Upper GI Tract

PHOENIX, ARIZ. – Cost and quality are not always synonymous, particularly when it comes to complex surgical procedures such as esophagectomy.

A review of records on more than 6,700 patients who underwent esophagectomy during a 4-year period showed that factors such as patient age, severity of illness, and hospital/surgeon volume can have a major effect on resource utilization and costs, said Dr. Daniel E. Abbott, assistant professor of surgery at the University of Cincinnati.

"There are certainly actionable risk factors for poor outcomes, such as mortality, and increased resource utilization, including dollar costs, the opportunity costs of increased length of stay, readmission, and rehabilitation and skilled nursing facilities," he reported at the annual Society of Surgical Oncology Cancer Symposium.

"I would argue that careful patient selection can have profound influences on cost-effectiveness. I think that as our health care is evolving and our outcomes are increasingly scrutinized, there will be increasing pressure to have better outcomes at lower costs," he added.

Neil Osterweil/Frontline Medical News

Dr. Abbott and his colleagues examined clinical variables in the cases of 6,737 esophagectomy patients treated from 2009 through 2012 in the University Healthsystems Consortium (UHC), an organization comprising 120 university hospitals and 299 affiliates.

They evaluated patient characteristics such as age and race, severity of illness index (1-4), esophagectomy type, and center and surgeon volume, and evaluated the effects of these variables on clinical outcomes that contribute to resource utilization, including deaths, readmissions, length of stay (LOS), and discharge disposition.

They found that the median LOS for all patients was 10 days (interquartile range, 8-17 days), but for patients over age 70, the median LOS was 11 days (P less than .01 vs. patients 70 and under).

Older patients did not have significantly higher readmission rates, but of the 4.2% of all patients who died in hospital, those over age 70 had more than twice the death rate of younger patients (7.0% vs. 3.2%, P less than .01).

Older patients were also significantly more likely to be discharged to a skilled nursing or rehabilitation facility than were younger patients (31.9% vs. 10.6%; P less than .01).

Total median cost per patient was $25,952, but again, older patients accounted for more of the expenses, at a median of $27,628 vs. $25,841 for those 70 and under (P less than .01).

In a multivariate analysis, patients over 70 had a more than twofold increase in risk of death (odds ratio, 2.12; P less than .01). Other factors significantly associated with greater risk for death were greater severity of illness (OR, 14.0; P less than .01) and black race vs. other races (OR, 1.88; P less than .01).

Factors associated with more frequent readmissions included greater severity of illness (OR, 1.33; P less than .01), and black race (OR, 1.34; P = .01), while patients of high-volume surgeons were less likely to need readmission (OR, 0.87; P = .04).

Lengths of stay were greater among patients over age 70, with every year over 70 translating into a 6% greater LOS (OR, 1.06; P =.03); older patients had a 16% increase in LOS for every year over 70 (OR, 1.16; P less than .01).

Similarly, each increase in severity of illness index score above 2 was associated with a 31% increase in LOS (OR, 1.31) and a 475% increase in intensive care unit (ICU) days (OR, 4.75; P less than .01 for both LOS and ICU days).

Black patients had a 22% increase in LOS vs. other races (OR, 1.22; P less than .01) and a 31% relative increase in ICU days (OR, 1.31; P = .01).

Because age and severity of illness were both strong predictors for mortality, readmission, and other perioperative outcomes, the authors conducted a further analysis combining the two variables, and found that for every 5 years of age, there were significant increases in the risk for death among patients with a greater severity of illness, compared with low severity.

Dr. Abbott noted that some of the odds ratios for older, sicker patients were "ridiculously high," probably because of the smaller sample sizes.

In a multivariate analysis of cost, factors associated with higher costs were age (OR, 1.14; P less than .01), greater severity of illness (OR, 2.14; P less than .01), and black race (OR, 1.15; P less than .01).

And in an analysis of cumulative resource use, the authors found what Dr. Abbott called a "snowball effect," in that hospitals with the lowest total costs discharged the majority of patients home, and that as costs increased, hospitals were less likely to discharge patients home and more likely to discharge them either to home health services or to extended care. In addition, as costs rose, the percentage of patients who died in hospital also rose.

He acknowledged that because the study used administrative data from university hospitals, it was skewed toward high-volume centers, and that the database did not include survival data, information about longitudinal resource use, or procedure-specific complications.

The authors did not disclose the funding source of the study. Dr. Abbott reported having no financial disclosures.

PHOENIX, ARIZ. – Cost and quality are not always synonymous, particularly when it comes to complex surgical procedures such as esophagectomy.

