Upper GI Tract

Clinicians appear to be too quick to perform antireflux procedures in infants, compared with older children, according to a report published online Nov. 6 in JAMA Surgery.

In a retrospective cohort study involving 141,190 pediatric and adolescent hospitalizations for gastroesophageal reflux disease (GERD) across the country over an 8-year period, the proportional hazard ratio of undergoing antireflux surgery was markedly decreased for those aged 7 months to 4 years (0.63) or 5-17 years (0.43), compared with those aged 0-2 months or 2-6 months.

The reasons for this strong difference are not yet known for certain, but the data showed a lack of objective diagnostic studies preceding the surgery in all pediatric age groups, and most strikingly in the youngest patients. It may well be that clinicians are confusing physiologic regurgitation – which is common, benign, and self-resolving in infancy – with a more pathologic process, said Dr. Jarod McAteer of the division of pediatric general and thoracic surgery, Seattle Children’s Hospital, and his associates.

At the very least, it appears that many infants aren’t given an adequate trial of medical management, since most cases of gastroesophageal reflux in infancy will resolve with that alone within 3-6 months, they noted.

"Referral for surgical treatment of GERD is generally presumed to be a last resort after failure of medical management, with optimal candidates having undergone specific preoperative evaluations," the authors wrote. Diagnostic and treatment guidelines are well delineated for adults, but not so for children.

For example, "upper GI fluoroscopy is frequently used in the preoperative workup among children with GERD," even though it has been clearly demonstrated to be a poor predictor of pathologic reflux, the investigators said.

In what they described as the first study to examine the influence of patient age on progression to antireflux procedures, Dr. McAteer and his colleagues analyzed data from the Pediatric Health Information System database, which includes demographic and clinical information from 41 children’s hospitals that cover 85% of major metropolitan areas in the U.S.

Out of 141,190 patients aged 0-7 years who were hospitalized with gastroesophageal reflux or GERD, 64% were younger than 1 year of age, and 53% were younger than 6 months. These numbers highlight how common the diagnosis is in babies, they said.

They also "suggest that physicians may be more likely to apply the diagnosis in this patient group because of diagnostic uncertainty or because other characteristics of these hospitalized infants make it more likely that any regurgitation is perceived as pathologic and indicative of GERD."

Examples of such "other characteristics" include comorbidities such as neurodevelopmental delay, cardiopulmonary disorders, seizures, asthma, and cerebral palsy.

A total of 11,621 of the study population underwent antireflux procedures, of which 52.7% were aged 6 months or younger. Only 14% of these patients had first undergone upper GI endoscopy, 0.2% esophageal manometry, 1.3% a 24-hour esophageal pH study, 65% upper GI fluoroscopy, and 17.1% a gastric emptying study, the investigators said (JAMA Surg. 2013 Nov. 6 [doi: 10.1001/jamasurg.2013.2685]).

The study findings show that the threshold for performing antireflux procedures is lower in infants than in older children. And "despite the fact that expert guidelines urge the use of objective studies in the diagnosis of GERD and despite evidence that supports the use of objective studies before performing antireflux procedures, such a standardized evaluation is not common practice.

"A greater effort is needed to develop and disseminate best-practice standards for the diagnosis and treatment of children, especially infants, with possible GERD. We must clarify the indications for antireflux procedures," Dr. McAteer and his associates said.

No financial conflicts of interest were reported.

Clinicians appear to be too quick to perform antireflux procedures in infants, compared with older children, according to a report published online Nov. 6 in JAMA Surgery.

In a retrospective cohort study involving 141,190 pediatric and adolescent hospitalizations for gastroesophageal reflux disease (GERD) across the country over an 8-year period, the proportional hazard ratio of undergoing antireflux surgery was markedly decreased for those aged 7 months to 4 years (0.63) or 5-17 years (0.43), compared with those aged 0-2 months or 2-6 months.

The reasons for this strong difference are not yet known for certain, but the data showed a lack of objective diagnostic studies preceding the surgery in all pediatric age groups, and most strikingly in the youngest patients. It may well be that clinicians are confusing physiologic regurgitation – which is common, benign, and self-resolving in infancy – with a more pathologic process, said Dr. Jarod McAteer of the division of pediatric general and thoracic surgery, Seattle Children’s Hospital, and his associates.

At the very least, it appears that many infants aren’t given an adequate trial of medical management, since most cases of gastroesophageal reflux in infancy will resolve with that alone within 3-6 months, they noted.

"Referral for surgical treatment of GERD is generally presumed to be a last resort after failure of medical management, with optimal candidates having undergone specific preoperative evaluations," the authors wrote. Diagnostic and treatment guidelines are well delineated for adults, but not so for children.

For example, "upper GI fluoroscopy is frequently used in the preoperative workup among children with GERD," even though it has been clearly demonstrated to be a poor predictor of pathologic reflux, the investigators said.

In what they described as the first study to examine the influence of patient age on progression to antireflux procedures, Dr. McAteer and his colleagues analyzed data from the Pediatric Health Information System database, which includes demographic and clinical information from 41 children’s hospitals that cover 85% of major metropolitan areas in the U.S.

Out of 141,190 patients aged 0-7 years who were hospitalized with gastroesophageal reflux or GERD, 64% were younger than 1 year of age, and 53% were younger than 6 months. These numbers highlight how common the diagnosis is in babies, they said.

They also "suggest that physicians may be more likely to apply the diagnosis in this patient group because of diagnostic uncertainty or because other characteristics of these hospitalized infants make it more likely that any regurgitation is perceived as pathologic and indicative of GERD."

Examples of such "other characteristics" include comorbidities such as neurodevelopmental delay, cardiopulmonary disorders, seizures, asthma, and cerebral palsy.

A total of 11,621 of the study population underwent antireflux procedures, of which 52.7% were aged 6 months or younger. Only 14% of these patients had first undergone upper GI endoscopy, 0.2% esophageal manometry, 1.3% a 24-hour esophageal pH study, 65% upper GI fluoroscopy, and 17.1% a gastric emptying study, the investigators said (JAMA Surg. 2013 Nov. 6 [doi: 10.1001/jamasurg.2013.2685]).

The study findings show that the threshold for performing antireflux procedures is lower in infants than in older children. And "despite the fact that expert guidelines urge the use of objective studies in the diagnosis of GERD and despite evidence that supports the use of objective studies before performing antireflux procedures, such a standardized evaluation is not common practice.

"A greater effort is needed to develop and disseminate best-practice standards for the diagnosis and treatment of children, especially infants, with possible GERD. We must clarify the indications for antireflux procedures," Dr. McAteer and his associates said.

No financial conflicts of interest were reported.

Clinicians appear to be too quick to perform antireflux procedures in infants, compared with older children, according to a report published online Nov. 6 in JAMA Surgery.

In a retrospective cohort study involving 141,190 pediatric and adolescent hospitalizations for gastroesophageal reflux disease (GERD) across the country over an 8-year period, the proportional hazard ratio of undergoing antireflux surgery was markedly decreased for those aged 7 months to 4 years (0.63) or 5-17 years (0.43), compared with those aged 0-2 months or 2-6 months.

The reasons for this strong difference are not yet known for certain, but the data showed a lack of objective diagnostic studies preceding the surgery in all pediatric age groups, and most strikingly in the youngest patients. It may well be that clinicians are confusing physiologic regurgitation – which is common, benign, and self-resolving in infancy – with a more pathologic process, said Dr. Jarod McAteer of the division of pediatric general and thoracic surgery, Seattle Children’s Hospital, and his associates.

At the very least, it appears that many infants aren’t given an adequate trial of medical management, since most cases of gastroesophageal reflux in infancy will resolve with that alone within 3-6 months, they noted.

"Referral for surgical treatment of GERD is generally presumed to be a last resort after failure of medical management, with optimal candidates having undergone specific preoperative evaluations," the authors wrote. Diagnostic and treatment guidelines are well delineated for adults, but not so for children.

For example, "upper GI fluoroscopy is frequently used in the preoperative workup among children with GERD," even though it has been clearly demonstrated to be a poor predictor of pathologic reflux, the investigators said.

In what they described as the first study to examine the influence of patient age on progression to antireflux procedures, Dr. McAteer and his colleagues analyzed data from the Pediatric Health Information System database, which includes demographic and clinical information from 41 children’s hospitals that cover 85% of major metropolitan areas in the U.S.

Out of 141,190 patients aged 0-7 years who were hospitalized with gastroesophageal reflux or GERD, 64% were younger than 1 year of age, and 53% were younger than 6 months. These numbers highlight how common the diagnosis is in babies, they said.

They also "suggest that physicians may be more likely to apply the diagnosis in this patient group because of diagnostic uncertainty or because other characteristics of these hospitalized infants make it more likely that any regurgitation is perceived as pathologic and indicative of GERD."

Examples of such "other characteristics" include comorbidities such as neurodevelopmental delay, cardiopulmonary disorders, seizures, asthma, and cerebral palsy.

A total of 11,621 of the study population underwent antireflux procedures, of which 52.7% were aged 6 months or younger. Only 14% of these patients had first undergone upper GI endoscopy, 0.2% esophageal manometry, 1.3% a 24-hour esophageal pH study, 65% upper GI fluoroscopy, and 17.1% a gastric emptying study, the investigators said (JAMA Surg. 2013 Nov. 6 [doi: 10.1001/jamasurg.2013.2685]).

The study findings show that the threshold for performing antireflux procedures is lower in infants than in older children. And "despite the fact that expert guidelines urge the use of objective studies in the diagnosis of GERD and despite evidence that supports the use of objective studies before performing antireflux procedures, such a standardized evaluation is not common practice.

"A greater effort is needed to develop and disseminate best-practice standards for the diagnosis and treatment of children, especially infants, with possible GERD. We must clarify the indications for antireflux procedures," Dr. McAteer and his associates said.

No financial conflicts of interest were reported.

Excess abdominal fat increases the risk for both Barrett’s esophagus and erosive esophagitis even after body mass index is accounted for, according to a recent meta-analysis. Extra fat around the middle also increases the risk for esophageal adenocarcinoma.

"Central adiposity has a strong and consistent association with development of esophageal inflammation, metaplasia, and neoplasia, independent of BMI [body mass index]," reported Dr. Siddharth Singh and his colleagues in the November issue of Clinical Gastroenterology and Hepatology (doi: 10.1016/j.cgh.2013.05.009). "In addition, central adiposity may be more highly associated with a reflux-independent effect on the development of Barrett’s esophagus and perhaps explains the predominance of esophageal adenocarcinoma in this population," said Dr. Singh of the Mayo Clinic in Rochester, Minn., and his coauthors.

The researchers conducted a systematic review and meta-analysis of all studies published through March 2013 in PubMed, Embase, or Web of Science that investigated associations between central adiposity and the risk of erosive esophagitis, Barrett’s esophagus, or esophageal adenocarcinoma. Included studies used computed tomography, waist-hip ratio, or waist circumference to assess central adiposity or visceral adipose tissue area or volume.

The researchers identified 40 studies, including 19 on erosive esophagitis, 17 on Barrett’s esophagus, and 6 on esophageal adenocarcinoma (including studies of overlapping conditions). Of the 37 independent populations covered in these studies, 18 involved Asian populations and the rest involved Western populations.

Compared with study participants in the lowest body-type category, participants with the highest central adiposity had 1.87 greater odds of erosive esophagitis, based on analysis of 18 heterogeneous studies (adjusted odds ratio, 1.87; 95% CI, 1.51-2.31). When the researchers analyzed only the eight studies that controlled for BMI, the risk remained (aOR, 1.93; 95% CI, 1.38-2.71). Although the researchers lacked data to assess the influence of gastroesophageal reflux disease (GERD) symptoms, they did find a dose-response relationship for higher central adiposity and higher erosive esophagitis risk.

An analysis of 15 studies similarly showed a greater risk for Barrett’s esophagus with greater central adiposity – even after accounting for BMI – and a dose-response relationship. Compared with participants in the lowest category of central adiposity, those in the highest group had about double the odds of Barrett’s esophagus (aOR, 1.98; 95% CI, 1.52-2.57). When the researchers evaluated Barrett’s esophagus risk in the five studies that allowed for BMI adjustment, the risk remained high (aOR, 1.88; 95% CI, 1.20-2.95).

In the 11 Barrett’s esophagus studies that controlled for GERD or used control-group participants with GERD, abdominal fat still doubled the odds for Barrett’s esophagus (aOR, 2.04; 95% CI, 1.44-2.90). Meanwhile, overall obesity had no impact on Barrett’s esophagus risk (aOR, 1.15; 95% CI, 0.89-1.47).

Even when the investigators analyzed only the seven studies in which GERD patients without Barrett’s esophagus were compared to Barrett’s esophagus patients, they found an increased risk of central adiposity (aOR, 2.51; 95% CI, 1.48-4.25). Meanwhile, BMI showed no effect on risk in these studies (aOR, 1.23; 95% CI, 0.90-1.66). "These results suggest that central adiposity, rather than overall obesity, may have a GERD symptom-independent effect on development of esophageal metaplasia," the researchers wrote.

