The current study was designed to investigate the potential association of serum interleukin-10 and interleukin-12 with HCV infection in chronic liver disease and to evaluate their possible role as new biomarkers in HCC development.Material and Methods. Forty-one patients suffering from chronic liver disease (33 patients harbor HCV infection and 8 are HCV-negative patients) were enrolled in the present study and histopathologically diagnosed into 15 patients with HCC, 16 patients with LC, and 10 patients with liver histology compatible with precirrhotic hepatitis (PCH). Ten patients complaining of cholecystitis were included as nondisease control. Serum levels of IL-10 and IL-12 were measured by enzyme linked immunosorbent assay (ELISA).Results. HCV-infected patients showed elevated expression of IL-10 and IL-12 compared to nondisease controls (P<0.0001) but there is no significant difference with respect to their expression in HCV-negative patients. Serum IL-10 and IL-12 were elevated significantly with disease progression (P<0.0001) and a positive correlation coefficient was detected between IL-10, IL-12 (r=0.785,P<0.0001), and transaminase values suggesting their possible role in chronic inflammation progression leading to HCC.Conclusion. IL-10 and IL-12 might be involved in chronic inflammation progression leading to HCC and their evaluation could be used as new biomarkers to reflect the degree of inflammation in HCC development.

Helicobacter pylori (H. pylori) infection is reported to be associated with various extragastrointestinal conditions such as insulin resistance, diabetes mellitus and metabolic syndrome. H. pylori infection and type 2 diabetes mellitus (T2DM) are associated with oxidative stress, this cross-relation between H. pylori induced infection in T2DM and oxidative damage is still debated. Thus, the question arises whether an increase in the serum level of 8-OHdG and Ox-LDL will occurs in patients with T2DM infected H. pylori; this will be through determination and compare frequency of H. pylori infection in T2DM and non-diabetic patients. 100 patients presented with history of epigastric discomfort for more than 1 month; 50 patients with T2DM and 50 non-diabetics. Anti-H. pylori IgG using ELISA, fasting and postprandial glucose level, glycated hemoglobin (HbA1c) and body mass index (BMI) was calculated. Serum 8-OHdG and Ox-LDL was measured using ELISA for the 100 patients and 50 control subject. Rates of H. pylori infection of T2DM and non-diabetic were 66 and 58 %, respectively, (p = 0.001). H. pylori IgG antibody was not correlated with HbA1c either in T2DM (p = 0.06) or non-diabetic (p = 0.25). Serum 8-OHdG level in T2DM with positive H. pylori infection showed a significant difference compared to non-diabetics with positive H. pylori infection (p = 0.001) and higher than that in T2DM with negative H. pylori. A correlation between 8-OHdG concentration and HbA1c in T2DM patients infected with H. pylori was observed (r = 0.39, p = 0.02). Serum Ox-LDL level in T2DM with positive H. pylori infection showed a significant difference compared to diabetics with both negative H. pylori infection and in non-diabetics with positive H. pylori infection (p = 0.001). Increased levels of oxidative DNA damage (8-OHdG) and Ox-LDL suggest the mechanistic link between H. pylori infection combined with diabetes and increased generation of ROS and could play as an important image for high risk to atherosclerosis.

Background. Several noninvasive predictive models were developed to substitute liver biopsy for fibrosis assessment. Aim. To evaluate the diagnostic value of fibronectin which reflect extracellular matrix metabolism and standard liver functions tests which reflect alterations in hepatic functions. Material and methods. Chronic hepatitis C (CHC) patients (n = 145) were evaluated using ROC curves and stepwise multivariate discriminant analysis (MDA) and was validated in 180 additional patients. Liver biochemical profile including transaminases, bilirubin, alkaline phosphatase, albumin, complete blood count were estimated. Fibronectin concentration was determined using monoclonal antibody and ELISA. Results. A novel index named fibronectin discriminant score (FDS) based on fibronectin, APRI and albumin was developed. FDS produced areas under ROC curves (AUC) of 0.91 for significant fibrosis and 0.81 for advanced fibrosis. The FDS correctly classified 79% of the significant liver fibrosis patients (F2–F4) with 87% sensitivity and 75% specificity. The relative risk [odds ratio (OR)] of having significant liver fibrosis using the cut-off values determined by ROC curve analyses were 6.1 for fibronectin, 4.9 for APRI, and 4.2 for albumin. FDS predicted liver fibrosis with an OR of 16.8 for significant fibrosis and 8.6 for advanced fibrosis. The FDS had similar AUC and OR in the validation group to the estimation group without statistically significant difference. Conclusion. FDS predicted liver fibrosis with high degree of accuracy, potentially decreasing the number of liver biopsy required.