A review of records on more than 6,700 patients who underwent esophagectomy during a 4-year period showed that factors such as patient age, severity of illness, and hospital/surgeon volume can have a major effect on resource utilization and costs, said Dr. Daniel E. Abbott, assistant professor of surgery at the University of Cincinnati.

"There are certainly actionable risk factors for poor outcomes, such as mortality, and increased resource utilization, including dollar costs, the opportunity costs of increased length of stay, readmission, and rehabilitation and skilled nursing facilities," he reported at the annual Society of Surgical Oncology Cancer Symposium.

"I would argue that careful patient selection can have profound influences on cost-effectiveness. I think that as our health care is evolving and our outcomes are increasingly scrutinized, there will be increasing pressure to have better outcomes at lower costs," he added.

Neil Osterweil/Frontline Medical News

Dr. Abbott and his colleagues examined clinical variables in the cases of 6,737 esophagectomy patients treated from 2009 through 2012 in the University Healthsystems Consortium (UHC), an organization comprising 120 university hospitals and 299 affiliates.

They evaluated patient characteristics such as age and race, severity of illness index (1-4), esophagectomy type, and center and surgeon volume, and evaluated the effects of these variables on clinical outcomes that contribute to resource utilization, including deaths, readmissions, length of stay (LOS), and discharge disposition.

They found that the median LOS for all patients was 10 days (interquartile range, 8-17 days), but for patients over age 70, the median LOS was 11 days (P less than .01 vs. patients 70 and under).

Older patients did not have significantly higher readmission rates, but of the 4.2% of all patients who died in hospital, those over age 70 had more than twice the death rate of younger patients (7.0% vs. 3.2%, P less than .01).

Older patients were also significantly more likely to be discharged to a skilled nursing or rehabilitation facility than were younger patients (31.9% vs. 10.6%; P less than .01).

Total median cost per patient was $25,952, but again, older patients accounted for more of the expenses, at a median of $27,628 vs. $25,841 for those 70 and under (P less than .01).

In a multivariate analysis, patients over 70 had a more than twofold increase in risk of death (odds ratio, 2.12; P less than .01). Other factors significantly associated with greater risk for death were greater severity of illness (OR, 14.0; P less than .01) and black race vs. other races (OR, 1.88; P less than .01).

Factors associated with more frequent readmissions included greater severity of illness (OR, 1.33; P less than .01), and black race (OR, 1.34; P = .01), while patients of high-volume surgeons were less likely to need readmission (OR, 0.87; P = .04).

Lengths of stay were greater among patients over age 70, with every year over 70 translating into a 6% greater LOS (OR, 1.06; P =.03); older patients had a 16% increase in LOS for every year over 70 (OR, 1.16; P less than .01).

Similarly, each increase in severity of illness index score above 2 was associated with a 31% increase in LOS (OR, 1.31) and a 475% increase in intensive care unit (ICU) days (OR, 4.75; P less than .01 for both LOS and ICU days).

Black patients had a 22% increase in LOS vs. other races (OR, 1.22; P less than .01) and a 31% relative increase in ICU days (OR, 1.31; P = .01).

Because age and severity of illness were both strong predictors for mortality, readmission, and other perioperative outcomes, the authors conducted a further analysis combining the two variables, and found that for every 5 years of age, there were significant increases in the risk for death among patients with a greater severity of illness, compared with low severity.

Dr. Abbott noted that some of the odds ratios for older, sicker patients were "ridiculously high," probably because of the smaller sample sizes.

In a multivariate analysis of cost, factors associated with higher costs were age (OR, 1.14; P less than .01), greater severity of illness (OR, 2.14; P less than .01), and black race (OR, 1.15; P less than .01).

And in an analysis of cumulative resource use, the authors found what Dr. Abbott called a "snowball effect," in that hospitals with the lowest total costs discharged the majority of patients home, and that as costs increased, hospitals were less likely to discharge patients home and more likely to discharge them either to home health services or to extended care. In addition, as costs rose, the percentage of patients who died in hospital also rose.

He acknowledged that because the study used administrative data from university hospitals, it was skewed toward high-volume centers, and that the database did not include survival data, information about longitudinal resource use, or procedure-specific complications.

The authors did not disclose the funding source of the study. Dr. Abbott reported having no financial disclosures.

PHOENIX, ARIZ. – Cost and quality are not always synonymous, particularly when it comes to complex surgical procedures such as esophagectomy.

A review of records on more than 6,700 patients who underwent esophagectomy during a 4-year period showed that factors such as patient age, severity of illness, and hospital/surgeon volume can have a major effect on resource utilization and costs, said Dr. Daniel E. Abbott, assistant professor of surgery at the University of Cincinnati.

