Proton Pump Inhibitor Cessation Research Articles

To wean or not to wean: proton pump inhibitor management after anti-reflux surgery amongst foregut experts

To wean or not to wean: proton pump inhibitor management after anti-reflux surgery amongst foregut experts

Timely Cessation of Proton Pump Inhibitors in Critically Ill Patients Impacts Morbidity and Mortality: A Propensity Score-Matched Cohort Study.

Proton pump inhibitors (PPIs) are among the drugs most commonly used in critically ill patients. Although mainly applied temporarily for stress ulcer prophylaxis, their application is frequently not terminated. Potential adverse effects of PPI treatment could impact the outcome in case of unnecessary and, therefore, avoidable long-term continuation. We tested the hypotheses that nonindicated PPI therapy continued beyond hospital discharge is associated with increased morbidity, rehospitalization rate, and mortality. Nationwide retrospective cohort study considering critically ill patients treated on German ICUs between January, 2017, and December, 2018 with a 2-year follow-up. A total of 591,207 patient datasets of a German healthcare insurer were screened. We identified 11,576 ICU patients who received PPI therapy for the first time during their index ICU stay without having an indication for its continuation. The cohort was stratified into two groups: 1) patients without further PPI therapy and 2) patients with continuation of PPI therapy beyond 8 weeks after hospital discharge. Frequency of predescribed adverse events associated with PPI therapy, 1-year rehospitalization rate, and 2-year mortality were determined. The proportion of patients with continued PPI therapy without an objectifiable indication was 41.7% (4,825 of 11,576 patients). These patients had a 27% greater risk of pneumonia (odds ratio [OR] 1.27; 95% CI, 1.15-1.39; p < 0.001) and a 17% greater risk of cardiovascular events (OR 1.17; 95% CI, 1.08-1.26; p < 0.001). Continued PPI therapy was associated with a 34% greater risk of rehospitalization (OR 1.34; 95% CI, 1.23-1.47) and a nearly 20% greater 2-year mortality risk (hazard ratio 1.17; 95% CI, 1.08-1.27; p = 0.006). These data demonstrate that an unnecessary continuation of PPI therapy after hospital discharge may significantly impact morbidity and mortality. To avoid potentially harmful overuse of a PPIs, intensivists should ensure timely cessation of a temporarily indicated PPI therapy.

Proton Pump Inhibitor Treatment Has Little Effects on Secretion of Saliva in Patients with Proton Pump Inhibitor-Responsive Mild Reflux Esophagitis and Non-Erosive Reflux Disease

Introduction: The secretion of saliva, which is triggered by acid reflux into the esophagus via the esophagosalivary reflex, plays a crucial role in the defensive mechanisms of the esophagus. The volume of saliva secreted in patients with gastroesophageal reflux disease (GERD) is reduced. However, the effects of proton pump inhibitors (PPI) on the secretion of saliva have rarely been reported. Therefore, the present study investigated changes in the volume and pH of saliva after the cessation of PPI. Materials and Methods: We retrospectively reviewed the records of consecutive patients previously diagnosed with mild reflux esophagitis (RE) or non-erosive reflux disease (NERD) controlled with PPI (including vonoprazan) who performed the salivary secretion test before and after a 2-week cessation of PPI. The volume, pH, and pH after acid loading (buffering capacity) of saliva were compared before and after the cessation of PPI. Results: Thirty-two patients (25 NERD, 7 mild RE) were included. The second saliva test was performed a median interval of 14 months [12.0–15.3] after the first test. No significant differences were observed in the volume of saliva secreted before and after the cessation of PPI (before 4.0 mL [2.7–6.0] vs. after 4.0 mL [2.3–5.9], p = 0.894). No significant differences were noted in pH or changes in pH after acid loading before and after the cessation of PPI (pH: before 7.1 ± 0.24 vs. after 7.0 ± 0.24, p = 0.1. Delta pH after acid loading: before 1.0 [0.8–1.2] vs. after 1.0 [0.8–1.2], p = 0.844). Conclusion: The cessation of PPI did not appear to affect the volume, pH, or buffering capacity of saliva in patients with PPI-responsive mild RE and NERD.