The six studies on esophageal adenocarcinoma revealed an increased risk for the cancer with increased abdominal adiposity (aOR, 2.51; 95% CI, 1.56-4.04), though too little data existed to evaluate a dose-response relationship or to calculate risk independent of BMI or GERD symptoms.

For all these analyses, data on the following confounders was also included when available: "age, sex, race, BMI, smoking status, alcohol consumption, GERD symptoms, use of proton pump inhibitors or histamine receptor antagonists, presence of hiatal hernia, family history of esophageal adenocarcinoma, caffeine intake, Helicobacter pylori infection, use of putative chemopreventive agents (aspirin, nonsteroidal anti-inflammatory drugs, statins), and for studies reporting EAC [esophageal adenocarcinoma] as outcome, presence, length, and histology of Barrett’s esophagus."

The authors suggested several possible reasons for the findings, starting with the higher risk for reflux that exists with more abdominal fat. They also noted that abdominal fat may cause systemic or inflammatory effects that could lead to Barrett’s esophagus and cancer, whether independently or in conjunction with other factors.

Past research has already shown an increased risk for colon and pancreatic cancer resulting from visceral fat’s "adipocytokine-mediated carcinogenic effect," the researchers wrote. They also noted the link between abdominal fat and insulin resistance and pointed out that recent research has found evidence for the "role of the insulin–insulin growth factor-1 axis in promoting esophageal neoplasia."

The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases and the American College of Gastroenterology. The authors had no disclosures.

Excess abdominal fat increases the risk for both Barrett’s esophagus and erosive esophagitis even after body mass index is accounted for, according to a recent meta-analysis. Extra fat around the middle also increases the risk for esophageal adenocarcinoma.

"Central adiposity has a strong and consistent association with development of esophageal inflammation, metaplasia, and neoplasia, independent of BMI [body mass index]," reported Dr. Siddharth Singh and his colleagues in the November issue of Clinical Gastroenterology and Hepatology (doi: 10.1016/j.cgh.2013.05.009). "In addition, central adiposity may be more highly associated with a reflux-independent effect on the development of Barrett’s esophagus and perhaps explains the predominance of esophageal adenocarcinoma in this population," said Dr. Singh of the Mayo Clinic in Rochester, Minn., and his coauthors.

The researchers conducted a systematic review and meta-analysis of all studies published through March 2013 in PubMed, Embase, or Web of Science that investigated associations between central adiposity and the risk of erosive esophagitis, Barrett’s esophagus, or esophageal adenocarcinoma. Included studies used computed tomography, waist-hip ratio, or waist circumference to assess central adiposity or visceral adipose tissue area or volume.

The researchers identified 40 studies, including 19 on erosive esophagitis, 17 on Barrett’s esophagus, and 6 on esophageal adenocarcinoma (including studies of overlapping conditions). Of the 37 independent populations covered in these studies, 18 involved Asian populations and the rest involved Western populations.

Compared with study participants in the lowest body-type category, participants with the highest central adiposity had 1.87 greater odds of erosive esophagitis, based on analysis of 18 heterogeneous studies (adjusted odds ratio, 1.87; 95% CI, 1.51-2.31). When the researchers analyzed only the eight studies that controlled for BMI, the risk remained (aOR, 1.93; 95% CI, 1.38-2.71). Although the researchers lacked data to assess the influence of gastroesophageal reflux disease (GERD) symptoms, they did find a dose-response relationship for higher central adiposity and higher erosive esophagitis risk.

An analysis of 15 studies similarly showed a greater risk for Barrett’s esophagus with greater central adiposity – even after accounting for BMI – and a dose-response relationship. Compared with participants in the lowest category of central adiposity, those in the highest group had about double the odds of Barrett’s esophagus (aOR, 1.98; 95% CI, 1.52-2.57). When the researchers evaluated Barrett’s esophagus risk in the five studies that allowed for BMI adjustment, the risk remained high (aOR, 1.88; 95% CI, 1.20-2.95).

In the 11 Barrett’s esophagus studies that controlled for GERD or used control-group participants with GERD, abdominal fat still doubled the odds for Barrett’s esophagus (aOR, 2.04; 95% CI, 1.44-2.90). Meanwhile, overall obesity had no impact on Barrett’s esophagus risk (aOR, 1.15; 95% CI, 0.89-1.47).

Even when the investigators analyzed only the seven studies in which GERD patients without Barrett’s esophagus were compared to Barrett’s esophagus patients, they found an increased risk of central adiposity (aOR, 2.51; 95% CI, 1.48-4.25). Meanwhile, BMI showed no effect on risk in these studies (aOR, 1.23; 95% CI, 0.90-1.66). "These results suggest that central adiposity, rather than overall obesity, may have a GERD symptom-independent effect on development of esophageal metaplasia," the researchers wrote.

The six studies on esophageal adenocarcinoma revealed an increased risk for the cancer with increased abdominal adiposity (aOR, 2.51; 95% CI, 1.56-4.04), though too little data existed to evaluate a dose-response relationship or to calculate risk independent of BMI or GERD symptoms.

For all these analyses, data on the following confounders was also included when available: "age, sex, race, BMI, smoking status, alcohol consumption, GERD symptoms, use of proton pump inhibitors or histamine receptor antagonists, presence of hiatal hernia, family history of esophageal adenocarcinoma, caffeine intake, Helicobacter pylori infection, use of putative chemopreventive agents (aspirin, nonsteroidal anti-inflammatory drugs, statins), and for studies reporting EAC [esophageal adenocarcinoma] as outcome, presence, length, and histology of Barrett’s esophagus."

The authors suggested several possible reasons for the findings, starting with the higher risk for reflux that exists with more abdominal fat. They also noted that abdominal fat may cause systemic or inflammatory effects that could lead to Barrett’s esophagus and cancer, whether independently or in conjunction with other factors.

Past research has already shown an increased risk for colon and pancreatic cancer resulting from visceral fat’s "adipocytokine-mediated carcinogenic effect," the researchers wrote. They also noted the link between abdominal fat and insulin resistance and pointed out that recent research has found evidence for the "role of the insulin–insulin growth factor-1 axis in promoting esophageal neoplasia."

The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases and the American College of Gastroenterology. The authors had no disclosures.

Excess abdominal fat increases the risk for both Barrett’s esophagus and erosive esophagitis even after body mass index is accounted for, according to a recent meta-analysis. Extra fat around the middle also increases the risk for esophageal adenocarcinoma.

"Central adiposity has a strong and consistent association with development of esophageal inflammation, metaplasia, and neoplasia, independent of BMI [body mass index]," reported Dr. Siddharth Singh and his colleagues in the November issue of Clinical Gastroenterology and Hepatology (doi: 10.1016/j.cgh.2013.05.009). "In addition, central adiposity may be more highly associated with a reflux-independent effect on the development of Barrett’s esophagus and perhaps explains the predominance of esophageal adenocarcinoma in this population," said Dr. Singh of the Mayo Clinic in Rochester, Minn., and his coauthors.

The researchers conducted a systematic review and meta-analysis of all studies published through March 2013 in PubMed, Embase, or Web of Science that investigated associations between central adiposity and the risk of erosive esophagitis, Barrett’s esophagus, or esophageal adenocarcinoma. Included studies used computed tomography, waist-hip ratio, or waist circumference to assess central adiposity or visceral adipose tissue area or volume.

The researchers identified 40 studies, including 19 on erosive esophagitis, 17 on Barrett’s esophagus, and 6 on esophageal adenocarcinoma (including studies of overlapping conditions). Of the 37 independent populations covered in these studies, 18 involved Asian populations and the rest involved Western populations.

Compared with study participants in the lowest body-type category, participants with the highest central adiposity had 1.87 greater odds of erosive esophagitis, based on analysis of 18 heterogeneous studies (adjusted odds ratio, 1.87; 95% CI, 1.51-2.31). When the researchers analyzed only the eight studies that controlled for BMI, the risk remained (aOR, 1.93; 95% CI, 1.38-2.71). Although the researchers lacked data to assess the influence of gastroesophageal reflux disease (GERD) symptoms, they did find a dose-response relationship for higher central adiposity and higher erosive esophagitis risk.

An analysis of 15 studies similarly showed a greater risk for Barrett’s esophagus with greater central adiposity – even after accounting for BMI – and a dose-response relationship. Compared with participants in the lowest category of central adiposity, those in the highest group had about double the odds of Barrett’s esophagus (aOR, 1.98; 95% CI, 1.52-2.57). When the researchers evaluated Barrett’s esophagus risk in the five studies that allowed for BMI adjustment, the risk remained high (aOR, 1.88; 95% CI, 1.20-2.95).

In the 11 Barrett’s esophagus studies that controlled for GERD or used control-group participants with GERD, abdominal fat still doubled the odds for Barrett’s esophagus (aOR, 2.04; 95% CI, 1.44-2.90). Meanwhile, overall obesity had no impact on Barrett’s esophagus risk (aOR, 1.15; 95% CI, 0.89-1.47).

Even when the investigators analyzed only the seven studies in which GERD patients without Barrett’s esophagus were compared to Barrett’s esophagus patients, they found an increased risk of central adiposity (aOR, 2.51; 95% CI, 1.48-4.25). Meanwhile, BMI showed no effect on risk in these studies (aOR, 1.23; 95% CI, 0.90-1.66). "These results suggest that central adiposity, rather than overall obesity, may have a GERD symptom-independent effect on development of esophageal metaplasia," the researchers wrote.

The six studies on esophageal adenocarcinoma revealed an increased risk for the cancer with increased abdominal adiposity (aOR, 2.51; 95% CI, 1.56-4.04), though too little data existed to evaluate a dose-response relationship or to calculate risk independent of BMI or GERD symptoms.

For all these analyses, data on the following confounders was also included when available: "age, sex, race, BMI, smoking status, alcohol consumption, GERD symptoms, use of proton pump inhibitors or histamine receptor antagonists, presence of hiatal hernia, family history of esophageal adenocarcinoma, caffeine intake, Helicobacter pylori infection, use of putative chemopreventive agents (aspirin, nonsteroidal anti-inflammatory drugs, statins), and for studies reporting EAC [esophageal adenocarcinoma] as outcome, presence, length, and histology of Barrett’s esophagus."

The authors suggested several possible reasons for the findings, starting with the higher risk for reflux that exists with more abdominal fat. They also noted that abdominal fat may cause systemic or inflammatory effects that could lead to Barrett’s esophagus and cancer, whether independently or in conjunction with other factors.

Past research has already shown an increased risk for colon and pancreatic cancer resulting from visceral fat’s "adipocytokine-mediated carcinogenic effect," the researchers wrote. They also noted the link between abdominal fat and insulin resistance and pointed out that recent research has found evidence for the "role of the insulin–insulin growth factor-1 axis in promoting esophageal neoplasia."

The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases and the American College of Gastroenterology. The authors had no disclosures.

Dr. Yu-Xiao Yang reported at the 2013 AGA Spring Postgraduate Course that proton pump inhibitor’ therapy has been associated with a variety of potential side effects. The exact underlying biological mechanism for all side effects remains to be elucidated. For example, literature analysis revealed that PPI use may not be associated with a clinically important increase in community-acquired pneumonia risk. The marked increase in risk of community-acquired pneumonia that has been associated with newly started PPI therapy is likely due to protopathic bias. The latter suggests that use of a drug to treat early signs of an outcome gives the appearance that the drug is associated with the outcome. In the case of PPI therapy and bone health the evidence is retrospective and observational only. Short-term and standard-dose PPI therapy is associated with very modest increased risk, if any. In contrast, long-term and/or high-dose PPI therapy may be associated with clinically important increased risk. Thus far, there are no data to support the benefit of altering existing diagnostic and treatment practices for osteoporosis in patients on long-term treatment with a PPI.

Dr. Doug Corley stated that the availability of effective ablative techniques for Barrett’s esophagus (BE) require us to come up with clear recommendations about who to watch and who to treat. Patients with nondysplastic BE, unifocal low-grade dysplasia on a single examination, low-grade dysplasia not confirmed by a second pathologist, and no intestinal metaplasia without dysplasia should be watched. Patients with high-grade dysplasia and those with true low-grade dysplasia (persistent, multifocal, confirmed by a second pathologist) should be considered for esophageal ablation and, if needed, endoscopic mucosal resection (EMR). Aspirin should be considered in proper patients and all should be treated aggressively for gastroesophageal reflux disease.

Dr. Loren Laine provided tips for the treatment of nonvariceal upper GI bleeding. In patients with ulcer bleeding, endoscopic therapy should be performed for active bleeding, a visible vessel, and considered for an adherent clot. In general, epinephrine should not be used as monotherapy. In contrast, thermal and sclerosant treatment and clips may all be used alone. However, sclerosant and clips may be less effective if there is active bleeding. In patients with non-ulcer bleeding, endoscopic therapy should be done for Dieulafoy lesions and actively bleeding Mallory-Weiss tears. Importantly, epinephrine should not be used as monotherapy.