"There are certainly actionable risk factors for poor outcomes, such as mortality, and increased resource utilization, including dollar costs, the opportunity costs of increased length of stay, readmission, and rehabilitation and skilled nursing facilities," he reported at the annual Society of Surgical Oncology Cancer Symposium.

"I would argue that careful patient selection can have profound influences on cost-effectiveness. I think that as our health care is evolving and our outcomes are increasingly scrutinized, there will be increasing pressure to have better outcomes at lower costs," he added.

Neil Osterweil/Frontline Medical News

Dr. Abbott and his colleagues examined clinical variables in the cases of 6,737 esophagectomy patients treated from 2009 through 2012 in the University Healthsystems Consortium (UHC), an organization comprising 120 university hospitals and 299 affiliates.

They evaluated patient characteristics such as age and race, severity of illness index (1-4), esophagectomy type, and center and surgeon volume, and evaluated the effects of these variables on clinical outcomes that contribute to resource utilization, including deaths, readmissions, length of stay (LOS), and discharge disposition.

They found that the median LOS for all patients was 10 days (interquartile range, 8-17 days), but for patients over age 70, the median LOS was 11 days (P less than .01 vs. patients 70 and under).

Older patients did not have significantly higher readmission rates, but of the 4.2% of all patients who died in hospital, those over age 70 had more than twice the death rate of younger patients (7.0% vs. 3.2%, P less than .01).

Older patients were also significantly more likely to be discharged to a skilled nursing or rehabilitation facility than were younger patients (31.9% vs. 10.6%; P less than .01).

Total median cost per patient was $25,952, but again, older patients accounted for more of the expenses, at a median of $27,628 vs. $25,841 for those 70 and under (P less than .01).

In a multivariate analysis, patients over 70 had a more than twofold increase in risk of death (odds ratio, 2.12; P less than .01). Other factors significantly associated with greater risk for death were greater severity of illness (OR, 14.0; P less than .01) and black race vs. other races (OR, 1.88; P less than .01).

Factors associated with more frequent readmissions included greater severity of illness (OR, 1.33; P less than .01), and black race (OR, 1.34; P = .01), while patients of high-volume surgeons were less likely to need readmission (OR, 0.87; P = .04).

Lengths of stay were greater among patients over age 70, with every year over 70 translating into a 6% greater LOS (OR, 1.06; P =.03); older patients had a 16% increase in LOS for every year over 70 (OR, 1.16; P less than .01).

Similarly, each increase in severity of illness index score above 2 was associated with a 31% increase in LOS (OR, 1.31) and a 475% increase in intensive care unit (ICU) days (OR, 4.75; P less than .01 for both LOS and ICU days).

Black patients had a 22% increase in LOS vs. other races (OR, 1.22; P less than .01) and a 31% relative increase in ICU days (OR, 1.31; P = .01).

Because age and severity of illness were both strong predictors for mortality, readmission, and other perioperative outcomes, the authors conducted a further analysis combining the two variables, and found that for every 5 years of age, there were significant increases in the risk for death among patients with a greater severity of illness, compared with low severity.

Dr. Abbott noted that some of the odds ratios for older, sicker patients were "ridiculously high," probably because of the smaller sample sizes.

In a multivariate analysis of cost, factors associated with higher costs were age (OR, 1.14; P less than .01), greater severity of illness (OR, 2.14; P less than .01), and black race (OR, 1.15; P less than .01).

And in an analysis of cumulative resource use, the authors found what Dr. Abbott called a "snowball effect," in that hospitals with the lowest total costs discharged the majority of patients home, and that as costs increased, hospitals were less likely to discharge patients home and more likely to discharge them either to home health services or to extended care. In addition, as costs rose, the percentage of patients who died in hospital also rose.

He acknowledged that because the study used administrative data from university hospitals, it was skewed toward high-volume centers, and that the database did not include survival data, information about longitudinal resource use, or procedure-specific complications.

The authors did not disclose the funding source of the study. Dr. Abbott reported having no financial disclosures.

SAN DIEGO – Seventeen of 425 children who had eosinophilic esophagitis caused by a specific food developed the condition after outgrowing the allergy to that food, a retrospective study found.

People who outgrow a food allergy may be at risk of developing eosinophilic esophagitis (EoE) to the same food, Dr. Jonathan Spergel said during a press briefing at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

He and his associates studied data on 1,025 children with EoE seen at the Children’s Hospital of Philadelphia in 2000-2012 to assess the prevalence of food allergy. In 425 children (42%), a specific food was identified as the EoE culprit – reintroducing the food to the diet caused esophageal changes on biopsy or biopsy changes normalized when the food was removed from the diet.

