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Hepatic vein (HV) stenosis after liver transplantation is a rare but life-threatening complication that leads to graft loss. The incidence of HV stenosis after living-donor liver transplantation (LDLT) and split liver transplantation is not so rare, and is reported to range from 2 to 8.6%. Recently, the minimal invasiveness of radiologic interventions and the innovative techniques have led to their widespread adoption for the treatment of various complications after liver transplantation. We report a five-year-old boy with HV stenosis post-LDLT with only scarcity of clinical information including edema with hypoalbuminemia and elevated hyaluronic acid value. Doppler ultrasonography was effective to suggest stenosis, and angiography confirmed its diagnosis. The stenosis was successfully treated with balloon dilatation using interventional radiologic technique through the jugular vein. In conclusion, we suggest that if liver transplanted patients manifest ascites or/and edema with hypoalbuminemia and elevated hyaluronic acid in sera, HV stenosis should be suspected even if the other laboratory values are normal.

Chronic ethanol consumption elicits detrimental changes of liver metabolism. By employing a 12-week-long feeding regimen, we investigated the effects of chronic ethanol consumption on the expression and localization of bile salt export pump (Bsep), a major canalicular exporter of bile salts, and multidrug resistance protein 2 (Mrp2), a canalicular organic anion transporter, in the rat liver. RT-PCR, confocal immunofluorescence microscopy, immunoblotting, and quantitative colocalization analysis were used to examine their gene and protein expression, and changes in the distribution of antigenic sites. Bsep mRNA was upregulated, while Mrp2 mRNA responded by downregulation. In agreement with mRNA, the expression of Bsep protein increased, while the expression of Mrp2 protein responded with a decrease, suggesting that the expression of both of them is transcriptionally regulated. Confocal immunofluorescence microscopy showed disruption of the colocalization of Bsep and Mrp2 proteins at the hepatocyte canalicular membrane and their relocation intracellularly. Quantitative colocalization analysis of Bsep and Mrp2 proteins revealed a steady decrease in the degree of colocalization and Mrp2 expression, indicating that although the properties of both transporters are affected, Mrp2 is altered more. These findings provide evidence that ethanol alters Bsep and Mrp2 canalicular transporters in the rat liver, at both the mRNA and protein levels. Mrp2 shows deeper involvement. Eight weeks appears to be a critical time point in this process.

Background/aims: The aim of this study is to prove the hemodynamic change in distribution of splenic venous flow in the liver, especially in the cirrhotic liver, and to reveal and evaluate a participation of splenic venous flow in regeneration or enlargement of the hepatic lobe., Methodology: We studied the distribution of splenic venous flow in the liver of patients with normal liver (NL group, n=15), chronic hepatitis (CH group, n=8), and liver cirrhosis (LC group, n=13) with the technique of scintiphotosplenoportography after percutaneous intrasplenic injection of Technetium-99m-diethylenetriaminepentaacetic acid-galactosyl-human serum albumin. The index of splenic venous flow volume per unit hepatocytes (Vunit) was calculated in each hepatic lobe. To compare V value of the left lobe (VLunit) with that of the right lobe (VRunit), predominant index of the left lobe (L/R index) was defined as L/R index = VLunit/VRunit., Results: The median (interquartile range) of L/R index of the LC group; 1.22 (1.06-1.70) was significantly higher than that of the NL group; 0.83 (0.66-0.92), p<0.001 and the CH group; 0.79 (0.69-0.92), p<0.001., Conclusions: L/R index reflects the change of portal hemodynamics in cirrhotic liver and is useful for discrimination between noncirrhosis and cirrhosis. These results suggest that in the liver exposed to continuous damages, splenic venous blood promotes liver fibrosis in the right lobe and eventually flows more into the left lobe with milder fibrosis.

