Critical Illness-Related Alterations in Plasma Phosphatidylcholine Species Reveal Selective Induction of PC 32:0.

Circulating lipoprotein concentrations decrease in critical illness, suggesting that plasma phosphatidylcholine (PC) levels may also decline. However, published data on individual PC species in critical illness are conflicting, and underlying liver cirrhosis may substantially influence systemic lipid profiles. We therefore examined the impact of systemic inflammatory response syndrome (SIRS)/sepsis, with and without liver cirrhosis, on circulating PC species. We quantified 21 plasma PC species in 160 patients with SIRS, sepsis, or septic shock, including 31 patients with liver cirrhosis. PC profiles were compared with those of healthy controls and across clinically relevant subgroups. In patients with SIRS/sepsis without liver cirrhosis, 15 PC species were reduced compared with healthy controls, whereas PC 32:0 was increased. In patients with SIRS/sepsis and concomitant liver cirrhosis, 12 PC species were lower than in septic patients without cirrhosis, while PC 32:0 was again increased. Because a proportion of circulating PC is derived from phosphatidylethanolamine (PE), we explored whether altered PE-to-PC conversion could account for these changes; however, the observed pattern did not support this mechanism. No significant differences in PC species were observed between survivors and non-survivors. In summary, critical illness is associated with a broad reduction in circulating PC species, and this decrease is accentuated by coexisting liver cirrhosis. In contrast, PC 32:0 is consistently increased in both SIRS/sepsis and SIRS/sepsis with cirrhosis, suggesting a distinct biological role that warrants further investigation.