Role Of Gastroesophageal Reflux Research Articles

A novel laparoscopic proximal gastrectomy esophagogastric anastomosis procedure with left placket muscle flap plasty (modified Kamikawa anastomosis): Two cases report and brief literature review

Background: The use of left placket single muscle flap covered anastomosis in proximal gastrectomy has not been reported in the literature. The occurrence of gastroesophageal reflux after proximal gastrectomy is closely related to the mode of digestive tract reconstruction. The currently available digestive tract reconstruction approach affects patient’s postoperative quality of life due to the disadvantages of gastroesophageal reflux and anastomotic stenosis. Therefore, the use of left open flap single muscle flap covered anastomosis in proximal gastrectomy may improve the postoperative quality of life of patients. We present a case report and literature review to illustrate the therapeutic results of left-opening single muscle flap covered anastomosis in proximal gastrectomy. Case presentation: Two male patients with average age of 70.5 years and average BMI of 20.5 underwent laparoscopic proximal gastrectomy with an intraoperative left open flap single muscle flap covered overlap anastomosis. The average duration of surgery was 277.5 min, with average intraoperative bleeding of 100 ml, and no anastomotic stenosis was detected by contrast examination on the sixth postoperative day. The postoperative exhaust time was 3 days in both cases, liquid diet was given for 7 days and discharged from the hospital on the 8th day after operation. On an average 19 lymph nodes were dissected. The postoperative pathological stages were T3N2M0 and T1bN0M0. No gastroesophageal reflux or anastomotic fistula was detected in the recent follow-up. Conclusion: The application of the left flap covering the overlap anastomosis in laparoscopic proximal gastrectomy has achieved good results. Multi center large sample clinical studies are needed to further determine its role in gastroesophageal reflux.

Controversies of Gastro-oesophageal Junction and “Gastric cardia” and the role of Gastro-oesophageal reflux in it

Sri Lanka Journal of Medicine is the official journal of the Kandy Society of Medicine. It is a peer-reviewed journal currently published biannually. Original articles, reviews, brief reports, case reports, points of view, and letters to the editor, in all fields of medical science and practice are accepted for publication.The Sri Lanka Journal of Medicine is now indexed in DOAJ

Association Between Antibodies Against Lung Self-Antigens and Gastroesophageal Reflux in Lung Transplant Candidates

Gastroesophageal reflux (GER) and pretransplant antibodies against lung self-antigens (SAbs) collagen-V and/or k-alpha 1 tubulin are both independently associated with allograft dysfunction after lung transplantation (LTx). The role of GER in inducing lung injury and SAbs is unknown. We aimed to study the association between pre-LTx GER and SAbs. After IRB approval, we retrieved SAb assays conducted between 2015 and 2019 and collected 24 hour GER data for these patients. Patients were divided into 2 groups: no reflux (GER-) and pathologic reflux (GER+) to compare the prevalence of SAbs. Multivariate analysis was used to study the association between GER and SAbs in the whole cohort and in restrictive lung disease (RLD) and obstructive lung disease (OLD) subsets. Proximal esophageal reflux (PER) events ≥5 was considered abnormal. Patients (n=134; 73 men) were divided into groups: GER- (54.5%, n=73) and GER+ (45.5%, n=61). The prevalence of GER was higher in the RLD than in the OLD subset (p < 0.001). The overall prevalence of SAbs was 53.7% (n=72), higher in the GER+ than the GER- group (65.6% vs 43.8%, p=0.012), but comparable between RLD and OLD subsets. Overall, SAbs were associated with GER (p=0.012) and abnormal PER (p=0.017). GER and abnormal PER increased the odds of SAbs in the RLD subset (OR [95% CI]: 2.825 [1.033-7.725], p=0.040 and OR [95% CI]: 3.551 [1.271-9.925], p=0.014, respectively) but not in the OLD subset. LTx candidates have a high prevalence of SAbs, which are significantly associated with GER and abnormal PER in patients with RLD.

Distress in Infants and Young Children: Don't Blame Acid Reflux.