Dr. Neena Abraham discussed the challenging topic of endoscopy in patients requiring antithrombotics. Dr. Abraham reviewed the currently available literature and provided the following tips; it is safe to perform endoscopy on patients taking aspirin monotherapy, avoid stopping P2Y12 receptor antagonists (clopidogrel, prasugrel, and ticagrelor) in the first 90 days post acute coronary syndrome (ACS) and continue aspirin therapy when stopping a P2Y12 receptor antagonists. In addition, patients with GI bleed leading to ACS should be scoped within 48-72 hours post ACS, which will increase the chance of finding high-risk bleeding stigmata that is treatable by endoscopy and will lead to faster cardiac catheterization in 43% of the patients. Another important tip is that endoscopic therapy is effective in patients with moderately elevated International Normalized Ratios (INRs) (less than 2.7). There is no need to normalize the INR. Warfarin should be resumed within 4-7 days post GI-bleed. The introduction of new oral anticoagulants revealed an increase in GI bleed risk. Dual antiplatelet therapy plus a new oral anticoagulant (triple antithrombotic therapy) is associated with threefold increase risk of GI bleed. In general, dabigatran-related bleeding requires support of patient’s hemodynamics to promote renal excretion of the drug.

Dr. Fass is director, division of gastroenterology and hepatology, and Head, Esophageal and Swallowing Center, MetroHealth Medical Center, Cleveland.

Dr. Yu-Xiao Yang reported at the 2013 AGA Spring Postgraduate Course that proton pump inhibitor’ therapy has been associated with a variety of potential side effects. The exact underlying biological mechanism for all side effects remains to be elucidated. For example, literature analysis revealed that PPI use may not be associated with a clinically important increase in community-acquired pneumonia risk. The marked increase in risk of community-acquired pneumonia that has been associated with newly started PPI therapy is likely due to protopathic bias. The latter suggests that use of a drug to treat early signs of an outcome gives the appearance that the drug is associated with the outcome. In the case of PPI therapy and bone health the evidence is retrospective and observational only. Short-term and standard-dose PPI therapy is associated with very modest increased risk, if any. In contrast, long-term and/or high-dose PPI therapy may be associated with clinically important increased risk. Thus far, there are no data to support the benefit of altering existing diagnostic and treatment practices for osteoporosis in patients on long-term treatment with a PPI.

Dr. Doug Corley stated that the availability of effective ablative techniques for Barrett’s esophagus (BE) require us to come up with clear recommendations about who to watch and who to treat. Patients with nondysplastic BE, unifocal low-grade dysplasia on a single examination, low-grade dysplasia not confirmed by a second pathologist, and no intestinal metaplasia without dysplasia should be watched. Patients with high-grade dysplasia and those with true low-grade dysplasia (persistent, multifocal, confirmed by a second pathologist) should be considered for esophageal ablation and, if needed, endoscopic mucosal resection (EMR). Aspirin should be considered in proper patients and all should be treated aggressively for gastroesophageal reflux disease.

Dr. Loren Laine provided tips for the treatment of nonvariceal upper GI bleeding. In patients with ulcer bleeding, endoscopic therapy should be performed for active bleeding, a visible vessel, and considered for an adherent clot. In general, epinephrine should not be used as monotherapy. In contrast, thermal and sclerosant treatment and clips may all be used alone. However, sclerosant and clips may be less effective if there is active bleeding. In patients with non-ulcer bleeding, endoscopic therapy should be done for Dieulafoy lesions and actively bleeding Mallory-Weiss tears. Importantly, epinephrine should not be used as monotherapy.

Dr. Neena Abraham discussed the challenging topic of endoscopy in patients requiring antithrombotics. Dr. Abraham reviewed the currently available literature and provided the following tips; it is safe to perform endoscopy on patients taking aspirin monotherapy, avoid stopping P2Y12 receptor antagonists (clopidogrel, prasugrel, and ticagrelor) in the first 90 days post acute coronary syndrome (ACS) and continue aspirin therapy when stopping a P2Y12 receptor antagonists. In addition, patients with GI bleed leading to ACS should be scoped within 48-72 hours post ACS, which will increase the chance of finding high-risk bleeding stigmata that is treatable by endoscopy and will lead to faster cardiac catheterization in 43% of the patients. Another important tip is that endoscopic therapy is effective in patients with moderately elevated International Normalized Ratios (INRs) (less than 2.7). There is no need to normalize the INR. Warfarin should be resumed within 4-7 days post GI-bleed. The introduction of new oral anticoagulants revealed an increase in GI bleed risk. Dual antiplatelet therapy plus a new oral anticoagulant (triple antithrombotic therapy) is associated with threefold increase risk of GI bleed. In general, dabigatran-related bleeding requires support of patient’s hemodynamics to promote renal excretion of the drug.

Dr. Fass is director, division of gastroenterology and hepatology, and Head, Esophageal and Swallowing Center, MetroHealth Medical Center, Cleveland.

Dr. Yu-Xiao Yang reported at the 2013 AGA Spring Postgraduate Course that proton pump inhibitor’ therapy has been associated with a variety of potential side effects. The exact underlying biological mechanism for all side effects remains to be elucidated. For example, literature analysis revealed that PPI use may not be associated with a clinically important increase in community-acquired pneumonia risk. The marked increase in risk of community-acquired pneumonia that has been associated with newly started PPI therapy is likely due to protopathic bias. The latter suggests that use of a drug to treat early signs of an outcome gives the appearance that the drug is associated with the outcome. In the case of PPI therapy and bone health the evidence is retrospective and observational only. Short-term and standard-dose PPI therapy is associated with very modest increased risk, if any. In contrast, long-term and/or high-dose PPI therapy may be associated with clinically important increased risk. Thus far, there are no data to support the benefit of altering existing diagnostic and treatment practices for osteoporosis in patients on long-term treatment with a PPI.

Dr. Doug Corley stated that the availability of effective ablative techniques for Barrett’s esophagus (BE) require us to come up with clear recommendations about who to watch and who to treat. Patients with nondysplastic BE, unifocal low-grade dysplasia on a single examination, low-grade dysplasia not confirmed by a second pathologist, and no intestinal metaplasia without dysplasia should be watched. Patients with high-grade dysplasia and those with true low-grade dysplasia (persistent, multifocal, confirmed by a second pathologist) should be considered for esophageal ablation and, if needed, endoscopic mucosal resection (EMR). Aspirin should be considered in proper patients and all should be treated aggressively for gastroesophageal reflux disease.

Dr. Loren Laine provided tips for the treatment of nonvariceal upper GI bleeding. In patients with ulcer bleeding, endoscopic therapy should be performed for active bleeding, a visible vessel, and considered for an adherent clot. In general, epinephrine should not be used as monotherapy. In contrast, thermal and sclerosant treatment and clips may all be used alone. However, sclerosant and clips may be less effective if there is active bleeding. In patients with non-ulcer bleeding, endoscopic therapy should be done for Dieulafoy lesions and actively bleeding Mallory-Weiss tears. Importantly, epinephrine should not be used as monotherapy.

Dr. Neena Abraham discussed the challenging topic of endoscopy in patients requiring antithrombotics. Dr. Abraham reviewed the currently available literature and provided the following tips; it is safe to perform endoscopy on patients taking aspirin monotherapy, avoid stopping P2Y12 receptor antagonists (clopidogrel, prasugrel, and ticagrelor) in the first 90 days post acute coronary syndrome (ACS) and continue aspirin therapy when stopping a P2Y12 receptor antagonists. In addition, patients with GI bleed leading to ACS should be scoped within 48-72 hours post ACS, which will increase the chance of finding high-risk bleeding stigmata that is treatable by endoscopy and will lead to faster cardiac catheterization in 43% of the patients. Another important tip is that endoscopic therapy is effective in patients with moderately elevated International Normalized Ratios (INRs) (less than 2.7). There is no need to normalize the INR. Warfarin should be resumed within 4-7 days post GI-bleed. The introduction of new oral anticoagulants revealed an increase in GI bleed risk. Dual antiplatelet therapy plus a new oral anticoagulant (triple antithrombotic therapy) is associated with threefold increase risk of GI bleed. In general, dabigatran-related bleeding requires support of patient’s hemodynamics to promote renal excretion of the drug.

Dr. Fass is director, division of gastroenterology and hepatology, and Head, Esophageal and Swallowing Center, MetroHealth Medical Center, Cleveland.

Obstructive sleep apnea is a risk factor for Barrett’s esophagus, according to findings published online September 11 in Clinical Gastroenterology and Hepatology.

Researchers from the Mayo Clinic in Rochester, Minn., studied 7,482 patients who had undergone both a diagnostic polysomnogram and esophagogastroduodenoscopy from January 2000 to November 2011.

"In this subset of patients, the presence of OSA [obstructive sleep apnea] was associated with an 80% increased risk of [Barrett’s esophagus], compared to subjects without OSA and [Barrett’s esophagus]," wrote study author Dr. Prasad G. Iyer and his colleagues (Clin. Gastroenterol. Hepatol. 2013 September;11:1108-14.e5).

Several overlapping risk factors exist for obstructive sleep apnea and Barrett’s esophagus (BE), including obesity, gastroesophageal reflux disease (GERD), male gender, and older age. This study was designed to explore whether there is a relationship between obstructive sleep apnea and Barrett’s esophagus independent of these factors.

Subjects were categorized into four groups: diagnosis of BE but not OSA; OSA but not BE; both; or neither. Of the 7,482 patients, 2,480 did not have a diagnosis of OSA or BE; 83 had BE but not OSA; 4,641 had OSA but not BE; and 278 had a diagnosis of both.

The study authors used univariable models assessing age, sex, body mass index, GERD, and smoking history to determine the association between OSA and BE. GERD and OSA were associated with Barrett’s esophagus. A multiple-variable analysis was performed to observe the association of OSA with BE, adjusting for other factors. Patients with OSA were about 80% more at risk for having Barrett’s esophagus than were subjects without OSA or Barrett’s esophagus.

"This association was dose dependent, with an increase in severity of OSA being associated with an increased risk of Barrett’s esophagus," wrote the authors.

Additionally, since "the association of [Barrett’s esophagus] and OSA could be confounded by gastroesophageal reflux," the researchers also performed analyses to determine whether this relationship was independent of a GERD diagnosis. In a univariate analysis, both OSA and GERD were associated with BE, and in a multiple-variable analysis demonstrated that "both OSA and GERD were "independently associated with an increased risk of Barrett’s esophagus."

Dr. Iyer and his colleagues cited a few limitations to this study. First, the study’s design did not allow for exploration of a specific mechanism for how OSA predisposes individuals to Barrett’s esophagus. Second, the ability to accurately assess the association of OSA with GERD was limited by a lack of an established clinical definition of GERD. Finally, the use of ICD-9 codes to diagnose conditions may have resulted in overestimates in the sample.

The authors concluded that further research is needed to confirm that these findings can be applied to the general population and to explore whether treatment for OSA may help reverse this risk.

They also added that given the "asymptomatic nature" of Barrett’s esophagus and the higher risk of esophageal adenocarcinoma, patients with OSA may benefit from BE screening.

Dr. Iyer and his colleagues disclosed that this study was supported in part by the American College of Gastroenterology, the National Institute of Diabetes, Digestive and Kidney Disease; and the Edward C. Rosenow Endowed Professorship Internal Medicine Residency Award at the Mayo Clinic.

mrajaraman@frontlinemedcom.com

Obstructive sleep apnea is a risk factor for Barrett’s esophagus, according to findings published online September 11 in Clinical Gastroenterology and Hepatology.

Researchers from the Mayo Clinic in Rochester, Minn., studied 7,482 patients who had undergone both a diagnostic polysomnogram and esophagogastroduodenoscopy from January 2000 to November 2011.

"In this subset of patients, the presence of OSA [obstructive sleep apnea] was associated with an 80% increased risk of [Barrett’s esophagus], compared to subjects without OSA and [Barrett’s esophagus]," wrote study author Dr. Prasad G. Iyer and his colleagues (Clin. Gastroenterol. Hepatol. 2013 September;11:1108-14.e5).

Several overlapping risk factors exist for obstructive sleep apnea and Barrett’s esophagus (BE), including obesity, gastroesophageal reflux disease (GERD), male gender, and older age. This study was designed to explore whether there is a relationship between obstructive sleep apnea and Barrett’s esophagus independent of these factors.

Subjects were categorized into four groups: diagnosis of BE but not OSA; OSA but not BE; both; or neither. Of the 7,482 patients, 2,480 did not have a diagnosis of OSA or BE; 83 had BE but not OSA; 4,641 had OSA but not BE; and 278 had a diagnosis of both.

The study authors used univariable models assessing age, sex, body mass index, GERD, and smoking history to determine the association between OSA and BE. GERD and OSA were associated with Barrett’s esophagus. A multiple-variable analysis was performed to observe the association of OSA with BE, adjusting for other factors. Patients with OSA were about 80% more at risk for having Barrett’s esophagus than were subjects without OSA or Barrett’s esophagus.

"This association was dose dependent, with an increase in severity of OSA being associated with an increased risk of Barrett’s esophagus," wrote the authors.

