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Synergistic Effect of Alcohol Consumption and Body Mass on Serum Concentrations of Cytokeratin‐18
Author(s) -
GonzalezQuintela Arturo,
Tomé Santiago,
FernandezMerino Carmen,
Rey Jesus,
Meijide Luis,
Gude Francisco
Publication year - 2011
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.2011.01570.x
Subject(s) - cytokeratin , body mass index , obesity , metabolic syndrome , medicine , endocrinology , population , odds ratio , alcohol , physiology , biology , biochemistry , environmental health , immunohistochemistry
Background: Cytokeratin‐18 is an essential component of the cytoskeleton of epithelial cells (including hepatocytes). Serum concentrations of cytokeratin‐18 (tissue polypeptide‐specific antigen [TPS]) are used as a marker of epithelial neoplasms. Here, we investigated the potential interaction between alcohol and obesity in relation to serum TPS concentrations. Methods: Alcohol consumption, body mass index, and components of metabolic syndrome were measured in a random sample ( n = 420) of the adult population (aged 18 to 92 years, 45% men) from a single municipality. Regular alcohol intake of >20 g/d (women) or >30 g/d (men) was considered risky drinking. Serum TPS was measured with a commercial immunoassay. Results: Risky drinking was associated with increased serum concentrations of TPS, which was particularly evident among obese individuals. Among individuals without risky drinking, TPS concentrations were similar for all levels of body mass. Conversely, among risky drinkers, serum TPS concentrations increased in parallel with body mass ( p = 0.002). The odds ratio of a high (>100 U/l) TPS concentration for the combination of risky drinking and obesity was greater than the additive effect of the 2 separate factors, after adjusting for age and sex. A similar interaction was observed between risky drinking and abdominal adiposity, a major component of the metabolic syndrome. Serum TPS concentrations were correlated with markers of liver damage. Serum TPS was not superior to standard markers (gamma‐glutamyl transferase and red blood cell mean volume) for the detection of risky drinking. Conclusions: There is a synergism between risky alcohol consumption and common metabolic disorders (particularly obesity) in relation to serum concentrations of cytokeratin‐18 (TPS), which probably reflect liver disease.