The role of gastroesophageal reflux (GER) causing distress in infants is controversial but acid inhibitors are often empirically prescribed. We evaluated the relation between distress assessed by the Face, Legs, Activity, Cry, Consolability (FLACC) scale and GER in infants. We analyzed multiple intraluminal impedance-pH (MII-pH) monitoring tracings of infants with persistent unexplained fussiness or distress. Symptoms occurring during investigation were scored by parents using the FLACC scale and were grouped as "distress" episodes. We recruited 62 children (ages 15 days to 23 months, median age 3.5 months). During MII-pH, 452 episodes of distress were registered: 217 (48%) were temporally associated with GER and 235 (52%) were not, with no difference in the median value of FLACC between the 2 groups. Infants with abnormal acid exposure index had a significantly lower FLACC compared with the group with acid reflux index <7% (P < 0.001). When associated with symptoms, GER occurred significantly more often before than simultaneously or after an episode of distress (P = 0.001). Age, proximal extension, and duration of GER did not correlate with FLACC scores. Episodes of distress associated with nonacid reflux presented a significant higher FLACC compared with the ones with acid content (FLACC 6 vs 5, P = 0.011). In infants, episodes of distress do not significantly correlate with GER. No difference in infant distress was noted between proximal and distal GER. Non-acid reflux is perceived at least as painful than acid GER. Our results stress that acid inhibitors should not be started in infants presenting distress unless a clear association with acid GER is demonstrated.

Prevalence of Helicobacter pylori infection in sexual partners of H. pylori-infected subjects: Role of gastroesophageal reflux.

Helicobacter pylori is transmitted through faecal-oral or oral-oral routes. Whether H. pylori infection is more prevalent in sexual partners of H. pylori-infected subjects is unclear. We evaluated 1) the prevalence of H. pylori infection in sexual partners of H. pylori-infected subjects; and 2) whether presence of gastroesophageal reflux in H. pylori-infected subjects was associated with transmission of infection to their sexual partners. We evaluated H. pylori infection by 13C Urea Breath Test in sexual partners of 161 consecutive patients with H. pylori-related dyspepsia. The case-control group consisted of 161 dyspeptic subjects undergoing the 13C Urea Breath Test. The prevalence of reflux symptoms was noted through the Leeds scale. The role of gastroesophageal reflux in transmission of H. pylori infection was evaluated by binary logistic regression. A two-tailed p value of 0.05 or less was considered significant. Prevalence of H. pylori infection in sexual partners of H. pylori-infected subjects is 74.5% whereas prevalence of H. pylori infection in the control group is 32.3%, p<0.05. At the logistic regression analysis, the presence of reflux symptoms in H. pylori-infected subjects is independently associated with concomitant infection in both members of the couple (odds ratio 4.41, 95% confidence interval 1.6-12.3) and with length of cohabitation (odds ratio 2.39, 95% confidence interval 1.0-5.7). The prevalence of H. pylori infection is significantly higher in sexual partners of H. pylori-infected subjects than in controls. Members of a couple are four times more likely to be both H. pylori infected if one of the couple has reflux symptoms.

Facts and Fantasies on Extraesophageal Reflux: A Gastroenterologist Perspective.

Gastroesophageal reflux disease encompasses a wide spectrum of disorders related to the reflux of gastric contents into the esophagus. Extraesophageal reflux (EER) may be suspected in patients with unexplained chronic cough, pharyngolaryngeal symptoms, and asthma. For physicians, suspected EER is challenging as there is currently no tool that can reliably make a definitive diagnosis. Endoscopic signs are not specific, pharyngeal and proximal reflux monitoring are not reliable, and if distal pH or pH-impedance monitoring can identify patients with abnormal reflux, they cannot predict the response to therapy. Controlled randomized trials have failed to reliably demonstrate any benefit of high-dose proton-pump inhibitors over placebo in patients with laryngeal symptoms, chronic cough, and asthma. Overall, the role of gastroesophageal reflux has been largely overestimated in patients with suspected EER. Especially when proton-pump inhibitors failed to improve symptoms, other diagnosis should be considered, such as functional laryngeal disorders which are probably much more prevalent in these patients than pathologic gastroesophageal reflux.

Bronchial reacutization and gastroesophageal reflux: is there a potential clinical correlation?