We describe an unusual case of extreme hepatic left lobar atrophy with hilar cholangiocarcinoma. A 67-year-old woman was referred to Nippon Medical School with obstructive jaundice. On admission, computed tomography revealed dilated intrahepatic bile ducts and a defect in the area drained by the left side of the middle hepatic vein. A Spiegel lobe was demonstrated, but the left lobe could not be detected to the left side of the gallbladder. Percutaneous transhepatic cholangiography was performed and demonstrated obstruction of the intrahepatic bile duct at the hepatic hilum. A drainage catheter was left in place. Angiography revealed that the left hepatic artery was present, but there was narrowing of the left portal vein. A diagnosis of agenesis of the left hepatic lobe with hilar cholangiocarcinoma was made. At surgery, the left lobe appeared extremely atrophic without atrophy of the Spiegel lobe. The right anterior branches of the hepatic artery and portal vein had been invaded by carcinoma, so a left trisegmentectomy was performed. Final pathology was advanced hilar cholangiocarcinoma with invasion of the hepatic parenchyma, portal vein, and nervous system. The left lobe was atrophic without hepatolithiasis. The left portal vein was narrow distal to the Spiegel branch. The serum total bilirubin concentration was elevated postoperatively, and the patient was treated for hepatic failure. The patient died of pneumonia without recurrence 7 months after surgery. This rare case of extreme hepatic left lobar atrophy with hilar cholangiocarcinoma was successfully treated by left trisegmentectomy. Preoperative portal embolization was unnecessary because the left lobe was already atrophic.

In the liver, function of the bile salt export pump (Bsep), a major canalicular exporter of bile salts, is complemented by activity of the multidrug resistance protein 2 (Mrp2), a canalicular organic anions transporter. Mrp2 was found capable of transporting various anticancer drugs out of cells, eventually undermining their therapeutic potential and contributing to multidrug resistance. We employed a RT-PCR, immunoblotting, and immunofluorescence to examine their gene, protein expression, and distribution of antigenic sites in the rat liver during development from 16-day-old fetus to adult animal. Bsep mRNA was almost undetectable before birth. It was first clearly expressed in the liver of newborn rats. On the contrary, Mrp2 mRNA was seen before birth, although at low levels. In concert with mRNA expression, Bsep protein was undetectable before birth, while Mrp2 protein was already expressed. Both proteins were clearly detectable in the postnatal period. Confocal immunofluorescent microscopy showed asynchronous appearance of Bsep and Mrp2 proteins during development but their colocalization in the bile canaliculi once each one is expressed. During the gestational period, a weak immunofluorescence for Mrp2 was observed only in livers of 16-day-old embryos. No fluorescence for Bsep was seen. Both proteins were clearly visualizable after birth, although the pattern of immunostaining varied. These findings provide molecular evidence that expression of both Bsep and Mrp2 during development is transcriptionally regulated. They also point out the differences in relevance to the liver function of the systems responsible for canalicular transport of bile salts versus organic anions.

Liver transplant aspiration cytology(TAC) contributes significantly to the differential diagnosis of transplanted liver graft dysfunction, since each of the possible causes induces characteristic cytological findings in the graft and peripheral blood. That is, TAC can differentiate various inflammatory changes as indicating acute rejection, viral infection, or bacterial infection. The key is the intensity of activated lymphocytes in the graft and in blood. Remarkable lymphocytic activation only in the liver graft indicates acute rejection, meanwhile in a case of viral infection the activation can be seen both in liver graft and blood. The patterns and degree of liver cell injury and cholestasis can also identify the reason for liver impairment. Several cases of acute rejection, viral infection, and subclinical acute rejection diagnosed by TAC were recognized on TAC slide preparations. Subclinical rejection, which means acute rejection appreciated only cytologically or histologically, can be followed without treatment unless the patient demonstrates jaundice and liver enzymes over 100 units. In a case of chronic rejection, TAC is not an appropriate method of diagnosis, because there are few infiltrating cells in the portal triad, and subsequently, no visible activated lymphocytes on TAC slides. Although TAC is not well accepted, it is an informative means preliminary to core biopsy, and its use is expected to become wide-spread in the future because it is a safe procedure with minimal invasiveness to patients, and useful for differential diagnosis. The use of TAC will lessen the frequency of performing more invasive core biopsy.