Apoptosis pathway of liver cells in chronic hepatitis.

AIM: To study the pathway of apoptosis in chronic liver disease and the role of mitochondria in programmed cell death. METHODS: Liver biopsy specimens from 72 cases of chronic hepatitis and 29 cases of post hepatitis cirrhosis were studied. The pro-apoptotic protein Fas, FasL, Bax and the anti-apoptotic protein Bcl-2, Bcl-x(L), Bcl-2 alpha were studied immunohistochemically by SP method. Specimens from 15 cases of chronic hepatitis and post hepatitis cirrhosis were examined for their ultramicrostructures with special attention to their mitochondrial changes. Specimens from 3 normal adults (demised in traffic accidents) were used as control. RESULTS: The expression of proapoptotic proteins (Fas, FasL, Bax) in hepatocytes was significantly higher in the chronic hepatitis group than in the cirrhosis group (P<0.001). In the study of ultramicrostructure 364 hepatocytes were examined, from 12 cases of chronic hepatitis (including 10 mild cases, 1 moderate case and 1 severe case). Out of 364 hepatocytes 40 (11.0%) hepatocytes were found with various kinds of destruction in their mitochondria. Rupture of the outer membrane of mitochondria and the leakage of matrix from the intermembrane space were definitely demonstrated. The ultramicrostructural changes of mitochondria in the chronic hepatitis group were statistically higher than that in normal adults control group (chi(2)=4.32, P<0.05). CONCLUSION: The result of the study was in support of the current view that the apoptotic process in chronic hepatitis patients were largely along the intrinsic pathway (mitochondrial pathway), given that the intrinsic and extrinsic pathways could interlinked (converged) at some point on their progression, also it is impossible at present to exclude the possibility that the two pathways could be chosen by hepatocytes in parallel simultaneously.

Expression of hepatitis B virus antigen and Helicobacter pylori infection in gastric mucosa of patients with chronic liver disease.

BACKGROUND: It is common for the gastroendoscopist to find patients infected simultaneously with hepatitis B virus (HBV) and Helicobacter pylori (H pylori). Considering that HBV infection is linked to hepatocellular carcinoma and H pylori to gastric cancer, we investigated the incidence in this kind of patients in the northern Jiangsu Province, China. Rational management of these patients was also discussed. METHODS: Seventy-two patients including 28 patients with chronic hepatitis B and 44 patients with post hepatitis B liver cirrhosis served as observation group. Thirty patients with gastritis but without liver disease were included as controls. Diagnostic endoscopy was performed in all the patients. Three biopsy specimens were taken from the pyloric antrum 3 cm from the pyloric ring. Urease test staining of hematoxylin and eosin or fuchsin, and immunohistochemical analysis of H pylori IgG antigen and HBV antigen (HBsAg, HBcAg) were performed. RESULTS: The extent and intensity of chronic inflammation were identified in 95.5% (42/44) of the antrum mucosa of the patients with cirrhosis and in 92.9% (26/28) of the patients with chronic hepatitis. The expression of H pylori in the mucosa was found in 29 of the 42 patients with cirrhosis associated with antrum inflammation (69.0%). The expression of H pylori was observed in 20 of the 26 patients with chronic hepatitis combined with antrum inflammation (76.9%). No significant difference existed between the cirrhosis group and the chronic hepatitis group. The rates of HBV antigen expression in the H pylori positive and negative gastric antrum mucosa were 69.8% (37/53)and 73.7% (14/19), respectively (P>0.05). CONCLUSIONS: Over-expression of HBV antigen (HBsAg and HBcAg) coexists with the expression of H pylori antigen in the H pylori infected gastric mucosa. Difficult clearance of HBsAg and HBcAg from gastric epithelial cells may be related to persistent H pylori infection. Early treatment of H pylori infection may be beneficial to the prognosis of patients with chronic liver disease.