Pepsin plays a role in gastroesophageal reflux (GER). Aims of this study were to verify if pepsin could be the cause of frequent bronchial exacerbations and to check if the persistence of chronic respiratory symptoms were correlated with pre-existing respiratory diseases. From January to May 2016, 42 patients underwent a diagnostic bronchoscopy. All patients had a history of at least one bronchial exacerbation during the previous year. Bronchial lavage fluid specimens were obtained. A semiquantitative assessment of pepsin in the samples was carried out based on the intensity of the test sample. Pepsin was present in 37 patients (88%), but in patients with bronchial asthma and chronic obstructive pulmonary disease (COPD), the finding of pepsin in the bronchoalveolar fluid was 100%. There was a strong positive statistical correlation between pepsin detection and radiological signs of GER (ρ=0.662), and between pepsin detection and diagnosis (ρ=0.682). No correlation was found between the bacteriology and the presence of pepsin in the airways (ρ=0.006). The presence of pepsin in the airways shows the occurrence of reflux. The persistence of respiratory symptoms by at least 2 months suggest an endoscopic bronchial examination. This straightforward test confirms the cause possible irritation of the airways and may prevent further diagnostic tests, such as an EGD or pH monitoring esophageal.

A study with pharyngeal and esophageal 24-hour pH-impedance monitoring in patients with laryngopharyngeal symptoms refractory to proton pump inhibitors.

The role of gastroesophageal reflux in chronic laryngeal symptoms is difficult to establish. The aim of this study was to characterize pharyngeal and esophageal pH-impedance reflux patterns in a group of patients with suspected laryngopharyngeal reflux and to determine predictive factors of response to proton pump inhibitors. Patients with chronic pharyngolaryngeal symptoms were evaluated with a symptom score questionnaire, laryngoscopy, and 24-hour pharyngeal and esophageal pH-impedance monitoring at baseline and after 8-week treatment with esomeprazole 40mg b.i.d. Response to treatment was defined by a diminution of more than 50% of the score for the primary symptom. Reflux patterns and baseline impedance values were compared to those obtained in 46 healthy subjects. Twenty-four patients were included (17 women, median age 54years), all previously refractory to antisecretory therapy. Symptom scores were 46 (32-62) and 40 (27-76) off and on therapy, respectively (P=.1). There was no significant difference between patients and controls for pH-impedance reflux parameters and baseline values off and on therapy in distal and proximal esophagus and in the pharynx. Median numbers of pharyngeal reflux were 0 and 0 off and on therapy, respectively. Only two patients were responders to treatment, both with excessive distal reflux but no pharyngeal reflux. Only one patient had abnormal pharyngeal reflux but did not respond to proton pump inhibitors. Patients with suspected laryngopharyngeal reflux refractory to therapy do not exhibit abnormal pharyngeal or esophageal pH-impedance reflux. In these patients, laryngopharyngeal reflux is unlikely.

The Role of Gastroesophageal Reflux and Other Factors during Progression to Esophageal Adenocarcinoma.

U.S. esophageal adenocarcinoma (EAC) incidence increased over 5-fold between 1975 and 2009. Symptomatic gastroesophageal reflux disease (sGERD) elevates the risk for EAC. However, a simple calculation suggests that changes in sGERD prevalence can explain at most approximately 16% of this trend. Importantly, a mechanistic understanding of the influence of sGERD and other factors (OF) on EAC is lacking. A multiscale model was developed to estimate temporal trends for sGERD and OF, and their mechanistic role during carcinogenesis. Model calibration was to Surveillance, Epidemiology, and End Results (SEER) incidence and age-dependent sGERD data using maximum likelihood and Markov chain Monte Carlo (MCMC) methods. Among men, 77.8% [95% credibility interval (CI), 64.9%-85.6%] of the incidence trend is attributable to OF, 13.4% (95% CI, 11.4%-17.3%) to sGERD, and 8.8% (95% CI, 4.2%-13.7%) to sGERD-OF interactions. Among women, 32.6% (95% CI, 27.0%-39.9%) of the trend is attributable to OF, 13.6% (95% CI, 12.5%-15.9%) to sGERD, and 47.4% (95% CI, 30.7%-64.6%) to interactions. The predicted trends were compared with historical trends for obesity, smoking, and proton pump inhibitor use. Interestingly, predicted OF cohort trends correlated most highly with median body mass index (BMI) at age 50 (r = 0.988 for men; r = 0.998 for women). sGERD and OF mechanistically increase premalignant cell promotion, which increases EAC risk exponentially with exposure duration. Surveillance should target individuals with long-duration sGERD and OF exposures.

