The impact of gastroesophageal reflux disease symptoms in scleroderma: effects on sleep quality.

Systemic scleroderma/sclerosis (SSc) is an autoimmune connective tissue disease, which can lead to esophageal motor dysfunction and gastroesophageal reflux disease (GERD). Nocturnal GERD symptoms may be associated with sleep disturbances, which in turn can drastically affect well-being and fatigue levels. We hypothesized that GERD symptoms would be associated with poorer sleep in patients with SSc. Rheumatologist established SSc patients completed the following questionnaires: the UCLA scleroderma clinical trial consortium gastrointestinal tract instrument (GIT) 2.0 questionnaire; the Pittsburgh sleep quality index (PSQI); the fatigue severity scale (FSS); the multidimensional gastrointestinal symptom severity index (GSSI). Poor sleep quality was defined by a PSQI total score >5. Questionnaires were completed by 287 patients [mean (SD) age = 59 (14) years; female = 243]. Poor sleep quality was identified in 194 (68%) patients. Patients with poor sleep quality reported less sleep time and increased fatigue compared to those with normal sleep scores. SSc patients with poor sleep had significantly higher GIT Reflux scores (P < .001), and poor sleep was more frequent in those with moderate/severe versus mild/no heartburn on GISSI (P < .001). Narcotic and antidepressant use was significantly more frequent in SSc patients with poor sleep quality. Multivariable logistic regression supported the association between GERD symptoms and poor sleep after controlling for age, sex, and body mass index (BMI) (2.53, 95% confidence interval (CI) 1.52-4.25; P < .001). The association remained after controlling for narcotic and antidepressant use (2.20, 95% CI 1.29-3.73; P < .001). SSc patients who reported GERD symptoms were also more likely to report poor sleep quality. Future studies should examine mechanisms underlying nocturnal GERD symptoms in SSc patients, and the impact of improved GERD symptom control on sleep quality.

The 2018 ISDE achalasia guidelines.

Achalasia is a relatively rare primary motor esophageal disorder, characterized by absence of relaxations of the lower esophageal sphincter and of peristalsis along the esophageal body. As a result, patients typically present with dysphagia, regurgitation and occasionally chest pain, pulmonary complication and malnutrition. New diagnostic methodologies and therapeutic techniques have been recently added to the armamentarium for treating achalasia. With the aim to offer clinicians and patients an up-to-date framework for making informed decisions on the management of this disease, the International Society for Diseases of the Esophagus Guidelines proposed and endorsed the Esophageal Achalasia Guidelines (I-GOAL). The guidelines were prepared according the Appraisal of Guidelines for Research and Evaluation (AGREE-REX) tool, accredited for guideline production by NICE UK. A systematic literature search was performed and the quality of evidence and the strength of recommendations were graded according to the Grading of Recommendations Assessment, Development and Evaluation (GRADE). Given the relative rarity of this disease and the paucity of high-level evidence in the literature, this process was integrated with a three-step process of anonymous voting on each statement (DELPHI). Only statements with an approval rate >80% were accepted in the guidelines. Fifty-one experts from 11 countries and 3 representatives from patient support associations participated to the preparations of the guidelines. These guidelines deal specifically with the following achalasia issues: Diagnostic workup, Definition of the disease, Severity of presentation, Medical treatment, Botulinum Toxin injection, Pneumatic dilatation, POEM, Other endoscopic treatments, Laparoscopic myotomy, Definition of recurrence, Follow up and risk of cancer, Management of end stage achalasia, Treatment options for failure, Achalasia in children, Achalasia secondary to Chagas' disease.

Obesity and GERD impair esophageal epithelial permeability through 2 distinct mechanisms.

