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To study the effects of habitual alcohol intake and cigarette smoking on the latency period for the development of hepatocellular carcinoma (HCC), 455 patients with HCC were analyzed with respect to age at diagnosis. They were divided into hepatitis B virus (HBV) positive and negative patients based on HbsAg and high titer anti-HBc in serum. HBV-positive and negative HCC patients were further subdivided into four subgroups based on the history of drinking more than one small bottle of Japanese 'sake' or its equivalent per day for more than 10 yr and the history of smoking more than one cigarette per day for more than 10 yr. Among HBV-positive HCC patients, the average age of those with a drinking and a smoking habit (50 ± 10 yr) was younger compared with that of patients with a drinking habit but without a smoking habit (56 ± 14 yr, not significant, NS), of those who were smokers and nondrinkers (55 ± 10 yr, NS) and of those who did not drink nor smoke (59 ± 8 yr, p < 0.005). Among HBV-negative HCC patients, patients with drinking and smoking habits (57 ± 9 yr) were younger compared with those with a drinking habit without smoking (59 ± 9 yr, NS), those who were smokers and nondrinkers (62 ± 9 yr, p < 0.005), and those who were nondrinkers and nonsmokers (63 ± 12 yr, p < 0.005). These data suggest that habitual alcohol intake may promote the development of HCC if the patients smoke cigarette regardless of the status of HBV seromakers. [ABSTRACT FROM AUTHOR]

Changes that occurred in splanchnic circulation with the progression of chronic liver disease were investigated using an ultrasonic Doppler flowmeter in healthy adults and in patients with chronic active hepatitis and liver cirrhosis in the supine position after an overnight fast. Superior mesenteric venous flow, splenic venous flow, and portal venous flow were significantly increased in patients with liver cirrhosis but not in patients with chronic active hepatitis compared with normal subjects. Portal venous flow (control value 10.5 ± 2.3 ml/min/kg body weight) minus the sum of superior mesenteric venous flow and splenic venous flow was 0.8 ± 2.1 ml/ min/kg body weight in the control, (O.1 ± 1.9) in chronic active hepatitis, and (-2.2 ± 4.3) in liver cirrhosis; the difference was significant between the control and cirrhosis groups. These results indicate that in patients with liver cirrhosis a hyperdynamic state occurs in the splanchnic circulation of the intestine and spleen and that some portion of splanchnic blood flow bypasses the liver into the systemic circulation. [ABSTRACT FROM AUTHOR]

The acute effects of histamine H2 receptor antagonist, famotidine, on hepatic hemodynamics were studied in six normal volunteers and eight patients with chronic liver disease, and its chronic effects on peptic ulcer, portal hemodynamics, and hepatic function were studied in 20 patients with chronic liver disease and peptic ulcer (16 with gastric ulcer, four with duodenal nicer). Infusion of 20 nag famotidine did not reduce hepatic blood flow and portal blood flow in normal subjects, nor did it reduce cardiac output, the gradient between wedged hepatic vein pressure and free hepatic vein pressure, hepatic blood flow, and portal blood flow in patients with chronic liver disease. An oral dose of 20 mg famotidine twice daily for 2 months healed peptic ulcer in 19 of 20 patients (95%) with chronic liver disease and peptic ulcer, without any change in portal blood flow and hepatic function. Thus famotidine does not appear to alter hepatic hemodynamics and hepatic function in normal subjects and patients with chronic liver disease. [ABSTRACT FROM AUTHOR]

In view of the variability in the magnitude of the response of portal venous pressure to vasopressin in man, we investigated the effect of vasopressin on portal hemodynamics in seven patients with portal hypertension by simultaneous catheterization of the portal and the hepatic vein and the measurement of portal venous flow hy an echo-Doppler flowmetry. Infusion of vasopressin (0.3 U/min) significantly decreased portal venous pressure (-36%), the gradient bemeen portal venous pressure and free hepatic venous pressure (-50.6%), and portal venous flow (-54.3%) but did not reduce mean arterial pressure and pulse rate. Thus, vasopressin seems to decrease portal venous pressure by reducing portal venous flow. [ABSTRACT FROM AUTHOR]

