Patients with cirrhosis had increased levels of plasma long chain fatty acids (LCFA) and venous ammonia (NH3) as compared to controls, and the level of these substances increased with greater severity of the disease. Blood NH3 was significantly higher in patients with hepatic encephalopathy (p <0.05) while the levels of LCFA were comparable in the noncomatose and comatose patients (p >0.05). In patients with cirrhosis, with or without coma, plasma LCFA levels did not correlate significantly with venous ammonia levels (r = 0.131, n = 38, p >0.05). In cirrhotics, plasma phospholipids and cholesteryl esters were significantly depressed, whereas triglycerides were normal. The abnormal plasma lipid pattern worsened with severity of cirrhosis but did not correlate with encephalopathy. The distribution pattern of LCFA in most plasma lipids in cirrhosis varied significantly from normal in that the percentages of 18:2 (linoleate) and 20:4 (arachidonate) were decreased and those of 1 6:1 (palmitoleate), 18:1 (oleate)and 1 6:0(palmitate) increased. We infer from these data that (1) LCFA per se do not contribute importantly to the induction of hepatic encephalopathy and do not influence significantly the steady state blood NH3 level; (2) plasma lipid levels in cirrhosis (with hepatocellular insufficiency) are abnormal as a result of impaired lipoprotein metabolism; and (3) the fatty acid composition of LCFA and esterified lipids in cirrhosis is altered suggestive of both essential fatty acid deficiency, probably reflecting malnutrition/malabsorption, and impaired hepatic fatty acid elongation and desaturation.