BACKGROUND: The mechanism by which obesity leads to damage independent of reflux is unclear. We aimed to determine the influence of obesity on mean nocturnal baseline impedance (MNBI), a functional measure of the epithelial barrier, in the presence and absence of acid reflux, using ambulatory pH impedance measurements. METHODS: Twenty-four-hour pH impedance studies performed off medications in Caucasian men with a normal endoscopic examination were assessed for level of acid exposure and MNBI. Four patient groups were studied: Group 1, Not obese and normal acid exposure; Group 2, Obese and normal acid exposure; Group 3, Not obese and increased acid exposure; and Group 4, Obese with increased acid exposure. RESULTS: One hundred patients were studied (25 in each group). Mean esophageal mucosal impedance (MI) was substantially lower in obese patients without reflux (Group 2) and non-obese patients with reflux (Group 3) compared to normal controls (non-obese, no reflux, Group 1). MI was progressively lower in the distal (vs the proximal) esophagus in GER patients, compared to those without GER. This difference persisted in the presence or absence of obesity. In contrast, in obese patients, the mean MI was significantly lower throughout the esophagus when compared to the non-obese patients and also persisted in the presence and absence of accompanying reflux. Obesity and reflux were both independently negatively correlated with MI. CONCLUSION: Obesity is associated with abnormal esophageal MNBI. In contrast to gastro-esophageal reflux, this decrease is pan-esophageal. These data may support a systemic mechanism by which obesity alters the esophageal barrier function.

Do recent reports about the adverse effects of proton pump inhibitors change providers' prescription practice?

Proton pump inhibitors (PPI) are utilized for a variety of indications, including treatment of gastroesophageal reflux disease, peptic ulcer disease, and prevention of gastrointestinal (GI) bleeding. Several studies have documented an increasing prevalence of inappropriate PPI use. Furthermore, recent media reports have highlighted new research data suggesting a possible association between chronic PPI use and several adverse medical outcomes, leading to frequent patient inquiries about these associations. Thus, providers face the challenge of counseling patients about the balance of risks and benefits related to PPI use. We aimed to explore providers' knowledge and attitudes toward reported adverse effects of PPI use and compare providers' prescription practices. A comprehensive, non-incentivized electronic survey was sent to all providers (residents, fellows, advanced practice providers, and consultants across 8 internal medicine specialties) at our tertiary academic medical center. The survey contained 21 questions covering provider demographics and responses to challenging clinical scenarios dealing with PPI use. Chi-square was used to compare responses from providers. The survey was distributed to 254 providers, of which 94 (24 GI and 70 non-GI) completed the survey (37% response rate). Among those 94 providers, 48 were consultants, 17 were advanced practice providers, and 29 were trainees. Non-GI providers included cardiology, pulmonary, endocrinology, family medicine, general internal medicine, hematology/oncology, and nephrology. Over half of the providers (51 [54%]) described their practice as outpatient setting, 29 (31%) providers defined their practice as a mixed setting (inpatient and outpatient), while 14 (15%) designated it as inpatient only. Nineteen (80%) GI providers and 48 (69%) non-GI providers discussed the risks and benefits with patients (P = 0.64). Fifteen (63%) GI providers and 33 (47%) non-GI providers indicated that recent reports changed their practice (P = 0.49). More GI providers (5 [21%]) lowered the dose of PPI compared with non-GI (1[1%]) (P = 0.004); 18 (26%) of non-GI and 3 (13%) of GI providers discontinued PPI and substituted it with a histamine 2 (H2) blocker (P = 0.29). A larger but nonsignificant percentage of trainees (8 [28%]) switched PPI to H2 blockers compared with consultants (8 [17%]; P = 0.39). Six (25%) of GI providers and 14 (20%) of non-GI providers were concerned about Clostridium difficile infection (P = 0.58). Twenty-four (34%) of the non-GI were worried about kidney diseases compared with 3 (13%) of the GI providers (P = 0.1). Ten (21%) consultants were concerned about risk of osteoporosis compared with 3 (10%) trainees (P = 0.38), while 8 (28%) trainees were worried about the risk of C. difficile infection compared with 10 (21%) consultants (P = 0.69). Most providers (85 [90%]) agreed that educational activities would be helpful to address these challenges. More GI providers lowered the dose of PPI compared with non-GI; non-GI providers were more likely to discontinue PPI and substitute it with an H2 blocker. Educating patients and providers about potential adverse effects of PPI is imperative.

Esophageal dysmotility according to Chicago classification v3.0 vs v2.0: Implications for association with reflux, bolus clearance, and allograft failure post-lung transplantation.

