Helicobacter pylori causes a lifelong infection in the stomach after exposure. H. pylorihas been shown to be associated with peptic ulcer and gastric cancer development. Moreover, it is held responsible for some other nongastric diseases. Among them, coronary heart disease attracts much debate. Many studies have demonstrated a close relationship between insulin resistance and atherosclerosis. Chronic inflammation and alterations in counter-regulatory hormones are deemed responsible for the etiology of insulin resistance. We aimed to examine the effect of H. pylori on insulin resistance. Sixty-three patients were enrolled in the study. Patients were divided into two groups according to H. pylori presence. HOMA-IR (homeostasis model assessment of insulin resistance) level was used to assess insülin resistance. Thirty-six patients were H. pylori positive and 27 were H. pylori negative. There was no difference between the two groups with regard to age, gender, or body mass index. HOMA-IR level was 1.73+/- 1.1 in the H. pylori-negative group, whereas it was 2.56 +/- 1.54 in the H. pylori-positive group (P < 0.05). This study provides the first direct evidence for an association between chronic H. pylori infection and insulin resistance.

The advantages of this method include accurate placement, preperitoneal fixation, and immediate use of the catheter for routine peritoneal dialysis. We also believe that because of the preperitoneal fixation of the catheter, this technique will decrease outflow obstruction, which usually occurs due to omental wrapping or displacement of the catheter tip.

BACKGROUND: Markers of an acute phase reaction, such as C-reactive protein (CRP) or tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6, are predictive for cardiovascular morbidity and mortality in normal subjects and in chronic renal failure patients. In this study, we aimed to investigate serum TNF-alpha, IL-6, IL-10 and CRP levels in continuous ambulatory peritoneal dialysis (CAPD) and hemodialysis (HD) patients. MATERIALS AND METHODS: Serum levels of TNF-alpha, IL-6, IL-10 and CRP levels were measured in 30 patients who were just diagnosed with end-stage renal failure and treated, with 16 CAPD (nine female, seven male) and 14 HD (eight female, six male) patients, before CAPD or HD treatment and after 3 months from the beginning of CAPD or HD in patients with no clinical signs of infection. The control groups were 20 healthy persons of similar age and sex. Serum levels of TNF-alpha, IL-6, IL-10 and CRP were measured by enzyme-linked immunosorbent assay in stable CAPD and HD patients and in healthy persons. RESULTS: The mean serum levels of TNF-alpha, IL-6, IL-10 and CRP showed no significant differences between the CAPD and HD patients for the beginning values and the third month of treatment. However, serum TNF-alpha, IL-6, IL-10 and CRP levels were higher than the control group in the CAPD and HD patients regarding the beginning values and the third month of treatment (p < 0.001). CONCLUSIONS: CAPD and HD of the renal replacement therapy have no effects on serum CRP and cytokines.

INTRODUCTION: Helicobacter pylori (H. pylori) is a non-invasive microorganism causing intense gastric mucosal inflammatory and immune reaction. H. pylori-induced gastric mucosal cytokine overproduction has been clearly documented previously. The stomach has a large surface area and continuous spill-over of locally produced cytokines into the blood stream is a possibility. There are few and conflicting data on circulatory proinflammatory cytokine levels in patients with H. pylori infection. MATERIALS AND METHODS: Forty-two dyspeptic patients were enrolled into the study. The presence of H. pylori infection was diagnosed with antral histopathologic examination. After overnight fasting; serum samples were obtained from each patient to determine circulating interleukin (IL)-6, IL-8 and tumor necrosis factor-alpha (TNF-alpha) levels. RESULTS: H. pylori was shown in 30 cases using Giemsa stain in antral histopathologic evaluation. Twelve cases were negative for H. pylori staining. Both the age and sex distribution had an insignificant difference in both H pylori-positive and H. pylori-negative groups. The mean circulatory levels of IL-6, IL-8 and TNF-a in both groups were not different. The situation was same in respect to the serum levels of these cytokines and the degree of inflammation, H. pylori density and activation scores according to Sydney classification. CONCLUSION: We could not show elevated circulatory levels of IL-6, IL-8 and TNF-alpha in H. pylori-infected cases. We believe that H. pylori-related cytokine activation become concentrated on gastric mucosa and this pathogen-induced local inflammatory cascade does not cause changes in circulatory levels of these cytokines. Moreover, there is no correlation between the levels of serum cytokines and Sydney parameters.

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.