Gastroesophageal reflux disease and the lung transplant recipient

Lung transplantation is today a valid treatment for end-stage lung disorders, although long-term survival is still limited by chronic lung allograft dysfunction (CLAD). Repeat evidence has indicated gastroesophageal reflux and consequent retrograde chronic and silent microaspiration as a non-alloimmunogenic inflammatory risk factor for CLAD and/or bronchiolitis obliterans syndrome (BOS). Unfortunately, to date a gold standard methodology for detecting penetrance of refluxed duodenogastric secretions into the lung is lacking, and a definitive marker of retrograde microaspiration secondary to gastroesophageal reflux that identifies patients at risk for lung allograft dysfunction needs to be determined. Appropriately, designed clinical trials should be performed to understand better the role of gastroesophageal reflux in CLAD and/or BOS and to identify appropriate treatment algorithms.

The Role of Gastroesophageal Reflux and Microaspiration in Idiopathic Pulmonary Fibrosis.

There has been controversy regarding the relationship between gastroesophageal reflux, microaspiration, and idiopathic pulmonary fibrosis (IPF). In the last decade, there is increasing evidence supporting a relationship between gastroesophageal reflux, microaspiration, and IPF. Specifically, gastroesophageal reflux is common in IPF, is often asymptomatic in this population, and may impact disease progression and the natural history of IPF. More intriguing are the data suggesting that treatment of gastroesophageal reflux, either medical or surgical, may slow disease progression, as measured by change in forced vital capacity, and improve survival in IPF. Despite the growing evidence, there are still many gaps in our understanding of this relationship. Some of the major gaps include the discrepancy between the prevalence of gastroesophageal reflux in the general population compared to the prevalence of IPF, the unclear causative agent leading to injury, the lack of reliable methods to evaluate for gastroesophageal reflux and microaspiration, and the role of treatment. Further research, including a randomized controlled trial of anti-reflux therapy, needs to be done to clarify the relationship between gastroesophageal reflux, microaspiration, and IPF.

Bolus retention in hiatal hernia identified by high-resolution esophageal manometry with impedance

Esophageal acid retention in a hiatal hernia (HH) may play a role in gastro-esophageal reflux. The aims of this study were to determine the prevalence of bolus retention (BR) in HH and to compare pressure profiles in patients with HH with BR in the hernia to those with bolus clearance (BC) through the hernia using high-resolution esophageal manometry with impedance (HREMI). Clinical HREMI studies with HH ≥1.5cm were analyzed for lower esophageal sphincter (LES) and crural diaphragm (CD) pressures and pressure profiles during 12 saline swallows. Impedance was analyzed for swallow retention in the HH. Bolus retention in a HH was present in 35 of 53 (66%) patients with a HH. Patients with BR had overall lower pressure profiles including a lower basal LES pressure (14.8±10.6 vs 28.9±16.8mmHg; p=0.0001), LES-CD gradient (6.8±17.9 vs 20.6±12.2mmHg; p=0.002), residual LES pressure (2.5±4.6 vs 6.1±12.2mmHg; p=0.017), amplitude of distal esophageal contractions (83.2±38.8 vs 111.2±42.8mmHg; p=0.020), and distal contractile integral (1487±1016 vs 2608±1221mmHg-cm-sec; p=0.001) compared to the BC group. Patients with BR were more likely to have a larger sized HH compared to the BC group (3.1±1.6 vs 2.1±0.6cm; p=0.016); similar pressure changes were found when the groups were divided up by HH sizes. Bolus retention was seen in 66% of patients with HH. Bolus retention in the HH was associated with larger HH size, lower LES pressure, and lower esophageal contractile pressures compared to those with BC.

