Impaired ability of neutrophils to produce oxygen-derived free radicals in patients with chronic liver disease and hepatocellular carcinoma.
To evaluate whether neutrophil bactericidal function, the ability to produce oxygen-derived free radicals, is altered in patients with chronic liver disease, we measured chemiluminescence amplified by a luciferin analog (Cypridina luciferin analog-dependent chemiluminescence) and luminol (luminol-dependent chemiluminescence) in response to N-formyl-Met-Lue-Phe by neutrophils from patients with chronic liver diseases due to C and/or B type hepatitis: chronic active hepatitis, cirrhosis and hepatocellular carcinoma. Both Cypridina luciferin analog-dependent chemiluminescence and luminol-dependent chemiluminescence were significantly decreased in neutrophils from patients with chronic liver disease (hepatocellular carcinoma < cirrhosis < chronic active hepatitis) when they were compared with normal healthy subjects. The reduction of Cypridina luciferin analog-dependent chemiluminescence in chronic active hepatitis and cirrhosis was more sensitive than Cypridina luciferin analog-dependent chemiluminescence; however, in hepatocellular carcinoma, luminol-dependent chemiluminescence was more reduced than luminol-dependent chemiluminescence. Although there were not significant correlations between glutamic pyruvic transaminase and Cypridina luciferin analog-dependent chemiluminescence/luminol-dependent chemiluminescence, there were significant negative correlations between total bilirubin and Cypridina luciferin analog-dependent chemiluminescence/luminol-dependent chemiluminescence. Furthermore, there were significant positive correlations between albumin/prothrombin time and Cypridina luciferin analog-dependent chemiluminescence/luminol-dependent chemiluminescence. These data suggest that an impaired ability to produce oxygen-derived free radicals may contribute to the susceptibility to infection in patients with chronic liver disease.
Uehara
M
M
First Department of Internal Medicine, Gunma University School of Medicine, Japan.
Sato
N
N
D000410:Alanine Transaminase / Q000097:blood; D001663:Bilirubin / Q000097:blood; D006528:Carcinoma, Hepatocellular / Q000097:blood / Q000276:immunology*; D002908:Chronic Disease; D005260:Female; D005609:Free Radicals; D006521:Hepatitis, Chronic / Q000276:immunology; D006801:Humans; D008103:Liver Cirrhosis / Q000276:immunology; D008107:Liver Diseases / Q000097:blood / Q000276:immunology*; D008113:Liver Neoplasms / Q000097:blood / Q000276:immunology*; D008163:Luminescent Measurements; D008165:Luminol; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism*; D011517:Prothrombin Time; D011719:Pyrazines; D012709:Serum Albumin / Q000032:analysis
D005609:Free Radicals; D011719:Pyrazines; D012709:Serum Albumin; C048193:2-methyl-6-phenyl-3,7-dihydroimidazo(1,2-a)pyrazin-3-one; D008165:Luminol; D000410:Alanine Transaminase; D001663:Bilirubin; D010100:Oxygen