NAFLD is one of the most common forms of chronic liver diseases among obese patients and as one of the features of the metabolic syndrome . It is characterized by accumulation of large triglyceride droplets within the liver cells .
Serum PTX3 level increases rapidly in inflammatory conditions, reaching its peak values after 6–8 h of any inflammatory condition; its elevation on the early phase is due to rapid release of stored PTX3 by the activated neutrophils [11, 12]. The short pentraxins, CRP, and serum amyloid protein are produced by the liver as a systemic response to local inflammation, whereas expression of the long pentraxin (PTX3) is induced by the damaged tissues .
In the current study, the aim was to evaluate plasma PTX3 levels in NAFLD patients in comparison to patients with hepatic steatosis and concomitant chronic hepatitis C.
The diagnosis of NAFLD in this study relied on the characteristic abdominal ultrasonographic features such as the presence of diffuse hyperechoic echo texture (bright liver), increased liver echo texture compared with the kidney, vascular blurring, and deep attenuation, together with the exclusion of other causes of fatty liver such as significant alcohol consumption, drug induced hepatitis, and chronic viral hepatitis.
Although liver biopsy is the gold standard diagnostic test of NAFLD, liver biopsy is an invasive procedure that carries a risk of complications together with sampling errors and intra- and interobserver variability. For that reasons, liver biopsy is considered an “imperfect Gold Standard diagnostic tool” . Depending solely on ultrasound in the diagnosis of NAFLD is considered a weak point in the current study as it is less sensitive than liver biopsy or magnetic resonance elastography. On the other hand, ultrasound is widely available, of low cost and non-invasive. Most of the recent studies relied on the ultrasonographic diagnosis of NAFLD after exclusion of other causes of liver diseases .
We found that plasma levels of PTX3 were significantly higher in patients with NAFLD in comparison to controls. Our results agreed with the study of Yoneda et al.  which revealed that PTX3 levels were significantly higher in NAFLD patients than healthy control subjects. Kadir et al.  had demonstrated that PTX3 levels in NAFLD patients with fibrosis were higher than NAFLD patients without fibrosis and healthy subjects, independent of metabolic syndrome components. On the other hand, Maleki et al.  found no significant difference between NAFLD and healthy control subjects regarding plasma PTX3.
In the present study, there was non-significant difference between NAFLD patients with and without chronic HCV regarding plasma PTX3. PTX3 is directly produced by damaged tissues, and a rapid increase indicates inflammation. Elevated PTX3 concentrations are related to liver-associated pathological conditions such as liver infections, NAFLD, NASH, and hepatic tumors . In a study performed by Carmo et al. , patients with hepatocellular carcinoma (HCC) on top of HCV were found to have higher PTX3 plasma levels than individuals with mild or severe fibrosis. They concluded that PTX3 seems to be a risk factor for the occurrence of HCC in chronic hepatitis C .
Significant positive correlation between plasma PTX3 and HCV quantitative PCR was found in the current study. PTX3, the prototype of the long pentraxin group, is a critical component of the humoral arm of innate immunity and opsonic activity. It facilitates pathogen recognition and produced by a variety of tissues and cells in response to pro-inflammatory signals and Toll-like receptor engagement . The persistent elevation in PTX3 levels is associated with disease severity and increased morbidity in several clinical conditions. Persistently elevated PTX3 may represent a novel and promising biomarker of liver disease .
In the present study, significant positive correlations were found between serum PTX3 levels and body mass index (BMI), waist circumference, fasting blood sugar (FBS), TG, ALT, AST, total and direct bilirubin, while it correlated negatively with platelet count and HDL. Also, patients with metabolic syndrome in the current study showed higher levels of PTX3 than those without metabolic syndrome. A cut-off value for PTX3 ≥ 1.8 ng/ml was the best in predicting metabolic syndrome with a high sensitivity and a moderate specificity. Similarly, Kardas et al.  found significant higher concentrations of plasma PTX3 in obese children and adolescents with metabolic syndrome and higher triglyceride levels, and PTX3 levels correlated negatively with HDL cholesterol in their study. This is contrary to others in the literature who found PTX3 inversely related to obesity and that it increases with weight loss and exercise [23, 24].
Significantly high body mass index and waist circumference were found in NAFLD patients with or without chronic HCV infection in comparison to healthy control subjects. This is like the results of Kowdley et al. , Sobhonslidsuk et al. , Marchesini et al. , and the Rotterdam study of Edith et al. . Steatosis results from enhanced lipogenesis, increased stability of lipid droplets, reduced lipoprotein secretion, and altered mitochondrial function . Hepatic steatosis is present in about 50% of patients with HCV. Genotype 3 was found to be independently associated with hepatic steatosis. In those with other genotypes of HCV, steatosis was associated with features of the metabolic syndrome. The presence of hepatic steatosis was related to the presence of insulin resistance .
Several studies, including the current one, revealed significant higher ALT and AST levels in NAFLD with or without HCV patients than control subjects. Increased hepatic enzyme levels are indicators of hepatocellular necrosis whether due to NAFLD or chronic HCV [24, 31, 32].
The current study revealed significant higher levels of FBS, post prandial blood sugar, triglycerides, total cholesterol, LDL, and significant lower HDL in NAFLD patients with or without chronic HCV infection than in healthy controls. This agreed with Marchesini et al. , the Rotterdam study by Edith et al. , Dixon et al. , Nakahara et al. , and Poynard et al. . NAFLD and type 2 diabetes mellitus (T2DM) frequently coexist because these conditions share common risk factors of excess adiposity, higher lipids, and insulin resistance.