ObjectiveTo evaluate laparoscopic anti-reflux surgery for treatment of chronic obstructive pulmonary disease (COPD) associated with gastroesophageal reflux disease (GERD).MethodsA total of 20 patients with GERD and COPD underwent laparoscopic anti-reflux procedure in the First Affiliated Hospital of Zhengzhou University from January 2016 to December 2017. The reflux diagnostic questionnaire, pulmonary function, COPD assessment test scale, 24-hour esophageal pH-impedance monitoring and esophageal pressure measurement were performed in all patients. All drug-refractory patients underwent the laparoscopic anti-reflux surgery. After 12 months follow-up, the parameters of COPD and GERD were evaluated again.ResultsTwenty patients with COPD and GERD were successfully performed laparoscopic anti-reflux surgery, no hernia patch repair patient and death patient occurred. There was no esophageal rupture, bleeding, infection, and other serious postoperative complications. Although 8 patients had the different degree dysphagia and 10 patients had the different degree abdominal distention, they all relieved themselves. Twenty patients with GERD and COPD were followed up for 1 year. Compared with the values before treatment, the GERD symptom score, reflux times, DeMeester score, and COPD assessment test score of the patients were significantly reduced (P<0.05), the lower esophageal sphincter pressure, percentage of forced expiratory volume in one second (FEV1) in the predicted value and FEV1/forced vital capacity (FVC) were significantly increased (P<0.05) after the treatment. According to the grading standard of The Global Initiative for Chronic Obstructive Lung Disease (GOLD), 5 cases of grade Ⅰ, 2 cases of grade Ⅱ and 1 case of grade Ⅲ were cured; 1 case of grade Ⅰ, 4 cases of grade Ⅱ and 4 cases of grade Ⅲ were improved; 1 case of grade Ⅰ, 1 case of grade Ⅱ and 1 case of grade Ⅳ were ineffective. The total effective rate was 85% (17/20).ConclusionsCOPD is closely related to GERD. Laparoscopic anti-reflux surgery can not only effectively treat GERD, but also markedly improve COPD.
ObjectiveTo develop an experimental model of gastroesophageal reflux-induced esophageal stricture in rats and explore the mechanism of esophageal stricture. MethodsA total of 30 male Sprague-Dawley (SD) rats by random number table method were randomly divided into three groups as follows: an operation+acid perfusion group, first the models of lower esophageal sphincter relaxation and hiatal hernia were made, and then the rats’ esophagus were perfused with hydrochloric acid-pepsin; acid perfusion group, the rats’ esophagus were directly perfused with hydrochloric acid-pepsin; and control group, rats’ esophagus were perfused with normal saline. After 4 weeks of continuous perfusion, the esophageal mucosal injury of SD rats in each group were observed, and the concentrations of inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-18] in esophageal tissues were detected by enzyme-linked immunosorbent assay. ResultsIn the operation+acid perfusion group, esophageal stricture was formed in 2 SD rats, but no esophageal stenosis was found in the acid perfusion group and the control group. The body weight of rats in the operation+acid perfusion group and the acid perfusion group were lower than that in the control group (P<0.05). The esophageal mucosal injury scores of rats in the operation+acid perfusion group and the acid perfusion group were higher than that in the control group (P<0.001), and the operation+acid perfusion group was higher than that in the acid perfusion group (P=0.014). The concentrations of TNF-α, IL-1β and IL-18 in esophageal tissues were higher in the operation+acid perfusion group and the acid perfusion group than that in the control group (P<0.001), and the operation+acid perfusion group was higher than that in the acid perfusion group (P<0.001). ConclusionsThe anti-reflux barrier is an important part of preventing gastroesophageal reflux disease. The destruction of anti-reflux barrier, hydrochloric acid-pepsin perfusion and inflammatory cytokines jointly induced esophageal inflammation and injury, and even caused esophageal stricture.
Barrett’s esophagus (BE) is currently recognized as a precancerous lesion of esophageal adenocarcinoma. Gender, age, obesity, smoking and some other factors are closely related to BE, but the exact pathogenesis is still unclear. Gastrointestinal microecology is of great significance to the human body. It is closely related to human immunity, tumor, chronic inflammation, nutrient absorption, material metabolism. It may be closely related to the occurrence and development of BE. This article reviews the research progress of the relationship between BE and gastrointestinal microecology, aiming to provide a basis for further clarifying the pathogenesis of BE and targeting intervention in BE.