Background and Aims: Oncogenes and tumor suppressor genes expression are well described in bladder cancer associated with schistosomiasis especially in Egypt. Scarce studies were directed to colorectal cancer (CRC) associated with Schistosoma mansoni (S. mansoni). Apoptosis (programmed cell death) and the genes regulating this process (e.g., Bcl-2) have recently become a focus of interest in the study of cancer development and progression. In the present study, we aimed to investigate the expression pattern of p53, Bcl-2 and C-Myc in CRC tissues obtained from Egyptian colorectal cancer patients divided in two different groups, one associated with Schistosoma mansoni (CRC-Sm) and the other without Schistosoma mansoni (CRC-NSm). Methods: Seventy-five CRC tumors containing 36 draining lymph node metastatic tumors were immunohistochemically stained using specific monoclonal antibodies for p53, Bcl-2 and C-Myc, in addition the apoptotic activity of these tumors were analyzed. Results and Conclusions: Regardless of the S. mansoni infection, the obtained Results showed that the apoptotic activity was more evident in p53 diffuse positive tumors (P=0.021). There was a significant correlation between p53 diffuse positive staining and Bcl-2 positive immunostaining (P=0.011). Signet ring cell carcinoma and mucinous adenocarcinoma exhibited both intense C-Myc expression than non-mucinous carcinoma (P=0.001). When adjusting for S. mansoni infection, 58.3% of CRC-Sm cases were Bcl-2 positive compared to only (33.3%) of CRC-NSm (P=0.046). Apoptotic activity was more evident in the latter group than of CRC-Sm tumors (P=0.009). p53 and C-Myc expressions were found insignificantly different in CRC-Sm compared with CRC-NSm (P>0.05). These observations suggest that the genotoxic agents produced endogenously through the course of schistosomiasis mansoni may play a role in CRC-Sm pathogenesis through the dysregulation of apoptosis by alteration the expression pattern of Bcl-2 protein differently from CRC-NSm suggesting a different biological behavior.

Lead (Pb) is known to disrupt the pro-oxidant/antioxidant balance of tissues leading to biochemical and physiological dysfunction. The present study was designed to investigate the effect of tannic acid on some biochemical parameters in Swiss albino mice exposed to lead acetate. The levels of thiobarbaturic acid-reactive substances (TBARS) as an index of lipid peroxidation, nitric oxide (NO), and serum lead (Pb) were significantly increased following intragastric administration of 50 mmole lead acetate/kg body weight three times a week, every other day for three weeks, compared to the corresponding control values. On the other hand, the activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione-S-transferase (GST) and glutathione content (GSH) and serum copper (Cu) and zinc (Zn) were significantly diminished relative to the control values. The administration of 20 mg tannic acid/kg body weight three times a week every other day for three weeks, enhanced the endogenous antioxidant capacity of the cells by increasing the activities of antioxidant enzymes (SOD, CAT, GSH-R, GST), GSH content and serum Cu and Zn levels. Compared to the lead acetate-exposed group, the levels of TBARS, NO and Pb were decreased in the lead acetate exposed group treated with tannic acid. These results afford evidence supporting the hypothesis that lead induces oxidative stress in hepatic cells. Moreover, tannic acid has a potential in sustaining global antioxidant effect in hepatic cells leading to decreased oxidative stress and cellular damage initiated through free radical production by lead acetate.