Increased Exhaled 8‐Isoprostane and Interleukin‐6 in Patients with <i>Helicobacter pylori</i> Infection

Yıldırım, Zeki; Bozkurt, Bülent; Özol, Duygu; Armutçu, Ferah; Akgedik, Recep; Karamanli, Harun; Kızılırmak, Deniz; Ikizek, Mustafa

doi:10.1111/hel.12302

Cited by 21 publications

(14 citation statements)

References 32 publications

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“…The existing literature shows that patients with NAFLD have higher BUN values 61 . In summary, a previous study showed that in NAFLD patients, an elevated GGT concentration was associated with an increase in the risk of CKD among nondiabetic, non-hypertensive Korean men, regardless of whether metabolic syndrome was present 62 . However, our study supports the notion that ALD and H. pylori infection specifically influence BUN levels.…”

Section: Discussionmentioning

confidence: 74%

The Correlation and Risk Factors between Carotid Intima-Media Thickening and Alcoholic Liver Disease Coupled with Helicobacter pylori Infection

Wang

Jia

et al. 2017

Sci Rep

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The aim of this study was to explore the associations and differences in influencing factors between alcoholic liver disease (ALD) coupled with Helicobacter pylori infection and atherosclerosis and to determine whether there is a “double hit phenomenon” in atherosclerosis patients with ALD and H. pylori infections. Included cases (n = 160) were categorized into 4 groups: 41 cases of ALD coupled with H. pylori infections (group A), 35 cases of H. pylori infections without ALD (group B), 37 cases of ALD without H. pylori infections (group C), and 47 normal control cases (group D). CIMT was significantly greater in group A than in groups B and D (P = 0.005 and P = 0.001, respectively). The GLM univariate analysis found that CIMT was significantly greater in group A than in groups B, C and D (P = 0.018, P = 0.001 and P = 0.009, respectively). We found that BMI and ALT, AST and ApoB levels were independent predictors of CIMT (P = 0.000, P = 0.000, P = 0.012 and P = 0.014, respectively). ALD coupled with H. pylori infection may result in significant CIMT thickening, but H. pylori infection without ALD and ALD without H. pylori infection does not, suggesting that a “double hit phenomenon” occurs. Additionally, BMI, and ALT, AST and ApoB levels were independent risk factors for increased CIMT.

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Section: Discussionmentioning

confidence: 74%

The Correlation and Risk Factors between Carotid Intima-Media Thickening and Alcoholic Liver Disease Coupled with Helicobacter pylori Infection

Wang

Jia

et al. 2017

Sci Rep

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“…In addition to urinary samples [133–135], other noninvasive and low-cost tools for the screening of oxidative stress, such as salivary [136–138] or exhaled breath [139–141] analysis, have been proposed. However, it has been reported that creatinine urinary markers are not suitable in patients with impaired renal function [135].…”

Section: Markers Based On Ros-induced Modificationsmentioning

confidence: 99%

Measurement and Clinical Significance of Biomarkers of Oxidative Stress in Humans

Marrocco

Altieri

Peluso

2017

Oxidative Medicine and Cellular Longevity

611

500

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Oxidative stress is the result of the imbalance between reactive oxygen species (ROS) formation and enzymatic and nonenzymatic antioxidants. Biomarkers of oxidative stress are relevant in the evaluation of the disease status and of the health-enhancing effects of antioxidants. We aim to discuss the major methodological bias of methods used for the evaluation of oxidative stress in humans. There is a lack of consensus concerning the validation, standardization, and reproducibility of methods for the measurement of the following: (1) ROS in leukocytes and platelets by flow cytometry, (2) markers based on ROS-induced modifications of lipids, DNA, and proteins, (3) enzymatic players of redox status, and (4) total antioxidant capacity of human body fluids. It has been suggested that the bias of each method could be overcome by using indexes of oxidative stress that include more than one marker. However, the choice of the markers considered in the global index should be dictated by the aim of the study and its design, as well as by the clinical relevance in the selected subjects. In conclusion, the clinical significance of biomarkers of oxidative stress in humans must come from a critical analysis of the markers that should give an overall index of redox status in particular conditions.

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“…34 Reports have confirmed that H. pylori-induced chronic inflammation may enhance the production of IL-6, TNFα, and CRP. 35,36 These proinflammatory cytokines would stimulate a series of kinases like JNK, and IKK/NF-kB, leading to enhance IR by suppression of the autophosphorylation of the tyrosyl of the insulin receptor substrate (IRS)-1 37 or upregulating Ser phosphorylation. 38 A recent study was in agreement with our finding that H. pylori infection was related to increased serum leptin.…”

Section: Data From a Follow-up Assessment Extra 3 Months After Compmentioning

confidence: 99%

Helicobacter pylori and non‐alcoholic fatty liver disease: A new enigma?

et al. 2018

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Background and Aim The relationship between Helicobacter pylori (H. pylori) and nonalcoholic fatty liver disease (NAFLD) is a matter of debate. We achieved this prospective work to study whether H. pylori infection is a risk factor for NAFLD. Methods A cohort multicenter pilot study of 369 adults without NAFLD at baseline was followed up for 2 years. Serum leptin, insulin, tumor necrosis factor‐α, adiponectin, and interleukin‐6 were measured using an enzyme‐linked immunosorbent assay (ELISA). Homeostasis model assessment of insulin resistance (HOMA‐IR) and leptin/adiponectin ratio (LAR) were calculated. Fecal H. pylori antigen was measured by ELISA. A total of 127 participants with H. pylori positive were treated and then followed up for 3 months. Results Helicobacter pylori‐positive patients (46.3%) were associated with an increase in IR, proinflammatory cytokines, C‐reactive protein (CRP), LAR, NAFLD‐liver fat score (NAFLD‐LFS), and hepatic steatosis index (HSI) (all P < 0.01). Multivariate analysis of NAFLD according to HSI and NAFLD‐LFS reported that presence of H. pylori, LAR, CRP, IL‐6, smoking, and age (all P < 0.01) were independent risk factors for the presence of NAFLD. Multiple models adjusted for potential mediators or confounders such as metabolic, inflammatory, and biochemical factors were constructed. After therapy of H. pylori infection, there was a significant reduction in lipogenic profile, IR, leptin, LAR, CRP, proinflammatory cytokines, HSI, and NAFLD‐LFS, as well as, increasing HDL. Conclusion Helicobacter pylori infection was related to an increased risk of NAFLD development, through increased markers of IR, inflammatory mediators, and lipid metabolism. Moreover, its eradication can recover these NAFLD risk factors.

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Increased Exhaled 8‐Isoprostane and Interleukin‐6 in Patients with Helicobacter pylori Infection

Abstract: H. pylori infection causes an asymptomatic airway inflammation which can be detected by exhaled breath condensate. The clinical importance of this inflammation remains unclear.

Cited by 21 publications

References 32 publications

The Correlation and Risk Factors between Carotid Intima-Media Thickening and Alcoholic Liver Disease Coupled with Helicobacter pylori Infection

The Correlation and Risk Factors between Carotid Intima-Media Thickening and Alcoholic Liver Disease Coupled with Helicobacter pylori Infection

Measurement and Clinical Significance of Biomarkers of Oxidative Stress in Humans

Helicobacter pylori and non‐alcoholic fatty liver disease: A new enigma?

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