Background & Aims. Hepatocyte apoptosis may play a role in progression of
nonalcoholic fatty liver and oxidative stress seems one of the key mechanisms responsible for liver damage. The aim was to determine the association of oxidative stress with
cytokeratin-18 M30 fragment levels, a marker of hepatocyte apoptosis. Methods. Steatosis severity was defined according to Hamaguchi's echographic criteria in 209 patients with
nonalcoholic fatty liver. Serum
cytokeratin-18, urinary 8-iso-prostaglandin F2 α , soluble NOX2-derived
peptide, and
adiponectin were measured. Results. Serum
cytokeratin-18 progressively increased with steatosis severity (from 169.5 (129.3/183.8) to 176 (140/190) and 180 (169.5/192.5) μ IU/mL in mild, moderate, and severe steatosis, respectively; P < 0.01). After stratification by
cytokeratin-18 tertiles, a significant progression of body mass index, HOMA-IR,
triglycerides, urinary 8-iso-PGF2 α , soluble NOX2-derived
peptide, and of the prevalence of diabetes and severe steatosis was found, while
HDL-cholesterol and
adiponectin progressively decreased. A positive correlation between
cytokeratin-18 and body mass index, HOMA-IR, Hamaguchi's score, urinary 8-iso-PGF2 α , and soluble NOX2-derived
peptide and a negative correlation between
cytokeratin-18 and
HDL-cholesterol and
adiponectin were found. Body mass index,
adiponectin, and soluble NOX2-derived
peptide were independent predictors of serum
cytokeratin-18 levels (adjusted R (2) = 0.36). Conclusion. We support an association between oxidative stress and severity of liver damage in patients with
nonalcoholic fatty liver.