TU1.9 Oesophageal manometry and ambulatory pH monitoring prior to laparoscopic anti-reflux surgery – is it a necessity? An evaluation of a newly established anti-reflux surgery service at a district general hospital

Abstract Background Laparoscopic fundoplication is an effective surgical option for patients with symptoms of reflux refractory to proton-pump inhibitor (PPI) use. Oesophageal manometry and ambulatory pH monitoring are typically advocated as part of the evaluation of gastro-oesophgeal reflux disease, when anti-reflux surgery is considered. However, the requirement for these as a mandatory procedure remains controversial, particularly in the context of large hiatus hernia or presence of endoscopic reflux oesophagitis. Methods A retrospective review of all cases performed since the inception of the anti-reflux service at a single-centre district general hospital was undertaken. All patients who underwent an elective laparoscopic anti-reflux operation were included. Data pertaining to preoperative symptoms, preoperative investigations and postoperative outcomes (resolution of symptoms and PPI cessation) was collected. Results Over the three-year period, 22 anti-reflux operations were performed, of which 17 were followed up. The mean length of follow-up was 9.5 months. Most patients (91%) had typical reflux symptoms with a large hiatus hernia or endoscopic reflux oesophagitis. Only 4 (18.2%) patients underwent oesophageal manometry and ambulatory pH monitoring—each of these had either a normal preoperative OGD or barium swallow, or atypical symptoms. Alleviation of symptoms was achieved in 14 (82.3%) patients; 9 (52.9%) of which achieved complete resolution. PPI cessation was achieved in 12 (70.1%) patients, comparable with current literature. Conclusion Anti-reflux surgery can safely be performed without routine oesophageal manometry and ambulatory pH monitoring in the context of typical symptoms, a large hiatal defect or evidence of endoscopic reflux oesophagitis, as exemplified in our newly established anti-reflux service.

Magnetic sphincter augmentation in treating refractory gastroesophageal reflux disease: A systematic review and meta-analysis.

In this systematic review and meta-analysis we aimed to determine the efficacy and safety of magnetic sphincter augmentation (MSA) in the management of refractory gastroesophageal reflux disease (rGERD). Literature search was conducted in PubMed, the Cochrane Library, EMBASE, Web of Science, OpenGrey and ClincalTrials.gov for single-arm studies evaluating the efficacy and safety of MSA in rGERD or comparative studies with proton pump inhibitor (PPI) or laparoscopic Nissen fundoplication (LNF) serving as the control published until April 2020. Primary outcome was the rate of postoperative PPI use, and secondary outcomes included postoperative GERD-health-related quality of life (GERD-HRQL), normalization of acid exposure time (AET) and incidence of procedure-related adverse events (AE). Ten single-arm studies, one randomized controlled trial and three cohort studies involving 1138 participants were included. Post-MSA PPI withdrawal, significant GERD-HRQL improvement and AET normalization were achieved in 87.0%, 88.0% and 75.0% of the patients, respectively. The incidence of postoperative dysphagia was 29% and endoscopic dilation was required in 7.4% of patients undergoing MSA. MSA showed a better efficacy in symptom control than PPI (PPI cessation: 91% vs 0%; GERD-HRQL improvement: 81% vs 8%) and similar effectiveness but a lower risk of gas-bloat syndrome (risk ratio [RR] 0.69, 95% confidence interval [CI] 0.51-0.93, P=0.01) and better reserved ability to belch (RR 1.48, 95% CI 0.76-2.86, P=0.25) compared with LNF. MSA was an effective and safe therapy for rGERD. Well-designed randomized trials that compare the efficacy of MSA with other therapies are needed.

Gastric NET Subtypes: Do We Need An Additional One?