BACKGROUND: Proximal reflux and incomplete transit of boluses swallowed are risk factors for obstructive chronic lung allograft dysfunction (o-CLAD) post-lung transplantation (LTx). Likewise, so is esophagogastric junction outflow obstruction (EGJOO), but not hypo-contractility, when diagnosed using Chicago Classification (CC) v3.0. Given, peristaltic breaks as defined using CCv2.0 can prolong esophageal clearance, both swallowed and refluxed, but which are deemed within normality using CCv3.0, our aim was to determine whether hypo-contractility as diagnosed using CCv2.0, influences the association with reflux, along with its clearance, and that of boluses swallowed, and thus its association to allograft failure. METHODS: Esophageal motility abnormalities were classified using CC v3.0 and v2.0 in 50 patients post-LTx (26 female, 55 years (20-73 years)). RESULTS: Reclassification from CCv3.0 to v2.0 resulted in 7 patients with normal motility being reclassified to hypo-contractility (n = 6) or hyper-contractility (n = 1); 2 patients with hypo-contractility to normal motility; and 3 patients with EGJOO without hyper-contractility to EGJOO with hyper-contractility. The main consequence of reclassification was that the sub-group exhibiting hypo-contractility became more likely to have abnormal numbers of reflux events (P = .025) and incomplete bolus transit (P = .002) than those with normal motility using CCv2.0; associations not seen using CCv3.0. Irrespective of CC used only patients with EGJOO appeared more likely to develop o-CLAD than those with normal motility (P < .05). CONCLUSIONS: Irrespective of CC used, o-CLAD appears linked to EGJOO. CCv2.0 however, accentuates the increased reflux and incomplete bolus transit associated with hypo-contractility post-LTx, suggesting that these motor abnormalities, though considered minor, may be of importance after lung transplant.

Longitudinal outcomes of radiofrequency ablation versus surveillance endoscopy for Barrett's esophagus with low-grade dysplasia.

Radiofrequency ablation of Barrett's esophagus with low-grade dysplasia is recommended in recent American College of Gastroenterology guidelines, with endoscopic surveillance considered a reasonable alternative. Few studies have directly compared outcomes of radiofrequency ablation to surveillance and those that have are limited by short duration of follow-up. This study aims to compare the long-term effectiveness of radiofrequency ablation versus endoscopic surveillance in a large, longitudinal cohort of patients with Barrett's esophagus, and low-grade dysplasia.We conducted a retrospective analysis of patients with confirmed low-grade dysplasia at a single academic medical center from 1991 to 2014. Patients progressing to high-grade dysplasia or esophageal adenocarcinoma within one year of index LGD endoscopy were defined as missed dysplasia and excluded. Risk factors for progression were assessed via Cox proportional hazards model. Comparison of progression risk was conducted using a Kaplan-Meier analysis. Subset analyses were conducted to examine the effect of reintroducing early progressors and excluding patients diagnosed prior to the advent of ablative therapy. Of 173 total patients, 79 (45.7%) underwent radiofrequency ablation while 94 (54.3%) were untreated, with median follow up of 90 months. Seven (8.9%) patients progressed to high-grade dysplasia or adenocarcinoma despite ablation, compared with 14 (14.9%) undergoing surveillance (P = 0.44). This effect was preserved when patients diagnosed prior to the introduction of radiofrequency ablation were excluded (8.9% vs 13%, P = 0.68). Reintroduction of patients progressing within the first year of follow-up resulted in a trend toward significance for ablation versus surveillance (11.1% vs 23.8%, P = 0.053).In conclusion, progression to high-grade dysplasia or adenocarcinoma was not significantly reduced in the radiofrequency ablation cohort when compared to surveillance. Despite recent studies suggesting the superiority of radiofrequency ablation in reducing progression, diligent endoscopic surveillance may provide similar long-term outcomes.

The clinical significance of hypercontractile peristalsis: comparison of high-resolution manometric features, demographics, symptom presentation, and response to therapy in patients with Jackhammer esophagus versus Nutcracker esophagus.