Objective To investigate the different clinical features of chronic cough induced by rhinitis /sinusitis or gastro-esophageal reflux, and its significance for etiological diagnosis of chronic cough.Methods Chronic cough patients were recruited from respiratory medicine clinic in Chongqing Xinqiao Hospital from December 2009 to December 2010. Medical history, symptoms and signs were recorded from all selected patients. The patients with chronic rhinitis / sinusitis, but without gastro-esophageal reflux symptoms were suspected upper airway cough syndrome ( UACS) , and given chlorpheniramine, nasal decongestant, and corticosteroid treatment for 1 week. The patients with clinical symptoms associated with gastroesophageal reflux or with history of gastric diseases were suspected gastroesophaged reflux-related cough ( GERC) , were given esomeprazole ( 40 mg, bid) , combined prokinetic agent for 2 weeks. The patients were confirmed the diagnosis of UACS or GERC when their cough was relieved after the above targeted treatment.Results 114 patients were enrolled in this study. 47 patients were suspected GERC, of which 32 were confirmed, and 67 patients were suspected UACS, of which 43 were confirmed. There was no significant difference in age, duration of disease, severity of cough, proportion of night cough, proportion of clear throat symptom, or proportion of cobblestone sign between the UACS patients and the GERC patients ( P gt;0. 05) .There were more females in the GERC patients and more males in the UACS patients ( P lt; 0. 05) . Cough with sputum, throat symptoms and signs were more common in the UACS patients ( P lt;0. 05) . The hoarseness and sore throat symptoms were found only in the GERC patients, but postnasal drip symptoms were found only in the UACS patients. Conclusions Throat signs and symptoms are not completely similiar in the GERC and the UACS patients. Comprehensive judgments combining with patient history,characteristics of concurrent cough, throat symptoms, and signs can provide important references for the clinical diagnosis of chronic cough caused by rhinitis/ sinusitis or gastro-esophageal reflux.
Objective We aimed to evaluate the prevalence of H.pylori infection and the prevalence of cagA+ strains in patients with and without Barrett’s esophagus. Methods A full literature search to February 2008 was conducted in PubMed, MEDLINE and EMbase databases to identify case-control studies or cohort studies evaluating the prevalence of H.pylori in patients with or without Barrett’s esophagus. Summary odds ratios (OR) and 95% confidence interval (CI) were calculated by RevMan 4.2.8. Results Nineteen studies were identified (16 case-controlled studies and 3 cohort studies). In case controlled studies, the prevalence of H.pylori infection significantly decreased in patients with Barrett’s esophagus as compared subjects with normal endoscopic appearance, with a overall OR of 0.56 (95%CI 0.40 to 0.79). The prevalence of H.pylori infection was no statistically significant difference in patients with Barrett’s esophagus as compared to those with gastroesophageal reflux disease, with a overall OR of 0.86 (95% CI 0.74 to 1.00). In cohort studies, the prevalence of H. pylori was no statistically significant difference in patients with Barrett’s esophagus as compared to patients with normal endoscopic appearance or patients with gastroesophageal reflux disease, with a overall OR of 1.12 (95%CI 0.77 to 1.61) and 1.10 (95%CI 0.32 to 3.83). When the analysis was stratified by the status of cagA, the prevalence of cagA positive strains significantly decreased in patients with Barrett’s esophagus as compared both to subjects with normal endoscopic appearance with OR 0.30 and 95% CI 0.12 to 0.74, and to those with gastroesophageal reflux disease (OR 0.55; 95%CI 0.33 to 0.94). Irrespective of the presence of intestinal metaplasia, similar magnitude for the reduction of H.pylori infection was observed for patients with Barrett’s esophagus and those with normal endoscopic appearance. While accompared with the presence of intestinal metaplasia, Barrett’s esophagus was associated with a significantly reduction as compared to the patients with gastroesophageal reflux disease (OR 0.81, 95%CI 0.68 to 0.98). When stratified analyses were performed, a significant reduction of H.pylori infection was observed only in patients with long-segment Barrett’s esophagus (OR 0.54; 95%CI 0.35 to 0.82), but not in those with short-segment Barrett’s esophagus (OR 0.72; 95%CI 0.43 to 1.20). Conclusion This meta-analysis indicated that the prevalence of H.pylori infection, especially the prevalence of cagA positive strains was significantly lower in patients with Barrett’s esophagus than in subjects with normal endoscopic appearance. However, the prevalence of H. pylori infection was no statistical difference in patients with Barrett’s esophagus as compared to those with gastroesophageal reflux disease. Colonization with cagA positive strains may be protective against the formation of Barrett’s esophagus.
Non-erosive gastroesophageal reflux disease (NERD) refers to a disease with symptoms such as acid reflux, heartburn and pathological reflux, but no significant esophageal mucosal damage under endoscopy. Its pathogenesis may be related to factors such as lower esophageal sphincter dysfunction, weakened esophageal clearance ability, visceral hypersensitivity, and disordered intestinal microecology, but the specific mechanism is still unclear. Small intestinal bacterial overgrowth (SIBO) is a common intestinal flora disorder syndrome. A number of studies have shown that SIBO has a certain correlation with NERD, and SIBO may be involved in the occurrence and development of NERD through mechanisms such as inflammatory response, gas production, and increased short-chain fatty acids. Therefore, this article reviews the correlation between NERD and SIBO, aiming to provide new ideas for the diagnosis and treatment of NERD.
