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Relationship between serum concentrations of keratin-18 and apoptosis in chronic hepatitis C

Apoptosis is a relevant feature in hepatitis C (1). Keratin-18, the major component of the hepatocyte cytoskeleton, is cleaved by caspases during apoptosis and keratin-18 fragments are released to the extracellular space (2). Serum keratin-18 (tissue polypeptide specific antigen; TPS) is used as a tumour marker in clinical practice (3). Serum keratin-18 (TPS) is increased in a variety of liver diseases, including hepatitis C (4–6). Furthermore, serum keratin-18 concentrations decrease after therapy for hepatitis C (4). We hypothesised that the increase in serum keratin-18 (TPS) in liver disease may reflect enhanced apoptosis. Indeed, serum concentrations of TPS are markedly increased in patients with alcoholic hepatitis (7–9) in relation to the presence of Mallory bodies (keratin-18 aggregates) (7) and immunostaining to M30 (9), a neo-epitope in keratin-18 (K18-Asp396) which is generated during apoptosis (10). We investigated the potential relationship between serum keratin-18 (TPS) concentrations and liver cell apoptosis in patients with hepatitis C. The study included 68 patients from a single institution (2005–2007) (median age 40 years, range 20–71 years, 48 males) with positive hepatitis C virus-RNA and untreated chronic hepatitis. Cases with additional causes for liver disease or HIV infection were excluded. The study was approved by the regional Ethics Committee and conformed to the Helsinki Declaration. Serum TPS was measured with a commercial immunoassay (Immulite-TPS, Siemens, Gwynedd, UK), which employs the M3 monoclonal antibody to residues 322–340 in keratin-18 (3). The limit of detection is 15 U/L and the upper reference value is 80 U/L. Serum TPS