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Biomedical subjects

H Musha

Publications and source records attributed to H Musha.

At least 37 records · Page 2Linked to original sources

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.

Ammonia↗

Esophageal varices: correlation of left gastric venography and endoscopy in patients with portal hypertension.

Selective left gastric venography was performed via percutaneous transheptic catheterization in 100 patients with portal hypertension to study hemodynamics and left gastric collaterals. Flow was hepatofugal in 81 patients, while 63 had varices supplied by the left gastric vein; azygos/hemiazygos collaterals were seen in 27 patients, gastrorenal shunts in 18, and other collaterals in 58. In 79 cases, enlarged, tortuous veins arising from thin parallel vessels at the esophagogastric junction on venography corresponded with varices on endoscopy in both size and course. Venography failed to show small varices which were seen endoscopically, whereas endoscopy often interpreted non-tortuous veins as varices. Using endoscopy as a reference, the sensitivity of venography for varices was 76%, specificity 100%, and accuracy 78%. There was a significant correlation between venographic demonstration of varices and previous hematemesis. Left gastric venography is necessary prior to embolization of varices and is also useful in their diagnosis as well as study of hemodynamics and assessment of bleeding risk.

Esophageal and Gastric Varices↗

Sonographic detection of large spontaneous spleno-renal shunts and its clinical significance.

The ultrasonographic findings of large spleno-renal shunts seen in five patients with liver cirrhosis and confirmed by CT and/or portography, are described. These spleno-renal shunts were seen in the left inter- or subcostal sections as transonic, mass-like lesions located between the splenic hilum and the left kidney, and by continuous scanning, they were found to be part of a tortuous, large tubular structure. Oesophageal varices were absent or minimal in these patients, and none of them had ever bled.

Aged↗

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.

Adolescent↗

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 using 131I-macroaggregated albumin and 99mTc-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.

Glucose Tolerance Test↗

False-positive liver scans due to portal hypertension: correlation with percutaneous transhepatic portograms in 33 patients.

Tc-99m-phytate scanning of the liver and percutaneous transhepatic catheterization of the portal vein were performed in 33 patients--26 with cirrhosis, 3 with chronic active hepatitis, 2 with idiopathic portal hypertension, and 2 with unresolved acute hepatitis. A discrete defect in the porta hepatis area was seen in 6 of 28 patients who had portal vein pressure above 200 mm H2O. In 5 of the 6 patients with a false-positive scan, the umbilical portion of the left portal vein branch was dilated (larger than 25 x 20 mm) on the portogram, with or without a patent paraumbilical vein. The anatomical basis of this phenomenon is discussed, and it is suggested that this area be given special attention.

Adult↗

The effect of chronic habitual alcohol intake on the development of liver cirrhosis and hepatocellular carcinoma: relation to hepatitis B surface antigen carriage.

To study the effects of habitual alcohol intake on the latency period for the development of liver cirrhosis and hepatocellular carcinoma (HCC), 158 patients with cirrhosis and 79 with HCC were analyzed with respect to age at the time of diagnosis. They were classified into four groups based on hepatitis B surface antigen (HBsAg) in serum, and the history of intake of more than one small bottle of Japanese "sake" or an equivalent per day for more than 10 years. The average age of HBsAg positive male cirrhotics with a drinking habit (n = 10) was 38.8 years, 10.5 years younger than that of those without a drinking habit (n = 8) (P less than 0.05). The average age of HBsAg negative cirrhotics with a drinking habit (n = 97) was 47.9 years, eight years younger than that of those not drinking (n = 36) (P less than 0.001). There was no significant difference in the laboratory data between these groups. The average age of the HBsAg positive HCC patients with a drinking habit (n = 20) was 48.9 years, nine years younger than that of those without a drinking habit (n = 12) (P less than 0.05). The average age of HBsAg negative male HCC cases with habitual intake of more than 126 ml of ethanol per day was 51.0 years (n = 8), ten years younger than that of nondrinking male HCC cases (n = 11) (P less than 0.05). These data suggest that habitual alcohol intake may promote the development of liver cirrhosis and HCC, especially in HBsAg carriers.

Adult↗

Spontaneous reversal of portal blood flow demonstrated by percutaneous transhepatic catheterization: report of two cases.

