The chronic inflammation and damage to the gastric epithelium induced by Helicobacter pylori (H. pylori) are the main risk factors for gastric cancer development. Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) induce chronic inflammation and have been found in gastric tumors. The objectives this observational study were to determine the frequency of multiple infections by Helicobacter pylori, Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) and to relate the infection by EBV and HCMV with H. pylori vacA/cagA genotypes in patients with chronic gastritis or gastric cancer. DNA from H. pylori, EBV and HCMV was detected by PCR in biopsies from 106 Mexican patients with chronic gastritis and 32 from gastric cancer. The cagA status and the vacA genotypes of H. pylori were determined by PCR. In chronic gastritis and gastric cancer EBV was found in 69.8% and 87.5%, HCMV in 52.8% and 53.1%, and H. pylori in 48.1% and 40.6%, respectively. In chronic gastritis, 53% of H. pylori+ patients were EBV+ and 33% were both EBV+/HCMV+; in gastric cancer, 92.3% of H. pylori-infected individuals were EBV+ and 46.1% were EVB+/HCMV+. All the intestinal- and mixed-type tumors and the 83.3% of diffuse-type tumors were EBV+. No significant differences were found between single infections or coinfections with the diagnosis or the cancer type. The H. pylori genotypes were not related to EBV or HCMV infection. The frequency of dual infections by H. pylori, EBV and HCMV is higher in patients from southwest Mexico than other populations. It is likely that these pathogens act synergistically to induce inflammation and gastric cancer.

MMP9 expression is enhanced in gastric cancer compared to normal mucosa; interpretation of differential expression of MMP2 is difficult to establish.

Background. During progression of gastric cancer (GC), degradation of the extracellular matrix is mediated by the matrix metalloproteases (MMPs) and their tissue inhibitors (TIMPs): changes in the expression of these have been related to unfavorable prognosis in GC. Objective. To analyze the expression of certain MMPs and TIMPs in chronic superficial gastritis (SG) and GC. Methods. The expression of MMPs and TIMPs was determined using qRT-PCR; the expression was classified, using threshold cycle (C T) values, as very high (C T ≤ 25), high (C T = 26–30), moderate (C T = 31–35), low (C T = 36–39), or not detected (C T = 40). Strength of association was estimated between the proteins, which were detected by Western blot, and the risk of developing GC. Results. We found a high expression of MMP1, MMP2, MMP14, TIMP1, and TIMP3; moderate one of MMP9 and MMP25, and low one of MMP13 and MMP24 in both tissues. In absolute mRNA levels, significant differences were found in expression of MMP2, MMP24, and MMP25, which are overexpressed in GC compared with SG. The presence of the proteins MMP-14 and TIMP-3 was associated with the risk of developing GC. Conclusions. We consider that MMP2, MMP24, and MMP25 and the proteins MMP-14 and TIMP-3 could be candidates for prognostic molecular markers in GC.

alteration in IL-1, adiponectin and oxidative stress levels were found to be related to overweight and obesity; also, iodine levels decreased when BMI increased, contributing to loss of redox equilibrium. All this data may play an important role in etiopathogenesis of chronic disease related to the increase of BMI.

Background Vancomycin resistant enterococci (VRE) infections are of increasing concern in many hospitalized patients. Patients with cirrhosis are at added risk of infection with VRE, with associated increased risk for complications from infections. The goals of this study were to: [ 1 ] identify risk factors for VRE amongst cirrhotic patients before liver transplantation, and [ 2 ] evaluate risk of morbidity and mortality at 30-days and one-year after VRE infection. Methods Chart review of 533 cirrhotic patients hospitalized at a tertiary medical center was performed. Patients infected with VRE ( n = 65) were separately compared to patients infected with gram-negative organisms ( n = 80) and uninfected patients ( n = 306). Results In multivariable logistic regression analyses, female gender (OR 3.73(95% CI1.64,8.49)), severity of liver disease measured by higher Child Pugh scores (OR 0.37(95%CI 0.16,0.84)), presence of ascites (OR 9.43(95% CI 3.22,27.65) and any type of dialysis (OR 3.31,95% CI (1.21,9.04), oral antibiotic prophylaxis for spontaneous bacterial peritonitis and rifaximin use were statistically significantly associated with VRE infection (OR 2.37 (95%CI 1.27, 4.42)). VRE-infected patients had significantly longer mean ICU and total hospital stays (both p < 0.0001), with increased one-year mortality compared to cirrhotic patients without VRE infection, adjusted for age, sex, Hispanic ethnicity, and disease severity. Conclusions It is unclear whether VRE infection serves as an independent risk factor for increased mortality or an indicator for patients with more severe illnesses and thus a higher risk for death.