Patients with end-stage liver disease (ESLD) manifest a wide variety of fun
ctional abnormalities that lead eventually to their death. Such patients al
so often have low levels of long-chain polyunsaturated fatty acids (PUFA) o
f carbon length 20 or greater in plasma total lipids, triacylglycerols, cho
lesterol esters, and phospholipids. We hypothesize that, due to hepatic dam
age, 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 t
hat normally takes place principally in the liver. This results in a "condi
tional" essential fatty acid deficiency that may, in fact, be responsible f
or some of the pathophysiologic effects in ESLD. We propose that direct sup
plementation with very long-chain PUFA will provide a unique advantage in t
he correction of this "conditional" essential fatty acid deficiency in pati
ents with ESLD and lead to improvements in their clinical condition. Nutrit
ion 1999;15:302-304. (C) Elsevier Science Inc. 1999.