The role of gastro-esophageal reflux (GER) in systemic sclerosis and lung fibrosis

Systemic sclerosis (SSc) is an autoimmune condition characterized by tissue fibrosis of the skin and internal organs. A significant subgroup of SSc patients develops progressive interstitial lung disease(ILD) leading to pulmonary fibrosis similar to IPF (idiopathic pulmonary fibrosis). Gastro-esophageal reflux (GER) has been suggested as a driving factor in the pathogenesis of both SSc-ILD and IPF. The esophagus is affected in 50-82% of patients with SSc. Gastric reflux may be liquid, gaseous, or particulate; acid or nonacid; distal (localized to the distal oesophagus) or proximal (reaching the proximal oesophagus and pharynx). Reflux to the proximal oesophagus, which is intuitively linked to microaspiration into the lungs, appears to be quite common in patients with ILD-SSc and IPF. Importantly, a significant proportion of GER reflux is asymptomatic. Concentration of pepsin and bile acids in broncho-alveolar lavage (BAL) and exhaled breath condensate (EBC) have been investigated as biomarkers of microaspiration in various respiratory diseases. The confirmation of a causative link of microaspiration in the genesis and progression of lung fibrosis would have a major impact in the management of ILD-SSc patients. It is likely that proteases such as pepsin, and not the acidity, are the primary target for future therapies. Potent inhibitors specific for proteases, e.g. pepstatin, are available and have been tested in phase-III clinical trials.

The Role of Gastroesophageal Reflux in Relation to Symptom Onset in Patients with Proton Pump Inhibitor-Refractory Nonerosive Reflux Disease Accompanied by an Underlying Esophageal Motor Disorder

Background: The symptom improvement rate is low with proton pump inhibitors (PPIs) in nonerosive reflux disease (NERD). The underlying pathogenic mechanism is complex. Esophageal motility disorders (EMDs) are thought to be a factor, but their prevalence, type, symptoms and the role played by gastroesophageal reflux (GER) in symptom onset have not been fully investigated. Aim: To investigate the role of GER in symptom onset in PPI-refractory NERD patients with EMDs. Methods: This study comprised 76 patients with PPI-refractory NERD. Manometry was performed during PPI treatment and patients were divided into an EMD group and normal motility (non-EMD) group. Then, multichannel intraluminal impedance-pH monitoring was performed and medical interviews were conducted. Results: Nineteen patients (25%) had an EMD. Data were compared between 17 patients, excluding 2 with achalasia and 57 non-EMD patients. No significant differences were observed between groups in 24-hour intraesophageal pH <4 holding time (HT), mean number of GER episodes or mean number of proximal reflux episodes. The reflux-related symptom index (≥50%) showed a relationship between reflux and symptoms in 70.5% of EMD patients and 75% of non-EMD patients. In the EMD group, the score for FSSG (Frequency Scale for the Symptoms of GERD) question (Q)10 was significantly correlated with the number of GER episodes (r = 0.58, p = 0.02) and the number of proximal reflux episodes (r = 0.63, p = 0.02). In addition, the score for Q9 tended to be correlated with the number of GER episodes (r = 0.44, p = 0.06). Conclusion: Our results suggest that some PPI-refractory NERD patients have EMDs, and that GER plays a role in symptom onset.

Gastroesophageal Reflux in Infants

Rarely have the best methods of diagnosis or the treatment of a disease engendered more controversy than gastroesophageal reflux (GER), a highly prevalent condition in infants. To discuss the latest controversies in the diagnosis and treatment of GER in infants. All articles related to the diagnosis and treatment of GER were reviewed and, whenever possible, literature about infants was weighted with greater importance than literature about older children and adults. Although as many as 60% of infants have signs of GER, the role of GER in causing disease is difficult to elucidate. Despite new diagnostic tools to detect acid and nonacid reflux, our understanding of the relationship between reflux events and symptoms is complex. Furthermore, acid suppression, the mainstay of therapy for GER, increases the burden of nonacid reflux, which is already much higher in infants than in older children and which may worsen symptoms. Therefore, more conservative therapies are recommended for symptomatic infants. Although GER is a common reason for visits to primary care providers and specialists, few data suggest that GER results in many of the symptoms to which it has been attributed. A strong shift away from acid-suppression therapy in infants has occurred because of the adverse effects, lack of efficacy, and increase of nonacid reflux burden relative to acid burden. Nonpharmacologic measures should be used whenever possible because most infant GER will resolve without intervention.

