Is Metabolic Syndrome Considered to Be a Risk Factor for Gastroesophageal Reflux Disease (Non-Erosive or Erosive Esophagitis)?: A Systematic Review of the Evidence

Mohammadi, Mohammad Hossein; Jolfaie, Nahid Ramezani; Alipour, Rooya; Zarrati, Mitra

doi:10.5812/ircmj.30363

Cited by 20 publications

(26 citation statements)

References 63 publications

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“…The major ubiquitous signs of GERD include heartburn and acid regurgitation, while other commonly reported symptoms include sore throat, nausea, eructation, chest pain and cough [2]. Among European and American populations, the approximate prevalence rate of GERD has been reported to be between 10%-20%, while in Asia, this number is below 10% [3,4].…”

Section: Introductionmentioning

confidence: 99%

Involvement of the TLR4/NF-κB Signaling Pathway in the Repair of Esophageal Mucosa Injury in Rats with Gastroesophageal Reflux Disease

Yu¹,

Wang²,

Zhang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Numerous studies have highlighted the activation of NF-κB in the esophageal mucosa during the early stages of gastroesophageal reflux disease (GERD). The present study aimed to investigate the role of the TLR4/NF-κB signaling pathway in GERD rat models. Methods: Wistar rats (n = 60) were recruited to establish a GERD animal model. Distal esophageal pH was assessed, followed by determination of the contents of thiobarbituric acid-reactive species (TBARS) and reactive oxygen species (ROS) in esophageal mucosa homogenate. ELISA was employed to detect the levels of inflammatory factors (IL-6, IL-8, IL-10 and TNF-α) in esophageal mucosa. The expression of MMP-3, MPP-9, Cldn1 and Cldn4 was determined by immunohistochemistry. RT-qPCR and western blot analysis were applied to evaluate the protein expressions in TLR4/NF-κB signaling pathway, while TUNEL staining was utilized to examine the apoptosis rate in the esophageal mucosal tissues. Results: Distal esophageal pH of the rats was higher in the GERD + PDTC group than in other groups. Levels of inflammatory factors in esophageal mucosal tissues were downregulated with the inhibition of NF-κB, which was determined to be associated with the decreased contents of TBARS and ROS. Moreover, decreased MMP-3 and MPP-9 in addition to elevated Cldn1 and Cldn4 were detected in the esophageal mucosa as a result of the inactivation of NF-κB. The TLR4/NF-κB signaling pathway-related proteins (TLR4, NF-κB and IκBα); the rate of apoptosis was demonstrated to be suppressed in the GERD + PDTC group, while inactivating NF-κB was found to alleviate the tissue damage observed in the esophageal mucosa. Conclusion: The key findings of the current study demonstrate that the inactivation of the TLR4/NF-κB signaling pathway alleviates oxidative stress injury and promotes the repair of esophageal mucosal injury among rats with GERD, highlighting a potential novel GERD mechanism.

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Section: Introductionmentioning

confidence: 99%

Involvement of the TLR4/NF-κB Signaling Pathway in the Repair of Esophageal Mucosa Injury in Rats with Gastroesophageal Reflux Disease

Yu¹,

Wang²,

Zhang³

et al. 2018

Cell Physiol Biochem

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“…Calcium channel blockers are widely used to treat hypertension. Some studies have reported that calcium channel blockers are important associated factors for RE as they inhibit esophageal muscle contraction and reduce lower esophageal sphincter pressure leading to RE [9, 12, 30]. However, in addition to the side effects of antihypertensive treatment, the influence of hypertension itself must be taken into account.…”

Section: Discussionmentioning

confidence: 99%

“…Recent aspirin or non-steroid anti-inflammatory drugs use may increase the risk of reflux esophagitis. Otherwise, taking proton-pump inhibitor or histamine-2 receptor antagonists may improve reflux esophagitis [12]. Third, self-reported medical and pharmacology history (such as anti-dyslipidemia medicine use) may result in misclassification bias.…”

Section: Discussionmentioning

confidence: 99%

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What is the impact of metabolic syndrome and its components on reflux esophagitis? A cross-sectional study

