Arachidonic acid in mononuclear cells and its clinical significance in HCV cirrhotic patients

Objective An abnormal fatty acid pattern in patients with advanced liver cirrhosis (LC) has been reported in plasma phospholipids and some other tissues. To elucidate the significance of arachidonic acid deficiency on the clinical pathophysiology of LC and hepatocellular carcinoma (HCC), we analyzed the fatty acid compositions of mononuclear cell phospholipids, plasma α-tocopherol, and thiobarbituric acid-reactive substances and serum tumor necrosis factor-α (TNF-α) in cirrhotic patients infected with the hepatitis C virus with and without HCC. Methods Twelve cirrhotic patients without HCC (LC patients) and 11 with HCC (HCC patients) were enrolled. Fatty acids were analyzed with gas chromatography. α-Tocopherol and TNF-α were analyzed by high-performance liquid chromatography and enzyme-linked immunosorbent assay, respectively. Statistical analysis was performed by using the unpaired t test with Welch’s correction and Spearman’s rank-correlation analysis. Results Significantly low levels of linoleic, dihomo-γ-linolenic, arachidonic, and eicosapentaenoic acids from mononuclear cell phospholipids were observed in LC and HCC patients compared with control subjects. Plasma α-tocopherol was lower and thiobarbituric acid-reactive substances were higher in HCC patients than in controls. Arachidonic acid molar percentage in mononuclear cell phospholipids correlated significantly with lymphocyte count (r = 0.460, P < 0.05) in the cirrhotic patients and with lymphocyte (r = 0.680, P < 0.01) and platelet (r = 0.763, P < 0.01) counts in all subjects. Conclusion These results suggested that arachidonic acid in mononuclear cells may have an important role in the pathophysiology of hepatitis C virus associated with cirrhosis and that nutritional management preventing arachidonic acid deficiency may have some beneficial effects on the progression of LC.