Biliary lipids, faecal steroids, andliver function in patients withchronic active hepatitis andprimary biliary cirrhosis: significance ofhepatic orcein-stained complexes

SUMMARY Biliary lipids, faecal steroids, andserum bile acids were studied inpatients withchronic active hepatitis andprimary biliary cirrhosis. Theresults were correlated withexcretory andparenchymal liver function testsandwiththepresenceorabsence oforcein-positive copperprotein complexes inhistological liver specimens. Ingeneral, faecal bile acids, butnotneutral and total sterols, correlated negatively withthepercentage ofbiliary cholic acid, serum cholesterol, and serum bile acids andpositively withthepercentage ofbiliary deoxycholic acid. Inorcein-positive subjects-indicative oflong-standing cholestasis-the bile was undersaturated withcholesterol, biliary deoxycholic acid was subnormal, cholic acidcorrespondingly increased, andserum cholesterol andbile acids were raised. Onlythepatients withmarkedimpairment ofbothexcretory andparenchymal liver functions hada decreased outputofneutral sterols, bile acids, andtotal steroids, and,thus, lowbileacidandcholesterol synthesis. Thefindings indicate thatmild disturbances inparenchymal liver function infrequently cause majorchanges incholesterol metabolism, whileabnormalities insecretoryliver function-in orcein-positive subjects especially-are frequently associated withproportionate changes inparameters ofcholesterol metabolism. Patients withliver disease exhibit analmost complete lack ofbiliary andplasma deoxycholic acid,'-3 raised plasma bile acids,45 adecrease incholic acidpool size," andadiminution inthehepatic clearance of labelled bile acids.89 Biliary cholesterol secretion is reduced morethanthesecretion ofbile acids and phospholipids,'° andmicellar solubilisation ofintestinal lipids andsterols canbemarkedly reduced. " Faecal bile acids andneutral sterols ofcholesterol origin aredecreased inpatients withsevere chronic liver disease, while urinary bile acids areconstantly, butnevergreatly, increased,'2 indicating thatthe production ofcholesterol anditsconversion tobile acids isdecreased. Theabnormalities ofbiliary lipids inliver diseases havebeenmainly reported inalcoholic cirrhosis and factors affecting different aspects ofsterol metabolism arepoorly understood. Inthepresent study thebiliary lipids, faecal steroids, andserumbileacids were