Portal hemodynamics were studied in 69 patients with cirrhosis and 29 patients with idiopathic portal hypertension to investigate the effects of an operative procedure for varices that consists of transabdominal esophageal mucosal transection, paraesophagogastric devascularization, pyloroplasty, and splenectomy. Portal venous flow measured by the pulsed Doppler flowmeter in 14 patients with cirrhosis and nine patients with idiopathic portal hypertension, who underwent operation 2-5 yr earlier, was significantly reduced compared with that in unoperated 49 patients with cirrhosis and 17 patients with idiopathic portal hypertension who had esophageal varices (410 ± 158 versus 660 ± 263 ml/ min in cirrhosis; 443 ± 185 versus 912 ± 189 ml/min in idiopathic potal hypertension). In nine patients (six cirrhosis, three idiopathic portal hypertension), portal venous flow and portal vein pressure were measured before and after operation. In patients with cirrhosis, portal vein pressure did not change significantly postoperatively even though portal venous flow was reduced. In contrast, portal vein pressure decreased in two patients with idiopathic portal hypertension in whom portal venous flow was reduced. Portal vein pressure was elevated in one patient with idiopathic portal hypertension in whom portal venous flow was increased postoperatively as a result of resection of a large gastro- and splenorenal shunt conducted additionally. [ABSTRACT FROM AUTHOR]

On the premise that extensive intrahepatic portal-venous anastomoses known to occur in cirrhosis would be demonstrated by contrast medium directly placed in the portal vein, percutaneous transhepatic portograms were analyzed in 82 patients with liver cirrhosis in relation to the estimated degree of shunting. The degree of intrahepatic shunt was measured during transhepatic portography using 99mTc-macroaggregated albumin. Hepatic veins began to opacify at 4 to 10 s after the start of injection of contrast medium during portography in 20 patients with cirrhosis who had intrahepatic shunt indices of 58.5 ± 18.5%, but it was not visualized in 62 patients with cirrhosis whose shunt indices were 19.9 ± 14.1%. Anomalous large anastomoses of 1 or 2 mm in size between the right portal vein and the right hepatic vein were clearly visualized during portography in 18 of 20 patients in whom the hepatic vein was opacified. Frequency and time of beginning opacification of the hepatic vein were closely correlated with the degree of intrahepatic shunt. Thus, opacification of the hepatic vein and abnormal anastomoses between the portal and hepatic vein systems in an early phase of portography indicates extensive intrahepatic shunts. [ABSTRACT FROM AUTHOR]

Clinical and portal hemodynamic features in 28 cirrhotic subjects with a large spontaneous spleno- and/or gastrorenal shunt were studied in comparison with 30 control cirrhotic cases without such collaterals. Forty-six percent of the former had chronic hepatic encephalopathy, but none of the latter was encephalopathic. These patients with large renal shunts were divided into those with and those without encephalopathy. Large esophageal varices were significantly less common in patients with a large shunt and encephalopathy compared with those who had a large shunt but no encephalopathy, and the control. But there was no significant difference of past variceal bleeding among these three groups. In all those with encephalopathy, part of superior mesenteric venous blood was shunting through these collaterals into the left renal vein or inferior vena cava, but the same was not demonstrable in patients with a large shunt and no encephalopathy and control cirrhotics. In the chronic encephalopathic, portal venous flow was estimated to he less than one-half of that in control cirrhotics, and the portion of superior mesenteric venous blood that was flowing hepatofugally through a large shunt into the left renal vein seemed about the same or greater than the portal venous flow. Thus, a large spontaneous spleno- and/or gastrorenal shunt might prevent development of large esophageal varices but not variceal hemorrhage and it increased a risk of chronic hepatic encephalopathy. [ABSTRACT FROM AUTHOR]