Depending on etiology, prognosis and malignant potential, recent S2k guideline differentiates gastric neuroendocrine tumors (gNET) in 4 types with different treatment implications.We report on a 55-year-old patient with the accidental finding of a 15 mm gNET. Apart from a prolonged use of proton pump inhibitors (PPI) for 20 years as a treatment for gastroesophageal reflux disease, there were no other associations or risk factors for gNETs. Formally, this patient would have been classified as a type III gNET, implicating gastric surgery. From a pathophysiological point of view, however, the assumed prolonged gastrin hypersecretion would have justified an assignment as a type I gNET. The gNET was resected by ESD, but histology showed an R1 situation. After cessation of PPIs, there is no recurrence so far. Besides, the initially documented numerous and large gland polyps showed an impressive regression only a few weeks after cessation of PPI.This case points to a probably underestimated gap in the present gNET classification. On the basis of present literature, the therapeutic dilemma of PPI-associated gNETs is discussed. A new assignment of PPI associated gNETs as type Ib could help to overcome this dilemma.

Colitis Nucleomigrans: A Proposal for The Third Type of Microscopic Colitis

Recently, we proposed the third entity of microscopic colitis (MC), termed colitis nucleomigrans (CN). The present review describes clinicopathological features of CN. CN shares clinical and endoscopic features of MC with collagenous colitis and lymphocytic colitis. We analyzed endoscopic biopsy specimens of nonspecific colitis clinically manifesting chronic watery diarrhea or inflammatory bowel disease (IBD)-like symptoms, but with minor endoscopic abnormality. The histopathological criteria of CN are as follows: a) chained nuclear migration to the middle part of the surface-lining columnar epithelia, b) apoptotic nuclear debris scattered below the nuclei, and c) mild to moderate chronic inflammation in the lamina propria. Thirty-three patients (M: F=20:13, median 63 years; range 17-88) fulfilled the above criteria. Seven cases accompanied MC-like clinical/endoscopic features. Mucosal reddening with or without erosions/aphthae was endoscopically observed in the remaining 26 cases with IBD-like clinical features: occult/gross hematochezia (n=19), abdominal pain (n=2) and mucin secretion (n=2). Apoptotic debris immunoreactive for cleaved caspase-3 appeared more frequently in IBD-like CN than in MC-like CN. CD8-positive intraepithelial lymphocytes were comparable in both types. Proton pump inhibitors (PPIs) were administered in five (71%) CN cases with MC-like features, and the diarrhea improved after cessation of PPIs in three. In IBD-like CN cases, eight (31%) received PPIs. Altered apoptotic processes in the colorectal surface-lining epithelia, predominantly with a debris pattern of apoptosis, may be involved in the pathogenesis. Mechanisms of nuclear migration to the unusual position and the impairment of nuclear anchoring to the basal situation in the surface-lining epithelia remain to be established.

S2933 Vanishing Polyps: Can Switching From a PPI to an H2 Blocker Cause Regression of Fundic Gland Polyps?

INTRODUCTION: Fundic gland polyps (FGPs) are identified as a sequalae of prolonged acid suppression. Though some studies show that acid suppression with a proton pump inhibitor (PPI) or Histamine 2 receptor blockers (H2RB) may cause FGPs, stronger evidence supports PPIs as a culprit. Studies have shown improvement of FGPs with cessation of acid suppression, but few studies investigated the effect of changing therapy to an H2RB. This case demonstrates a reduction of polyp size and number upon transition to an H2RB in a patient who developed FGPs as a result of long-term PPI use. CASE DESCRIPTION/METHODS: An 85-year-old female with rheumatoid arthritis on methotrexate and prednisone and on chronic PPI for 15 years for acid reflux presented to the gastroenterology clinic for possible gastritis. Upper endoscopy was performed and showed multiple 5–50 mm pedunculated and sessile polyps throughout the entire stomach. A majority of the polyps were about 3–5 cm. A hot snare and a Roth net were used to remove polyps to confirm histopathology (Figure 1). Gastric biopsies revealed FGPs without evidence of H. pylori, intestinal metaplasia, dysplasia or malignancy. Despite concern for FAP, malignancy, or high-grade dysplasia, the patient elected for continued endoscopic surveillance. She transitioned from a PPI to an H2RB. Serial endoscopies showed marked improvement in the size and number of gastric polyps at 6-months (Figure 2) and at 1-year (Figure 3). DISCUSSION: Some studies have shown a 4 fold increased risk of FGP formation in patients on chronic PPI. These polyps likely form as a response to low acid production causing increased parietal cell growth due to increased gastrin and chromogranin-A circulation causing gland proliferation. Few case reports demonstrate improvement of polyp size and number with transitioning therapy from PPI to H2RB and no large trials support changing therapy to H2RB. Still, H2RBs may be an ideal alternative since studies have shown an improvement in polyp size with cessation of PPI. Though FGPs are benign, PPI may increase the risk of adenomatous polyps and biopsy is necessary to differentiate these, particularly in patients with FAP. Our case demonstrates that discontinuing PPI for H2RB may lead to a sheer reduction in both number of polyps and polyp size, making lesions more amenable to continued resection and sampling and, therefore decreasing and minimizing risk of malignancy.Figure 1.: Initial endoscopy showing multiple large Fundic Gland Polyps in patient on chronic PPI for 15 years.Figure 2.: Repeat Endoscopy 6 months after transitioning from PPI to H2RB and showing smaller and fewer number of Fundic Gland Polyps.Figure 3.: Repeat Endoscopy 1 year after transitioning to H2RB and demonstrating continued, marked improvement in the size and number of Fundic Gland Polyps.