Additionally, since "the association of [Barrett’s esophagus] and OSA could be confounded by gastroesophageal reflux," the researchers also performed analyses to determine whether this relationship was independent of a GERD diagnosis. In a univariate analysis, both OSA and GERD were associated with BE, and in a multiple-variable analysis demonstrated that "both OSA and GERD were "independently associated with an increased risk of Barrett’s esophagus."

Dr. Iyer and his colleagues cited a few limitations to this study. First, the study’s design did not allow for exploration of a specific mechanism for how OSA predisposes individuals to Barrett’s esophagus. Second, the ability to accurately assess the association of OSA with GERD was limited by a lack of an established clinical definition of GERD. Finally, the use of ICD-9 codes to diagnose conditions may have resulted in overestimates in the sample.

The authors concluded that further research is needed to confirm that these findings can be applied to the general population and to explore whether treatment for OSA may help reverse this risk.

They also added that given the "asymptomatic nature" of Barrett’s esophagus and the higher risk of esophageal adenocarcinoma, patients with OSA may benefit from BE screening.

Dr. Iyer and his colleagues disclosed that this study was supported in part by the American College of Gastroenterology, the National Institute of Diabetes, Digestive and Kidney Disease; and the Edward C. Rosenow Endowed Professorship Internal Medicine Residency Award at the Mayo Clinic.

mrajaraman@frontlinemedcom.com

Obstructive sleep apnea is a risk factor for Barrett’s esophagus, according to findings published online September 11 in Clinical Gastroenterology and Hepatology.

Researchers from the Mayo Clinic in Rochester, Minn., studied 7,482 patients who had undergone both a diagnostic polysomnogram and esophagogastroduodenoscopy from January 2000 to November 2011.

"In this subset of patients, the presence of OSA [obstructive sleep apnea] was associated with an 80% increased risk of [Barrett’s esophagus], compared to subjects without OSA and [Barrett’s esophagus]," wrote study author Dr. Prasad G. Iyer and his colleagues (Clin. Gastroenterol. Hepatol. 2013 September;11:1108-14.e5).

Several overlapping risk factors exist for obstructive sleep apnea and Barrett’s esophagus (BE), including obesity, gastroesophageal reflux disease (GERD), male gender, and older age. This study was designed to explore whether there is a relationship between obstructive sleep apnea and Barrett’s esophagus independent of these factors.

Subjects were categorized into four groups: diagnosis of BE but not OSA; OSA but not BE; both; or neither. Of the 7,482 patients, 2,480 did not have a diagnosis of OSA or BE; 83 had BE but not OSA; 4,641 had OSA but not BE; and 278 had a diagnosis of both.

The study authors used univariable models assessing age, sex, body mass index, GERD, and smoking history to determine the association between OSA and BE. GERD and OSA were associated with Barrett’s esophagus. A multiple-variable analysis was performed to observe the association of OSA with BE, adjusting for other factors. Patients with OSA were about 80% more at risk for having Barrett’s esophagus than were subjects without OSA or Barrett’s esophagus.

"This association was dose dependent, with an increase in severity of OSA being associated with an increased risk of Barrett’s esophagus," wrote the authors.

Additionally, since "the association of [Barrett’s esophagus] and OSA could be confounded by gastroesophageal reflux," the researchers also performed analyses to determine whether this relationship was independent of a GERD diagnosis. In a univariate analysis, both OSA and GERD were associated with BE, and in a multiple-variable analysis demonstrated that "both OSA and GERD were "independently associated with an increased risk of Barrett’s esophagus."

Dr. Iyer and his colleagues cited a few limitations to this study. First, the study’s design did not allow for exploration of a specific mechanism for how OSA predisposes individuals to Barrett’s esophagus. Second, the ability to accurately assess the association of OSA with GERD was limited by a lack of an established clinical definition of GERD. Finally, the use of ICD-9 codes to diagnose conditions may have resulted in overestimates in the sample.

The authors concluded that further research is needed to confirm that these findings can be applied to the general population and to explore whether treatment for OSA may help reverse this risk.

They also added that given the "asymptomatic nature" of Barrett’s esophagus and the higher risk of esophageal adenocarcinoma, patients with OSA may benefit from BE screening.

Dr. Iyer and his colleagues disclosed that this study was supported in part by the American College of Gastroenterology, the National Institute of Diabetes, Digestive and Kidney Disease; and the Edward C. Rosenow Endowed Professorship Internal Medicine Residency Award at the Mayo Clinic.

mrajaraman@frontlinemedcom.com

Helicobacter pylori was found to have a strong inverse link with Barrett’s esophagus, but not with symptoms of gastroesophageal reflux disease. Erosive esophagitis also was seen to trend toward an inverse association with H. pylori.

Previous reports have attributed a protective effect against gastroesophageal reflux disease (GERD), esophageal adenocarcinoma, and Barrett’s esophagus to H. pylori infection, particularly the cytotoxin-associated gene A (cagA+) strain. Having determined the studies associating H. pylori with GERD either yielded weak support for an inverse relationship, were prone to bias, or were otherwise flawed, a team led by Dr. Joel Rubenstein of the Veterans Affairs Center for Clinical Management Research, Washington, and the University of Michigan Medical School in Ann Arbor analyzed the associations of the three disease outcomes occurring in the same populations with the bacterium.

They constructed a case-control study of men between the ages of 50 and 79 years (n = 533), who had colorectal cancer screening at one of two tertiary medical centers in Michigan between 2008 and 2011, and who were recruited to have upper endoscopy. The study served as a secondary analysis of the Newly Diagnosed Barrett’s Esophagus Study, and included three non–mutually exclusive case groups: Barrett’s esophagus, erosive esophagitis, and GERD symptoms. An additional group of men in the same age group (n = 80) found to have Barrett’s esophagus during clinically indicated upper endoscopy exams was also assessed.

Using logistic regression, the investigators estimated any associations between serum antibodies against H. pylori and cagA+ in the study group, and GERD symptoms, esophagitis, and Barrett’s esophagus. These results were compared with a control group of randomly selected men (n = 177) who did not have any of the three conditions and who were having colorectal screens.

Women were not studied, because of their typically low rates of Barrett’s esophagus. Also excluded were men with any history of upper endoscopy, Barrett’s esophagus, or esophagectomy; diagnostic indication for colonoscopy; inflammatory* bowel disease; known ascites or esophageal varices; any cancers other than melanoma in the previous 5 years; or notable coagulopathy.

The study did include consecutive men between the ages of 50 and 79 years, newly diagnosed at either of the two study sites with Barrett’s esophagus by way of a clinically indicated upper endoscopy.

To determine the presence of GERD, the study group was given a survey that was not formally validated, about their use of proton pump inhibitors (PPI) and histamine₂ receptor agonists (HR₂A) in relation to the frequency they experienced heartburn and regurgitation. Patients who reported weekly heartburn and regurgitation while not using medication were considered to have GERD. A validated survey, the Mayo Clinic’s Gastroesophageal Reflux Questionnaire (GERQ), was applied during the last quarter of the study, although because the GERQ does not address the role of acid-reducing medications, the investigators wrote that there is the chance that patients with GERD managed by medication could have been misclassified by the questionnaire as non-GERD controls.

The study group also underwent colonoscopy, followed by upper endoscopy. If Barrett’s esophagus was suspected, biopsies were obtained. Using the Los Angeles Classification scheme, if class C or D esophagitis was found, patients repeated the endoscopy while taking a PPI before investigators determined if the patient had Barrett’s esophagus. Patients who were not taking any acid-reducing medications at the time of the endoscopy who reported at least weekly symptoms of GERD and had a normal endoscopy without erosive esophagitis or Barrett’s esophagus were considered to have nonerosive reflux symptoms. Patients with Barrett’s esophagus identified on a clinically indicated upper endoscopy were included with the same as those identified among the the people screened for colorectal cancer. Blood samples were drawn from all subjects and assayed for H. pylori.

The results were that 822 of the colorectal cancer patients had upper endoscopy; 328 were randomly selected for descriptive analysis of assays, 22.3% of which were found to have antibodies against H. pylori, with 1.8% equivocal for H. pylori on two assays. Of those positive for H. pylori, nearly half (49.3%) were found to have antibodies against cagA while none of those who were equivocal for H. pylori were found to have antibodies against cagA. Compared with study group members who were seropositive for H. pylori, those who were seronegative were less likely to be smokers and to have higher education and income.

Noting that classification errors for GERD might have biased the estimated associations with H. pylori toward the null, the investigators discovered that while there was a strong inverse connection between H. pylori, especially the cagA+ strain, and erosive esophagus (H. pylori adjusted odds ratio, 0.63; 95% confidence interval: 0.37-1.08 and cagA+ OR, 0.47; 95% CI: 0.21-1.03) and Barrett’s esophagus (OR, 0.53; 95% CI: 0.29 -0.97), especially the cagA+ strain (OR, 0.36; 95% CI: 0.14-0.90), they could not make a decisive link between GERD symptoms and H. pylori infection (OR, 0.948; 95% CI: 0.548-1.64 and cagA+ OR, 0.967; 95% CI: 0.461-2.03) (Clin. Gastroenterol. Hepatol. 2013 [doi: 10.1016/j.cgh.2013.08.029]).

Dr. Rubenstein and his colleagues theorized that since the GERD link was not found, the mechanism of H. pylori’s negative association with Barrett’s esophagus might be from the direct impact of the bacteria on the inflammatory or mucosal response; its indirect effects on the production of leptin or ghrelin; or a confounding effect created by genetic regulation of cytokines or prior alterations in the esophageal and gastric microbiota.

The study was underwritten by the National Institutes of Health and by a senior marketing grant from the American Society for Gastrointestinal Endoscopy. Dr. Rubenstein and his associates reported no relevant disclosures.

wmcknight@frontlinemedcom.com

*Correction, 9/20/2013: An earlier version of this story incorrectly identified inflammatory bowel disease.

Helicobacter pylori was found to have a strong inverse link with Barrett’s esophagus, but not with symptoms of gastroesophageal reflux disease. Erosive esophagitis also was seen to trend toward an inverse association with H. pylori.

Previous reports have attributed a protective effect against gastroesophageal reflux disease (GERD), esophageal adenocarcinoma, and Barrett’s esophagus to H. pylori infection, particularly the cytotoxin-associated gene A (cagA+) strain. Having determined the studies associating H. pylori with GERD either yielded weak support for an inverse relationship, were prone to bias, or were otherwise flawed, a team led by Dr. Joel Rubenstein of the Veterans Affairs Center for Clinical Management Research, Washington, and the University of Michigan Medical School in Ann Arbor analyzed the associations of the three disease outcomes occurring in the same populations with the bacterium.

They constructed a case-control study of men between the ages of 50 and 79 years (n = 533), who had colorectal cancer screening at one of two tertiary medical centers in Michigan between 2008 and 2011, and who were recruited to have upper endoscopy. The study served as a secondary analysis of the Newly Diagnosed Barrett’s Esophagus Study, and included three non–mutually exclusive case groups: Barrett’s esophagus, erosive esophagitis, and GERD symptoms. An additional group of men in the same age group (n = 80) found to have Barrett’s esophagus during clinically indicated upper endoscopy exams was also assessed.

Using logistic regression, the investigators estimated any associations between serum antibodies against H. pylori and cagA+ in the study group, and GERD symptoms, esophagitis, and Barrett’s esophagus. These results were compared with a control group of randomly selected men (n = 177) who did not have any of the three conditions and who were having colorectal screens.

Women were not studied, because of their typically low rates of Barrett’s esophagus. Also excluded were men with any history of upper endoscopy, Barrett’s esophagus, or esophagectomy; diagnostic indication for colonoscopy; inflammatory* bowel disease; known ascites or esophageal varices; any cancers other than melanoma in the previous 5 years; or notable coagulopathy.

The study did include consecutive men between the ages of 50 and 79 years, newly diagnosed at either of the two study sites with Barrett’s esophagus by way of a clinically indicated upper endoscopy.

To determine the presence of GERD, the study group was given a survey that was not formally validated, about their use of proton pump inhibitors (PPI) and histamine₂ receptor agonists (HR₂A) in relation to the frequency they experienced heartburn and regurgitation. Patients who reported weekly heartburn and regurgitation while not using medication were considered to have GERD. A validated survey, the Mayo Clinic’s Gastroesophageal Reflux Questionnaire (GERQ), was applied during the last quarter of the study, although because the GERQ does not address the role of acid-reducing medications, the investigators wrote that there is the chance that patients with GERD managed by medication could have been misclassified by the questionnaire as non-GERD controls.

The study group also underwent colonoscopy, followed by upper endoscopy. If Barrett’s esophagus was suspected, biopsies were obtained. Using the Los Angeles Classification scheme, if class C or D esophagitis was found, patients repeated the endoscopy while taking a PPI before investigators determined if the patient had Barrett’s esophagus. Patients who were not taking any acid-reducing medications at the time of the endoscopy who reported at least weekly symptoms of GERD and had a normal endoscopy without erosive esophagitis or Barrett’s esophagus were considered to have nonerosive reflux symptoms. Patients with Barrett’s esophagus identified on a clinically indicated upper endoscopy were included with the same as those identified among the the people screened for colorectal cancer. Blood samples were drawn from all subjects and assayed for H. pylori.

