Association of Helicobacter Pylori Infection with Endothelial Dysfunction in Metabolic Syndrome

Background: Metabolic risk factors play a critical role in metabolic syndrome (MetS), and endothelial dysfunction is important in its development. On the other hand, Helicobacter pylori (H. pylori) infection has an essential role in MetS. The goal of present study was to evaluate the effect of H. pylori infection on endothelial dysfunction in MetS patients. Methods: Based on the International Diabetes Federation (IDF) criteria, 80 MetS patients (59 females and 21 males, mean age: 48.94 ± 10.00 years) were selected. Plasma samples were assayed for H. pylori IgG using the ELISA method. Endothelial function was also evaluated by measuring plasma concentrations of endothelin-1 (ET-1), E-selectin, and intracellular adhesion molecule-1 (ICAM-1) using ELISA method. Also, NO2– and NO3– concentrations were measured by Griess method. Results: Fifty patients (62.5%) had H. pylori infection. Plasma concentrations of ET- 1, NO2–, and NO3– were significantly higher in MetS patients with positive H. pylori infection than in MetS patients with negative H. pylori infection (ET-1: 2.92 ± 2.33 vs 1.9 ± 1.4 pg/ml; P = 0.037; NO2–:19.46 ± 7.11 vs 15.46 ± 4.56 μM; P = 0.003; NO3–: 20.8 ± 10.53 vs 16.85 ± 6.03 μM, P = 0.036). However, plasma concentrations of ICAM-1 and E-selectin did not show any significant difference in the two groups. Conclusion: The results showed a relationship between H. pylori infection and endothelial dysfunction. H. pylori infection can lead to atherosclerosis by causing chronic inflammation and affecting the factors contributing to the MetS

The effect of Helicobacter pylori infection on oxidative stress status in erosive reflux disease

Background and Objectives: Helicobacter pylori (H. pylori) infection has been associated with increased production of reactive oxygen species, which leads to oxidative stress in the gastrointestinal mucosa. Nevertheless, the association of H. pylori infection and oxidative stress in erosive reflux disease (ERD) is still unclear. We sought to investigate the association between oxidative stress status and H. pylori infection in ERD. Materials and Methods: Eighty-three ERD patients (45 male/ 38 female; mean age: 40.4 ± 14.3 years) who had heartburn and/or regurgitation and erosion(s)-confirmed by endoscopy-in the distal esophagus were enrolled. Two antral biopsies were taken from the patients for rapid urease test. Blood samples were drawn for measurement of oxidative stress parameters, including malondialdehyde (MDA), ferric reducing antioxidant power (FRAP), superoxide dismutase (SOD) activity, and glutathione peroxidase (GPX) activity. Data were compared among H. pylori(+) and H. pylori(-) patients. Results : The overall prevalence of H. pylori infection was 71% (59/83). There was a significant increase in the levels of MDA in H. pylori(+) patients (0.98 ± 0.28 μmol/l) when compared with H. pylori(-) patients (0.84 ± 0.33 μmol/l; P = 0.048). However, the levels of FRAP in the H. pylori-infected patients were significantly lower than in those without infection (941 ± 211.8 vs. 1060.3 ± 216.6 μmol/l, respectively; P = 0.028). There were no significant differences in SOD activity, GPX activity, age, sex, and body mass index (BMI) of H. pylori(+) vs. H. pylori(-) patients (P > 0.05). Conclusion: Increased levels of MDA in H. pylori(+) patients showed association between oxidative stress and H. pylori infection in EDR patients. Also, considerable changes of antioxidant concentrations indicate a compensatory mechanism to cope with the increased oxidant status in H. pylori(+) patients. It may be concluded that oxidative stress increases in the presence of H. pylori in ERD patients, and antioxidant defense mechanisms, try to minimize oxidative stress damage

Oxidative stress status in patients with cardiac syndrome X

ABSTRACT: Cardiac syndrome X (CSX) is characterized by chest pain, typical angina pectoris, abnormal exercise test result and normal coronary arteries. Microvascular dysfunction and enhanced oxidative stress are the mechanisms suspected to play an important role in the pathogenesis of CSX. Thus we aimed to evaluate the oxidative stress status of 28 patients with CSX (14 male/14 female, mean age 49.5 ± 9.3 years) and 24 age-and gender-matched healthy controls (10 male/14 female, mean age 45.6 ± 5.7 years). Blood samples were drawn for measurement of malodialdehyde (MDA), as a marker of lipid peroxidation, glutathione (GSH) and superoxide dismutase (SOD) activity, as antioxidant markers and ferric reducing ability of plasma (FRAP), as a marker of total antioxidant capacity. There was significant increase in the levels of MDA in CSX patients comparing to controls (3.8 ± 0.12 vs 3.3 ± 0.14 mM, respectively; p = 0.006). But the levels of FRAP in CSX patients were significantly lower than those controls (504 ± 19 vs 568 ± 26 µM, respectively; p = 0.046). Also, GSH levels and SOD activity in patients were significantly lower than those of the controls (GSH: 133.6 ± 5.4 vs 152.5 ± 7.8 mmol/g Hb, p = 0.048; SOD: 386 ± 34 vs 578 ± 38 U/g Hb, p = 0.0001). It may be concluded that there is systemic oxidative stress in CSX patients. Considerable changes of antioxidant concentrations, indicating a compensatory mechanism to cope with increased oxidative stress in CSX patients and the body's antioxidant defence mechanisms try to minimize oxidative stress damage

