Conditionally essential fatty acid deficiencies in end-stage liver disease.

Patients with end-stage liver disease (ESLD) manifest a wide variety of functional abnormalities that lead eventually to their death. Such patients also often have low levels of long-chain polyunsaturated fatty acids (PUFA) of carbon length 20 or greater in plasma total lipids, triacylglycerols, cholesterol esters, and phospholipids. We hypothesize that, due to hepatic damage, there is an impairment in de novo synthesis of very long-chain (20-22) carbon PUFA from their essential fatty acid 18 carbon dietary precursors that normally takes place principally in the liver. This results in a "conditional" essential fatty acid deficiency that may, in fact, be responsible for some of the pathophysiologic effects in ESLD. We propose that direct supplementation with very long-chain PUFA will provide a unique advantage in the correction of this "conditional" essential fatty acid deficiency in patients with ESLD and lead to improvements in their clinical condition.