The recently developed Doppler flowmetry system that consists of an electronic sector and a pulsed Doppler flowmeter, is capable of determining the direction of blood flow in large veins visible by ultrasonography and measuring blood flow. It is noninvasive and can be performed in patients on ambulatory basis at the time of routine ultrasound examination. In this communication, clinical utility of pulsed Doppler flowmetry was tested in 20 patients with portal hypertension. Doppler flowmetry proved useful in differential diagnosis of splenorenal shunt and cystic disease, diagnosis of arterioportal shunt, diagnosis of portal vein occlusion, demonstration of hepatofugal flow in the splenic vein, and prediction of esophageal varices by the demonstration of hepatofugal flow in an enlarged left gastric vein. [ABSTRACT FROM AUTHOR]

The interrelationship between the type and degree of spontaneous portal systemic shunting, and portal vein pressure was studied in 155 patients with liver disease by catheterizing the portal vein. The degree of portal vein shunting was measured in 100 patients and that of splenic vein shunting in 50 and that of total portal systemic shunting in 52, using macroaggregated radioalbumin. Increasing portal vein pressures were associated with progressively higher indices of portal vein shunt, splenic vein shunt, and total portal systemic shunt up to a certain level. Beyond this level, portal vein pressure did not increase further, and rather it decreased with further increasing degrees of splenic vein shunt and total portal systemic shunt. These results indicate that spontaneous portal systemic shunt keeps the portal vein pressure within certain limits or decreases it. [ABSTRACT FROM AUTHOR]

Effects of two histamine H2 receptor antagonists, cimetidine and ranitidine, on systemic and splanchnic hemodynamics were studied in patients with chronic liver disease by simultaneous catheterization of the portal vein and the right hepatic vein and measurement of portal venous flow using the ultrasound doppler system or cineangiography. Neither infusion of 200 mg of cimetidine nor 50 mg of ranitidine reduced cardiac output, portal venous pressure, the gradient between wedged hepatic venous pressure and free hepatic venous pressure, hepatic blood flow, and portal venous flow. It is unlikely that histamine is an important modulator of flow via the H2 receptor. [ABSTRACT FROM AUTHOR]

To elucidate the mechanism by which propranolol reportedly affects portal hemodynamics, we investigated the effect of propranolol on systemic and splanchnic hemodynamics in 15 patients with portal hypertension and esophageal varices by simultaneous catheterization of the portal vein and the right hepatic vein and measurement of portal venous flow using an ultrasound doppler system. Infusion of 5 mg of propranolol significantly decreased pulse rate (-12.6%), cardiac output (-24.5%), portal venous flow (-22.3%), portal venous pressure (-13.3%), and gradient between portal venous pressure and free hepatic venous pressure (-24.8%). Thus, propranolol seems to decrease portal venous pressure by reducing portal venous flow, at least in part, as a result of reduction of cardiac output due to its β1 adrenergic receptor blocking action. [ABSTRACT FROM AUTHOR]

Extensive intrahepatic portal-hepatic venous anastomosis is very rare. This report describes a 47-year-old man with cirrhosis who presented with mental confusion and flapping tremor, and in whom percutaneous trans-hepatic portography and superior mesenteric angiography demonstrated shunting between the portal vein branches and the right hepatic vein. Measurements of pressure, ammonia, and immunoreactive insulin in blood of the portal and right hepatic veins clearly indicated that a large amount of portal vein blood was being shunted into the right hepatic vein. These findings suggest that hepatic encephalopathy in this patient is accounted for at least in part by an intrahepatic portal-hepatic venous shunting. [ABSTRACT FROM AUTHOR]

Spontaneous disappearance of limy bile is extremely rare, and only four cases have so far been reported. This is the account of the fifth case, a 42-year-old woman, who spontaneously lost a stone incarcerated in the neck of the gallbladder and all of the limy bile, after symptoms suggestive of a transient obstructive jaundice. Various investigations including ultrasound, computed tomography, and percutaneous transhepatic cholangiography suggested spontaneous passage of the stone through the cystic duct and the papilla of Vater, followed by limy bile. Apparently the patient's gallbladder had a contracting capacity. The literature on this subject is briefly reviewed. [ABSTRACT FROM AUTHOR]

Looks at an endoscopic observations of gastric varices. Occurrence of gastric varices in portal hypertension; Description of gastric varices; Information on the treatment of gastric varices.