Open AccessElevation of Serum Levels of Advanced Glycation End Products in Patients With Non‐B or Non‐C Hepatocellular Carcinoma
Author(s) -
Kan Hiromi,
Yamagishi Shoichi,
Ojima Ayako,
Fukami Kei,
Ueda Seiji,
Takeuchi Masayoshi,
Hyogo Hideyuki,
Aikata Hiroshi,
Chayama Kazuaki
Publication year - 2015
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.21797
Subject(s) - hepatocellular carcinoma , elevation (ballistics) , glycation , medicine , oncology , carcinoma , gastroenterology , cancer research , engineering , receptor , structural engineering
Background The prevalence of non‐B or non‐C hepatocellular carcinoma (NBNC‐HCC) has been increasing all over the world. Advanced glycation end products (AGE) play a role in the pathogenesis of alcoholic liver injury or nonalcoholic steatohepatitis (NASH). Methods We examined here whether serum levels of AGE were elevated in NBNC‐HCC patients compared with NASH subjects without HCC and investigated which anthropometric and clinical variables were independent determinants of AGE. Results Ninety NBNC‐HCC, 56 NASH, and 27 control subjects underwent a complete history and physical examination, determination of blood chemistries, including AGE levels. Serum levels of AGE were significantly higher in NBNC‐HCC patients compared with NASH and control subjects [9.1 ± 2.7, 5.2 ± 1.7, 3.5 ± 1.2 (U/ml), respectively, P < 0.05]. Univariate analysis showed that AGE levels were associated with male ( P < 0.05), age ( P < 0.01), aspartate aminotransferase ( P < 0.05), γ‐glutamyl transpeptidase (GGT) ( P < 0.01), HDL‐cholesterol (inversely, P < 0.01), fasting plasma glucose ( P < 0.01), and HbA1c ( P < 0.05). By the use of multiple stepwise regression analysis, age, GGT, and HDL‐cholesterol (inversely) remained significant and were independently related to AGE levels ( R 2 = 0.406). Conclusion The present results suggest that AGE might be involved in the pathogenesis of NBNC‐HCC, thereby being a biomarker that could discriminate NBNC‐HCC from NASH.