G. Barbaro et al., Serum ferritin and hepatic glutathione concentrations in chronic hepatitisC patients related to the hepatitis C virus genotype, J HEPATOL, 30(5), 1999, pp. 774-782
Background/Aims: Increased serum ferritin is thought to be responsible for
activation of glutathione turnover in patients with chronic hepatitis C, Th
e aim of the study was to evaluate a possible correlation between levels of
serum ferritin and concentrations of hepatic, plasmatic and lymphocytic gl
utathione in a selected cohort of chronic hepatitis C patients in relation
to the hepatitis C virus genotype,
Methods: The study considered 130 chronic hepatitis C patients and 23 contr
ol subjects, Hepatic glutathione was determined from biopsy liver specimens
by high performance liquid chromatography, Total Iron Score was assessed b
y scoring iron separately within hepatocytes, sinusoidal cells and portal t
racts. Blood samples mere tested for determination of serum ferritin, and p
lasmatic and lymphocytic glutathione levels, Hepatic and erythocyte malonyl
dialdehyde were also determined along with peripheral blood mononuclear cel
l cytotoxic assay,
Results: Patients with genotype 1b showed higher levels of serum ferritin c
ompared to patients with genotype 2a/2c and 3a and to controls, along with
a significant reduction of the concentrations of hepatic, plasmatic and lym
phocytic glutathione and peripheral blood mononuclear cell cytotoxic activi
ty, The levels of serum ferritin correlated significantly to Total Iron Sco
re, to hepatic, plasmatic and lymphocytic glutathione, to hepatic and eryth
rocyte malonyldialdehyde and to peripheral blood mononuclear cell cytotoxic
activity,
Conclusions: The levels of serum ferritin correlate significantly to lipope
roxidation markers in chronic hepatitis C patients. The increased productio
n of free radicals with a reduced peripheral blood mononuclear cell cytotox
ic activity may represent, especially in patients with genotype 1b, a facto
r underlying the resistance to interferon therapy and may influence the evo
lution of the liver disease by enhancement of the cytopathic effect of hepa
titis C virus.