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The relationship between Helicobacter pylori (H. pylori) infection and Portal hypertensive gastropathy (PHG) is still a debatable matter. The aim of this study is to find out how common H. pylori infection is in cirrhotic patients with PHG and to see if there’s a link between H. pylori infection and PHG severity. Out of 340 cirrhotic patients who had upper Gastrointestinal Tract (GIT) endoscopy for early varices screening, 160 cirrhotic patients were selected and divided into 2 groups; 80 cirrhotic patients with PHG (cases) and 80 cirrhotic patients without PHG (controls). Gastric biopsies were taken from all enrolled patients for histological evaluation for the presence or absence of H. pylori infection. H. pylori was found in 44 cirrhotic patients (55%) who had PHG (cases), compared to 22 cirrhotic patients (27.5%) who did not have PHG (controls). The prevalence of H. pylori infection was significantly higher in patients with PHG (p < 0.001). The severity of PHG was associated with H. pylori infection (p < 0.001). The response to eradication therapy of H. pylori infection was must better in patients without PHG (p = 0.045). By multi-variant analysis, H. pylori infection, splenic diameter, and portal vein diameter were independent predictors for PHG presence. After treating H. pylori infection in patients who tested positive for H. pylori, there was a significant reduction in PHG severity (p < 0.001). Patients with PHG have a greater prevalence of H. pylori infection. PHG is more severe in patients infected with H. pylori. To improve PHG severity, cirrhotic patients must have their H. pylori infection eradicated.

Background and PurposeThe advanced glycation end products (AGEs) have been implicated in different diseases’ pathogenesis, but their role in hepatocellular carcinoma (HCC) is still a matter of debate. This study aims to investigate the association of AGEs with HCC development in patients with hepatitis C-related cirrhosis.MethodsOnly 153 of the 181 non-diabetic patients with cirrhosis were consecutively involved in this pilot cohort prospective study, along with 34 healthy control participants. Demographic characteristics, biochemical parameters, clinical data, and AGEs levels in all subjects at the starting point and every year after that for two years were assessed. Multivariable Cox regression analysis was used to settle variables that could predict HCC development within this period.ResultsHCC developed in 13 (8.5%) patients. Univariate Cox regression analysis reported that body mass index (P=0.013), homeostatic model assessment-insulin resistance (P=0.006), alpha-fetoprotein (P <0.001), and AGEs levels (P <0.001) were related to HCC development. After adjusting multiple confounders, the multivariable Cox regression model has revealed that AFP and AGEs were the powerful parameters related to the HCC occurrence (all P<0.05). AGEs at a cutoff value of more than 79.6 ng/ml had 100% sensitivity, 96.4% specificity, and 0.999 area under the curve (all P<0.001), using the receiver operating characteristic curve, for prediction of HCC development.ConclusionThis work suggests that AGEs are associated with an increased incidence of HCC, particularly in cirrhosis, which is encouraging in decreasing the risk of HCC in these patients.

Individual differences in IBD illness severity, behavior, progression, and therapy response are evident. Since a break in the intestinal epithelial barrier causes IBD to begin, mucosal gene expression in IBD is crucial. Due to its high sensitivity and dynamic nature, molecular analysis of biomarkers in intestinal biopsies is feasible and provides a reliable means of evaluating localized inflammation. The goal of this investigation was to discover alterations in gene expression in the inflamed mucosa of IBD patients undergoing treatment with 5-amino salicylic acid (5ASA) (N = 39) or anti-TNF drugs (N = 22). The mucosal expression of numerous IBD-related genes was evaluated using qPCR. We discovered that the levels of the proteins Lipocalin-2 (LCN2), Nitric Oxide Synthase 2 (NOS2), Mucin 2 (MUC2), Mucin 5AC (MUC5AC), and Trefoil factor 1 (TFF1), which are overexpressed in untreated IBD patients compared to non-IBD subjects, are decreased by both therapy regimens. On the other hand, anti-TNF medicine helped the levels of ABCB1 and E-cadherin return to normal in IBD patients who were not receiving treatment.

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