The Chicago Classification version 3.0 (CC v 3.0) defines hypercontractile peristalsis as Jackhammer esophagus (JE); Nutcracker esophagus (NE) is no longer recognized. Data regarding patient characteristics and treatment response for JE versus NE are limited. We aimed to compare demographic characteristics, high resolution manometry (HRM) features, clinical presentation, management strategies, and treatment outcomes in patients with JE versus NE. We performed a retrospective analysis of adult patients diagnosed with NE (CC v 2.0) or JE (CC v 3.0) by HRM from January 2012 to August 2015. Demographics, symptoms, treatments, and response to therapy (none or partial/complete) were ascertained by chart review, for statistical comparisons. In 45 patients with JE and 29 with NE, there was no significant difference in rate of dysphagia (73% and 59%) or chest pain (44% and 59%). Treatment data were available in 29 JE (smooth muscle relaxants in 4, pain modulators in 3, botulinum toxin injection (BTX) in 10, endoscopic dilation in 5, multimodal treatment in 7), and 20 NE patients (smooth muscle relaxants in 2, pain modulators in 2, (BTX) in 6, endoscopic dilation in 3, multimodal treatment in 7). Follow-up data on 26/29 JE and 20/20 NE patients showed similar treatment response (96.4% vs. 82.1%, p= 0.08) after mean follow-up of 11.2 and 11 months, respectively. There were no major differences for JE versus NE in demographics, symptoms, or type of and response to therapy. Larger prospective, controlled trials are needed to clarify the clinical significance and response to treatment in JE and NE.

Baseline impedance measured during high-resolution esophageal impedance manometry reliably discriminates GERD patients.

BACKGROUND: Baseline impedance measured with ambulatory impedance pH monitoring (MII-pH) and a mucosal impedance catheter detects gastroesophageal reflux disease (GERD). However, these tools are limited by cost or patient tolerance. We investigated whether baseline impedance measured during high-resolution impedance manometry (HRIM) distinguishes GERD patients from controls. METHODS: Consecutive patients with clinical HRIM and MII-pH testing were identified. Gastroesophageal reflux disease was defined by esophageal pH <4 for ≥5% of both the supine and total study time, whereas controls had an esophageal pH <4 for ≤3% of the study performed off PPI. Baseline impedance was measured over 15 seconds during the landmark period of HRIM and over three 10 minute intervals during the overnight period of MII-pH. KEY RESULTS: Among 29 GERD patients and 26 controls, GERD patients had a mean esophageal acid exposure time of 22.7% compared to 1.2% in controls (P<.0001). Mean baseline impedance during HRIM was lower in GERD (1061 Ω) than controls (2814 Ω) (P<.0001). Baseline mucosal impedance measured during HRIM and MII-pH correlated (r=0.59, P<.0001). High-resolution esophageal manometry baseline impedance had high diagnostic accuracy for GERD, with an area under the curve (AUC) of 0.931 on receiver operating characteristics (ROC) analysis. A HRIM baseline impedance threshold of 1582 Ω had a sensitivity of 86.2% and specificity of 88.5% for GERD, with a positive predictive value of 89.3% and negative predictive value of 85.2%. CONCLUSIONS & INFERENCES: Baseline impedance measured during HRIM can reliably discriminate GERD patients with at least moderate esophageal acid exposure from controls. This diagnostic tool may represent an accurate, cost-effective, and less invasive test for GERD.

The impact of obesity on oesophageal acid exposure time on and off proton pump inhibitor therapy.

BACKGROUND: Obesity is associated with increased oesophageal acid exposure time (AET) in patients with gastro-oesophageal reflux (GER), and may decrease the effects of proton pump inhibitors (PPIs). AIM: To evaluate the effects of increased body mass on the ability of PPI therapy to decrease AET in patients with reflux symptoms. METHODS: Acid exposure time profiles collected from adult patients using wireless pH-metry while on or off PPI therapy was retrospectively reviewed. Patients were separated into five body mass index (BMI) categories as defined by the World Health Organization. A multivariable logistic regression evaluated the association between abnormal AET and BMI groups while controlling for age, gender and pH capsule placement methods. RESULTS: The study group comprised 968 patients with 336 (34.7%) studied on a PPI and 632 (65.3%) studied off PPI therapy. AET (total greater than 5.3%) was found more frequently in the overweight (67%) and obese classes (74-80%) compared to those who were normal weight (40%) while off acid-suppressing medications (P < 0.001). No significant differences were found between these groups when studied on acid-suppressing medications, and the proportion of patients with abnormal AET across BMI classes was similar regardless of taking a PPI either once or twice daily. CONCLUSIONS: This is the largest study to report on the relationship between BMI and oesophageal acid exposure time in patients with GER on and off PPI therapy. We conclude that obesity is related to increased acid exposure time, but with no significant difference in acid exposure time among different weight-based groups when taking a once or twice-daily PPI.

