. Modeling the impact of interferon alfa treatment on liver fibrosis progression in chronic hepatitis C: A dynamic view. Gastroenterology 999; 6: Lau DTY, Kleiner DE, Ghany MG et al. 0- year follow-up after interferon-alfa therapy for 62

7 C SVR 2 chronic hepatitis C. Hepatology 998; 28: Marcellin P, Boyer N, Gervais A et al. Longterm histologic improvement and loss of detectable intrahepatic HCV RNA in patients with chronic hepatitis C and sustained response to interferon-alfa therapy. Ann. Intern. Med 997; 27: Manesis EK, Papaioannou C, Gioustozi A et al. Biochemical and virological outcome of patients with chronic hepatitis C treated with interferon alfa-2b for 6 or 2 months : A 4-year follow-up of 2 patients. Hepatology 997; 26: Reichard O, Glaumann H, Fryden A et al. Two-year biochemical, virological, and histological follow-up in patients with chronic hepatitis C responding in a sustained fashion to interferon alfa-2b treatment. Hepatology 995; 2: Shiratori Y, Imazeki F, Moriyama M et al. Histologic improvement of fibrosis in patients with hepatitis C patients who have sustained response to interferon therapy. Annals of Internal Medicine 2000; 32: Lindsay KL. Therapy of hepatitis C: overview. Hepatology 997; 26: s ; 62: IFN C 2000; 4: C ; 99: C 999; 96: Stuart K, Tessitore J, Huberman M et al. 5- Fluorouracil and alfa-interferon in hepatocellular carcinoma. Am J Clin. Oncol 996; 9: C 8 C 998; 39: Yamamura T, Matumoto A, Rokuhara A et al. Development of small hepatocellular carcinoma in a patient with chronic hepatitis C after 77 months of a sustained and complete response to interferon therapy. J. Gastoenterol. Heptol 2002; 7: Kasahara A, Hayashi N, Mochizuki K et al. Risk Factors for Hepatocellular Carcinoma and Its Incidence After Interferon Treatment in patients With Chronic Hepatitis C. Hepatology 998; 27: Ikeda K, Saitoh S, Arase Y et al. E#ect of Interferon Therapy on Hepatocellular Carcinogenesis in Patients With Chronic Hepatitits Type C: A Long-Term Observation Study of 643 Patients Using Stastical Bias Correction With Proportional Hazard Analysis. Hepatology 999: 29; Yoshida H, Shiratori Y, Moriyama M et al. Interferon Therapy Reduces the Risk for Hepatocellular Carcinoma: National Survaillance Program of Cirrhotic and Noncirrhotic Patients with Chronic Hepatitis C in Japan. Annals of Internal Medicine 999; 3: Okanoue T, Ito Y. Hepatocellular carcinoma in sustained responders of interferon-treated chronic hepatitis C. J. Gastroenterol. Hepatol. 2003; 8: Schwaltz M. A biomathmatical approach to clinical tumor growth. Cancer 96; 4: Toyoda H, Kumada T, Honda T et al. Analysis of hepatocellular carcinoma tumor growth detected in sustained responders to interferon in patients with chronic hepatitis C. J. Gastroenterol. Hepatol. 200; 6: Takase S, Takeda N, Sawada M et al. Relationship between alcoholic liver disease and HCV infection. Alcohol Alcohol 993; 28 A:

8 HBs HCV HBV 999; 40: Parterlini P, Driss F, Nalpas B et al. Persistance of hepatitis B and hepatitis C viral genomes in primary liver cancers from HBs Agnegative patients: A study of a low-endemic area. Hepatology 993; 7: Chung H-T, Lai C-L and Lok A. S. F. Pathogenic role of hepatitis B virus in hepatitis B surface antigen-negative decompensated cirrhosis. Hepatology 995; 22:

9 C SVR 23 Abstract A Case of Hepatocellular Carcinoma Ten Years after Successful Interferon Therapy for Chronic Hepatitis C. Minoru Kobayashi, Michihiro Suzuki, Norie Yamada, Masayo Yamaguchi, Hiroki Ikeda, Hideaki Takahashi, Yoshihiko Nagase, Yoshiki Katakura, Koutarou Matunaga, Toshiya Ishii, Nobuyuki Matsumoto, Chiaki Okuse, Satoshi Kitajima, Junki Koike 2 and Fumio Itoh A 63-year-old man was pointed out liver dysfunction on his medical check-up in 986. He was diagnosed as chronic hepatitis C in 990 on the basis of liver biopsy finding, which showed A F2 in November 993. He was treated with interferon, using 9MIU of interferon-alfa2a, 3 times a week for 24 weeks. He got sustained virological response and normalization of transaminase was observed after the treatment. In Februrary 995, liver biopsy was performed again, fibrosis was improved from F2 to F, and the inflammation had disappeared. In May 2004, a 20 mm liver tumor was noted in S8 on abdominal ultrasonography. He was admitted to our hospital in June of 2004 for further examination. Laboratory data showed elevated alpha-fetoprotein 3.5ng ml and lectin-reactive AFP 40. The tumor showed enhancement on CT arteriography, and defect on CT during arterial portography study. In MRI enhanced with super paramagnetic iron oxide, the lesion was detected with high intensity on T2 weighted image. These data led to the diagnosis of hepatocellular carcinoma HCC and a biopsy was performed. Histological findings of the tumor lesion revealed a high cellularity and high ratio of N C with scattered fatty droplets. These findings strongly suggested a suspected well di#erentiated adenocarcinoma. The tumor was treated with RFA. No recurrence has been found since then. Department of Gastroenterology and Hepatology, St. Marianna University School of Medicine 2 Department of Pathology, St. Marianna University School of Medicine 65