Abstract
Hepatocellular carcinoma (HCC) is the most common liver cancer, accountable for 90% cases. Visfatin and vaspin are adipocytokines with various suggested functions and proven significant correlations between BMI and percentage of body fat. The aim was to assess visfatin and vaspin serum levels in HCC patients and controls, compare their levels in patients with different cancer etiology and grade assessed according to the Barcelona-Clinic Liver Cancer (BCLC) staging system. The additional aim was to analyze relationship between analyzed adipokines and metabolic abnormalities and liver disfunction severity. The study was performed on 69 cirrhotic patients (54 males/15 females) with HCC, aged 59.0 ± 12.1 years, and with BMI 29.0 ± 4.5 kg/m2 compared to 20 healthy volunteers. Serum visfatin and vaspin concentrations were significantly increased in HCC patients compared to controls (p = 0.01 and p = 0.02, respectively). Serum vaspin was significantly higher in HCC patients with viral compared to those with non-viral etiology (p = 0.02), with more evident increase in chronic hepatitis C patients (CHC). Serum visfatin levels were significantly higher in patients with higher insulin resistance (p = 0.04) and with platelets count > 100 000/mm3 (p<0.001). Patients with BMI >30 kg/m2 had markedly up-regulated vaspin levels (p = 0.04). There was no difference in vaspin and visfatin serum levels with respect to liver dysfunction and BCLC classification. In conclusion, our study revealed serum vaspin and visfatin to be significantly increased in HCC patients independently of cancer etiology compared to controls. Additionally, serum vaspin was elevated in viral disease, especially in CHC. Vaspin up-regulation can be a compensatory mechanism against IR in HCC patients. Serum visfatin and vaspin, although up-regulated, seem not to be associated with cancer grade and cirrhosis severity.
Highlights
Hepatocellular carcinoma (HCC) is the growing problem worldwide
Chronic hepatitis C confirmed by the presence of HCV genotype 1b RNA was diagnosed in 35 patients
nonalcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH) derived cirrhosis was found in 26 patients
Summary
Hepatocellular carcinoma (HCC) is the growing problem worldwide. HCC constitutes the 6th most frequent worldwide malignancy and is 3rd cause of malignancy-related mortality. Many factors influence the development of nonalcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH) and carcinogenesis in the course of obesity and related metabolic abnormalities They comprise common pathway of intracellular insulin signaling and affecting insulin sensitivity. Dysregulation of adipose tissue derived hormones (adipocytokines/adipokines) might be involved in obesity-related liver carcinogenesis [3,4,5,6,7] Adipokines disbalance, such as dysregulation in level of adiponectin, leptin, resistin, chemerin, visfatin and some others, have been identified as a factor increasing fibrosis progression, inflammation and steatosis in chronic liver diseases including NAFLD/NASH, CHB and alcoholic liver disease (ALD) [4,5,6,7,8,9]
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