Management strategies for achalasia.

Treatment options for achalasia include oral pharmacologic therapy, endoscopic injection of botulinum toxin, pneumatic dilation, and myotomy (conventionally by laparoscopy, but more recently by an endoscopic approach). Oral pharmacologic agents have fallen out of use because of insufficient efficacy and frequent side effects. Endoscopic injection of botulinum toxin is safe and has good short-term effectiveness, but as the effect invariably wears off after a few months, this treatment is reserved for patients who are not candidates for more definitive treatments. Pneumatic dilation and surgical myotomy are currently considered the most effective treatments, with similar effectiveness in randomized controlled trials with follow-up of up to 2 years. The risk/benefit ratio and choice of therapy depend on patient characteristics (age, comorbidities, disease stage, prior treatments), patient's preference, and locally available expertise. Treatment of patients who fail or relapse after initial therapy is challenging and the success rate of pneumatic dilation or myotomy in this group is lower compared with previously untreated patients. The recently developed peroral endoscopic approach to myotomy has achieved excellent results in early uncontrolled studies, but high-quality randomized trials are needed to ensure widespread adoption is reasonable. Finally, retrospective data suggest that achalasia subtypes as defined by high-resolution esophageal pressure topography may guide treatment choice, but confirmation in prospective outcome studies is awaited.

Poor sleep quality and obstructive sleep apnea in patients with GERD and Barrett's esophagus.

BACKGROUND: Gastroesophageal reflux disease (GERD) reduces sleep quality. Whether Barrett's esophagus (BE) affects sleep differently is unknown. Obstructive sleep apnea (OSA) often coexists with GERD and may disrupt sleep; whether GERD reduces sleep quality independently of OSA is unknown. Our aims were to compare the effect of GERD and BE on sleep quality, and assess the impact of OSA on this association. METHODS: Validated questionnaires for GERD symptoms, sleep quality, and OSA risk were prospectively administered to subjects undergoing upper endoscopy. GERD was defined by erosive esophagitis and/or reflux symptoms >1/week. BE was defined histologically. Controls had normal endoscopy and were asymptomatic. Poor sleep quality was defined by a Pittsburgh Sleep Quality Index score >5. Risk of OSA was defined by a positive Berlin Questionnaire. The risk poor sleep quality in GERD, BE, and controls was evaluated in multivariate models. KEY RESULTS: 83 GERD, 63 BE, and 75 controls were included. OSA and poor sleep quality were significantly more frequent in GERD (65% and 60%) but not BE (52% and 46%) compared with controls (48% and 39%). Controlling for age, race, gender, smoking, body mass index, and hypertension, the risk of poor sleep quality was significantly increased in GERD compared with controls (odds ratio [OR] = 2.79, 95% confidence interval [CI]: 1.08-6.80), significance was lost after adding OSA to the model (OR = 2.27, 95% CI: 0.87-5.85). CONCLUSIONS & INFERENCES: GERD but not BE increases the risk of poor sleep quality. This association is not independent of OSA.

Utilization of wireless pH monitoring technologies: a summary of the proceedings from the esophageal diagnostic working group.