Age–sex differences in the global burden of lower respiratory infections and risk factors, 1990–2019: results from the Global Burden of Disease Study 2019

Summary Background The global burden of lower respiratory infections (LRIs) and corresponding risk factors in children older than 5 years and adults has not been studied as comprehensively as it has been in children younger than 5 years. We assessed the burden and trends of LRIs and risk factors across all age groups by sex, for 204 countries and territories. Methods In this analysis of data for the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019, we used clinician-diagnosed pneumonia or bronchiolitis as our case definition for LRIs. We included International Classification of Diseases 9th edition codes 079.6, 466–469, 470.0, 480–482.8, 483.0–483.9, 484.1–484.2, 484.6–484.7, and 487–489 and International Classification of Diseases 10th edition codes A48.1, A70, B97.4–B97.6, J09–J15.8, J16–J16.9, J20–J21.9, J91.0, P23.0–P23.4, and U04–U04.9. We used the Cause of Death Ensemble modelling strategy to analyse 23 109 site-years of vital registration data, 825 site-years of sample vital registration data, 1766 site-years of verbal autopsy data, and 681 site-years of mortality surveillance data. We used DisMod-MR 2.1, a Bayesian meta-regression tool, to analyse age–sex-specific incidence and prevalence data identified via systematic reviews of the literature, population-based survey data, and claims and inpatient data. Additionally, we estimated age–sex-specific LRI mortality that is attributable to the independent effects of 14 risk factors. Findings Globally, in 2019, we estimated that there were 257 million (95% uncertainty interval [UI] 240–275) LRI incident episodes in males and 232 million (217–248) in females. In the same year, LRIs accounted for 1·30 million (95% UI 1·18–1·42) male deaths and 1·20 million (1·07–1·33) female deaths. Age-standardised incidence and mortality rates were 1·17 times (95% UI 1·16–1·18) and 1·31 times (95% UI 1·23–1·41) greater in males than in females in 2019. Between 1990 and 2019, LRI incidence and mortality rates declined at different rates across age groups and an increase in LRI episodes and deaths was estimated among all adult age groups, with males aged 70 years and older having the highest increase in LRI episodes (126·0% [95% UI 121·4–131·1]) and deaths (100·0% [83·4–115·9]). During the same period, LRI episodes and deaths in children younger than 15 years were estimated to have decreased, and the greatest decline was observed for LRI deaths in males younger than 5 years (–70·7% [–77·2 to –61·8]). The leading risk factors for LRI mortality varied across age groups and sex. More than half of global LRI deaths in children younger than 5 years were attributable to child wasting (population attributable fraction [PAF] 53·0% [95% UI 37·7–61·8] in males and 56·4% [40·7–65·1] in females), and more than a quarter of LRI deaths among those aged 5–14 years were attributable to household air pollution (PAF 26·0% [95% UI 16·6–35·5] for males and PAF 25·8% [16·3–35·4] for females). PAFs of male LRI deaths attributed to smoking were 20·4% (95% UI 15·4–25·2) in those aged 15–49 years, 30·5% (24·1–36·9) in those aged 50–69 years, and 21·9% (16·8–27·3) in those aged 70 years and older. PAFs of female LRI deaths attributed to household air pollution were 21·1% (95% UI 14·5–27·9) in those aged 15–49 years and 18·2% (12·5–24·5) in those aged 50–69 years. For females aged 70 years and older, the leading risk factor, ambient particulate matter, was responsible for 11·7% (95% UI 8·2–15·8) of LRI deaths. Interpretation The patterns and progress in reducing the burden of LRIs and key risk factors for mortality varied across age groups and sexes. The progress seen in children younger than 5 years was clearly a result of targeted interventions, such as vaccination and reduction of exposure to risk factors. Similar interventions for other age groups could contribute to the achievement of multiple Sustainable Development Goals targets, including promoting wellbeing at all ages and reducing health inequalities. Interventions, including addressing risk factors such as child wasting, smoking, ambient particulate matter pollution, and household air pollution, would prevent deaths and reduce health disparities