Eighty-four children had a history of IgE-mediated food allergy. Milk, egg, wheat, and soy were the most common food triggers of EoE in the 425 children in the study and in a subset of 17 who had outgrown IgE-mediated allergy to the specific food, reported Dr. Spergel, chief of the allergy section at the Children’s Hospital of Philadelphia. Sixteen of the 17 patients had atopic disease. The most common foods causing IgE-mediated allergy were peanuts, tree nuts, eggs, and milk.

The development of EoE coincided with reintroducing the food triggers. The time between outgrowing an allergy and reintroducing the food, triggering EoE, averaged 2 years but ranged from 6 months to 5 years.

Notably, two of the children who outgrew their food allergy had a normal biopsy of the esophagus when they had the food allergy, he said.

The findings support other recent studies suggesting that the pathophysiologies of EoE and IgE-mediated food allergy are distinct from each other, and that both can occur in the same individual to the same food, Dr. Spergel said. The mechanism by which EoE develops is poorly understood.

"I think these kids probably always had EoE to the food, but they weren’t eating it" because of the allergy, he said. "From 1% to 15% on oral immunotherapy get EoE, depending on which group you look at. I don’t think we caused" EoE by giving oral immunotherapy, he added. "We uncovered it."

Although it is rare for children who outgrow a food allergy to later develop EoE to that food, it’s worth keeping in mind if a child starts vomiting often or complains of stomachaches months or years later, Dr. Spergel said. Keeping the possibility in mind may help clinicians rule out other etiologies and detect EoE faster. "You have to take it seriously and get it checked out," he said.

Of the 84 patients with IgE-mediated food allergy, the 17 who outgrew the allergy and then developed EoE to the same food were significantly older (12 years, on average), compared with 67 patients who developed EoE from a different food from the one that caused their allergy.

The lead author on the study was Dr. Solrun Melkorka Meggadottir, a fellow at the Children’s Hospital of Philadelphia. The findings have been submitted to the Journal of Allergy and Clinical Immunology.

Dr. Spergel and Dr. Meggadottir reported having no disclosures.

[email protected] On Twitter @sherryboschert

SAN DIEGO – Seventeen of 425 children who had eosinophilic esophagitis caused by a specific food developed the condition after outgrowing the allergy to that food, a retrospective study found.

People who outgrow a food allergy may be at risk of developing eosinophilic esophagitis (EoE) to the same food, Dr. Jonathan Spergel said during a press briefing at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

He and his associates studied data on 1,025 children with EoE seen at the Children’s Hospital of Philadelphia in 2000-2012 to assess the prevalence of food allergy. In 425 children (42%), a specific food was identified as the EoE culprit – reintroducing the food to the diet caused esophageal changes on biopsy or biopsy changes normalized when the food was removed from the diet.

Eighty-four children had a history of IgE-mediated food allergy. Milk, egg, wheat, and soy were the most common food triggers of EoE in the 425 children in the study and in a subset of 17 who had outgrown IgE-mediated allergy to the specific food, reported Dr. Spergel, chief of the allergy section at the Children’s Hospital of Philadelphia. Sixteen of the 17 patients had atopic disease. The most common foods causing IgE-mediated allergy were peanuts, tree nuts, eggs, and milk.

The development of EoE coincided with reintroducing the food triggers. The time between outgrowing an allergy and reintroducing the food, triggering EoE, averaged 2 years but ranged from 6 months to 5 years.

Notably, two of the children who outgrew their food allergy had a normal biopsy of the esophagus when they had the food allergy, he said.

The findings support other recent studies suggesting that the pathophysiologies of EoE and IgE-mediated food allergy are distinct from each other, and that both can occur in the same individual to the same food, Dr. Spergel said. The mechanism by which EoE develops is poorly understood.

"I think these kids probably always had EoE to the food, but they weren’t eating it" because of the allergy, he said. "From 1% to 15% on oral immunotherapy get EoE, depending on which group you look at. I don’t think we caused" EoE by giving oral immunotherapy, he added. "We uncovered it."

Although it is rare for children who outgrow a food allergy to later develop EoE to that food, it’s worth keeping in mind if a child starts vomiting often or complains of stomachaches months or years later, Dr. Spergel said. Keeping the possibility in mind may help clinicians rule out other etiologies and detect EoE faster. "You have to take it seriously and get it checked out," he said.

Of the 84 patients with IgE-mediated food allergy, the 17 who outgrew the allergy and then developed EoE to the same food were significantly older (12 years, on average), compared with 67 patients who developed EoE from a different food from the one that caused their allergy.

