Liver damage and alterations in the exocrine function of the gland lead to a profound alteration of the :,rna lipoprotein profile. To determine whether hepatic disease results in changes in the lipoprotein fatty acid ·,,cnposition, i.e. to determine whether liver function influences the homeostasis of complex lipids in plasma, we ~,i.ltcd the fatty acid profile of lipids from VLDL, LDL and HDL, as well as from total plasma, in thirty-one .,.m:nts of both sexes with hepatobiliary pathology ( compensated liver cirrhosis, uncompensated liver cirrhosis, -t:rnary biliary cirrhosis, other intrahepatic cholestasis, and acute viral hepatitis). We also studied a group of healthy ,.lulls as controls. We present the lipoprotein profile and the fatty acid composition (myristic Cl4, palmitic Cl6, ,,ilrnitoleic Cl6: l, stearic C18, oleic C18: 1, linoleic Cl8: 2, eicosatrienoic C20: 3co6 and arachidonic C20: 4) ,i ltpoprotein and total plasma triacylglycerols, cholesteryl esters and phospholipids. The main observation of this .n,Jy is that, despite the profound changes in the lipoprotein profile and the lower abundance of polyunsaturated t,nr acids in complex lipids, the composition of all triagylglycerols, cholesteryl esters and phospholipids is .~- similar for the corresponding lipoproteins of patients with hepatobiliary disease and of control subjects. nu~ indicates that in the controls as in the studied patients, the exchange of lipids between plasmatic 3P'Proteins is very rapid and demonstrates the possible importance of the extrahepatic synthesis of cholesteryl e11er transfer protein.