Objective To investigate the inhibitory effects and related mechanisms of NOD like receptor protein 3 (NLRP-3) inflammasome inhibitor MCC950 on oxidative stress, inflammation, and pyroptosis in human esophageal epithelial cells (HEECs). MethodsHEECs cells were passaged and divided into blank control group, acid stimulation group (stimulated 3 times a day with pH 4 acidic medium for 15 minutes each time, cultured for 48 hours), bile salt stimulation group (stimulated 3 times a day with 400 μmol/L bile salt mixture for 15 minutes each time, cultured for 48 hours), lipopolysaccharide (LPS) group (stimulated with 10 μL of 100 ng/mL LPS for 48 hours), MCC950 group (stimulated with 10 μL of 7.5 ng/mL MCC950 for 4 hours, then stimulated with acid, bile hydrochloric acid, and LPS for 48 hours), and N-acetyl-L-cysteine (NAC) group (stimulated with 1 mmol/L NAC for 4 hours, then stimulated with acid, bile hydrochloric acid, and LPS 48 hours). Three culture dishes were used in each group to detect the mRNA and protein expression levels of oxidative protein/antioxidant protein [Nox-4 (NADPH oxidase 4), nuclearfactor erythroidderived 2-like 2 (Nrf-2), heme oxygenase-1 (HO-1)], NLRP-3 signaling pathway [NLRP-3/caspase-1/intereukin (IL)-1β/IL-18], and cell apoptosis pathway [caspase-4/caspase-5/GSDMD] using real-time reverse transcription polymerase chain reaction (RT-PCR) and Western blotting experiments. Cell apoptosis were observed through Hoechst33342 staining. ResultsMCC950 intervention (0.023) and NAC intervention (0.031) effectively inhibited HEECs apoptosis induced by acid (0.042), bile salt (0.047), and LPS (0.054). The results of RT-PCR experiments showed that MCC950 intervention and NAC intervention significantly inhibited the high expression of Nox-4 mRNA (MCC950: 1.68; NAC: 1.62) in HEECs cells induced by acid (2.40), bile salt (3.07), and LPS (3.52), and significantly upregulated the mRNA expression levels of antioxidant proteins Nrf-2 (MCC950: 0.72; NAC: 0.57) and HO-1 (MCC950: 0.74; NAC: 0.57). MCC950 intervention and antioxidant NAC intervention effectively inhibited the mRNA expression levels of NLRP-3 (MCC950: 1.58; NAC: 1.47), ASC (MCC950: 1.56; NAC: 1.93), caspase-1 (MCC950: 1.64; NAC: 1.96), IL-1β (MCC950: 1.66; NAC: 1.82), IL-18 (MCC950: 1.58; NAC: 1.84) in HEECs cells induced by acid stimulated, bile salt stimulated, and LPS. MCC950 intervention and antioxidant NAC intervention effectively inhibited the mRNA expression levels of apoptosis pathway markers such as caspase-4 (MCC950: 1.51; NAC: 1.61), caspase-5 (MCC950: 1.38; NAC: 1.64), and GSDMD (MCC950: 1.41; NAC: 1.54) induced by acid stimulation, bile salt stimulation, and LPS in HEECs cells. The electrophoresis results were similar with RT-PCR. ConclusionAcid, bile salt, and LPS can all induce the overexpression of oxidative stress markers in HEECs, reduce the expression of antioxidant proteins, and activate the NLRP-3 inflammasome signaling pathway and cell pyroptosis pathway, promoting cellular inflammatory damage, but MCC950 has a protective effect.
ObjectiveTo investigate the causal relationship between gastroesophageal reflux disease (GERD) and obstructive sleep apnea (OSA) with its typical symptoms (snoring and daytime sleepiness) by using Mendelian randomization (MR). MethodsThe inverse-variance weighted method was used as the main analysis method to assess the causal effect. Sensitivity and pleiotropy analyses were carried out using leave-one-out and MR-Egger analysis, and then heterogeneity tests were conducted. ResultsIn the MR analysis, genetically predicted GERD was associated with a greater risk of OSA (IVW: OR=1.528, 95%CI 1.374 to 1.699, P=5.315E?15). Additional MR results were consistent with the IVW results, and no pleiotropy or heterogeneity was found. We also discovered a significant causal relationship between GRED and snoring (IVW: OR=0.959, 95%CI 0.949 to 0.969, P=1.507E?15), and daytime sleepiness (IVW: OR=1.024, 95%CI 1.021 to 1.036, P=4.580E?5), with no evidence of pleiotropy. ConclusionThe MR study supports a causal effect between GERD and OSA with its typical symptoms (daytime sleepiness and snoring).
Gastroesophageal reflux (GER) is one of the most common postoperative complications in patients with esophageal cancer, which mainly manifests as heartburn sensation and acid reflux, and has a serious impact on patients' postoperative recovery and quality of life. This article reviews five aspects of postoperative reflux: main manifestations, hazards, assessment tools, influencing factors, and nonpharmacological interventions, in order to enhance the awareness of clinical healthcare professionals in recognizing and managing patients with postoperative reflux, and to provide a reference for carrying out the assessment and developing the intervention program.