PROTON PUMP INHIBITORS AND THE RISK OF CHRONIC KIDNEY DISEASES: A CRITICAL REVIEW

Proton pump inhibitors (PPIs) are most widely used medications for acid related gastrointestinal disorders. Accessible evidence based studies suggest that the increased use of PPI is linked to a greater risk of developing kidney diseases. This review aims to determine the association of kidney disease with the use of proton pump inhibitor with various study designs. PubMed, Scopus and Google Scholar databases as well as a reference list of relevant articles were systematically searched for studies by using the following search terms; ‘proton pump inhibitors’, ‘acute kidney injury’, ‘chronic kidney disease’ and ‘end stage renal disease’. Both observational and randomized controlled trials (RCTs) exploring the association of PPI use with kidney disease were eligible for inclusion. A total of 8 articles, including 9 studies (n = 794,349 participants) were identified and included in the review. Majority of the studies showed a higher risk of kidney outcomes in patients taking PPIs, with effect higher of acute kidney injury (4-to 6-fold) compared with chronic kidney disease and end stage renal disease (1.5-to 2.5-fold). However, the studies suggest that the strength of evidence is weak and could not prove causation. The risk increased considerably with the use of high dose of PPIs and prolonged duration of exposure necessitates the monitoring of renal function. Exercising vigilance in PPI use and cessation of proton pump inhibitor when there is no clear indication may be a reasonable approach to reduce the population burden of kidney diseases.

Ambulatory Reflux Monitoring Guides Proton Pump Inhibitor Discontinuation in Patients With Gastroesophageal Reflux Symptoms: A Clinical Trial

Proton pump inhibitor (PPI) therapy fails to provide adequate symptom control in up to 50% of patients with gastroesophageal reflux symptoms. Although a proportion do not require ongoing PPI therapy, a diagnostic approach to identify candidates appropriate for PPI cessation is not available. This study aimed to examine the clinical utility of prolonged wireless reflux monitoring to predict the ability to discontinue PPIs. This double-blinded clinical trial performed over 3 years at 2 centers enrolled adults with troublesome esophageal symptoms of heartburn, regurgitation, and/or chest pain and inadequate PPI response. Participants underwent prolonged wireless reflux monitoring (off PPIs for ≥7 days) and a 3-week PPI cessation intervention. Primary outcome was tolerance of PPI cessation (discontinued or resumed PPIs). Symptom burden was quantified using the Reflux Symptom Questionnaire electronic Diary (RESQ-eD). Of 128 enrolled, 100 participants met inclusion criteria (mean age, 48.6 years; 41 men). Thirty-four participants (34%) discontinued PPIs. The strongest predictor of PPI discontinuation was number of days with acid exposure time (AET) > 4.0% (odds ratio, 1.82; P < .001). Participants with 0 days of AET > 4.0% had a 10 times increased odds of discontinuing PPI than participants with 4 days of AET > 4.0%. Reduction in symptom burden was greater among the discontinued versus resumed PPI group (RESQ-eD, -43.7% vs -5.3%; P= .04). Among patients with typical reflux symptoms, inadequate PPI response, and absence of severe esophagitis, acid exposure on reflux monitoring predicted the ability to discontinue PPIs without symptom escalation. Upfront reflux monitoring off acid suppression can limit unnecessary PPI use and guide personalized management. (ClinicalTrials.gov, Number: NCT03202537).

