Abstract
BackgroundElevated pentraxin-3 (PTX3) is related to liver pathologies such as infections, non-alcoholic fatty liver disease (NAFLD), and tumors. Aim of this study is to evaluate serum PTX3 levels in NAFLD and its affection by concomitant chronic hepatitis C viral infection (HCV). Seventy subjects were included and divided into 3 groups. Group I included 25 patients with NAFLD. Group II included 25 patients with NAFLD and chronic HCV. Group III included 20 controls. Chronic hepatitis C was diagnosed using quantitative PCR. Plasma pentraxin-3 was measured using ELISA.ResultsPlasma PTX3 was significantly high in group Ι and group ΙΙ, when compared to controls. There was non-significant difference between groups Ι and ΙΙ as regard PTX3 level. Higher PTX3 levels were detected in relation to metabolic syndrome. Cut-off value of PTX3 ≥ 1.8 was the best to predict metabolic syndrome with 91.4% sensitivity, 60.0% specificity, 65.7% PPV, and 56.7% NPV.ConclusionSerum PTX level in patients with concomitant NAFLD and HCV infection apparently reflects inflammatory response due to changes in metabolic profile, rather than that caused by infection itself, making PTX possibly useful in identifying those at risk of developing metabolic syndrome.
Highlights
Elevated pentraxin-3 (PTX3) is related to liver pathologies such as infections, non-alcoholic fatty liver disease (NAFLD), and tumors
Non-alcoholic fatty liver disease (NAFLD) represents a group of conditions ranging from asymptomatic simple liver steatosis to non-alcoholic steatohepatitis (NASH), that may progress to cryptogenic cirrhosis and hepatocellular carcinoma [1, 2]
The current study aimed to evaluate plasma PTX3 levels in NAFLD patients in comparison to patients with hepatic steatosis and concomitant chronic hepatitis C
Summary
Elevated pentraxin-3 (PTX3) is related to liver pathologies such as infections, non-alcoholic fatty liver disease (NAFLD), and tumors. Group I included 25 patients with NAFLD. Group II included 25 patients with NAFLD and chronic HCV. Non-alcoholic fatty liver disease (NAFLD) represents a group of conditions ranging from asymptomatic simple liver steatosis to non-alcoholic steatohepatitis (NASH), that may progress to cryptogenic cirrhosis and hepatocellular carcinoma [1, 2]. PTX3 is produced from several cells of the innate immune system, primarily the dendritic cells, macrophages, fibroblasts, and activated endothelial cells in response to pro-inflammatory stimuli, such as tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and lipopolysaccharides (LPS), all Hepatic steatosis is present in about 50% of HCV patients. Whether HCV replication and hepatic steatosis may lead to liver disease progression and elevation of inflammatory markers is still a wide field for investigation
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