The lead author on the study was Dr. Solrun Melkorka Meggadottir, a fellow at the Children’s Hospital of Philadelphia. The findings have been submitted to the Journal of Allergy and Clinical Immunology.

Dr. Spergel and Dr. Meggadottir reported having no disclosures.

[email protected] On Twitter @sherryboschert

SAN DIEGO – Seventeen of 425 children who had eosinophilic esophagitis caused by a specific food developed the condition after outgrowing the allergy to that food, a retrospective study found.

People who outgrow a food allergy may be at risk of developing eosinophilic esophagitis (EoE) to the same food, Dr. Jonathan Spergel said during a press briefing at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

He and his associates studied data on 1,025 children with EoE seen at the Children’s Hospital of Philadelphia in 2000-2012 to assess the prevalence of food allergy. In 425 children (42%), a specific food was identified as the EoE culprit – reintroducing the food to the diet caused esophageal changes on biopsy or biopsy changes normalized when the food was removed from the diet.

Eighty-four children had a history of IgE-mediated food allergy. Milk, egg, wheat, and soy were the most common food triggers of EoE in the 425 children in the study and in a subset of 17 who had outgrown IgE-mediated allergy to the specific food, reported Dr. Spergel, chief of the allergy section at the Children’s Hospital of Philadelphia. Sixteen of the 17 patients had atopic disease. The most common foods causing IgE-mediated allergy were peanuts, tree nuts, eggs, and milk.

The development of EoE coincided with reintroducing the food triggers. The time between outgrowing an allergy and reintroducing the food, triggering EoE, averaged 2 years but ranged from 6 months to 5 years.

Notably, two of the children who outgrew their food allergy had a normal biopsy of the esophagus when they had the food allergy, he said.

The findings support other recent studies suggesting that the pathophysiologies of EoE and IgE-mediated food allergy are distinct from each other, and that both can occur in the same individual to the same food, Dr. Spergel said. The mechanism by which EoE develops is poorly understood.

"I think these kids probably always had EoE to the food, but they weren’t eating it" because of the allergy, he said. "From 1% to 15% on oral immunotherapy get EoE, depending on which group you look at. I don’t think we caused" EoE by giving oral immunotherapy, he added. "We uncovered it."

Although it is rare for children who outgrow a food allergy to later develop EoE to that food, it’s worth keeping in mind if a child starts vomiting often or complains of stomachaches months or years later, Dr. Spergel said. Keeping the possibility in mind may help clinicians rule out other etiologies and detect EoE faster. "You have to take it seriously and get it checked out," he said.

Of the 84 patients with IgE-mediated food allergy, the 17 who outgrew the allergy and then developed EoE to the same food were significantly older (12 years, on average), compared with 67 patients who developed EoE from a different food from the one that caused their allergy.

The lead author on the study was Dr. Solrun Melkorka Meggadottir, a fellow at the Children’s Hospital of Philadelphia. The findings have been submitted to the Journal of Allergy and Clinical Immunology.

Dr. Spergel and Dr. Meggadottir reported having no disclosures.

[email protected] On Twitter @sherryboschert

MIAMI BEACH – Intraoperative fluorescent cholangiography is just as effective as traditional cholangiography but costs hundreds of dollars less and is significantly faster to perform.

It’s also a great teaching tool, Dr. Fernando Dip said at the annual meeting of the Americas Hepato-Pancreato-Biliary Association. In just one session, all of the third- and fourth-year surgical residents were able to correctly identify 100% of the biliary structures.

"It appears to be an additional tool for the laparoscopic surgeon," said Dr. Dip, chief of surgical research at the Cleveland Clinic in Weston, Fla. "It’s quick, inexpensive, real-time, there are no adverse events, and it’s an inciscionless procedure."

Common bile duct injury is the most frequent injury seen in laparoscopic cholecystectomy, he said, and although the overall incidence is low, the number of injuries each year is not inconsiderable, since more than 750,000 laparoscopic cholecystectomies are performed in the United States annually.

"Only 3% of these injuries are due to problems with technical skill," Dr. Dip said. "The other 97% are problems of visual perception – illusions of where the ducts are."

Intraoperative cholangiography helps surgeons visualize this anatomy, but its true usefulness is somewhat controversial. Dr. Dip cited a recent study of almost 93,000 patients – 40% of whom underwent the procedure. It showed that intraoperative cholangiography is not effective as a preventive strategy against common duct injury during cholecystectomy.

Intraoperative fluorescent cholangiography is sometimes used to identify biliary anatomy in extrahepatic surgery. Dr. Dip and his colleagues examined its usefulness in 45 patients undergoing laparoscopic cholecystectomy. Senior residents performed all of the procedures under the supervision of experienced laparoscopic surgeons. All patients underwent the investigational procedure, followed by standard cholangiography.

