Background/Aims
Most liver diseases lead to a pathobiochemical reaction termed liver fibrosis. Hepatic fibrosis is not a uniform phenomenon and it comprises increased deposition of the liver connective tissue components(collagen, noncollagenous glycoprotein, proteoglycan) in the intercellular space, leading to disturbances of intrahepatic blood flow and hindrance of exchange processes between blood and cells, Fibrosis can be determined by morphological examination o f the liver, but this approach cannot be used to assess accurately the activity of collagen synthesis at any given point in time, Thus, the development of biochemical markers of hepatic fihrosis might allow a promising diagnostic approach for the identification and quantitation of this process, Aminoterminal procollagen III pn)peptide(PIIINP) and carboxytermina1 procollagen I propeptide(PICP) are known as the most widely used parameter for evaluating liver fibrosis, but it is diAicult to find previous report discribing the correlation ot each other. To elucidate the clinical significance of the corretation of PICP(x) and PIIINP(y) concentrations in patients with chronic liver diseases, radioimmunoassay was employed in this investigation. Methods:Sera tested were obtained from pathologically proven 43 patients;4 cases of fatly liver, 11 cases of chronic persistent hepatitis, 13 cases of chronic active hepatitis, l5 cases of liver cirrhosis. All the patients except 4 cases ot fatty liver were shown positivity of HBsAg. PICP and PIIlNP radioimmunoassay kits(Farrnos Diagnostica, Oulunsalo, Finland) wcre purchased for this study. Results:In the patients among the three groups of chronic active hepatitis, liver cirrhosis, chmnic persistent hepatitis, the correlations were significant in orders(y= - 10.27 +0.l3938x, r=0.92286, p=0.000007;y=-1.185+0.06611x, r=0.73656, p=0.001737;y=1.1174+0.03273x, r=0.56879, p=0.067849). Four cases of fatty liver reveal no signiticant correlation(y=4,8671- 0,0079x, r= 0.1959, p=0.804054). Conclusion:0n the basis of these data, we s st that the correlation of each showed a significant increase with heightening degree of inflammation, activity of diseases and fibrosis.

Backgroud:Liver fibrosis by the progression of the chronic processes of the liver diseases induces deforrned microcirculations of the hepatic lobules. And this eventually resolted in portal hypertension. On the other hands, angiogenic stimu4nt factors are physiologically activated in order to repair the tissue damage. Overexpression of angiogenic factors, however, can stimulate neovascularization as in a fonnation of the tumor that liberates uncontrolled overgrowing of the tumor cells. Methods: To elucidate the dynamic changes of the serum concentration of angiogenin in chronic liver diseases, this study is intended to employ an ELISA in 44 pathologically proven patients. Quantikiae human angiogenin kit (R & D,systems Inc. Mmneapolis, MN) was used for this investigation. Results:Mean value and standard error of angiogenin concentration (ng/ml) of the sera was 238.92+ 50.95 in 5 cases of chronic persistent hepatitis, 184.47+ 12.75 in 6 cases of chronic active hepatitis, 131.36+ 10.99 in 19 cases of liver cirrhosis, and 211.03+ 19.08 in 14 cases of hepatocellular carcinoma, respectively. Serum angiogenin level in the liver cirrhosis was significantly lower than in chronic persistent hepatitis(p=0.00336), and than in chronic active hepatitis(p=0.018673). Angiogenin concentration in hepatocellular carcinomas was significantly higher than the level of the liver cirrhosis investigated(p=0.00569). Conclusions:These data support that persistent inflammatory insults in the chronic hepatitis were compensated by the elevation of angiogenin but complete fibrosis as in liver cirrhosis showed the depressed level. And emerging of the hepatocellular carcinoma is accompanied by the elevated stimuli of angiogenin for the neovascularization.

Background/Aims
The spectrum of clinical features of chronic liver disease bas wide range from asymptomatic cases to hepatic failure, The natural course and long-term prognosis of chronic liver disease also varies greately, and this diversity makes it diflicult to predict the clinical course of individual patient. The two majar approaches to the treatment of chronic liver disease are 1) directed toward the eradication of the virus and 2)designed to modulate cellular and humeral immunity. Progress has been made in the development of antiviral chernotherapeutic agents for hepatitis. But as yet no safe and reliably effective treatment or combination of treatrnents is available. In tkis study, we performed trial of diphenyl-dimethyl-dicarboxylate to evaluate the therapeutic effect and safety of it. Methods: The ciinical trials of DDB(complex capsule of diphenyl dimethyl dicarboxylate 7.5mg and polysorbate 80 1,5mg and polyethylene glycol 6000 66mg) were carried out in 30 patients with chronic liver disease for 6 months. All patients had abnormal liver function test ouer a period of 6 months. Results:In selected groups mean serum aspartate aminotransferase and alanine aminotrans- ferase dropped from pretreatment level of' 115.9+ 74.1 IU/L and 201.6+ 173.0 1U/L to posttreatment level of46.6+ 21.6 UU/L and 28.7- 15.4IU/L, respectively(p<0.01). There was no significant hernatological and biochemical change after administration of DDB. Untoward side effects were easily controlled by discontinuing the drugs, Conclusions:Administration of DDB(for 6 months) appears to be effective for decrement of transaminase level and safe for the treatment of patients with chronic liver disease.

Background
/Aim: Transforming growth factor-a(TGF-a) is a polypeptide cytokine related to cell proliferation and transformation. TGF- a binds to EGF receptor and stimulating DNA synthesis in liver cell. The hepatitis B virus (HBV) by itself is also believed to play a role in the hepatic carcinogenesis. Recently, it was reported that TGF- a and HBV were synergistic in action with rapid appearance of hepatocelluar carcinoma in bitransgenic mice. Although TGF- a is thought to play an important role in hepatocarcinogenesis, its expression during the natural history of HBV hepatitis was poorly understood. This investigation was performed to elucidate the dynamic changes and distinct immunohistochemical staining patterns in the course of chronic HBV hepatitis with specific reference to hepatocelluar carcinoma and to explain the role of TGF- a in the pathogenesis of hepatocelluar carcinoma. Materials/Methods: Employing TGF- a monoclonal antibody, signal detection was carried out by peroxidase-conjugated streptavidin in deparaffinized liver tissue sections taken from HBsAg positive patients. All of the liver tissue sections were proven HBV DNA positive by in situ hybridization. Immunohistochemical staining was performed in the tissue sections obtained from four normal controls, six from patients with chronic persistent hepatitis, five with chronic active hepatitis, eight with liver cirrhosis and eleven with hepatocellular carcinoma. Results: The patterns of TGF- a immunoreactivity were cytoplasmic-grain types in normal controls and chronic persistent hepatitis, honeycomb types in chronic active hepatitis, occasional cytoplasmic-flooding types in liver cirrhosis, and cytoplasmic-grape types in hepatocellular carcinoma. A Shapiro-Wilk W test for frequency table analysis for the expression of TGF- a in these different disease groups was statistically significant. Conclusion: These data suggest that step-wise distinct expression of TGF-a enhancement in HBV associated chranic liver diseases which eventually resulted in the development of hepatocellular carcinoma were conceivably due to dysregulation of liver cell cycles by both HBV and TGF- a during the persistent repetition of cell cycles. (Korean J Hepatol 1997;7:316 328)