Phosphatidylcholine (PC) is an essential lipid for liver health and lipoprotein metabolism,
but its circulating levels have rarely been studied in patients with cirrhosis. Chronic hepatitis C
virus (HCV) infection causes lipid abnormalities and is a major cause of cirrhosis. Effective HCV
elimination with direct-acting antivirals (DAAs) is associated with the normalization of serum lowdensity
lipoprotein cholesterol levels. Since PC is abundant in all lipoprotein particles, this study
analyzed the association between serum PC species levels and liver cirrhosis before and after HCV
eradication. Therefore, 27 PC species were measured by Fourier Transform Mass Spectrometry in
the serum of 178 patients with chronic HCV infection at baseline and in 176 of these patients at the
end of therapy. The PC species did not correlate with viral load, and the levels of 13 PC species were
reduced in patients infected with genotype 3a compared to those affected with genotype 1. Four PC
species were slightly elevated 12 weeks after DAA initiation, and genotype-related changes were
largely normalized. Patients with HCV and cirrhosis had higher serum levels of PC 30:0 and 32:0
before and at the end of therapy. PC species containing polyunsaturated fatty acids were mostly
decreased in cirrhosis. The levels of polyunsaturated, but not saturated, PC species were inversely
correlated with the model of the end-stage liver disease score. A receiver operating characteristic
curve analysis showed area under the curve values of 0.814 and 0.826 for PC 32:0 and 0.917 and 0.914
for % PC 32:0 (relative to the total PC levels) for the classification of cirrhosis at baseline and at the
end of therapy, respectively. In conclusion, the specific upregulation of PC 32:0 in cirrhosis before
and after therapy may be of diagnostic value in HCV-related cirrhosis.