Tobacco use is not associated with increased risk of recurrent reflux 5 years after laparoscopic anti-reflux surgery.

Tobacco use worsens gastrointestinal reflux disease (GERD). Smoking cessation improves GERD symptoms, but its impact on the efficacy of laparoscopic anti-reflux surgery (LARS) is unclear. In this retrospective cohort study, we hypothesized that non-smokers would demonstrate greater long-term improvements in disease-specific quality of life than active smokers. Data were maintained in an IRB-approved prospective database, and patients were stratified according to tobacco use. Postoperative follow-up occurred in clinic and long-term follow-up via telephone interview. Outcomes measured were gastroesophageal health-related quality of life (GERD-HRQL) and GERD symptom scale (GERSS) scores, proton pump inhibitor (PPI) cessation, and satisfaction with surgery. Two hundred and thirty-five patients underwent primary LARS, and 31 (13%) were active smokers with 18 median pack-years [10-30]. Baseline PPI use (96% vs. 94%, p=0.64), presence of a hiatal hernia (79% vs. 68%, p=0.13), esophagitis (28% vs. 45%, p=0.13), and DeMeester score (41.9 vs. 33.6, p=0.47) were similar. Baseline GERD-HRQL and GERSS scores and their post-surgical decreases were also similar between groups. PPI cessation was achieved in 92% of non-smokers and 94% of smokers (p=0.79), and GERD-HRQL scores decreased to 4 [1-7] and 5 [0-12], respectively (p=0.53). After 59 [25-74] months, GERD-HRQL scores were 5 [2-11] and 2 [0-13] (p=0.61) and PPI cessation was maintained in 69% and 79% of patients (p=0.59). Satisfaction with surgery was similar between smokers and non-smokers (88% vs. 87%, p=0.85). Female gender was significantly associated withincreased improvements in GERD-HRQL (p<0.01) and GERSS scores (p=0.04) postoperatively but not at long-term follow-up. Patients without a hiatal hernia were less likely to achieve long-term PPI cessation compared to those with a hernia (OR 0.23, p<0.01). After 5years, smokers demonstrate similar symptom resolution, PPI cessation rates, and satisfaction with surgery as non-smokers. Active smoking does not appear to negatively impact long-term symptomatic outcomes of LARS.

2923 A Prospective Longitudinal Study of Proton Pump Inhibitors Effect on Inflammatory Bowel Disease Flares and Activity

INTRODUCTION: Proton pump inhibitors (PPIs) are one of the most commonly prescribed medications in the United States. Some recent studies have suggested that PPIs may have a negative effect on the gut microbiome. Dysbiosis of the gut microbiome has been linked with inflammatory bowel disease (IBD). We hypothesized that PPI use is associated with increased IBD flares and activity. This study was aimed to assess the effect of PPIs on IBD flares and activity. METHODS: We conducted a prospective longitudinal study of Veterans from the IBD clinic at the Michael E. DeBakey VA Medical Center from 2014 to 2018. Our eligibility criteria included patients who were at least 18 years of age, who were diagnosed with Crohn's Disease (CD) or Ulcerative Colitis (UC), and who had at least 1 clinic visit. IBD flare was defined by patient self-report of IBD flare between clinical encounters. IBD activity was quantified using the partial Mayo Score (pMayo) for UC, and the Harvey Bradshaw Index (HBI) for CD. Remission was defined by pMayo &lt;2 for UC and HBI &lt;5 for CD. Exposure of PPI was confirmed by chart review. Associations of PPI use with IBD flare and activity were assessed using T-tests and Chi-squared tests. RESULTS: A total of 132 patients were included in the analysis of which 74 had CD and 58 had UC. 40 patients were PPI users, and IBD flares occurred in 60 patients. No significant association between PPI usage and IBD flares were observed: 42.5% of PPI users developed flares compared to 46.7% of non-PPI users who developed flares, P-value = 0.658. In patients with CD, PPI use was associated with non-remission status (RR 2.53; 95% CI 1.04-6.15). In UC patients, PPI use was not associated with non- remission status (RR 1.10; 95% CI 0.67-1.79). 13 CD patients on PPIs discontinued the PPI between encounters, which was associated with a statistically significant decrease in HBI (3.62- &gt;2.54, P-value = 0.005). Among UC patients who discontinued PPIs, there was a non-significant trend towards decreased pMayo (2.26- &gt;1.59, P-value = 0.069). CONCLUSION: Amongst CD patients, PPI use was not associated with interval flare however, it was associated with non-remission status. Cessation of PPIs was associated with a statistically significant decrease in HBI in CD patients. In UC patients, no significant association between PPI use and flare or activity were observed. Decreasing unnecessary PPI use in patients with CD may decrease disease severity.