Gastroesophageal reflux disease (GERD) can be difficult to diagnose - symptoms alone are often not enough, and thus, objective testing is often required. GERD is a manifestation of pathologic levels of reflux into the esophagus of acidic, nonacidic, and/or bilious gastric content. However, in our current evidence-based knowledge approach, we only have reasonable outcome data in regards to acid reflux, as this particular type of refluxate predictably causes symptoms and mucosal damage, which improves with medical or surgical therapy. While there are data suggesting that nonacid reflux may be responsible for ongoing symptoms despite acid suppression in some patients, outcome data about this issue are limited. Therefore, this working group believes that it is essential to confirm the presence of acid reflux in patients with 'refractory' GERD symptoms or extraesophageal symptoms thought to be caused by gastroesophageal reflux before an escalation of antireflux therapy is considered. If patients do not have pathologic acid reflux off antisecretory therapy, they are unlikely to have clinically significant nonacid or bile reflux. Patients who do not have pathologic acid gastroesophageal reflux parameters on ambulatory pH monitoring then: (i) could attempt to discontinue antisecretory medications like proton pump inhibitors and H2-receptor antagonists (which are expensive and which carry risks - i.e. C. diff, etc.); (ii) may undergo further evaluation for other causes of their esophageal symptoms (e.g. functional heartburn or chest pain, eosinophilic esophagitis, gastroparesis, achalasia, other esophageal motor disorders); and (iii) can be referred to an ear, nose, and throat/pulmonary/allergy physician for assessment of non-GERD causes of their extraesophageal symptoms.

[If no-acid, no-heartburn? New physiopathological mechanisms of the gastroesophageal reflux disease]. / ¿Si no hay ácido no hay pirosis? Nuevos mecanismos fisiopatológicos de la enfermedad por reflujo gastroesofágico.

The role of acid is very well established in the pathogenesis of gastroesophageal reflux disease (GERD). In the current era of frequent use of proton pump inhibitors, we are seeing increasing numbers of patients with symptoms that are refractory to acid suppression. Recent studies suggest that in patients being treated with proton pump inhibitors, non-acid reflux (composed of buffered gastric contents), esophageal hypersensitivity, esophageal motor dysfunction and psychological comorbidity can cause persistent symptoms. Concepts surrounding possible pathogenetic mechanisms leading to heartburn as a result of nonacid reflux and other mechanisms are explored, and potential treatments for this type of reflux are outlined in this review.

Systematic review: Proton pump inhibitor-associated acute interstitial nephritis.

BACKGROUND: A number of recent case reports and case series suggest that proton pump inhibitors may cause acute interstitial nephritis. AIM: To establish the nature of the relationship (cause or association) between proton pump inhibitor use and development of interstitial nephritis. DATA COLLECTION: Two researchers independently searched electronic databases (MEDLINE, EMBASE, GOOGLE, LILACS, COCHRANE) for articles from 1970 to 2006, including all study designs, populations and languages. Two independent reviewers assessed study quality and collected the data. SELECTION CRITERIA: absence of baseline renal failure, development of interstitial nephritis after proton pump inhibitor exposure, nephritis confirmed by creatinine plus either renal biopsy or recurrence upon reinitiating proton pump inhibitor. RESULTS: Sixty four cases (60% females, mean age 78 years) of proton pump inhibitor-associated interstitial nephritis were found, 60 included in this review (59 confirmed by renal biopsy, one by recurrence upon reinitiating proton pump inhibitor). The most common symptoms were non-specific. The mean proton pump inhibitor treatment duration before diagnosing nephritis was 13 weeks, average recovery time was 35.5 weeks, one patient required permanent dialysis, there were no deaths. CONCLUSION: Proton pump inhibitor-related interstitial nephritis is rare, idiosyncratic and difficult to predict. It requires a high level of clinical suspicion. While there is not sufficient evidence to establish a causal relationship with certainty, there does appear to be a low-prevalence association.

Baclofen decreases acid and non-acid post-prandial gastro-oesophageal reflux measured by combined multichannel intraluminal impedance and pH.

