Faculty Bibliography

To study mechanisms and anatomic correlates of precirrhotic portal hypertension, we measured portal pressure either at laparotomy (in the portal vein) or by hepatic vein catheterization (wedge pressure) in 24 pairs of baboons fed 50% of energy either as ethanol or isocaloric carbohydrate (controls) for 4 mo-9 yr. On liver biopsy 7 had simple fatty liver; none had portal pressure exceeding the control range (2.7-13.0 cmH2O). The remaining 17 alcohol-fed baboons had fibrous tissue deposition around the terminal hepatic venules and adjacent sinusoids. The mean portal pressure was significantly increased (15.0 +/- 1.4 cmH2O) compared with the value in baboons with fatty liver (9.6 +/- 0.9 cmH2O) and in controls (8.0 +/- 0.6 cmH2O), with 8 animals exceeding the control range. Estimated hepatic blood flow was unchanged. Alcohol feeding resulted in increased hepatocyte size in both the fatty liver and fatty liver with fibrosis group; however, portal pressure did not correlate with alterations of cell size, liver volume, hepatic triacylglycerol, and protein contents. By contrast, for veins of comparable size, there was a significant correlation (r = 0.6666, p less than 0.01) between the thickness of the perivenular fibrous rim and portal pressure. Perivenular fibrosis was commonly associated with adjacent perisinusoidal fibrosis and this lesion also correlated with portal pressure. Furthermore, if one postulates that increased cell size causes enhanced pressure with secondary fibrosis, the latter should have first occurred 'upstream,' in the mid and portal zones. Sequential biopsy specimens, however, showed that fibrosis first appeared in the perivenular areas, suggesting that, in most instances, increased pressure is in fact secondary to the perivenular fibrosis

Evolution in the diagnosis and non-surgical management of biliary tract disease is outlined and analyzed. The relative roles of endoscopic and percutaneous techniques are weighed in terms of risk, technical difficulty and clinical value. Initial diagnosis and treatment should be by endoscopic retrograde cholangiopancreatography (ERCP) when feasible because of lower diagnostic and treatment risk. When technical or clinical circumstances dictate, a prompt shift to percutaneous techniques is indicated. The complimentary roles of endoscopic, percutaneous and surgical methods are emphasized. Therapy by nonsurgical methods is closely linked to diagnosis by direct cholangiography. Close coordination reduces hazard and improves likelihood of successful resolution in these difficult clinical problems