To evaluate susceptibility of Helicobacter pylori to amoxicillin and clarithromycin in end-stage renal disease (ESRD) patients and non-uremic controls. The subjects with dyspeptic complaints were 33 ESRD patients and 46 age- and sex-matched non-uremic controls who exhibited H pylori on antral biopsy specimens. The two groups were age and sex matched. The H pylori strains' pattern of susceptibility to amoxicillin and clarithromycin was investigated with the agar dilution technique. None of the H pylori strains from either group showed resistance to amoxicillin with the agar dilution method. Twelve (36.4%) of the ESRD group strains and 7 (15.2%) of the control group strains showed resistance to clarithromycin, and this difference was statistically significant (P<0.05). Resistance to amoxicillin does not appear to be an important problem in H pylori-infected ESRD and non-uremic patients in our region. In contrast, the rates of resistance to clarithromycin are high, particularly in the ESRD population.

Heart failure (HF) remains a significant health problem despite advances in diagnosis and treatment options. Malnutrition and increased inflammation predict poor disease prognosis. The parameters of the Naples prognostic score (NPS) include albumin, total cholesterol, neutrophil-lymphocyte ratio (NLR), and lymphocyte-monocyte ratio (LMR). We aimed to assess the potential of NPS as a predictor of long-term mortality in patients with HF. A total of 1728 patients with HF who applied to our center between 2018 and 2022 were included in this study. The NPS was computed and the patients were divided into three groups according to their NPS values as follows: NPS = 0 (Group 1), NPS = 1-2 (Group 2), and NPS = 3-4 (Group 3). We also evaluated the association between NPS value and HF mortality. The patients were followed for a mean follow-up duration of 30 months. The mortality rate was 8.3% (145 patients). We carried out Model-1 and -2 Cox regression analyses to identify long-term mortality determinants. Model-2 was constructed by adding NPS to Model-1. NPS was significantly associated with HF mortality (Hazard Ratio: 2.194, 95% Confidence Interval: 1.176-4.091, p = 0.014). According to the Kaplan-Meier plot and log-rank analyses, there was a statistically significant difference in the long-term mortality of patients with HF and their NPS values for the entire cohort. Based on our findings, NPS showed promise as an independent predictor of long-term mortality in individuals with HF.

INTRODUCTION: Helicobacter pylori is one of the main causes of gastroduodenal diseases, such as chronic gastritis and peptic ulcer. It has been shown that eosinophils increase in the stomach in H. pylori infection. Eosinophilic cationic protein (ECP) is a cytotoxic molecule secreted by the activated eosinophils. However, there are no sufficient data about the role of ECP in H. pylori infection and its effect on ulcer development. In this study we investigated the gastric eosinophilic infiltration, gastric juice and serum ECP levels in patients with chronic gastritis and gastric ulcer associated with H. pylori.Materials and methods: Forty‐four H. pylori‐positive and 20 H. pylori‐negative patients who underwent upper gastrointestinal system endoscopy after admitting with dyspeptic complaints were enrolled in the study. Twenty‐one of the H. Pylori‐positive patients had gastric ulcer while 23 patients had none. During endoscopy, multiple gastric biopsies and juices were taken. In gastric biopsies, H. pylori and eosinophilic infiltration were assessed. Additionally, gastric juice and serum ECP levels were measured.Results: Eosinophil infiltration, gastric juice ECP levels, and gastric juice/serum ECP ratios in the H. pylori‐positive group were greater than in the H. pylori‐negative group (p < 0.01). There was no statistically significant difference regarding serum ECP levels between the two groups (p > 0.05). When H. pylori‐positive patients were compared with regard to gastric ulcer presence, however, there was no significant difference in gastric eosinophil infiltration, gastric juice ECP levels, serum ECP levels, and gastric juice/serum ECP ratios (p > 0.05).Conclusion: The results of this study suggest that eosinophils and eosinophil‐released ECP may contribute to inflammatory changes seen in chronic gastritis, whereas there is no proof that they play a role in ulcer development.

Introduction. Microbial pathogens, one of them isHelicobacter pylori(H. pylori), have frequently been implicated in the atherogenesis. Endothelium-derived nitric oxide (NO) is synthesized from L-arginine by nitric oxide synthase (NOS) and plays a pivotal role in the regulation of vascular tone. Asymmetric dimethylarginine (ADMA) is the most potent endogenous NOS inhibitor. Elevated levels of ADMA have been reported in many circumstances associated with a high cardiovascular risk. The aim of the present study was to investigate whether the eradication ofH. pyloriinfection affects serum ADMA levels.Materials and Methods. Forty-twoH. pylori-positive patients were enrolled in the study. Triple therapy for 14 days were given to all patients. Serum ADMA levels were measured at baseline and 2 months after therapy.Results. Eradication was achieved in 34 (81%) patients. The mean serum ADMA levels before and after therapy were and ng/mL in the group withH. pylorieradicated and and ng/mL in the noneradicated, respectively. We detected statistically significant decreased serum ADMA levels after therapy inH. pylorieradicated group.Conclusion. These findings have indicated that eradication ofH. pyloriinfection may decrease the risk of atherosclerosis and cardiovascular events.