BACKGROUND: Omeprazole controls acid but not non-acid reflux. The GABA B agonist baclofen decreases acid reflux through the inhibition of transient lower oesophageal sphincter relaxations (TLESRs) and should similarly decrease non-acid reflux. Using combined multichannel intraluminal impedance and pH (MII/pH), we compared acid and non-acid reflux after placebo and baclofen. METHODS: Nine healthy volunteers and nine heartburn patients underwent two 2-h studies of combined MII/pH in right lateral decubitus after a refluxogenic meal in random order: on placebo and after baclofen 40 mg p.o. Tracings were analysed for acid and non-acid reflux episodes, re-reflux and symptoms in the heartburn patients. RESULTS: In normal subjects baclofen significantly reduced the median number of episodes of acid (7 vs. 1, P = 0.02), non-acid (2 vs. 0, P = 0.005), and all reflux combined (10 vs. 2, P = 0.006); re-reflux was not reduced (0 vs. 0, P = N.S.). In heartburn patients, baclofen significantly decreased the median number of episodes of acid (15 vs. 6, P = 0.004), non-acid (4 vs. 2, P = 0.003), re-reflux (2 vs. 0, P = 0.02), and all reflux combined (23 vs. 8, P = 0.004); it also reduced the median number of acid-related (9 vs. 1, P = 0.008) and non-acid-related (1 vs. 0, P = 0.04) symptoms. CONCLUSIONS: Baclofen reduces post-prandial acid and non-acid reflux and their associated symptoms. GABA B agonists may have a role in treating GERD.

Simultaneous intraesophageal impedance and pH measurement of acid and nonacid gastroesophageal reflux: effect of omeprazole.

BACKGROUND & AIMS: Nonacid reflux may explain symptoms in acid-suppressed patients. Simultaneous intraesophageal impedance and pH measurement was used to evaluate the frequencies of postprandial acid and nonacid reflux before and after omeprazole administration. METHODS: Twelve heartburn patients underwent two 2-hour studies of intraesophageal impedance and pH in the right lateral decubitus position after a refluxogenic meal; session 1 without medication, session 2 after 7 days of omeprazole twice daily. Acid and nonacid reflux were quantified. RESULTS: Two hundred seventeen reflux episodes were detected before and 261 after omeprazole treatment (P > 0.05). Percentage of acid reflux decreased (from 45% to 3%, P = 0.02) and nonacid reflux increased (from 55% to 97%, P = 0.03) after omeprazole. Heartburn and acid taste were more commonly linked to acid reflux but were also produced by nonacid reflux. Regurgitation was reported equally in acid and nonacid reflux. Delta(pH) > 1 did not help predict the presence of symptoms during nonacid reflux. CONCLUSIONS: During treatment with omeprazole, postprandial reflux becomes predominantly nonacid. Symptoms are more common with acid reflux but are also produced by nonacid reflux. Simultaneous intraesophageal impedance and pH may be useful in evaluating the role of nonacid reflux in symptoms that persist despite adequate acid suppression.

Maximal acid reflux control for Barrett's oesophagus: feasible and effective.

UNLABELLED: The treatment of patients with Barrett's oesophagus is controversial. Debate exists regarding the use and value of high dose acid suppression as the standard of practice. Despite prolonged use of high dose proton pump inhibitors (40 mg omeprazole, 60 mg lansoprazole), most studies have shown no convincing evidence of significant regression of Barrett's length. These studies, however, have used fixed doses of proton pump inhibitors and did not regularly document control of oesophageal acid exposure. AIM: To determine whether regression of Barrett's epithelium can be achieved with documented maximal acid suppression. METHODS: We have prospectively followed nine patients with Barrett's oesophagus (eight male; mean age 60 years) for more than 1 year. They were all treated using medical therapy with pH monitoring documenting oesophageal acid exposure over 24 h < 1.6% of the time, and with two or more esophagogastroduodenoscopies performed by the same endoscopist. RESULTS: Acid control was individually tailored and achieved with proton pump inhibitor b.d. (omeprazole 20 mg or lansoprazole 30 mg) and ranitidine at bedtime (HS) (Ran) if necessary. All nine patients (100%) showed some evidence of regression. All nine patients (100%) showed a decrease in Barrett's length (mean 2 cm, range 1-3 cm). Six out of nine (66.67%) patients showed evidence of squamous islands on the last oesophagogastroduodenoscopy. The mean total distal oesophageal acid exposure was 0.38% (range: 0-1.5%). The mean follow-up of patients was 54 months (range: 13-118 months). CONCLUSIONS: Consistent and individually tailored maximal acid suppression documented by pH-metry is achievable and may result in decreased length and development of squamous islands in patients with Barrett's epithelium. This approach should be further evaluated as potentially the preferred medical treatment for these patients.