Peptic ulcer bleeding patients with Rockall scores ≥6 are at risk of long-term ulcer rebleeding: A 3.5-year prospective longitudinal study.

Patients with high Rockall scores have increased risk of rebleeding and mortality within 30days after peptic ulcer bleeding, but long-term outcomes deserve follow-up after cessation of proton pump inhibitors. The paper aimed to validate whether patients with high Rockall scores have more recurrent ulcer bleeding in a 3.5-year longitudinal cohort. Between August 2011 and July 2014, 368 patients with peptic ulcer bleeding were prospectively enrolled after endoscopic hemostasis to receive proton pump inhibitors for at least 8 to 16weeks. These subjects were categorized into either a Rockall scores ≥6 group (n=257) or a Rockall scores <6 group (n=111) and followed up until July of 2015 to assess recurrent ulcer bleeding. The proportion of patients with rebleeding during the 3.5-year follow-up was higher in patients with Rockall scores ≥6 than in those with scores <6 (10.51 vs. 3.63 per 100person-year, P=0.004, log-rank test). Among patients with Rockall scores ≥6, activated partial thromboplastin time prolonged ≥1.5-fold (P=0.045), American Society of Anesthesiologists physical status class ≥III (P=0.02), and gastric ulcer (P=0.04) were three additional independent factors found to increase rebleeding risk. The cumulative rebleeding rate was higher in patients with Rockall scores ≥6 with more than or equal to any two additional factors than in those with fewer than two additional factors (15.69 vs. 7.63 per 100person-year, P=0.012, log-rank test). Patients with Rockall scores ≥6 are at risk of long-term recurrent peptic ulcer bleeding. The risk can be independently increased by the presence of activated partial thromboplastin time prolonged ≥1.5-fold, American Society of Anesthesiologists class ≥III, and gastric ulcer in patients with Rockall scores ≥6.

Fundic Gland Polyposis Associated with Proton-Pump Inhibitor Use.

We describe the case of a man with fundic gland polyposis associated with proton-pump inhibitor (PPI) use. Some investigators have reported an association between long-term PPI use and an increase in the risk of developing fundic gland polyps (FGPs). These FGPs are considered to be reversible on stopping PPI treatment. The current patient had used a PPI for 10 years, resulting in multiple FGPs in his gastric body. However, 6 months after cessation of the PPI, the FGPs had obvously regressed, even though a histamine-2 receptor antagonist had subsequently been prescribed. This case demonstrates a link between PPI treatment and FGPs.LEARNING POINTSLong-term proton-pump inhibitor (PPI) use can increase the risk of developing fundic gland polyps (FGPs).This phenomenon is thought to be reversible, and a few case reports have demonstrated spontaneous resolution of FGPs after cessation of PPI use.When fundic gland polyposis is detected, a family history of polyposis and a history of PPI use should both be sought.

Real-world Helicobacter pylori diagnosis in patients referred for esophagoduodenoscopy: The gap between guidelines and clinical practice.