Two patients are described in whom percutaneous transhepatic catheterization of the portal vein for a hemodynamic study demonstrated a continuous reversed blood flow in the portal vein, entering into a large collateral. The measurements made of blood pressure in the superior mesenteric, splenic, and left gastric veins, and of ammonia, immunoreactive insulin, and C-peptide in blood taken from these and peripheral veins all indicated reversed portal vein blood flow. The evidence for retrograde portal vein blood flow was obtained in only 2 of 203 patients with cirrhosis in whom portal hemodynamics were studied by the same procedure. Thus, spontaneous reversal of portal vein blood flow does occur, but very rarely.

Blood Pressure↗

Anatomical basis of hepatic venographic alterations in idiopathic portal hypertension.

Hepatic venograms made in 40 authentic cases of idiopathic portal hypertension (Banti's syndrome) were compared with 13 normal venograms and venograms obtained in 88 cases of cirrhosis, and analyzed in the light of the pathological changes seen in 16 postmortem liver specimens. There were frequent anastomoses between hepatic vein radicles, approximation of middle-size branches to the liver surface, reduction in the angles between the main hepatic vein and its tributaries, and difficulty in opacifying portal vein branches in wedged retrograde portography. These angiographic alterations were corroborated by gross pathological findings which comprised displacement of middle-size hepatic vein branches closer to the liver surface and their approximation among themselves, and seem to be accounted for by the disappearance of liver parenchyma secondary to the peripheral portal circulatory failure.

Hepatic Veins↗

Hepatic venography in noncirrhotic idiopathic portal hypertension. Comparison with cirrhosis of the liver.

Free and wedged hepatic venography were carried out in 37 patients with idiopathic portal hypertension (IPH) and the findings compared with those in 88 patients with cirrhosis of the liver. Characteristic changes in IPH included frequent vein-to-vein anastomoses, narrower angles between large veins and their tributaries, smooth and wavy middle-sized to large branches (giving a general "weeping willow" appearance), homogeneous sinusoidal filling, and minimal to absent filling of the portal venous system on wedged retrograde portography. In cirrhosis, by contrast, changes included rare vein-to-vein anastomoses, wide angles between veins and tributaries, irregular stenoses of large veins and branches at various levels, spotty sinusoidal filling, and frequent retrograde flow in the portal venous system. Hepatic venography is helpful in differentiating IPH from cirrhosis.

Adult↗

A dynamic study of rectally absorbed ammonia in liver cirrhosis using [13N]ammonia and a positron camera.

[13N]Ammonia produced by the cyclotron was instilled intrarectally in patients with cirrhosis and other liver diseases to study the turnover of rectally absorbed [13N]ammonia. A positron camera connected to an on-line computer system was used for the measurement of sequential changes of 13N activity in blood and for coincidence positron imaging of the liver and heart. 13N activity over the head was also recorded. Chromatographic analysis of 13N-labeled substances in blood was carried out using a Dowex 50Wx8 column at varying times after the administration. In the control, [13N]ammonia was absorbed quickly and visualized the liver, whereas in patients with cirrhosis, the lungs and heart were first visualized, and 13N activity over the head was also higher. It was suggested that a large proportion of absorbed [13N]ammonia bypassed hepatocytes and reached peripheral tissues in cirrhosis. The heart/liver ratio of 13N and 13N over the head were correlated with various indices of portal hypertension. The relative proportion of nonammonia 13N metabolites in blood was lower at 5 and 15 min after administration in cirrhosis, suggesting a reduced capacity of the liver to remove and metabolize ammonia.

Acute Disease↗

Portographic liver changes in idiopathic noncirrhotic portal hypertension.

Intraoperative and transhepatic portograms in patients with noncirrhotic portal hypertension, or idiopathic portal hypertension, were compared with portograms of patients with liver cirrhosis. Although the portograms in idiopathic portal hypertension varied from case to case, they were distinctly different from those in cirrhosis. The most common features of the former included a paucity of medium-sized portal branches, irregular and often obtuse-angled division of the peripheral branches, occasional abrupt interruptions of them, an avascular area beneath the liver surface, nonopacification of some of the large intrahepatic portal branches and of their periphery, and increase of very fine vasculature around large intrahepatic portal branches. These findings are compatible with occlusion of intrahepatic portal vessels at various levels.

Adult↗