The patients had a mean age of 49 years and were evenly split between men and women. The mean body mass index was 28 kg/m². Surgical indications were cholelithiasis (22), acute cholecystitis (17), chronic cholecystitis (5), and polyp (1). About 1 hour before surgery, patients received an infusion of indocyanine green 0.5 mg/kg. During the laparoscopic exploration, surgeons used near-infrared light to make the marker fluoresce as it was excreted by the liver.

In a picture review before surgery, all residents correctly identified 100% of the anatomic structures visualized by the fluorescent procedure. They were able to complete the fluorescent procedure in all of the patients. The completion rate for cholangiography was 93% (42 patients). In three patients, cholangiography failed because the cystic duct could not be cannulated.

The residents identified the cystic duct in 44 of the patients (98%), the common bile duct in 36 (80%), and the common hepatic ducts in 27 (60%). Neither technique identified any aberrant or accessory ducts.

Because fluorescent cholangiography is a real-time surgical procedure, it allowed checking of the transection and resection of the gallbladder pedicle before smooth dissection in all of the patients.

The procedure was significantly quicker than standard cholangiography (0.71 minutes vs. 7.15 minutes). It was also significantly cheaper, costing a mean of $14 vs. $778. There were no adverse surgical events, and no adverse reactions to the dye or at the infusion site, Dr. Dip said. Additionally, he noted, fluorescent cholangiography does not rely on x-rays, and so spared the patients any radiation exposure.

He added that the Cleveland Clinic, in conjunction with the University of Tokyo, will soon launch a randomized clinical trial comparing the two methods. An ongoing trial from another institution is evaluating fluorescent cholangiography compared with critical view technique in visualizing anatomy during laparoscopic cholecystectomy. It was set to wrap up in January, but according to the trial record on clinicaltrials.gov, is still recruiting patients.

Dr. Dip had no financial disclosures.

[email protected]

On Twitter @alz_gal

MIAMI BEACH – Intraoperative fluorescent cholangiography is just as effective as traditional cholangiography but costs hundreds of dollars less and is significantly faster to perform.

It’s also a great teaching tool, Dr. Fernando Dip said at the annual meeting of the Americas Hepato-Pancreato-Biliary Association. In just one session, all of the third- and fourth-year surgical residents were able to correctly identify 100% of the biliary structures.

"It appears to be an additional tool for the laparoscopic surgeon," said Dr. Dip, chief of surgical research at the Cleveland Clinic in Weston, Fla. "It’s quick, inexpensive, real-time, there are no adverse events, and it’s an inciscionless procedure."

Common bile duct injury is the most frequent injury seen in laparoscopic cholecystectomy, he said, and although the overall incidence is low, the number of injuries each year is not inconsiderable, since more than 750,000 laparoscopic cholecystectomies are performed in the United States annually.

"Only 3% of these injuries are due to problems with technical skill," Dr. Dip said. "The other 97% are problems of visual perception – illusions of where the ducts are."

Intraoperative cholangiography helps surgeons visualize this anatomy, but its true usefulness is somewhat controversial. Dr. Dip cited a recent study of almost 93,000 patients – 40% of whom underwent the procedure. It showed that intraoperative cholangiography is not effective as a preventive strategy against common duct injury during cholecystectomy.

Intraoperative fluorescent cholangiography is sometimes used to identify biliary anatomy in extrahepatic surgery. Dr. Dip and his colleagues examined its usefulness in 45 patients undergoing laparoscopic cholecystectomy. Senior residents performed all of the procedures under the supervision of experienced laparoscopic surgeons. All patients underwent the investigational procedure, followed by standard cholangiography.

The patients had a mean age of 49 years and were evenly split between men and women. The mean body mass index was 28 kg/m². Surgical indications were cholelithiasis (22), acute cholecystitis (17), chronic cholecystitis (5), and polyp (1). About 1 hour before surgery, patients received an infusion of indocyanine green 0.5 mg/kg. During the laparoscopic exploration, surgeons used near-infrared light to make the marker fluoresce as it was excreted by the liver.

In a picture review before surgery, all residents correctly identified 100% of the anatomic structures visualized by the fluorescent procedure. They were able to complete the fluorescent procedure in all of the patients. The completion rate for cholangiography was 93% (42 patients). In three patients, cholangiography failed because the cystic duct could not be cannulated.

The residents identified the cystic duct in 44 of the patients (98%), the common bile duct in 36 (80%), and the common hepatic ducts in 27 (60%). Neither technique identified any aberrant or accessory ducts.