Histopathology is the most accurate test to detect H. pylori when performed correctly with unknown validity in daily practice clinic settings. We aimed to determine the rate of potentially false-negative H. pylori results that might be due to continued use of proton pump inhibitors (PPIs) in routine endoscopy practice. We also aimed to establish whether gastroenterologists recommend routine cessation of PPIs before esophagogastroduodenoscopy (EGD) and whether they regularly document that biopsies for H. pylori testing have been taken while the patients are on PPI treatment. Detailed information about three known factors (PPIs, antibiotics and prior H. pylori eradication treatment), which may cause histology or rapid urease test (RUT) to be unreliable, had been prospectively collected through interviews using a questionnaire before each test. Gastric biopsies were stained with H&E for histological analysis. A total of 409 individuals at three academic gastroenterology institutions were tested 200 times with histology. Fifty-six per cent (68 of 122) of all negative tests fell in the category of continuing PPI use, which had the potential to make the histology and RUT results unreliable. These data demonstrate a clear and important gap between current guidelines and real-world practice with regards to the diagnosis of H. pylori during EGD. A negative histology or RUT should be considered false negative until potential protocol violations are excluded. Documentation of PPI use during the EGD should be an integral part of the EGD report. The current practice of taking biopsies for H. pylori testing in patients under PPIs should be reevaluated.

Gastric Polyps—To Worry or Not?

A 15-year-old white boy underwent upper endoscopy for persistent dyspepsia for which he had been receiving a proton pump inhibitor (PPI) (lansoprazole) for several years. The esophagus and duodenum were visually and histologically normal. Small, sessile polyps were seen on the gastric body (Fig. 1A). Biopsies of the gastric mucosa were normal; the polyps showed dilatation and hyperplasia of oxyntic glands (Fig. 1B) consistent with fundic gland polyps secondary to PPI therapy.FIGURE 1: Endoscopic (A) and histological (B) findings of fundic gland hyperplasia caused by long-term use of a protein pump inhibitor.Gastric polyps may be found at endoscopy as a spontaneous benign condition, part of an adenomatous polyp syndrome (familial adenomatous polyposis [FAP]), part of a hamartomatous polyp syndrome (juvenile polyposis syndrome, Peutz-Jegher syndrome, and PTEN hamartoma syndrome), or a result of medication (PPIs). Although patient history is important for developing a differential diagnosis of gastric polyps, diagnosis is confirmed by histological findings. Fundic gland polyps (FGPs) are seen in 2% to 12% of patients with no PPI exposure, 26% to 36% of patients on long-term (>12 months) PPI therapy, and in up to 81% of adults and 51% of children with FAP (1–5). FGPs are characterized by cystically dilated and irregularly budded fundic glands, which are lined by normal parietal cells, chief cells, or mucous neck cells. FGPs in FAP (Fig. 2A) are distinguished by foveolar dysplasia and may develop adenomatous transformation (Fig. 2B). Incipient hamartomatous polyps can mimic FGP endoscopically. These polyps are characterized by an edematous lamina propria with inflammatory cells and cystically dilated glands lined by cuboidal to columnar epithelium with reactive changes; Peutz-Jegher polyps are differentiated by arborization of smooth muscle.FIGURE 2: Endoscopic (A) and histological (B) findings of gastric polyps in a patient with familial adenomatous polyposis.FGPs in FAP carry a risk of malignant transformation necessitating surveillance endoscopy. Consensus as to when to initiate surveillance does not exist; recommendations are included at the time of initial colonoscopy or around age 20 years. Interval of surveillance endoscopy for gastric FAP is every 1 to 3 years (5,6). Although there is no need to worry about malignancy related to PPI-induced FGPs, long-term use (>5 years) of PPIs has been associated with osteopenia and osteoporosis-related fractures. Conflicting data are found regarding the role of PPIs in predisposing to small bowel bacterial overgrowth. The patient was informed of the risks of long-term PPI use, received dietary counseling; the PPI was discontinued and an H2-receptor antagonist started. No further surveillance was performed as the polyps regress with cessation of PPIs.

Resolution of Fundic Gland Polyposis following Laparoscopic Magnetic Sphincter Augmentation and Subsequent Cessation of Proton Pump Inhibitors.