The results were that 822 of the colorectal cancer patients had upper endoscopy; 328 were randomly selected for descriptive analysis of assays, 22.3% of which were found to have antibodies against H. pylori, with 1.8% equivocal for H. pylori on two assays. Of those positive for H. pylori, nearly half (49.3%) were found to have antibodies against cagA while none of those who were equivocal for H. pylori were found to have antibodies against cagA. Compared with study group members who were seropositive for H. pylori, those who were seronegative were less likely to be smokers and to have higher education and income.

Noting that classification errors for GERD might have biased the estimated associations with H. pylori toward the null, the investigators discovered that while there was a strong inverse connection between H. pylori, especially the cagA+ strain, and erosive esophagus (H. pylori adjusted odds ratio, 0.63; 95% confidence interval: 0.37-1.08 and cagA+ OR, 0.47; 95% CI: 0.21-1.03) and Barrett’s esophagus (OR, 0.53; 95% CI: 0.29 -0.97), especially the cagA+ strain (OR, 0.36; 95% CI: 0.14-0.90), they could not make a decisive link between GERD symptoms and H. pylori infection (OR, 0.948; 95% CI: 0.548-1.64 and cagA+ OR, 0.967; 95% CI: 0.461-2.03) (Clin. Gastroenterol. Hepatol. 2013 [doi: 10.1016/j.cgh.2013.08.029]).

Dr. Rubenstein and his colleagues theorized that since the GERD link was not found, the mechanism of H. pylori’s negative association with Barrett’s esophagus might be from the direct impact of the bacteria on the inflammatory or mucosal response; its indirect effects on the production of leptin or ghrelin; or a confounding effect created by genetic regulation of cytokines or prior alterations in the esophageal and gastric microbiota.

The study was underwritten by the National Institutes of Health and by a senior marketing grant from the American Society for Gastrointestinal Endoscopy. Dr. Rubenstein and his associates reported no relevant disclosures.

wmcknight@frontlinemedcom.com

*Correction, 9/20/2013: An earlier version of this story incorrectly identified inflammatory bowel disease.

Helicobacter pylori was found to have a strong inverse link with Barrett’s esophagus, but not with symptoms of gastroesophageal reflux disease. Erosive esophagitis also was seen to trend toward an inverse association with H. pylori.

Previous reports have attributed a protective effect against gastroesophageal reflux disease (GERD), esophageal adenocarcinoma, and Barrett’s esophagus to H. pylori infection, particularly the cytotoxin-associated gene A (cagA+) strain. Having determined the studies associating H. pylori with GERD either yielded weak support for an inverse relationship, were prone to bias, or were otherwise flawed, a team led by Dr. Joel Rubenstein of the Veterans Affairs Center for Clinical Management Research, Washington, and the University of Michigan Medical School in Ann Arbor analyzed the associations of the three disease outcomes occurring in the same populations with the bacterium.

They constructed a case-control study of men between the ages of 50 and 79 years (n = 533), who had colorectal cancer screening at one of two tertiary medical centers in Michigan between 2008 and 2011, and who were recruited to have upper endoscopy. The study served as a secondary analysis of the Newly Diagnosed Barrett’s Esophagus Study, and included three non–mutually exclusive case groups: Barrett’s esophagus, erosive esophagitis, and GERD symptoms. An additional group of men in the same age group (n = 80) found to have Barrett’s esophagus during clinically indicated upper endoscopy exams was also assessed.

Using logistic regression, the investigators estimated any associations between serum antibodies against H. pylori and cagA+ in the study group, and GERD symptoms, esophagitis, and Barrett’s esophagus. These results were compared with a control group of randomly selected men (n = 177) who did not have any of the three conditions and who were having colorectal screens.

Women were not studied, because of their typically low rates of Barrett’s esophagus. Also excluded were men with any history of upper endoscopy, Barrett’s esophagus, or esophagectomy; diagnostic indication for colonoscopy; inflammatory* bowel disease; known ascites or esophageal varices; any cancers other than melanoma in the previous 5 years; or notable coagulopathy.

The study did include consecutive men between the ages of 50 and 79 years, newly diagnosed at either of the two study sites with Barrett’s esophagus by way of a clinically indicated upper endoscopy.

To determine the presence of GERD, the study group was given a survey that was not formally validated, about their use of proton pump inhibitors (PPI) and histamine₂ receptor agonists (HR₂A) in relation to the frequency they experienced heartburn and regurgitation. Patients who reported weekly heartburn and regurgitation while not using medication were considered to have GERD. A validated survey, the Mayo Clinic’s Gastroesophageal Reflux Questionnaire (GERQ), was applied during the last quarter of the study, although because the GERQ does not address the role of acid-reducing medications, the investigators wrote that there is the chance that patients with GERD managed by medication could have been misclassified by the questionnaire as non-GERD controls.

The study group also underwent colonoscopy, followed by upper endoscopy. If Barrett’s esophagus was suspected, biopsies were obtained. Using the Los Angeles Classification scheme, if class C or D esophagitis was found, patients repeated the endoscopy while taking a PPI before investigators determined if the patient had Barrett’s esophagus. Patients who were not taking any acid-reducing medications at the time of the endoscopy who reported at least weekly symptoms of GERD and had a normal endoscopy without erosive esophagitis or Barrett’s esophagus were considered to have nonerosive reflux symptoms. Patients with Barrett’s esophagus identified on a clinically indicated upper endoscopy were included with the same as those identified among the the people screened for colorectal cancer. Blood samples were drawn from all subjects and assayed for H. pylori.

The results were that 822 of the colorectal cancer patients had upper endoscopy; 328 were randomly selected for descriptive analysis of assays, 22.3% of which were found to have antibodies against H. pylori, with 1.8% equivocal for H. pylori on two assays. Of those positive for H. pylori, nearly half (49.3%) were found to have antibodies against cagA while none of those who were equivocal for H. pylori were found to have antibodies against cagA. Compared with study group members who were seropositive for H. pylori, those who were seronegative were less likely to be smokers and to have higher education and income.

Noting that classification errors for GERD might have biased the estimated associations with H. pylori toward the null, the investigators discovered that while there was a strong inverse connection between H. pylori, especially the cagA+ strain, and erosive esophagus (H. pylori adjusted odds ratio, 0.63; 95% confidence interval: 0.37-1.08 and cagA+ OR, 0.47; 95% CI: 0.21-1.03) and Barrett’s esophagus (OR, 0.53; 95% CI: 0.29 -0.97), especially the cagA+ strain (OR, 0.36; 95% CI: 0.14-0.90), they could not make a decisive link between GERD symptoms and H. pylori infection (OR, 0.948; 95% CI: 0.548-1.64 and cagA+ OR, 0.967; 95% CI: 0.461-2.03) (Clin. Gastroenterol. Hepatol. 2013 [doi: 10.1016/j.cgh.2013.08.029]).

Dr. Rubenstein and his colleagues theorized that since the GERD link was not found, the mechanism of H. pylori’s negative association with Barrett’s esophagus might be from the direct impact of the bacteria on the inflammatory or mucosal response; its indirect effects on the production of leptin or ghrelin; or a confounding effect created by genetic regulation of cytokines or prior alterations in the esophageal and gastric microbiota.

The study was underwritten by the National Institutes of Health and by a senior marketing grant from the American Society for Gastrointestinal Endoscopy. Dr. Rubenstein and his associates reported no relevant disclosures.

wmcknight@frontlinemedcom.com

*Correction, 9/20/2013: An earlier version of this story incorrectly identified inflammatory bowel disease.

Among patients with community-associated Clostridium difficile infection, more than a third had not used antibiotics in the 12 weeks before diagnosis and more than half reported limited or no health care contact over the same period.

To assess possible sources of infection, Dr. Amit S. Chitnis and his colleagues at the Centers for Disease Control and Prevention reviewed the medical records of, and interviewed, 984 patients with new-onset community-associated C. difficile infection (CDI).

The patients’ median age was 51 years and median Charlson comorbidity index 0. Almost 90% were white; two-thirds were women; 41% had preceding outpatient care such as surgery or dialysis.

Investigators found that 400 patients (41%) reported low-level health care exposure, such as a visit to a physician or dentist, while 177 (18%) reported no exposure (JAMA Intern. Med. 2013;173:1359-67).

Sixty-four percent (631) reported antibiotic use within 12 weeks of diagnosis, while 28% (273) reported using a PPI, and 9% (90) reported using an H₂-receptor antagonist. Among 177 patients with no health care contact, 44% had used antibiotics, 24% used a PPI, and 12% had used H₂-receptor antagonists.

Patients with no, or limited, health care contact were significantly more likely to live with an active CDI case or have contact with infants under a year old, who can be asymptomatic CDI carriers. There were no associations between CDI and animal exposure. "Prevention of community-associated CDI should primarily focus on reducing inappropriate antibiotic use and better infection control practices in outpatient settings," the investigators concluded. They suggested evaluating CDI transmission in household settings and reduction of PPI use.

The CDC funded the work. The authors reported no conflicts of interest.

aotto@frontlinemedcom.com

Among patients with community-associated Clostridium difficile infection, more than a third had not used antibiotics in the 12 weeks before diagnosis and more than half reported limited or no health care contact over the same period.

To assess possible sources of infection, Dr. Amit S. Chitnis and his colleagues at the Centers for Disease Control and Prevention reviewed the medical records of, and interviewed, 984 patients with new-onset community-associated C. difficile infection (CDI).

The patients’ median age was 51 years and median Charlson comorbidity index 0. Almost 90% were white; two-thirds were women; 41% had preceding outpatient care such as surgery or dialysis.

Investigators found that 400 patients (41%) reported low-level health care exposure, such as a visit to a physician or dentist, while 177 (18%) reported no exposure (JAMA Intern. Med. 2013;173:1359-67).

Sixty-four percent (631) reported antibiotic use within 12 weeks of diagnosis, while 28% (273) reported using a PPI, and 9% (90) reported using an H₂-receptor antagonist. Among 177 patients with no health care contact, 44% had used antibiotics, 24% used a PPI, and 12% had used H₂-receptor antagonists.

Patients with no, or limited, health care contact were significantly more likely to live with an active CDI case or have contact with infants under a year old, who can be asymptomatic CDI carriers. There were no associations between CDI and animal exposure. "Prevention of community-associated CDI should primarily focus on reducing inappropriate antibiotic use and better infection control practices in outpatient settings," the investigators concluded. They suggested evaluating CDI transmission in household settings and reduction of PPI use.

The CDC funded the work. The authors reported no conflicts of interest.

aotto@frontlinemedcom.com

Among patients with community-associated Clostridium difficile infection, more than a third had not used antibiotics in the 12 weeks before diagnosis and more than half reported limited or no health care contact over the same period.

To assess possible sources of infection, Dr. Amit S. Chitnis and his colleagues at the Centers for Disease Control and Prevention reviewed the medical records of, and interviewed, 984 patients with new-onset community-associated C. difficile infection (CDI).

The patients’ median age was 51 years and median Charlson comorbidity index 0. Almost 90% were white; two-thirds were women; 41% had preceding outpatient care such as surgery or dialysis.

Investigators found that 400 patients (41%) reported low-level health care exposure, such as a visit to a physician or dentist, while 177 (18%) reported no exposure (JAMA Intern. Med. 2013;173:1359-67).

Sixty-four percent (631) reported antibiotic use within 12 weeks of diagnosis, while 28% (273) reported using a PPI, and 9% (90) reported using an H₂-receptor antagonist. Among 177 patients with no health care contact, 44% had used antibiotics, 24% used a PPI, and 12% had used H₂-receptor antagonists.

Patients with no, or limited, health care contact were significantly more likely to live with an active CDI case or have contact with infants under a year old, who can be asymptomatic CDI carriers. There were no associations between CDI and animal exposure. "Prevention of community-associated CDI should primarily focus on reducing inappropriate antibiotic use and better infection control practices in outpatient settings," the investigators concluded. They suggested evaluating CDI transmission in household settings and reduction of PPI use.

The CDC funded the work. The authors reported no conflicts of interest.

aotto@frontlinemedcom.com

Peroral endoscopic myotomy is a safe and effective therapy for achalasia, with 82% of patients in symptom remission at 12 months post treatment.

"With [peroral endoscopic myotomy] it seems possible to emulate the surgical principles of laparoscopic Heller myotomy without the need for skin incisions and to reduce the procedural trauma," reported Dr. Daniel Von Renteln and colleagues. The findings are in the August issue of Gastroenterology.

According to Dr. Von Renteln of the University Hospital Hamburg-Eppendorf in Hamburg, Germany, peroral endoscopic myotomy (POEM) is a novel alternative achalasia treatment.

As described previously (Endoscopy 2010;42:265-71), under general anesthesia and following endoscopy to visualize the gastroesophageal junction, a mucosal incision is made to create entry to the submucosal space. A submucosal tunnel is then created, extending downward, allowing myotomy of the esophageal sphincter. The mucosal entry site is then closed with hemostatic clips.