Because fluorescent cholangiography is a real-time surgical procedure, it allowed checking of the transection and resection of the gallbladder pedicle before smooth dissection in all of the patients.

The procedure was significantly quicker than standard cholangiography (0.71 minutes vs. 7.15 minutes). It was also significantly cheaper, costing a mean of $14 vs. $778. There were no adverse surgical events, and no adverse reactions to the dye or at the infusion site, Dr. Dip said. Additionally, he noted, fluorescent cholangiography does not rely on x-rays, and so spared the patients any radiation exposure.

He added that the Cleveland Clinic, in conjunction with the University of Tokyo, will soon launch a randomized clinical trial comparing the two methods. An ongoing trial from another institution is evaluating fluorescent cholangiography compared with critical view technique in visualizing anatomy during laparoscopic cholecystectomy. It was set to wrap up in January, but according to the trial record on clinicaltrials.gov, is still recruiting patients.

Dr. Dip had no financial disclosures.

[email protected]

On Twitter @alz_gal

MIAMI BEACH – Intraoperative fluorescent cholangiography is just as effective as traditional cholangiography but costs hundreds of dollars less and is significantly faster to perform.

It’s also a great teaching tool, Dr. Fernando Dip said at the annual meeting of the Americas Hepato-Pancreato-Biliary Association. In just one session, all of the third- and fourth-year surgical residents were able to correctly identify 100% of the biliary structures.

"It appears to be an additional tool for the laparoscopic surgeon," said Dr. Dip, chief of surgical research at the Cleveland Clinic in Weston, Fla. "It’s quick, inexpensive, real-time, there are no adverse events, and it’s an inciscionless procedure."

Common bile duct injury is the most frequent injury seen in laparoscopic cholecystectomy, he said, and although the overall incidence is low, the number of injuries each year is not inconsiderable, since more than 750,000 laparoscopic cholecystectomies are performed in the United States annually.

"Only 3% of these injuries are due to problems with technical skill," Dr. Dip said. "The other 97% are problems of visual perception – illusions of where the ducts are."

Intraoperative cholangiography helps surgeons visualize this anatomy, but its true usefulness is somewhat controversial. Dr. Dip cited a recent study of almost 93,000 patients – 40% of whom underwent the procedure. It showed that intraoperative cholangiography is not effective as a preventive strategy against common duct injury during cholecystectomy.

Intraoperative fluorescent cholangiography is sometimes used to identify biliary anatomy in extrahepatic surgery. Dr. Dip and his colleagues examined its usefulness in 45 patients undergoing laparoscopic cholecystectomy. Senior residents performed all of the procedures under the supervision of experienced laparoscopic surgeons. All patients underwent the investigational procedure, followed by standard cholangiography.

The patients had a mean age of 49 years and were evenly split between men and women. The mean body mass index was 28 kg/m². Surgical indications were cholelithiasis (22), acute cholecystitis (17), chronic cholecystitis (5), and polyp (1). About 1 hour before surgery, patients received an infusion of indocyanine green 0.5 mg/kg. During the laparoscopic exploration, surgeons used near-infrared light to make the marker fluoresce as it was excreted by the liver.

In a picture review before surgery, all residents correctly identified 100% of the anatomic structures visualized by the fluorescent procedure. They were able to complete the fluorescent procedure in all of the patients. The completion rate for cholangiography was 93% (42 patients). In three patients, cholangiography failed because the cystic duct could not be cannulated.

The residents identified the cystic duct in 44 of the patients (98%), the common bile duct in 36 (80%), and the common hepatic ducts in 27 (60%). Neither technique identified any aberrant or accessory ducts.

Because fluorescent cholangiography is a real-time surgical procedure, it allowed checking of the transection and resection of the gallbladder pedicle before smooth dissection in all of the patients.

The procedure was significantly quicker than standard cholangiography (0.71 minutes vs. 7.15 minutes). It was also significantly cheaper, costing a mean of $14 vs. $778. There were no adverse surgical events, and no adverse reactions to the dye or at the infusion site, Dr. Dip said. Additionally, he noted, fluorescent cholangiography does not rely on x-rays, and so spared the patients any radiation exposure.

He added that the Cleveland Clinic, in conjunction with the University of Tokyo, will soon launch a randomized clinical trial comparing the two methods. An ongoing trial from another institution is evaluating fluorescent cholangiography compared with critical view technique in visualizing anatomy during laparoscopic cholecystectomy. It was set to wrap up in January, but according to the trial record on clinicaltrials.gov, is still recruiting patients.

Dr. Dip had no financial disclosures.

[email protected]

On Twitter @alz_gal

The Affordable Care Act now requires health insurance companies to cover routine costs for clinical trial participants, the American Society of Clinical Oncology reminded clinicians in educational materials about the provision it released Feb. 4.

