Portal biliopathy is defined as abnormalities in the extra- and intrahepatic ducts and gallbladder of patients with portal hypertension. This condition is associated with extrahepatic venous obstruction and dilatation of the venous plexus of the common bile duct, resulting in mural irregularities and compression of the biliary tree. Most patients with portal biliopathy remain asymptomatic, but approximately 10% of them advance to symptomatic abdominal pain, jaundice, and fever. Magnetic resonance cholangiopancreatography and endoscopic retrograde cholangiopancreatography are currently used as diagnostic tools because they are noninvasive and can be used to assess the regularity, length, and degree of bile duct narrowing. Management of portal biliopathy is aimed at biliary decompression and reducing the portal pressure. Portal biliopathy has rarely been reported in Korea. We present a symptomatic case of portal biliopathy that was complicated by cholangitis and successfully treated with biliary endoscopic procedures.

Background/Aims
Hepatocytes on the hepatic lobule mipate from portal zone to centrilobular mea as the DNA synthesis within it. And also, the xenobiotic reactions reveal characteristic differences associated with zone specific metabolism in the liver acinus. In this study, the zonal distribution of ethylnitrosourea (ENU)-induced hepatic precancerous lesion was stereologically investigated. Methods: Nine B6C3F1 mices were given I.p. injection of ENU (60 ug/pn body weight) when the pups were 15 days old prior to sacrifices at 8 weeks of life. All the 150 consecutive sections, 3 p m in thickness, were stained with hematoxylin and eosin and identified the basophilic precancerous lesions with 80-165 p m diameter in equatorial plane by the Zeiss microprojector. And then the distances from the center of selected foci to terminal hepatic vein or portal vein branches were estimated under the microscopic fields. As a control group, the same estimations were performed from the random points by the appointments of random digit table. Results: Mean distance between ENU-induced 52 hepatocellular foci and the nearest terminal hepytic vein was 181.15+112.39 p m (Mean+ SD), but that of randomly selected 104 points was 291.73+157.98pm (Mean+5D) (Students t-test, p<0.0005). Substantially, 52.7% of ENU-induced 52 hepatocellular foci were within 300 p m from the terminal hepatic vein, but randomly selected 104 points were only 50.9% (Shapiro Wilk W test, w=0.819857, p=0.048038). Mean distance from ENU-induced 52 foci to portal vein was 398.85+149.98pm (Mean+SD), but that from the randomly selected 104 points was 315.87+145.79 pm (Mean+SD)(Students t-test, p<0.0005). Conclusion: Stereologically, ENU-induced mice liver cell foci distribute non-randomly to Zone III, centrilobular zone of mouse hepatic acini where promote invasion toward terminal hepatic veins. (Korean J Hepatol 1997;6:227 240)

Background/Aims
In order to elucidate the possible mechanism of increase of y -glutamyl transpeptidase (y-GTP) activity in cholestatic liver and serum was studied. Method: Rats were divided into eight groups: Normal, sham operated control, bile duct obstruction (BDO) alone (BDO group), BDO plus taurocholic acid (TCA) injection (BDO plus TCA group), BDO plus tauroursodeoxycholic acid (TUDCA) injection (BDO plus TUDCA group), choledoco-caval shunt (CCS) operation (CCS groups), CCS plus TCA injection (CCS plus TCA group), and CCS plus TUDCA injection (CCS plus TUDCA group). Y -GTP activity was determined in the serum and liver cytosolic, mitochondrial and microsomal preparations isolated from above experimental rats. The values of Km and Vmax in this hepatic enzyme was measured. Result: the activities of liver cytosolic and microsomal y -GTP showed a significant increase in the CCS group. The activities of liver cytosolic, mitochondrial and microsomal y -GTP showed a significant increase in the BDO group. And the activity of serum y -GTP showed a marked increase in teth CCS and BDO poups. However, y-GTP activities in the serum and in liver microsomal prepatation rose more rapidly in the BDO group tban CCS. Y -GTP activity in liver cytosolic and microsomal preparatians, and its Vmax value incmmxl significantly in both CCS plus TCA group, and BDO plus TCA group than each control group, such as CCS and BDO group. On the other hand, the values of Km of the hepatic subcellular y -GTP did not change in the all experimental groups. Sennn y -GTP activity increased significantly in both CCS plus 7CA group, and BDO plus TCA group than each control group. However, these serum and hepatic enzyme activities did not change in both CCS plus TUDCA group and BDO plus TUDCA group. Conclusions: The above results suggest that 7CA stimulates biosynthesis of the y-GTP in the liver. And the elevations of the serum enzymes activity thought to be caused by increase of hepatocyte membrane permeability by a physical property (detergency) of TCA, which cause the enzyme to leak into the blood in large quantities. (Korean J Hepatol 1997;6:210 226)