In the present study, the researchers looked at 70 patients who underwent the procedure at five centers in Europe and North America.

The mean procedure time for POEM was 105 minutes and the mean length of myotomy was 13 cm. Patients experienced a small but significant drop in hemoglobin post procedure (from 13 to 12 g/dL, P less than .001) as well as small but significant increases in leukocyte count and C-reactive protein levels.

At 3 months post procedure, treatment success was achieved in 97% of cases, with mean Eckhardt scores decreasing from 7 pre procedure to 1 post procedure (P less than .001).

Of the 61 patients who underwent manometry at 3 months, the researchers found that the mean pretreatment and posttreatment lower esophageal sphincter pressures were 28 mm Hg versus 9 mm Hg, respectively (P less than .001).

Results at 6 months and 12 months were comparable, with treatment success of 88.5% and 82.4%, respectively, and mean Eckhardt scores of 1.3 and 1.7, respectively (P less than .001 for both).

Patients who failed treatment subsequently underwent laparoscopic Heller myotomy (n = 3) or balloon dilatation (n = 5), with safe and effective outcomes, reported the authors.

"Because the target area for the myotomy during POEM is lateral (on the lesser curvature side) and the myotomy during LHM is anterior, subsequent LHM seems to be a feasible second-line treatment if POEM fails."

Moreover, roughly half of the patients in the current study had previously undergone endoscopic balloon dilatation or botulinum toxin injection before POEM, the researchers wrote. "This shows that POEM is safe and efficient after previous treatments."

Nevertheless, the procedure is not without risk. "Visible complete transmural openings into the mediastinum and into the peritoneal cavity occurred in the majority of patients," they pointed out. "Therefore, POEM potentially carries the risk of mediastinitis/peritonitis and/or damage to surrounding organs."

Clip dislocation at mucosal closure (n = 3), mucosal injury through electrocautery or laceration (n = 3), and bleeding requiring intervention also occurred (n = 1).

Finally, looking at postprocedure reflux rates, at 12 months, roughly 37% of patients complained of gastroesophageal reflux, with just under 8% of these patients reporting reflux symptoms daily.

Overall, 29% were prescribed a proton pump inhibitor; 19.6% of these used a PPI daily.

The authors disclosed no conflicts of interest. The study was supported by EURO-NOTES Foundation – a partnership between the European Association for Endoscopic Surgery and the European Society of Gastrointestinal Endoscopy – and Olympus, maker of endotherapeutic supplies.

Peroral endoscopic myotomy is a safe and effective therapy for achalasia, with 82% of patients in symptom remission at 12 months post treatment.

"With [peroral endoscopic myotomy] it seems possible to emulate the surgical principles of laparoscopic Heller myotomy without the need for skin incisions and to reduce the procedural trauma," reported Dr. Daniel Von Renteln and colleagues. The findings are in the August issue of Gastroenterology.

According to Dr. Von Renteln of the University Hospital Hamburg-Eppendorf in Hamburg, Germany, peroral endoscopic myotomy (POEM) is a novel alternative achalasia treatment.

As described previously (Endoscopy 2010;42:265-71), under general anesthesia and following endoscopy to visualize the gastroesophageal junction, a mucosal incision is made to create entry to the submucosal space. A submucosal tunnel is then created, extending downward, allowing myotomy of the esophageal sphincter. The mucosal entry site is then closed with hemostatic clips.

In the present study, the researchers looked at 70 patients who underwent the procedure at five centers in Europe and North America.

The mean procedure time for POEM was 105 minutes and the mean length of myotomy was 13 cm. Patients experienced a small but significant drop in hemoglobin post procedure (from 13 to 12 g/dL, P less than .001) as well as small but significant increases in leukocyte count and C-reactive protein levels.

At 3 months post procedure, treatment success was achieved in 97% of cases, with mean Eckhardt scores decreasing from 7 pre procedure to 1 post procedure (P less than .001).

Of the 61 patients who underwent manometry at 3 months, the researchers found that the mean pretreatment and posttreatment lower esophageal sphincter pressures were 28 mm Hg versus 9 mm Hg, respectively (P less than .001).

Results at 6 months and 12 months were comparable, with treatment success of 88.5% and 82.4%, respectively, and mean Eckhardt scores of 1.3 and 1.7, respectively (P less than .001 for both).

Patients who failed treatment subsequently underwent laparoscopic Heller myotomy (n = 3) or balloon dilatation (n = 5), with safe and effective outcomes, reported the authors.

"Because the target area for the myotomy during POEM is lateral (on the lesser curvature side) and the myotomy during LHM is anterior, subsequent LHM seems to be a feasible second-line treatment if POEM fails."

Moreover, roughly half of the patients in the current study had previously undergone endoscopic balloon dilatation or botulinum toxin injection before POEM, the researchers wrote. "This shows that POEM is safe and efficient after previous treatments."

Nevertheless, the procedure is not without risk. "Visible complete transmural openings into the mediastinum and into the peritoneal cavity occurred in the majority of patients," they pointed out. "Therefore, POEM potentially carries the risk of mediastinitis/peritonitis and/or damage to surrounding organs."

Clip dislocation at mucosal closure (n = 3), mucosal injury through electrocautery or laceration (n = 3), and bleeding requiring intervention also occurred (n = 1).

Finally, looking at postprocedure reflux rates, at 12 months, roughly 37% of patients complained of gastroesophageal reflux, with just under 8% of these patients reporting reflux symptoms daily.

Overall, 29% were prescribed a proton pump inhibitor; 19.6% of these used a PPI daily.

The authors disclosed no conflicts of interest. The study was supported by EURO-NOTES Foundation – a partnership between the European Association for Endoscopic Surgery and the European Society of Gastrointestinal Endoscopy – and Olympus, maker of endotherapeutic supplies.

Peroral endoscopic myotomy is a safe and effective therapy for achalasia, with 82% of patients in symptom remission at 12 months post treatment.

"With [peroral endoscopic myotomy] it seems possible to emulate the surgical principles of laparoscopic Heller myotomy without the need for skin incisions and to reduce the procedural trauma," reported Dr. Daniel Von Renteln and colleagues. The findings are in the August issue of Gastroenterology.

According to Dr. Von Renteln of the University Hospital Hamburg-Eppendorf in Hamburg, Germany, peroral endoscopic myotomy (POEM) is a novel alternative achalasia treatment.

As described previously (Endoscopy 2010;42:265-71), under general anesthesia and following endoscopy to visualize the gastroesophageal junction, a mucosal incision is made to create entry to the submucosal space. A submucosal tunnel is then created, extending downward, allowing myotomy of the esophageal sphincter. The mucosal entry site is then closed with hemostatic clips.

In the present study, the researchers looked at 70 patients who underwent the procedure at five centers in Europe and North America.

The mean procedure time for POEM was 105 minutes and the mean length of myotomy was 13 cm. Patients experienced a small but significant drop in hemoglobin post procedure (from 13 to 12 g/dL, P less than .001) as well as small but significant increases in leukocyte count and C-reactive protein levels.

At 3 months post procedure, treatment success was achieved in 97% of cases, with mean Eckhardt scores decreasing from 7 pre procedure to 1 post procedure (P less than .001).

Of the 61 patients who underwent manometry at 3 months, the researchers found that the mean pretreatment and posttreatment lower esophageal sphincter pressures were 28 mm Hg versus 9 mm Hg, respectively (P less than .001).

Results at 6 months and 12 months were comparable, with treatment success of 88.5% and 82.4%, respectively, and mean Eckhardt scores of 1.3 and 1.7, respectively (P less than .001 for both).

Patients who failed treatment subsequently underwent laparoscopic Heller myotomy (n = 3) or balloon dilatation (n = 5), with safe and effective outcomes, reported the authors.

"Because the target area for the myotomy during POEM is lateral (on the lesser curvature side) and the myotomy during LHM is anterior, subsequent LHM seems to be a feasible second-line treatment if POEM fails."

Moreover, roughly half of the patients in the current study had previously undergone endoscopic balloon dilatation or botulinum toxin injection before POEM, the researchers wrote. "This shows that POEM is safe and efficient after previous treatments."

Nevertheless, the procedure is not without risk. "Visible complete transmural openings into the mediastinum and into the peritoneal cavity occurred in the majority of patients," they pointed out. "Therefore, POEM potentially carries the risk of mediastinitis/peritonitis and/or damage to surrounding organs."

Clip dislocation at mucosal closure (n = 3), mucosal injury through electrocautery or laceration (n = 3), and bleeding requiring intervention also occurred (n = 1).

Finally, looking at postprocedure reflux rates, at 12 months, roughly 37% of patients complained of gastroesophageal reflux, with just under 8% of these patients reporting reflux symptoms daily.

Overall, 29% were prescribed a proton pump inhibitor; 19.6% of these used a PPI daily.

The authors disclosed no conflicts of interest. The study was supported by EURO-NOTES Foundation – a partnership between the European Association for Endoscopic Surgery and the European Society of Gastrointestinal Endoscopy – and Olympus, maker of endotherapeutic supplies.

At 5 years after radiofrequency ablation for Barrett’s esophagus, 93% of patients remained in complete, sustained remission.

That’s the finding from a Netherlands cohort with the "longest duration of follow-up of patients undergoing RFA for BE containing high-grade intraepithelial neoplasia and/or early-stage cancer," wrote Dr. K. Nadine Phoa and coauthors. The study, for the July issue of Gastroenterology, was published online April 1.

The investigators cautioned, however, that "both cancer recurrences occurred after almost 5 years of follow-up," demonstrating the need for long-term monitoring in this population (doi: 10.1053/j.gastro.2013.03.046).

Dr. Phoa, of the Academic Medical Center in Amsterdam, and her colleagues looked at data from four distinct consecutive cohort studies: AMC-I, which was the first pilot study of circumferential RFA using the HALO360 ablation device; AMC-II, the second, prospective study of the device; EURO-I, the first European multicenter RFA trial; and AMC-IV, a prospective, randomized, multicenter trial of the device.

Of the 55 patients who underwent one of the included trials and were treated at Dr. Phoa’s institution (45 men; mean age, 65 years), 72% underwent endoscopic resection before the first RFA treatment, either piecemeal or en bloc.

After RFA, complete remission of neoplasia and/or complete remission of intestinal metaplasia was achieved in 54 of 55 patients; of the 54 patients, 8 withdrew during follow-up due to unrelated death, comorbidity, or emigration, leaving 46 patients with a median follow-up of 61 months and six endoscopies for analysis.

The investigators found that among these, sustained complete remission of neoplasia and complete remission of intestinal metaplasia were maintained in 43 of 46 patients (93%; 95% confidence interval, 82.5-97.8).

Among the 3 patients who did have recurrence, one was 71 years old and initially presented with early-stage cancer and multifocal high-grade intraepithelial neoplasia. At the 5-year visit, a "small area with columnar mucosa with low-grade intraepithelial neoplasia was discovered," wrote the authors, and "18 months after argon plasma coagulation, no endoscopic or histological evidence of residual BE was found."

The second case was an 81-year-old patient with baseline early-stage cancer and residual BE with high-grade intraepithelial neoplasia. During the patient’s fifth endoscopy, at 52 months post RFA, "a 6-mm lesion was seen and radically removed en bloc by endoscopic resection-cap technique," the authors wrote.

"Histological evaluation showed a radically resected mucosal cancer without evidence of lymph-vascular invasion," they added, and at 3 and 9 months post resection, no endoscopic or histologic evidence of neoplasia was found.

Finally, the third case of recurrence was seen in a 62-year-old patient with baseline early-stage cancer and high-grade intraepithelial neoplasia, who, at the 5-year visit, had an elevated Barrett’s island containing carcinoma 2 cm above the neo-squamocolumnar junction.

"The lesion was radically removed en bloc by endoscopic resection-cap technique," wrote the authors, and as in the case of the prior two lesions, 3 months later, "no endoscopic or histological evidence of neoplasia or intestinal metaplasia was found."

Taking into account these three cases, the authors performed a Kaplan-Meier analysis and found a recurrence-free proportion of 90% of patients after 5 years.

According to the authors, even though remission was reestablished in all 3 patients who recurred, "this study also demonstrates how small and subtle recurrences can be."

Indeed, "even a minimal area of residual Barrett’s might be at risk for malignant progression, and this emphasizes the importance of a dedicated treatment protocol and careful endoscopic inspection to ensure complete eradication of all Barrett’s epithelium."

One of Dr. Phoa’s coauthors disclosed financial relationships with BÂRRX Medical, maker of the HALO device, and other pharmaceutical and device makers. The researchers wrote that BÂRRX Medical also supported this study.

At 5 years after radiofrequency ablation for Barrett’s esophagus, 93% of patients remained in complete, sustained remission.

That’s the finding from a Netherlands cohort with the "longest duration of follow-up of patients undergoing RFA for BE containing high-grade intraepithelial neoplasia and/or early-stage cancer," wrote Dr. K. Nadine Phoa and coauthors. The study, for the July issue of Gastroenterology, was published online April 1.