Hsieh

Yang

et al. 2019

BMC Gastroenterol

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Background The prevalence rate of reflux esophagitis (RE) in Asia, including Taiwan, has increased dramatically in recent years. However, few studies have discussed on its relationship with metabolic syndrome (MetS). This study aimed to evaluate the correlation between RE and MetS and its components. Methods We conducted a cross-sectional study during 2013 to 2014 in Taiwan. A total of 4895 subjects who completed upper gastrointestinal endoscopy at the Health Examination Center of Changhua Christian Hospital were enrolled. RE was defined according to the upper gastrointestinal endoscopic findings and MetS was defined according to the Taiwanese criteria. Univariate and multivariate logistic regression analyses were applied to calculate odds ratios and 95% confidence intervals for each variable to assess the associated features for RE. We analyzed the relationship between the number of MetS components and the severity of RE using the chi-square test for trend. Results The prevalence rates of MetS and RE were respectively 28.5 and 59.6%. According to univariate logistic regression analysis, MetS was significantly associated with RE and remained a positive association in multivariate logistic regression analysis (adjusted OR ß = 1.251; 95% CI = 1.071–1.462; p = 0.005). Furthermore, among the five MetS components, elevated blood pressure (adjusted OR γ = 1.163; 95% CI = 1.023–1.323; p = 0.021), abdominal obesity (adjusted OR γ = 1.173; 95% CI = 1.020–1.349; p = 0.026) and hyperglycemia (adjusted OR γ = 1.306; 95% CI = 1.142–1.495; p < 0.001) were positively associated with the presence of RE. A weak association was also found between elevated triglycerides and RE after adjusting for age and gender (adjusted OR α = 1.171; 95% CI = 1.022–1.343; p = 0.023). Reduced high-density lipoprotein cholesterol showed no significant difference between groups with and without RE. Older age (≥65 years), male gender, higher body mass index, higher uric acid, smoking, alcohol drinking, and hiatal hernia were found to be significant associated factors for RE. In addition, a dose-response relation between the number of MetS components and the presence of RE was demonstrated in the multivariate analysis. Furthermore, we performed a trend analysis and found the severity of RE got worse as the number of MetS components increased ( p < 0.001). Conclusion This study suggests that MetS is significantly related to the presence and the severity of RE.

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“…С одной стороны, мужской пол, ожирение, сахарный диабет, артериальная гипертензия, курение и злоупотребление алкоголем непосредственно влияют на ГЭРБ; клинические проявления и тяжесть РЭ связаны с метаболическими факторами. Продемонстрирована прямая зависимость между количеством компонентов метаболического синдрома, наличием и степенью тяжести РЭ [54][55][56][57]. Среди перечисленных состояний самым значимым независимым предиктором развития РЭ считается абдоминальное ожирение [54].…”

Section: гэрб как предиктор возникновения ибсunclassified

Gastroesophageal Reflux Disease and Coronary Heart Disease: Is There a “Mutual Burden” Syndrome?

Алексеева

Пикулев

2019

Rossijskij žurnal gastroènterologii, gepatologii, koloproktolog

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Aim. This review aims to generalize data on the mutual aggravating effect on the course of gastroesophageal reflux disease (GERD) and coronary heart disease (CHD).General findings. The combination of CHD and GERD is a common clinical situation. In recent years, more and more information has appeared indicating a non-accidental character of the comorbidity of both diseases. In addition to common risk factors, a number of pathophysiological mechanisms have been established that determine a pathogenetic relationship between CHD and GERD. Reflux disease contributes adversely to chronic coronary heart disease, e.g. by increasing the risk of developing myocardial infarction (MI). The co-occurrence of myocardial ischemia episodes (registered by ECG) with those of heartburn has been identified. A correlation between pathological reflux and ST segment depression has been found. A trigger role of reflux in relation to angina attacks and heart rhythm disturbances has been determined. The pro-arrhythmic effects of GERD on the myocardium are explained by an imbalance of the autonomic nervous system with a predominance of the parasympathetic tone. In turn, both stable angina and myocardial infarction contribute to a more aggressive and refractory course of reflux esophagitis (RE), thus triggering reflux symptoms.Conclusion. The comorbid course of coronary heart disease and GERD is based on complex associations; this clinical situation is characterized by a mutual burden syndrome. Given the high prevalence of a combination of both diseases, it seems relevant to develop pathogenetically substantiated approaches to the management of this category of patients.

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Is Metabolic Syndrome Considered to Be a Risk Factor for Gastroesophageal Reflux Disease (Non-Erosive or Erosive Esophagitis)?: A Systematic Review of the Evidence

Cited by 20 publications

References 63 publications

Involvement of the TLR4/NF-κB Signaling Pathway in the Repair of Esophageal Mucosa Injury in Rats with Gastroesophageal Reflux Disease

Involvement of the TLR4/NF-κB Signaling Pathway in the Repair of Esophageal Mucosa Injury in Rats with Gastroesophageal Reflux Disease

What is the impact of metabolic syndrome and its components on reflux esophagitis? A cross-sectional study

Gastroesophageal Reflux Disease and Coronary Heart Disease: Is There a “Mutual Burden” Syndrome?

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