Systemic saturated lysophosphatidylcholine is associated with hepatic function in patients with liver cirrhosis

• Saturated lysophosphatidylcholine (LPC) declines in decompensated liver cirrhosis.
• LPC 16:0 and 18:0 negatively correlate with model for end-stage liver disease score.
• LPC 15:0, 16:0 and 18:0 negatively correlate with galectin-3.
• Saturated LPC is not associated with ascites volume and variceal size.

Serum lysophosphatidylcholine (LPC) is described to decline in patients with chronic liver diseases. Here it was evaluated which of the LPC species are associated with liver function. LPC species were quantified by direct flow-injection electrospray ionization tandem mass spectrometry in serum of 45 patients with mainly alcoholic liver cirrhosis. Saturated LPC is 52.1 (31.7–110.0) μmol/l in serum of patients with CHILD-PUGH score C (decompensated liver cirrhosis) and significantly lower compared to patients with well-compensated disease (CHILD-PUGH score A) with 114.1 (12.3–401.4) μmol/l. Mono- and polyunsaturated LPC are not changed in these groups. Saturated LPC is negatively correlated with the model for end-stage liver disease score, bilirubin and galectin-3 and positively with Quick prothrombin time. Ascites and varices are complications of liver cirrhosis. Saturated LPC does, however, not correlate with hepatic venous pressure gradient, ascites volume and variceal size. Unexpectedly, saturated LPC measured in serum of 42 patients declines from 88.4 (27.8–177.5) μmol/l to 72.4 (27.6–141.8) μmol/l shortly after transjugular intrahepatic portosystemic shunt implantation. Hepatic vein saturated LPC (82.3 (12.4–161.7) μmol/l) is higher than portal vein levels (78.8 (10.1–161.0) μmol/l) suggesting hepatic release of this lipid species. Current data demonstrate that systemic saturated LPC species are reduced in patients with decompensated liver cirrhosis and associated with mortality risk.