Infant Colic and Functional Gastrointestinal Disorders

B y the time their child is 4 months old, up to 20% of parents have reported colicky symptoms in their infants. Is infant colic a disorder? Is it related to the intestine, as the term colic implies? Is any treatment other than reassurance of families regarding the transient nature of these symptoms indicated? In short, are we stepping in an evidence-based arena or are we dealing with ‘‘gut feelings’’? This supplement on infant crying, colic, and gastrointestinal (GI) disturbances in early childhood provides theoretical and clinical observations on this and other intriguing functional GI topics. The supplement provides the scientific and clinical evidence that should guide current clinical practice and serve future studies that will enable better understanding and appropriate management by physicians and families alike. Burns and Thapar review the embryonic and postnatal events related to the enteric nervous system (ENS), which is the regulator of gut secretion, blood flow, sensation, and coordinated motility (1). They provide evidence that a significant amount of modification of the ENS occurs not only during the fetal period but also postnatally; thus the ENS can be altered in a number of ways: stress, infections, and changes in nutrition. Indrio et al focus on the non-nutritive pathophysiology of colic, looking at the relation of colic to gastroesophageal reflux (GER), GI motility disorders, the role of gut hormones, and intestinal microflora (2). Their review raises the old debate of whether colic is a functional disorder (eg, troubling GER or ‘‘immature’’ motility) or should be regarded as a normal developmental occurrence. The authors correctly conclude that ‘‘little evidence supports a substantial role of GER or GERD in the majority of infants with colic,’’ and observations for the role of hormones such as ghrelin and motilin as well as the positive effect shown for probiotic supplementation should be studied further. Indrio and colleagues also elaborate on the role of probiotics in the management of infant colic and provide recent and exciting data on the clinical benefit of the administration of probiotics in treating functional disorders and organic diseases (3). This review explores the hypothesis that there is a window of time when the gut microbiota may affect the structure and the function of the brain. The review by Di Lorenzo on early life events brings us elegantly to the ‘‘vulnerable child,’’ summarizing what is known about factors that predispose an infant to become colicky (4). Much of the available data refers to the possible link among infectious, inflammatory, and psychological noxious events that may cause changes in enteric nerve reactivity, as well as immune responses or alterations in intestinal microbiota composition that can then lead to functional GI disorders later in life. For example, there is evidence that early pain experiences are associated with altered pain responses later in infancy. Although the genetic background cannot be changed and the stressful events may be unavoidable, identifying the child at risk may provide an opportunity for interventions that will attenuate or prevent later functional disorders. Ha-Vinh Leuchter et al discuss the possibility that the peak shape of the crying behavior found in colicky as opposed to noncolicky babies, the circadian rhythm of the crying, and the observation that these babies are not soothed by ordinary sensory stimulation reflect a difference in central nervous system functioning (eg, differences in circadian rhythm maturation, different response to stimuli) rather than GI dysfunction (5). Heine summarizes available data on the relation between cow’s-milk allergy and infant colic (6). He notes that in breast-fed infants, elimination of cow’s milk and other food proteins from the maternal diet was associated with a greater reduction in crying or fussiness duration, and that the treatment of formula-fed infants with extensively hydrolysed formula was associated with reduced crying in several clinical trials. The use of lactose-free formulae provides inconsistent results, however. A limited trial of an Infant Crying, Colic, and Gastrointestinal Discomfort in Early Childhood: A Review of the Evidence and Most Plausible Mechanisms

Exacerbations of COPD and symptoms of gastroesophageal reflux: a systematic review and meta-analysis

