Nobuaki Goto

Incidence of portal vein thrombosis in liver cirrhosis

Portal vein thrombosis was thought to be a common complication of liver cirrhosis in the past. The incidence of angiographically demonstrable portal vein thrombosis was studied in 708 consecutive patients with unequivocal cirrhosis seen in the past 10 yr in whom either transhepatic portography or superior mesenteric arterial portography clearly delineated the major portal vein system. Excluding 2 cases that were thought to be associated with past splenectomy, there were 4 cases of portal vein thrombosis related to cirrhosis, all in a decompensated stage. The calculated incidence of portal vein thrombosis was 0.573% of all cirrhotic patients without splenectomy in the past. They constituted 23.5% of the 17 cases of extrahepatic portal vein obstruction encountered during the same period. There were 78 cases of idiopathic portal hypertension similarly studied angiographically, and the incidence of portal vein thrombosis unrelated to splenectomy was 2.86%. A statistical survey based on 247,728 necropsies recorded in the Japan Autopsy Registries of 1975-1982 showed a 0.05489% incidence of portal vein thrombosis and a 6.58857% incidence of cirrhosis of all types among them, suggesting that portal vein thrombosis is not a common complication of cirrhosis in Japan in recent years.

Formation of Hilar Collaterals or Cavernous Transformation After Portal Vein Obstruction by Hepatocellular Carcinoma: Observations in Ten Patients

A total of 155 patients with hepatocellular carcinoma were studied by celiac and superior mesenteric angiography. Complete (9 patients) or near complete (1 patient) obstruction of the portal vein and formation of hepatopetal collateral veins in the porta hepatis, or the so-called cavernous transformation of the portal vein, were seen in 10 patients. In 4 patients, the first angiogram did not show cavernous transformation, but on the follow-up angiograms cavernous transformation was present. The suggested interval between obstruction of the portal vein and formation of cavernous transformation was no more than 5 wk. The mechanism of cavernous transformation and its clinical implications are briefly discussed.

Case Report: Congenital absence of the portal vein associated with nodular hyperplasia in the liver

Congenital absence of the terminal portion of the portal vein with visceral venous return to the suprahepatic inferior vena cava, a rare malformation, was demonstrated in an 18‐year‐old Japanese woman. She had nodular hyperplasia in the liver and a non‐functioning pancreatic endocrine tumour. It is generally believed that reduction of portal venous flow causes atrophic changes and, subsequently, nodular hyperplasia occurs in a well‐perfused area in the liver. However, the liver was not perfused by the portal vein in this case. It is suggested that nodular hyperplasia can occur without portal blood flow.

Portal hemodynamics in chronic portal-systemic encephalopathy: Angiographic study in seven cases

A portal hemodynamic study was made in 7 consecutive patients with chronic portal-systemic encephalopathy by percutaneous transhepatic catheterization of the portal vein and injecting contrast medium into the superior mesenteric vein or by superior mesenteric arterial portography in comparison with patients without encephalopathy studied by percutaneous catheterization of these veins. All 7 patients had a large gastro-renal or spleno-renal shunt, and a large proportion of superior mesenteric venous blood was being shunted as estimated from the diameter of the portal and the collateral vein, whereas in nonencephalopathic patients in whom part of the superior mesenteric venous blood was shunting this diversion was much less (P less than 0.001). Only one of the chronic portal-systemic encephalopathic patients had esophageal varices, insignificant in size, and the incidence of esophageal varices was significantly less compared to the 12 nonencephalopathic control patients with portal hypertension who had either a gastro-renal or spleno-renal shunt (P less than 0.05). It is suggested that chronic portal-systemic encephalopathy is a result of a large collateral route shunting a large proportion of the superior mesenteric venous blood into systemic circulation, and that development of such collaterals precludes formation of large esophageal varices.

Effect of Previous Interferon-based Therapy on Recurrence after Curative Treatment of Hepatitis C Virus-related Hepatocellular Carcinoma

Previous reports have shown that interferon (IFN)-based therapy decreases the risk of development of hepatocellular carcinoma (HCC) in patients with chronic hepatitis C virus (HCV) infection. However, it remains to be fully elucidated whether elimination of HCV by IFN-based therapy inhibits HCC recurrence after curative treatment, such as surgical resection and local ablation therapies. In this study, we aimed to clarify the influence of a sustained virological response (SVR) after IFN-based therapy on recurrence and survival after curative treatment of HCC. Fifty-one patients who underwent curative treatment of HCV-related HCC after receiving IFN-based therapy were analyzed retrospectively. They were classified into SVR (N = 14) and non-SVR groups (N = 37). In the SVR group, serum levels of aspartate aminotransferase and alanine aminotransferase, the indocyanine green retention rate at 15 min, and the percentages of patients with liver cirrhosis and HCV serotype 1 were significantly lower, whereas serum albumin level and platelet count were significantly higher upon HCC occurrence. Recurrence-free survival (RFS) for the first recurrence was significantly higher in the SVR group (P < 0.01). Multivariate analysis showed that SVR at initial HCC treatment (P < 0.01) and multiple tumors (P < 0.01) are prognostic factors for RFS. Moreover, RFS for the second recurrence showed a similar trend to that for the first recurrence. In conclusion, patients who underwent IFN-based therapy before initial curative treatment of HCC had a favorable clinical outcome compared with non-SVR patients.