The investigators cautioned, however, that "both cancer recurrences occurred after almost 5 years of follow-up," demonstrating the need for long-term monitoring in this population (doi: 10.1053/j.gastro.2013.03.046).

Dr. Phoa, of the Academic Medical Center in Amsterdam, and her colleagues looked at data from four distinct consecutive cohort studies: AMC-I, which was the first pilot study of circumferential RFA using the HALO360 ablation device; AMC-II, the second, prospective study of the device; EURO-I, the first European multicenter RFA trial; and AMC-IV, a prospective, randomized, multicenter trial of the device.

Of the 55 patients who underwent one of the included trials and were treated at Dr. Phoa’s institution (45 men; mean age, 65 years), 72% underwent endoscopic resection before the first RFA treatment, either piecemeal or en bloc.

After RFA, complete remission of neoplasia and/or complete remission of intestinal metaplasia was achieved in 54 of 55 patients; of the 54 patients, 8 withdrew during follow-up due to unrelated death, comorbidity, or emigration, leaving 46 patients with a median follow-up of 61 months and six endoscopies for analysis.

The investigators found that among these, sustained complete remission of neoplasia and complete remission of intestinal metaplasia were maintained in 43 of 46 patients (93%; 95% confidence interval, 82.5-97.8).

Among the 3 patients who did have recurrence, one was 71 years old and initially presented with early-stage cancer and multifocal high-grade intraepithelial neoplasia. At the 5-year visit, a "small area with columnar mucosa with low-grade intraepithelial neoplasia was discovered," wrote the authors, and "18 months after argon plasma coagulation, no endoscopic or histological evidence of residual BE was found."

The second case was an 81-year-old patient with baseline early-stage cancer and residual BE with high-grade intraepithelial neoplasia. During the patient’s fifth endoscopy, at 52 months post RFA, "a 6-mm lesion was seen and radically removed en bloc by endoscopic resection-cap technique," the authors wrote.

"Histological evaluation showed a radically resected mucosal cancer without evidence of lymph-vascular invasion," they added, and at 3 and 9 months post resection, no endoscopic or histologic evidence of neoplasia was found.

Finally, the third case of recurrence was seen in a 62-year-old patient with baseline early-stage cancer and high-grade intraepithelial neoplasia, who, at the 5-year visit, had an elevated Barrett’s island containing carcinoma 2 cm above the neo-squamocolumnar junction.

"The lesion was radically removed en bloc by endoscopic resection-cap technique," wrote the authors, and as in the case of the prior two lesions, 3 months later, "no endoscopic or histological evidence of neoplasia or intestinal metaplasia was found."

Taking into account these three cases, the authors performed a Kaplan-Meier analysis and found a recurrence-free proportion of 90% of patients after 5 years.

According to the authors, even though remission was reestablished in all 3 patients who recurred, "this study also demonstrates how small and subtle recurrences can be."

Indeed, "even a minimal area of residual Barrett’s might be at risk for malignant progression, and this emphasizes the importance of a dedicated treatment protocol and careful endoscopic inspection to ensure complete eradication of all Barrett’s epithelium."

One of Dr. Phoa’s coauthors disclosed financial relationships with BÂRRX Medical, maker of the HALO device, and other pharmaceutical and device makers. The researchers wrote that BÂRRX Medical also supported this study.

At 5 years after radiofrequency ablation for Barrett’s esophagus, 93% of patients remained in complete, sustained remission.

That’s the finding from a Netherlands cohort with the "longest duration of follow-up of patients undergoing RFA for BE containing high-grade intraepithelial neoplasia and/or early-stage cancer," wrote Dr. K. Nadine Phoa and coauthors. The study, for the July issue of Gastroenterology, was published online April 1.

The investigators cautioned, however, that "both cancer recurrences occurred after almost 5 years of follow-up," demonstrating the need for long-term monitoring in this population (doi: 10.1053/j.gastro.2013.03.046).

Dr. Phoa, of the Academic Medical Center in Amsterdam, and her colleagues looked at data from four distinct consecutive cohort studies: AMC-I, which was the first pilot study of circumferential RFA using the HALO360 ablation device; AMC-II, the second, prospective study of the device; EURO-I, the first European multicenter RFA trial; and AMC-IV, a prospective, randomized, multicenter trial of the device.

Of the 55 patients who underwent one of the included trials and were treated at Dr. Phoa’s institution (45 men; mean age, 65 years), 72% underwent endoscopic resection before the first RFA treatment, either piecemeal or en bloc.

After RFA, complete remission of neoplasia and/or complete remission of intestinal metaplasia was achieved in 54 of 55 patients; of the 54 patients, 8 withdrew during follow-up due to unrelated death, comorbidity, or emigration, leaving 46 patients with a median follow-up of 61 months and six endoscopies for analysis.

The investigators found that among these, sustained complete remission of neoplasia and complete remission of intestinal metaplasia were maintained in 43 of 46 patients (93%; 95% confidence interval, 82.5-97.8).

Among the 3 patients who did have recurrence, one was 71 years old and initially presented with early-stage cancer and multifocal high-grade intraepithelial neoplasia. At the 5-year visit, a "small area with columnar mucosa with low-grade intraepithelial neoplasia was discovered," wrote the authors, and "18 months after argon plasma coagulation, no endoscopic or histological evidence of residual BE was found."

The second case was an 81-year-old patient with baseline early-stage cancer and residual BE with high-grade intraepithelial neoplasia. During the patient’s fifth endoscopy, at 52 months post RFA, "a 6-mm lesion was seen and radically removed en bloc by endoscopic resection-cap technique," the authors wrote.

"Histological evaluation showed a radically resected mucosal cancer without evidence of lymph-vascular invasion," they added, and at 3 and 9 months post resection, no endoscopic or histologic evidence of neoplasia was found.

Finally, the third case of recurrence was seen in a 62-year-old patient with baseline early-stage cancer and high-grade intraepithelial neoplasia, who, at the 5-year visit, had an elevated Barrett’s island containing carcinoma 2 cm above the neo-squamocolumnar junction.

"The lesion was radically removed en bloc by endoscopic resection-cap technique," wrote the authors, and as in the case of the prior two lesions, 3 months later, "no endoscopic or histological evidence of neoplasia or intestinal metaplasia was found."

Taking into account these three cases, the authors performed a Kaplan-Meier analysis and found a recurrence-free proportion of 90% of patients after 5 years.

According to the authors, even though remission was reestablished in all 3 patients who recurred, "this study also demonstrates how small and subtle recurrences can be."

Indeed, "even a minimal area of residual Barrett’s might be at risk for malignant progression, and this emphasizes the importance of a dedicated treatment protocol and careful endoscopic inspection to ensure complete eradication of all Barrett’s epithelium."

One of Dr. Phoa’s coauthors disclosed financial relationships with BÂRRX Medical, maker of the HALO device, and other pharmaceutical and device makers. The researchers wrote that BÂRRX Medical also supported this study.

Data from a U.K. registry reveal that 86% of Barrett’s esophagus patients achieve complete remission of high-grade dysplasia after radiofrequency ablation, with only 9% reporting adverse events.

"The safety and short-term efficacy of radiofrequency ablation as a minimally invasive intervention for premalignant dysplastic Barrett’s esophagus are now beyond debate," wrote Dr. Rehan J. Haidry and his coauthors in the July issue of Gastroenterology (doi: 10.1053/j.gastro.2013.03.045).

Indeed, radiofrequency ablation (RFA) "has provided clinicians in specialist centers a valuable adjunct to more established surgical treatments."

Dr. Haidry, of the National Medical Laser Centre at University College London, and his colleagues analyzed data from the U.K. National Halo RFA Registry, founded in 2008 to audit outcomes of all patients undergoing ablation using the Halo device for high-grade dysplasia and early cancer in Barrett’s esophagus.

The cohort included 335 patients (mean age, 68.1 years); 81% were men and 100% were white.

Dr. Haidry calculated that the median number of RFA treatments was 2 (range, 1-6), and they took place over a median period of 11.6 months. The mean length of Barrett’s esophagus to be ablated was 5.8 cm. In all, 72% of patients were classed as having high-grade dysplasia, 24% as having low-grade dysplasia, and 4% as having intramucosal cancer.

About half the patients (49%) underwent endoscopic resection before starting RFA.

The researchers then combed the records for evidence of the primary outcomes of this analysis: complete reversal of high-grade dysplasia and complete reversal of all dysplasia 12 months from the index RFA treatment.

They found that at 1 year post RFA, 86% of patients had achieved complete reversal of high-grade dysplasia, and 81% showed complete reversal of all dysplasia.

Nevertheless, the authors also found 12 cases of recurrent neoplasia after "apparently successful" ablation, occurring at a mean 8 months after completion of the protocol.

Additionally, "5.1% have progressed to invasive disease at their most recent follow-up biopsy," the authors wrote.

Looking at the safety profile of RFA, the investigators uncovered one case of perforation in a patient who was treated with a 34-mm balloon (since removed from the market, according to the researchers), and 30 cases (9%) of stricturing, all of which were managed endoscopically.

The authors conceded several limitations to this "real world" analysis of what they called "the largest series to date of patients with early Barrett’s neoplasia undergoing RFA."

For example, "the proposed protocol states that all patients should undergo ablation every 3 months until the 12-month period, at which point the end-of-protocol biopsy defines treatment success or failure," wrote Dr. Haidry.

"Within the confines of varied practice nationwide and diversity in resources, these strict timelines were difficult to achieve."

Moreover, "although the durability of favorable response appears promising, our median follow-up time of 19 months is short," added the authors, noting that two late relapses occurred more than 4 years after "apparently successful" ablation.

"This highlights the importance of long-term follow-up of these patients."

The researchers disclosed that one of their coauthors has financial ties to the makers of the Halo device. The work was supported by the Cancer Research UK (CRUK) University College London Early Cancer Medicine Centre, and was conducted at a facility sponsored by the U.K. Department of Health.

Data from a U.K. registry reveal that 86% of Barrett’s esophagus patients achieve complete remission of high-grade dysplasia after radiofrequency ablation, with only 9% reporting adverse events.

"The safety and short-term efficacy of radiofrequency ablation as a minimally invasive intervention for premalignant dysplastic Barrett’s esophagus are now beyond debate," wrote Dr. Rehan J. Haidry and his coauthors in the July issue of Gastroenterology (doi: 10.1053/j.gastro.2013.03.045).

Indeed, radiofrequency ablation (RFA) "has provided clinicians in specialist centers a valuable adjunct to more established surgical treatments."

Dr. Haidry, of the National Medical Laser Centre at University College London, and his colleagues analyzed data from the U.K. National Halo RFA Registry, founded in 2008 to audit outcomes of all patients undergoing ablation using the Halo device for high-grade dysplasia and early cancer in Barrett’s esophagus.

The cohort included 335 patients (mean age, 68.1 years); 81% were men and 100% were white.

Dr. Haidry calculated that the median number of RFA treatments was 2 (range, 1-6), and they took place over a median period of 11.6 months. The mean length of Barrett’s esophagus to be ablated was 5.8 cm. In all, 72% of patients were classed as having high-grade dysplasia, 24% as having low-grade dysplasia, and 4% as having intramucosal cancer.

About half the patients (49%) underwent endoscopic resection before starting RFA.

The researchers then combed the records for evidence of the primary outcomes of this analysis: complete reversal of high-grade dysplasia and complete reversal of all dysplasia 12 months from the index RFA treatment.

They found that at 1 year post RFA, 86% of patients had achieved complete reversal of high-grade dysplasia, and 81% showed complete reversal of all dysplasia.

Nevertheless, the authors also found 12 cases of recurrent neoplasia after "apparently successful" ablation, occurring at a mean 8 months after completion of the protocol.

Additionally, "5.1% have progressed to invasive disease at their most recent follow-up biopsy," the authors wrote.

Looking at the safety profile of RFA, the investigators uncovered one case of perforation in a patient who was treated with a 34-mm balloon (since removed from the market, according to the researchers), and 30 cases (9%) of stricturing, all of which were managed endoscopically.

The authors conceded several limitations to this "real world" analysis of what they called "the largest series to date of patients with early Barrett’s neoplasia undergoing RFA."

For example, "the proposed protocol states that all patients should undergo ablation every 3 months until the 12-month period, at which point the end-of-protocol biopsy defines treatment success or failure," wrote Dr. Haidry.

"Within the confines of varied practice nationwide and diversity in resources, these strict timelines were difficult to achieve."

Moreover, "although the durability of favorable response appears promising, our median follow-up time of 19 months is short," added the authors, noting that two late relapses occurred more than 4 years after "apparently successful" ablation.

"This highlights the importance of long-term follow-up of these patients."

The researchers disclosed that one of their coauthors has financial ties to the makers of the Halo device. The work was supported by the Cancer Research UK (CRUK) University College London Early Cancer Medicine Centre, and was conducted at a facility sponsored by the U.K. Department of Health.

Data from a U.K. registry reveal that 86% of Barrett’s esophagus patients achieve complete remission of high-grade dysplasia after radiofrequency ablation, with only 9% reporting adverse events.

