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Objective Fulminant hepatitis is a rare but fatal disease. In the present study, we examined the changes in etiology and prognosis of fulminant hepatitis in Nagasaki Prefecture, Japan between 1980 to 1999. Methods Eighty-one patients with fulminant hepatitis admitted to our hospitals from 1980 to 1999 were examined with respect to the etiology and prognosis. Results Fulminant hepatitis was due to hepatitis A virus in 2 (12%) cases, hepatitis B virus in 18 (22%) cases, unknown etiology in 50 (62%) cases, and drug-induced in 11(14%) cases. The number of cases in the first half of the study (1980-1989) was 47 and that of the latter half (1990-1999) was 34 cases. The incidence of fulminant hepatitis type B also decreased from 14 cases (30%) to 4 cases (12%) during these periods. The overall survival rate of fulminant hepatitis was 32%; it was equal in fulminant hepatitis type B, fulminant hepatitis of unknown etiology and fulminant drug-induced hepatitis. The survival rate of fulminant hepatitis type A was 100%, though only two cases were identified. Retrospectively, the survival rate in patients with a pre-encephalopathy period of ≤10 days and aged ≤39 years was significantly higher than in patients ≥40 years of age (p

A total of 44 patients with long-standing ulcerative colitis were studied to elucidate changes over time in colonoscopic and histological inflammatory activity. More than two years of symptomatic remission without melena or bloody diarrhea was achieved in 63.6% (28/44). All patients underwent total colonoscopic examinations. Compared with findings of the previously involved area, 70.5% (31/44) showed a reduction or disappearance of the inflammatory area on endoscopic and histological examinations; however, the rectal inflammation disappeared in 31.8% (14/44) of patients. Moreover, it became apparent that the remaining active inflammatory area tended to show discontinuous spread with patchy inflammatory foci. Thus, the mucosal inflammation in long-standing ulcerative colitis may be characterized by a reduction in both extent and degree.

The discovery of hepatitis C virus (HCV) has enabled the diagnosis of type C chronic liver disease, which had in the past been diagnosed as part of non-A, non-B chronic liver disease. Although most cases with chronic liver disease are caused by hepatitis B virus (HBV) or HCV infection, there are still cases of non-B, non-C chronic liver disease. Forty patients with chronic liver disease, who were seronegative for hepatitis B surface antigen and antibody to HCV, were followed for a mean period of 72 months. The clinical manifestations in these patients were compared with those reported for type B and type C chronic liver disease. Of the 40 patients, 22 were diagnosed with chronic hepatitis, 14 with liver cirrhosis and 4 with hepatocellular carcinoma (HCC). Twenty-seven (67.5%) patients showed mild alanine aminotransferase activity profiles, and the natural clinical course of most patients showed a slow progression compared with that reported for type B and type C patients. The yearly incidence of HCC was 9.7% in patients with liver cirrhosis and 3.9% in chronic hepatitis. These rates were similar to those in type B or type C patients. This suggests that our population sample contained a number of patients with type B, type C or other etiologic agent(s), because 66.7% of the patients who developed HCC had some evidence of exposure to HBV or HCV. Our results suggest that more detailed and accurate tests for detecting HBV and HCV should be considered before making the diagnosis of non-B, non-C chronic liver disease, and that there is the need to reveal unknown etiologic agent(s).

Background. The development of hepatocellular carcinoma (HCC) is associated closely with cirrhosis. In the present study, the cumulative risk of HCC in patients with cirrhosis was investigated. Methods. A total of 401 patients were registered from April 1977 and followed for a mean of 4.4 years. Of 401 patients, 255 (64%) were tested for hepatitis B surface antigen (HBsAg) and antibody (anti-) to the hepatitis C virus (HCV); 87 (34%) patients were positive for HBsAg but were negative for anti-HCV (hepatitis B virus [HBV] group), 126 (49%) were negative for HBsAg but were positive for anti-HCV (HCV group), 10 (4%) were positive for both and 32 (13%) were negative for both (non-B non-C group) Results. By the end of March 1993, HCC was diagnosed in 127 (31.6%) patients. The cumulative risk of HCC in the HCV group was slightly higher than that in HBV group (P = 0.3, 5-year risk: 36.9 versus 21.2%). In contrast, the rate was significantly lower in the non-B non-C group than in the HBV or HCV groups (P < 0.05 and P < 0.01, respectively, 5 year risk: 12.4%). Conclusions. These results suggest that not only HBV infection but also HCV infection increase the risk for HCC in patients with cirrhosis.