Gastric polyps occur from a variety of sources and are found commonly on upper endoscopy. We present the case of a 49-year-old female who presented for evaluation for antireflux surgery with a history of fundic gland polyposis who required twice-daily proton pump inhibitors (PPIs) for control of her gastric reflux. After verifying that she met criteria for surgery, she underwent an uncomplicated laparoscopic magnetic sphincter augmentation placement. With the cessation of PPIs following surgery, the fundic gland polyposis resolved. Fundic gland polyps may occur sporadically or within certain syndromes, such as familial adenomatous polyposis. Multiple possible inciting factors exist, including the use of PPIs. This is the first reported case of the resolution of numerous fundic gland polyps following the completion of laparoscopic magnetic sphincter augmentation.

Update in Procedural Therapy for GERD – Magnetic Sphincter Augmentation, Endoscopic Transoral Incisionless Fundoplication vs Laparoscopic Nissen Fundoplication

Gastroesophageal reflux disease (GERD) is a common and progressive condition manifested by heartburn or regurgitation. Though Nissen fundoplication has been and remains the gold standard for procedural therapy for GERD, two newer interventions have gained popularity: magnetic sphincter augmentation (MSA), which entails the placement of a self expanding magnetic ring around the gastroesophageal (GE) junction, and transoral incisionless fundoplication (TIF), an endoscopic approach that creates a neogastroesophageal valve near the fundus. Collective data gathered from four studies published within the past year suggest that the three modalities share comparable effectiveness in pH monitoring and patient satisfaction, TIF may have a lower proton pump inhibitor cessation rate, and Nissen fundoplication required longer recovery time and had a more serious adverse effects profile. Large, prospective, randomized controlled studies are needed to reliably compare the three procedures.

LINX® Reflux Management System in chronic gastroesophageal reflux: a novel effective technology for restoring the natural barrier to reflux

Gastroesophageal reflux disease (GERD) results from incompetency of the lower esophageal sphincter that allows the contents of the stomach to reflux into the esophagus, the airways, and the mouth. The disease affects about 10% of the western population and has a profound negative impact on quality of life. The majority of patients are successfully treated with proton-pump inhibitors, but up to 40% have incomplete relief of symptoms even after dose adjustment. The laparoscopic Nissen fundoplication represents the surgical gold standard, but is largely underused because of the level of technical difficulty and the prevalence of side effects. These factors have contributed to the propensity of patients to continue with medical therapy despite inadequate symptom control and complications of the disease. As a consequence, a significant 'therapy gap' in the treatment of GERD remains evident in current clinical practice. The LINX(®) Reflux Management System (Torax Medical, St. Paul, MN, USA) is designed to provide a permanent solution to GERD by augmenting the sphincter barrier with a standardized, reproducible laparoscopic procedure that does not alter gastric anatomy and is easily reversible. Two single-group trials confirmed that a magnetic device designed to augment the lower esophageal sphincter can be safely and effectively implanted using a standard laparoscopic approach. The device decreased esophageal acid exposure, improved reflux symptoms and quality of life, and allowed cessation of proton-pump inhibitors in the majority of patients.

Obscure bleeding colonic duplication responds to proton pump inhibitor therapy

We report the case of a 17-year-old male admitted to our academic hospital with massive rectal bleeding. Since childhood he had reported recurrent gastrointestinal bleeding and had two exploratory laparotomies 5 and 2 years previously. An emergency abdominal computed tomography scan, gastroscopy and colonoscopy, performed after hemodynamic stabilization, were considered normal. High-dose intravenous proton pump inhibitor (PPI) therapy was initiated and bleeding stopped spontaneously. Two other massive rectal bleeds occurred 8 h after each cessation of PPI which led to a hemostatic laparotomy after negative gastroscopy and small bowel capsule endoscopy. This showed long tubular duplication of the right colon, with fresh blood in the duplicated colon. Obscure lower gastrointestinal bleeding is a difficult medical situation and potentially life-threatening. The presence of ulcerated ectopic gastric mucosa in the colonic duplication explains the partial efficacy of PPI therapy. Obscure gastrointestinal bleeding responding to empiric anti-acid therapy should probably evoke the diagnosis of bleeding ectopic gastric mucosa such as Meckel's diverticulum or gastrointestinal duplication, and gastroenterologists should be aware of this potential medical situation.