Effects of intra- and extrahepatic portal systemic shunts on insulin metabolism

To study the effects of intra- and extrahepatic portal-systemic shunts on insulin degradation, 11 patients with liver cirrhosis and 7 noncirrhotic patients with liver disease were studied with percutaneous transhepatic catheterization. Insulin levels in portal and peripheral blood were measured simultaneously for 1–2 hr after intravenous administration of glucose. The degrees of intra- and extrahepatic portal-systemic shunting were measured with this technique using131I-macroaggregated albumin and99mTc-macroaggregated albumin. The amount of insulin secreted and insulin degraded were assessed from the areas under blood concentration curves for portal and peripheral blood. Insulin degradation was significantly reduced in cirrhotics compared to noncirrhotics with liver disease, although there was no difference in the amount of insulin secreted between these two groups. It was also correlated significantly with the degree of intrahepatic shunting but not with the degree of extrahepatic shunting. These results suggest that intrahepatic shunting plays an important role in the reduction of insulin degradation in cirrhosis.

Chronic Portal-Systemic Encephalopathy with Normal Portal Vein Pressure Possibly due to Noncirrhotic Portal Fibrosis

SummaryThis is the report of a 50-year-old man with a more than 20-year history of chronic progressive portal-systemic encephalopathy. Liver tests were normal except for increased serum ammonia and indocyanine green plasma retention. The liver pathology was compatible with idiopathic portal hypertension or noncirrhotic portal fibrosis, demonstrating localized surface nodularity and portal fibrosis. Percutaneous transhepatic catheterization of the portal vein revealed near top normal portal vein pressure and a large shunt connecting the left gastric or superior mesenteric vein and the left renal vein. Presumably, the patient had portal hypertension in the past and formation of a short, largecaliber shunt between the portal system and the renal vein effectively decompressed the portal circulation.

Efficacy of lamivudine or entecavir against virological rebound after achieving HBV DNA negativity in chronic hepatitis B patients.

Nucleos(t)ide analogues (NAs) lead to viral suppression and undetectable hepatitis B virus (HBV) DNA in some individuals infected with HBV, but the rate of virological rebound has been unknown in such patients. We examined the prevalence of virological rebound of HBV DNA among NA-treated patients with undetectable HBV DNA. We retrospectively analyzed 303 consecutive patients [158 entecavir (ETV)- and 145 lamivudine (LAM)-treated] who achieved HBV DNA negativity, defined as HBV DNA < 3.7 log IU/mL for at least 3 months. They were followed up and their features, including their rates of viral breakthrough, were determined. Viral rebound after HBV DNA negativity was not observed in the ETV-group. Viral rebound after HBV DNA negativity occurred in 38.7% of 62 HBe antigen-positive patients in the LAM-group. On multivariate analysis, age was an independent factor for viral breakthrough among these patients (P = 0.035). Viral rebound after HBV DNA negativity occurred in 29.1% of 79 HBe antigen-negative patients in the LAM-group. Differently from LAM, ETV could inhibit HBV replication once HBV DNA negativity was achieved. In contrast, LAM could not inhibit HBV replication even if HBV negativity was achieved in the early phase. Attention should be paid to these features in clinical practice.

Primary hepatic choriocarcinoma in an 83‐year‐old woman

We present a case of primary hepatic choriocarcinoma in an 83‐year‐old Japanese woman with gastric wall and lymph node metastases and a splenic vein tumor thrombus. Multiple irregular hepatic tumors with massive necrosis and hemorrhage were observed during autopsy. Syncytiotrophoblast‐like and mononucleated cytotrophoblast‐like cell morphology with focal hepatocellular carcinoma (HCC)‐like trabecular structures was observed. In immunohistochemical analyses, the tumor cells expressed human chorionic gonadotropin (hCG) and cytokeratins (AE1/AE3, CK7, CK19) but were negative for alpha‐fetoprotein (AFP), glypican‐3, and vimentin. Immunohistochemical findings did not reveal evidence of HCC or angiosarcoma. We concluded the liver tumor was primary hepatic choriocarcinoma.

Familial occurrence of idiopathic portal hypertension: Observations in two sisters

Abstract Idiopathic (non‐cirrhotic) portal hypertension is one of the major problems in developing countries, but the aetiology is not known. Two sisters with idiopathic portal hypertension diagnosed by percutaneous transhepatic catheterization of the portal vein and liver biopsy are reported. Both patients had large spontaneous portal‐systemic shunts. This seems to be the first report of a familial aggregation of this disorder.