The present study was designed to determine the frequency of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection in patients with hepatocellular carcinoma (HCC) in Nagasaki Prefecture, Japan. We examined the clinical features of 1019 patients with HCC who visited our hospitals between January and December 1999. The ratio of men to women was 709 : 310, and the peak incidence of HCC was in the seventh decade of life in both men and women. In the majority of the patients, HCC showed association with HCV infection (74%) compared with HBV infection (17%). HBV-associated HCC was more common in young patients, while HCV-associated HCC was more common in patients with a history as a "daily drinker", or with a history of blood transfusion, liver cirrhosis, and persistently high serum transaminases before the diagnosis of HCC. HCC was initially suspected by ultrasonography or computed tomography in 776 of the 874 patients for whom there was a history of mode of detection of HCC (89%). Tumor size at the time of diagnosis of HCC in patients who had been regularly followed up for liver diseases at our hospitals was significantly smaller than that in patients who were not followed up regularly before the diagnosis (P < 0.01). Our results indicate that the proportions of patients with HBV or with HCV infection among HCC patients in Nagasaki Prefecture are similar to those found in a nationwide survey in Japan, and there are some differences between the clinical manifestations of HBV- and HCV-associated HCC. Our results emphasize the importance of close follow-up for the high-risk group (i.e. those with HBV- or HCV-associated chronic liver diseases) for the early detection of HCC.

Objective The diagnostic criteria of autoimmune hepatitis (AIH) were recently modified by the International Autoimmune Hepatitis Group. This study was performed to assess the impact of the revised scoring system on the diagnosis of AIH. Patients and Methods We re-analyzed the clinical features of 89 patients diagnosed as AIH in Nagasaki Prefecture, Japan, using the revised scoring system, and compared the scores and final diagnosis with our previously published results using the original system. Results Of the 89 patients with AIH, 40 (45%) were classified using the new system as "definite" AIH, 41 (46%) as "probable" AIH, and 8 (9%) patients were categorized as "others". Of these, 37 (42%), 35 (39%), and 4 (4%) patients who were classified as "definite", "probable", and "others" by the original system remained in the same category by the revised system, respectively. However, 3, 4, and 6 patients were re-categorized as "definite" from "probable", "others" from "probable", and "probable" from "definite", respectively. The difference in aggregate scores between the above two systems ranged from -5 to +2. The main contributing factors to the changes in aggregate AIH score were "other autoimmune disease(s)" and "interface hepatitis without lobular involvement and bridging necrosis on liver histology". However, the main contributing factors to the demotions from "definite" to "probable" and form "probable" to "others" were those related to the characteristics of biliary diseases, i.e., antimitochondrial antibody positive, biliary changes in liver histology, and alkaline phosphatase: aspartate aminotransferase ratio between 1.5 and 3.0. Moreover, two patients who had no histological evidence of AIH were both re-categorized as "others" from "probable" AIH. Conclusion Our results indicated that the diagnosis, whether based on the revised or original system, was the same in the majority of AIH patients, but the revised scoring system excluded cases who had features suggestive of biliary diseases from "definite" AIH, and also confirmed that a diagnosis of "definite" AIH should not be made without liver histology.(Internal Medicine 39: 1008-1012, 2000)

症例は17歳女性.意識障害,黄疸,糖尿病を主訴として入院した.入院時の理学的所見では全身の黄疸と傾眠傾向を認め,入院時検査でプロトロンビン時間の延長,総ビリルビンの上昇,著明な尿糖,空腹時血糖の上昇が認められた.その意識障害の出現時期と併せ考えI型糖尿病と合併した亜急性肝炎と診断した.入院後,血漿交換などの種々の治療にも拘わらず意識障害が遷延化し,糖尿病のコントロールも困難な状態が続いたが,約3カ月後になって,肝機能は改善傾向を示し,6カ月後にはほぼ正常化して,糖尿病もコントロール可能となった.しかし,本患者はこのほか原発性甲状腺機能低下症も合併しておりその多彩な病態から興味ある症例と思われたので,文献的考察を加えて,ここに報告した.