OBJECTIVE: To examine the relationship between gastroesophageal reflux (GER) and COPD exacerbations. METHODS: We conducted a systematic search of various electronic databases for articles published up through December of 2012. Studies considered eligible for inclusion were those dealing with COPD, COPD exacerbations, and GER; comparing at least two groups (COPD vs. controls or GER vs. controls); and describing relative risks (RRs) and prevalence ratios-or ORs and their respective 95% CIs (or presenting enough data to allow further calculations) for the association between GER and COPD-as well as exacerbation rates. Using a standardized form, we extracted data related to the study design; criteria for GER diagnosis; age, gender, and number of participants; randomization method; severity scores; methods of evaluating GER symptoms; criteria for defining exacerbations; exacerbation rates (hospitalizations, ER visits, unscheduled clinic visits, prednisone use, and antibiotic use); GER symptoms in COPD group vs. controls; mean number of COPD exacerbations (with symptoms vs. without symptoms); annual frequency of exacerbations; GER treatment; and severity of airflow obstruction. RESULTS: Overall, GER was clearly identified as a risk factor for COPD exacerbations (RR = 7.57; 95% CI: 3.84-14.94), with an increased mean number of exacerbations per year (mean difference: 0.79; 95% CI: 0.22-1.36). The prevalence of GER was significantly higher in patients with COPD than in those without (RR = 13.06; 95% CI: 3.64-46.87; p < 0.001). CONCLUSIONS: GER is a risk factor for COPD exacerbations. The role of GER in COPD management should be studied in greater detail.

Role of Gastroesophageal Reflux in Children With Unexplained Chronic Cough

Role of Gastroesophageal Reflux in Children With Unexplained Chronic Cough

Role of Gastroesophageal Reflux in Children With Unexplained Chronic Cough

The relation between respiratory symptoms and gastroesophageal reflux (GER) is a matter of contention and debate, with limited data in children to substantiate or refute cause and effect. Moreover, there are few data on the relation between nonacid reflux and chronic cough in childhood. We aimed to describe the type and physical characteristics of reflux episodes in children with unexplained chronic cough. Forty-five children with chronic cough underwent 24-hour multichannel intraluminal impedance-pH monitoring (MII-pH monitoring). Symptom association probability (SAP) characterized the reflux-cough association. Twenty children with erosive reflux disease (ERD) served as controls. Twenty-four children had cough-related reflux (CRR), with 19 having no gastrointestinal symptoms. Twenty-one had cough-unrelated reflux (CUR). CRR and ERD had increased acid (AR), weakly acidic (WAc), and weakly alkaline (WAlk) reflux. Esophageal acid exposure time and acid clearance time were higher in ERD than in CRR and CUR. In the CRR group, of 158 cough episodes related to reflux episodes, 66% involved AR, 18% WAc, and 16% WAlk. Seventeen children had positive SAP, 7 for AR, 5 for both AR and WAc, 4 for both WAc and WAlk, and 1 for WAlk. In children with unexplained chronic cough, asymptomatic acid and nonacid GER is a potential etiologic factor. The increased acid exposure time and delayed acid clearance characteristic of ERD are absent in cough-related GER. MII-pH monitoring increases the likelihood of demonstrating a temporal association between the cough and all types of reflux.

Gastroesophageal Reflux during Enteral Feeding in Stroke Patients: A 24-hour Esophageal pH-monitoring Study

Patients who are unable to eat or drink after stroke may receive percutaneous endoscopic gastrostomy (PEG) or nasogastric tube feeding. Although the most common serious complication is well known to be aspiration pneumonia, the role of gastroesophageal reflux (GER) has not been fully assessed. The aim of this study was to examine, by means of 24-hour esophageal pH monitoring, whether GER is related to aspiration pneumonia and whether the size and laterality of brain lesions influence GER. Sixteen stroke patients were examined using a Degitrapper pH400 (Medtronic Japan Co., Tokyo, Japan) and Zinetics 24ME multiuse pH catheter (Medtronic). All patients had stroke lesions in the territory of the left or right middle cerebral artery that were confirmed by magnetic resonance imaging (MRI) and were receiving PEG or nasogastric feeding. Stroke volume was measured with MRIcron software. Nine patients (56%) were diagnosed with GER, and 10 (63%) developed aspiration pneumonia after enteral feeding. The rate of aspiration pneumonia was significantly higher in patients with GER (88.9%) than in those without GER (42.9%; P = .04). Patients with left hemispheric lesions had a significantly higher incidence of acid reflex than those with right lesions (116 ± 105 vs 13 ± 17; P = .04). There were no significant differences in total time of acid reflux or mean pH value between patients with left and right hemispheric lesions. The lesion volume had no significant effect on any of 3 indices of GER. GER is associated with aspiration pneumonia and occurs more often in patients with stroke lesions in the left hemisphere.