"The safety and short-term efficacy of radiofrequency ablation as a minimally invasive intervention for premalignant dysplastic Barrett’s esophagus are now beyond debate," wrote Dr. Rehan J. Haidry and his coauthors in the July issue of Gastroenterology (doi: 10.1053/j.gastro.2013.03.045).

Indeed, radiofrequency ablation (RFA) "has provided clinicians in specialist centers a valuable adjunct to more established surgical treatments."

Dr. Haidry, of the National Medical Laser Centre at University College London, and his colleagues analyzed data from the U.K. National Halo RFA Registry, founded in 2008 to audit outcomes of all patients undergoing ablation using the Halo device for high-grade dysplasia and early cancer in Barrett’s esophagus.

The cohort included 335 patients (mean age, 68.1 years); 81% were men and 100% were white.

Dr. Haidry calculated that the median number of RFA treatments was 2 (range, 1-6), and they took place over a median period of 11.6 months. The mean length of Barrett’s esophagus to be ablated was 5.8 cm. In all, 72% of patients were classed as having high-grade dysplasia, 24% as having low-grade dysplasia, and 4% as having intramucosal cancer.

About half the patients (49%) underwent endoscopic resection before starting RFA.

The researchers then combed the records for evidence of the primary outcomes of this analysis: complete reversal of high-grade dysplasia and complete reversal of all dysplasia 12 months from the index RFA treatment.

They found that at 1 year post RFA, 86% of patients had achieved complete reversal of high-grade dysplasia, and 81% showed complete reversal of all dysplasia.

Nevertheless, the authors also found 12 cases of recurrent neoplasia after "apparently successful" ablation, occurring at a mean 8 months after completion of the protocol.

Additionally, "5.1% have progressed to invasive disease at their most recent follow-up biopsy," the authors wrote.

Looking at the safety profile of RFA, the investigators uncovered one case of perforation in a patient who was treated with a 34-mm balloon (since removed from the market, according to the researchers), and 30 cases (9%) of stricturing, all of which were managed endoscopically.

The authors conceded several limitations to this "real world" analysis of what they called "the largest series to date of patients with early Barrett’s neoplasia undergoing RFA."

For example, "the proposed protocol states that all patients should undergo ablation every 3 months until the 12-month period, at which point the end-of-protocol biopsy defines treatment success or failure," wrote Dr. Haidry.

"Within the confines of varied practice nationwide and diversity in resources, these strict timelines were difficult to achieve."

Moreover, "although the durability of favorable response appears promising, our median follow-up time of 19 months is short," added the authors, noting that two late relapses occurred more than 4 years after "apparently successful" ablation.

"This highlights the importance of long-term follow-up of these patients."

The researchers disclosed that one of their coauthors has financial ties to the makers of the Halo device. The work was supported by the Cancer Research UK (CRUK) University College London Early Cancer Medicine Centre, and was conducted at a facility sponsored by the U.K. Department of Health.

About one-third of patients with Barrett’s esophagus can expect recurrence of intestinal metaplasia by 2 years after obtaining complete remission with radiofrequency ablation.

The finding highlights the importance of frequent endoscopic surveillance in these patients, even after remission is achieved, wrote Dr. Milli Gupta and colleagues in the July issue of Gastroenterology, which was published online in March.

In the study, Dr. Gupta, of the Mayo Clinic’s division of gastroenterology and hepatology in Rochester, Minn., and her associates looked at 448 patients with Barrett’s esophagus treated with radiofrequency ablation (RFA) at three different tertiary referral centers (doi: 10.1053/j.gastro.2013.03.008).

The data were collected from patients treated and followed up in these centers from January 2003 to November 2011 as part of the Barrett’s Esophagus Translational Research Network consortium.

The patients’ mean age was 64 years, 85% were men, and the mean length of Barrett’s esophagus that was treated was 4.1 cm, the authors reported.

Looking at the indication for RFA, 11% had intramucosal esophageal adenocarcinoma, 60% had high-grade dysplasia, 15% had low-grade dysplasia, and 14% had nondysplastic BE.

Slightly more than half (55%) of patients also underwent endoscopic mucosal resection before RFA, and 1% had received cryotherapy.

After RFA, the authors found that by 1 year, roughly 26% of patients achieved complete remission of intestinal metaplasia (CRIM), defined as two negative endoscopies and histology clear of intestinal metaplasia.

That figure climbed to 56% by 2 years, and to 71% by 3 years, with 29% of patients receiving one RFA treatment session, 35% receiving two sessions, and the remaining percentage of patients undergoing 3-10 sessions before remission.

Adverse events occurred in 6.5% of patients, with stricture formation being the most common, followed by bleeding, mucosal tears, and hospitalizations for dysrhythmias.

However, using a Kaplan-Meier survival curve, the authors found that after CRIM was attained, 20% of patients would go on to have recurrence of intestinal metaplasia by 1 year. Similarly, by 2 years after attainment of CRIM, the rate of recurrence was 33%.

"By 3 years, recurrences continued to occur, but precise estimates were difficult to establish because of the small number of at-risk subjects (n = 11), which made estimates of recurrence less precise," Dr. Gupta and her colleagues wrote.

According to the authors, the most common type of recurrence was intestinal metaplasia without dysplasia, which was seen in 78% of patients who recurred after CRIM.

The remaining patients who recurred (22%) developed dysplastic Barrett’s esophagus, with 11% showing high-grade dysplasia, 8% showing low-grade dysplasia, and 3% developing cancer.

There were no discernable endoscopic or patient factors associated with time to recurrence on univariate and multivariate analyses, the authors added.

"Despite the ability of RFA to achieve CRIM, recurrence of intestinal metaplasia and dysplasia appears to occur in a substantial proportion of subjects," wrote Dr. Gupta.

She pointed out that current recommendations call for intense surveillance at 3- to 6-month intervals, and if no recurrence is found, "surveillance generally is decreased to 6- to 12-month intervals."

However, "until predictive biomarkers are identified and available for clinical practice, endoscopic surveillance directed at the gastroesophageal junction and original BE [Barrett’s esophagus] segment should be continued."

Dr. Gupta had no conflicts of interest. Several of her coauthors disclosed financial relationships with drug makers, including the makers of therapies for Barrett’s esophagus. The study was funded by a grant from the National Institutes of Health. The Barrett’s Esophagus Translational Research Network consortium is funded by the National Cancer Institute.

About one-third of patients with Barrett’s esophagus can expect recurrence of intestinal metaplasia by 2 years after obtaining complete remission with radiofrequency ablation.

The finding highlights the importance of frequent endoscopic surveillance in these patients, even after remission is achieved, wrote Dr. Milli Gupta and colleagues in the July issue of Gastroenterology, which was published online in March.

In the study, Dr. Gupta, of the Mayo Clinic’s division of gastroenterology and hepatology in Rochester, Minn., and her associates looked at 448 patients with Barrett’s esophagus treated with radiofrequency ablation (RFA) at three different tertiary referral centers (doi: 10.1053/j.gastro.2013.03.008).

The data were collected from patients treated and followed up in these centers from January 2003 to November 2011 as part of the Barrett’s Esophagus Translational Research Network consortium.

The patients’ mean age was 64 years, 85% were men, and the mean length of Barrett’s esophagus that was treated was 4.1 cm, the authors reported.

Looking at the indication for RFA, 11% had intramucosal esophageal adenocarcinoma, 60% had high-grade dysplasia, 15% had low-grade dysplasia, and 14% had nondysplastic BE.

Slightly more than half (55%) of patients also underwent endoscopic mucosal resection before RFA, and 1% had received cryotherapy.

After RFA, the authors found that by 1 year, roughly 26% of patients achieved complete remission of intestinal metaplasia (CRIM), defined as two negative endoscopies and histology clear of intestinal metaplasia.

That figure climbed to 56% by 2 years, and to 71% by 3 years, with 29% of patients receiving one RFA treatment session, 35% receiving two sessions, and the remaining percentage of patients undergoing 3-10 sessions before remission.

Adverse events occurred in 6.5% of patients, with stricture formation being the most common, followed by bleeding, mucosal tears, and hospitalizations for dysrhythmias.

However, using a Kaplan-Meier survival curve, the authors found that after CRIM was attained, 20% of patients would go on to have recurrence of intestinal metaplasia by 1 year. Similarly, by 2 years after attainment of CRIM, the rate of recurrence was 33%.

"By 3 years, recurrences continued to occur, but precise estimates were difficult to establish because of the small number of at-risk subjects (n = 11), which made estimates of recurrence less precise," Dr. Gupta and her colleagues wrote.

According to the authors, the most common type of recurrence was intestinal metaplasia without dysplasia, which was seen in 78% of patients who recurred after CRIM.

The remaining patients who recurred (22%) developed dysplastic Barrett’s esophagus, with 11% showing high-grade dysplasia, 8% showing low-grade dysplasia, and 3% developing cancer.

There were no discernable endoscopic or patient factors associated with time to recurrence on univariate and multivariate analyses, the authors added.

"Despite the ability of RFA to achieve CRIM, recurrence of intestinal metaplasia and dysplasia appears to occur in a substantial proportion of subjects," wrote Dr. Gupta.

She pointed out that current recommendations call for intense surveillance at 3- to 6-month intervals, and if no recurrence is found, "surveillance generally is decreased to 6- to 12-month intervals."

However, "until predictive biomarkers are identified and available for clinical practice, endoscopic surveillance directed at the gastroesophageal junction and original BE [Barrett’s esophagus] segment should be continued."

Dr. Gupta had no conflicts of interest. Several of her coauthors disclosed financial relationships with drug makers, including the makers of therapies for Barrett’s esophagus. The study was funded by a grant from the National Institutes of Health. The Barrett’s Esophagus Translational Research Network consortium is funded by the National Cancer Institute.

About one-third of patients with Barrett’s esophagus can expect recurrence of intestinal metaplasia by 2 years after obtaining complete remission with radiofrequency ablation.

The finding highlights the importance of frequent endoscopic surveillance in these patients, even after remission is achieved, wrote Dr. Milli Gupta and colleagues in the July issue of Gastroenterology, which was published online in March.

In the study, Dr. Gupta, of the Mayo Clinic’s division of gastroenterology and hepatology in Rochester, Minn., and her associates looked at 448 patients with Barrett’s esophagus treated with radiofrequency ablation (RFA) at three different tertiary referral centers (doi: 10.1053/j.gastro.2013.03.008).

The data were collected from patients treated and followed up in these centers from January 2003 to November 2011 as part of the Barrett’s Esophagus Translational Research Network consortium.

The patients’ mean age was 64 years, 85% were men, and the mean length of Barrett’s esophagus that was treated was 4.1 cm, the authors reported.

Looking at the indication for RFA, 11% had intramucosal esophageal adenocarcinoma, 60% had high-grade dysplasia, 15% had low-grade dysplasia, and 14% had nondysplastic BE.

Slightly more than half (55%) of patients also underwent endoscopic mucosal resection before RFA, and 1% had received cryotherapy.

After RFA, the authors found that by 1 year, roughly 26% of patients achieved complete remission of intestinal metaplasia (CRIM), defined as two negative endoscopies and histology clear of intestinal metaplasia.

That figure climbed to 56% by 2 years, and to 71% by 3 years, with 29% of patients receiving one RFA treatment session, 35% receiving two sessions, and the remaining percentage of patients undergoing 3-10 sessions before remission.

Adverse events occurred in 6.5% of patients, with stricture formation being the most common, followed by bleeding, mucosal tears, and hospitalizations for dysrhythmias.

However, using a Kaplan-Meier survival curve, the authors found that after CRIM was attained, 20% of patients would go on to have recurrence of intestinal metaplasia by 1 year. Similarly, by 2 years after attainment of CRIM, the rate of recurrence was 33%.

"By 3 years, recurrences continued to occur, but precise estimates were difficult to establish because of the small number of at-risk subjects (n = 11), which made estimates of recurrence less precise," Dr. Gupta and her colleagues wrote.

According to the authors, the most common type of recurrence was intestinal metaplasia without dysplasia, which was seen in 78% of patients who recurred after CRIM.

The remaining patients who recurred (22%) developed dysplastic Barrett’s esophagus, with 11% showing high-grade dysplasia, 8% showing low-grade dysplasia, and 3% developing cancer.

There were no discernable endoscopic or patient factors associated with time to recurrence on univariate and multivariate analyses, the authors added.

"Despite the ability of RFA to achieve CRIM, recurrence of intestinal metaplasia and dysplasia appears to occur in a substantial proportion of subjects," wrote Dr. Gupta.

She pointed out that current recommendations call for intense surveillance at 3- to 6-month intervals, and if no recurrence is found, "surveillance generally is decreased to 6- to 12-month intervals."

However, "until predictive biomarkers are identified and available for clinical practice, endoscopic surveillance directed at the gastroesophageal junction and original BE [Barrett’s esophagus] segment should be continued."

Dr. Gupta had no conflicts of interest. Several of her coauthors disclosed financial relationships with drug makers, including the makers of therapies for Barrett’s esophagus. The study was funded by a grant from the National Institutes of Health. The Barrett’s Esophagus Translational Research Network consortium is funded by the National Cancer Institute.