Motohide Takashi

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.

Clinical Study of Eighty-six Cases of Idiopathic Portal Hypertension and Comparison With Cirrhosis With Splenomegaly

The clinical features of 86 cases of idiopathic portal hypertension, the equivalent of hepatoportal sclerosis in the United States and of noncirrhotic portal fibrosis in India, are presented. This disease is characterized by overt splenomegaly with pancytopenia, portal hypertension, and relatively mild abnormalities in liver function tests. Although differential diagnosis from liver cirrhosis is not always easy, liver histology, laparoscopy, portography, hepatic venography, and measurement of wedged hepatic vein pressure are useful in diagnosis. Prognosis is relatively benign if variceal bleeding is controlled or prevented, and the disease does not progress to cirrhosis. The etiology is still undetermined, but the liver pathology characterized by occlusive changes of the intrahepatic portal radicles, portal and periportal fibrosis, and irregularly distributed parenchymal atrophies suggests some sort of portal venopathy that causes decreased portal perfusion of peripheral liver parenchyma. These patients with idiopathic portal hypertension were compared with 63 cases of cirrhosis with splenomegaly and 80 cases of cirrhosis without splenomegaly. There was some similarity in hematologic findings between idiopathic portal hypertension and cirrhosis with splenomegaly, but the basic disease process seemed distinctly different. The cause of marked splenomegaly does not seem to be simply congestion, and remains an enigma.

Direction of splenic venous flow assessed by pulsed Doppler flowmetry in patients with a large splenorenal shunt

We studied the direction of blood flow in the splenic vein, using a combined ultrasonic system consisting of an electronic sector scanner and a pulsed Doppler flowmeter, in 21 patients with a large spontaneous splenorenal shunt demonstrated by angiography. Pulsed Doppler flowmetry revealed hepatofugal flow in the splenic vein in all 11 patients with chronic spontaneous hepatic encephalopathy, and hepatopetal flow in 10 patients without encephalopathy. In the former, hepatofugal flow of part of the superior mesenteric venous blood into the splenorenal shunt was corroborated by the venogram obtained after superior mesenteric arteriography. In 5 patients without a history of hepatic encephalopathy, superior mesenteric arteriography demonstrated hepatofugal flow of part of the superior mesenteric venous blood into the splenorenal shunt. Pulsed Doppler flowmetry, however, revealed hepatopetal flow in all of these patients, suggesting that the angiographic finding of hepatofugal flow may have represented an artifact.

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.

Transhepatic obliteration of esophageal varices using stainless coils combined with hypertonic glucose and gelfoam.

A total of 63 patients with variceal bleeding were included in this study. Fifty-six attempts at percutaneous transhepatic variceal obliteration were made using stainless steel coils followed by 50% glucose and Gelfoam in 27 emergency cases, in whom bleeding did not stop by conventional medical treatment; and in 18 elective cases, in whom bleeding did stop by conventional medical treatment. The remaining 18 patients, whose bleeding was controlled by conventional medical treatment, were used as a control for the elective cases (conservative cases). The overall success rate was 93%. In 92% of the 37 acute bleeders, bleeding ceased as soon as the varices were obliterated. In emergency cases, the cumulative variceal rebleeding rate at 1, 2, 3, 6, 9, and 12 months after obliteration was 16%, 29%, 34%, 44%, 56%, and 56%, respectively. Its mortality within 1 month after the first bleeding was only 11%. In elective cases, the rebleeding rate at 1, 2, and 12 months was significantly lower; and the survival rate at 1 and 2 months was significantly higher compared with conservative cases. Follow-up portography in 10 active rebleeders and two nonrebleeders demonstrated new vessel formation in six, and recanalization of previously completely occluded varices in two. Complications included transient hemiparesis and partial stenosis of intrahepatic portal branches, but none was fatal. When compared with a conventional treatment, transhepatic variceal obliteration using steel coils followed by 50% glucose and Gelfoam proved to be an effective, safe emergency treatment for variceal hemorrhage. However, since the rebleeding rate was high, this procedure should be followed by an elective operation or other procedures for a lasting prevention of bleeding.

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.

High sustained virologic response rate after interferon monotherapy in Japanese hepatitis C patients with a low HCV RNA titer and/or HCV genotype 2. A prospective study.

Objective: Hepatitis C virus (HCV) RNA titer and HCV genotype are considered to be major determinants of the outcome of interferon monotherapy. To clarify whether interferon monotherapy is really effective in patients with the appropriate viral parameters, we prospectively examined these parameters and treated the patients with interferon monotherapy. Methods: Sixty-four patients with an HCV RNA titer <100 kIU/ml and/or HCV genotype 2 were enrolled in the study. Eighteen patients with an HCV RNA titer >100 kIU/ml and genotype 1 were also enrolled as controls. All patients were treated with 10 megaunits of interferon-α2b every day for 2 weeks and then 3 times a week for 24 weeks. Results: Of the 64 patients with either HCV RNA <100 kIU/ml and/or genotype 2, seven dropped out from the study. Of the remaining 57 who completed the treatment, 48 (84%) showed a virologic sustained response. In contrast, only 4 of the 18 patients (22%) with HCV RNA >100 kIU/ml and genotype 1 were virologic sustained responders (p < 0.001). Conclusion: Our current study showed that the patients with HCV RNA <100 kIU/ml and/or HCV genotype 2 are good candidates for interferon monotherapy.

Paraesophageal Varices Mimicking a Mediastinal Tumor

This is the account of a patient with primary biliary cirrhosis, who had abnormal shadows in the mediastinum on the plain chest film, and in whom subsequent investigations including computed tomography and percutaneous trans-hepatic portography demonstrated them to be huge paraesophageal varices. Percutaneous transhepatic portography proved most diagnostic.

Direction of splenic venous flow assessed by pulsed doppler flowmetry in patients with a large splenorenal shunt. Relatin to spontaneous hepatic encephalopathy.

セクタ電子スキャンパルスドップラー複合装置を用いて,21例の巨大脾腎短絡路を有する患者の脾静脈の血流方向を調べた.肝性脳症を反復し,上腸間膜動脈造影の静脈相で上腸間膜静脈血の一部が脾腎短絡路に流入することを確認した反復性肝性脳症例全例(n=11)で,脾静脈血が脾腎短絡路へ流入する遠肝性血行を明らかにし得た.また上腸間膜動脈造影で遠肝性血行を示した5例と経皮経肝的上腸間膜静脈造影にて求肝性血行を示した5例の非脳症例全例(n=10)では脾静脈血が門脈へ流入する求肝性血行を明らかにした.以上より脾腎短絡路を有する患者でセクタ電子スキャンパルスドップラー複合装置を用いて,脾静脈の血流方向を測定することは,これら反復性肝性脳症群,非脳症群に分ける上で上腸間膜動脈造影に較べ非侵襲的でより正確であり,また脾静脈血流の逆流を示すものが近い将来脳症を発現するか否かを予測するのに有用と思われる.