In our study population, 21.8% had fatty liver diagnosed by USG, 9.3% were non-alcoholic with fatty liver, and 4.1% were non-alcoholic and non-overweight with fatty liver. Our results suggest that central body fat distribution can correlate with the development of fatty liver, and that measurement of percentage body fat is useful to assess the etiology of fatty liver in non-alcoholic and non-overweight participants, particularly women.

Spontaneous regression of hepatocellular carcinoma is a rare phenomenon. Abscopal regression of tumours resulting from the eVect of irradiation of a tissue on a remote non-irradiated tissue is also rare. The case of a 76 year old Japanese man with hepatocellular carcinoma that regressed after radiotherapy for thoracic vertebral bone metastasis is described. Serum levels of tumour necrosis factorincreased after radiotherapy. The findings suggests that such abscopal related regression may be associated with host immune response, involving cytokines such as tumour necrosis factor-. (Gut 1998;43:575-577)

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.

Mild acute intestinal inflammation induced by DSS can be inhibited by 4-CA and this action is associated with the suppression of COX-2 expression and activity.

Our results indicate that chemokines produced locally in the esophageal mucosa may be involved in the development and progression of RE.

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The HFC diet induced hepatic features of NASH and eventually progressed cirrhosis in Sprague-Dawley rats within 9 weeks.