The group is concerned, it said, because "the federal government has not yet issued regulations to guide implementation of the new law," and, at least so far, has characterized it as a "self-implementing" statute that insurers are "expected to implement ... using a good faith, reasonable interpretation of the law."

"While much of the statutory language is clear, in the absence of federal guidance, payers will likely vary on the legal interpretation of each element of the provision. It is likely that securing compliance with the law may require considerable negotiations with some insurers or health plans. There is no assurance that all parties will agree on the legal interpretation of each element of the provision," the group said.

To help, the American Society of Clinical Oncology (ASCO) issued a detailed explanation of the measure, plus educational materials for patients and a form investigators can fill out to demonstrate that a trial and potential subject meet the law’s requirements.

"ASCO and other groups fought long and hard for this law requiring insurers nationwide to cover the routine costs of care for individuals participating in clinical trials," ASCO president Dr. Clifford Hudis noted in a statement.

The hope is to counter poor study enrollment, the main reason that about 20% of cancer trials are never completed, according to a study reported at the 2014 Genitourinary Cancers Symposium earlier this year. Sometimes patients simply can’t afford to participate, because "some health plans have denied coverage ... of routine costs that are offered as part of the clinical trial." The new law might help patients afford clinical trial participation, the group said.

The law applies to plans newly issued or renewed after Jan. 1, 2014. Routine costs include all items and services that an insurance company would cover for a patient not enrolled in a clinical trial. Plans cannot prohibit participation in clinical trials; deny or limit coverage of routine patient costs for items and services furnished in connection with participation in a trial; or discriminate against an individual because they are enrolled in a trial.

The provision covers studies that are either federally funded, conducted under an Investigational New Drug Application, or exempt from an Investigational New Drug Application.

It does not apply to Medicaid plans, and payers are only required to cover routine costs delivered by out-of-network providers if out-of-network benefits are part of a patient’s insurance plan. "An insurer may attempt to deny coverage on the grounds that the service or item is ‘clearly inconsistent with the established standard of care.’ Providers may consider requesting that the insurers prove that the item or service is inconsistent with the standard of care," ASCO noted.

[email protected]

The Affordable Care Act now requires health insurance companies to cover routine costs for clinical trial participants, the American Society of Clinical Oncology reminded clinicians in educational materials about the provision it released Feb. 4.

The group is concerned, it said, because "the federal government has not yet issued regulations to guide implementation of the new law," and, at least so far, has characterized it as a "self-implementing" statute that insurers are "expected to implement ... using a good faith, reasonable interpretation of the law."

"While much of the statutory language is clear, in the absence of federal guidance, payers will likely vary on the legal interpretation of each element of the provision. It is likely that securing compliance with the law may require considerable negotiations with some insurers or health plans. There is no assurance that all parties will agree on the legal interpretation of each element of the provision," the group said.

To help, the American Society of Clinical Oncology (ASCO) issued a detailed explanation of the measure, plus educational materials for patients and a form investigators can fill out to demonstrate that a trial and potential subject meet the law’s requirements.

"ASCO and other groups fought long and hard for this law requiring insurers nationwide to cover the routine costs of care for individuals participating in clinical trials," ASCO president Dr. Clifford Hudis noted in a statement.

The hope is to counter poor study enrollment, the main reason that about 20% of cancer trials are never completed, according to a study reported at the 2014 Genitourinary Cancers Symposium earlier this year. Sometimes patients simply can’t afford to participate, because "some health plans have denied coverage ... of routine costs that are offered as part of the clinical trial." The new law might help patients afford clinical trial participation, the group said.

The law applies to plans newly issued or renewed after Jan. 1, 2014. Routine costs include all items and services that an insurance company would cover for a patient not enrolled in a clinical trial. Plans cannot prohibit participation in clinical trials; deny or limit coverage of routine patient costs for items and services furnished in connection with participation in a trial; or discriminate against an individual because they are enrolled in a trial.

The provision covers studies that are either federally funded, conducted under an Investigational New Drug Application, or exempt from an Investigational New Drug Application.

It does not apply to Medicaid plans, and payers are only required to cover routine costs delivered by out-of-network providers if out-of-network benefits are part of a patient’s insurance plan. "An insurer may attempt to deny coverage on the grounds that the service or item is ‘clearly inconsistent with the established standard of care.’ Providers may consider requesting that the insurers prove that the item or service is inconsistent with the standard of care," ASCO noted.

[email protected]

The Affordable Care Act now requires health insurance companies to cover routine costs for clinical trial participants, the American Society of Clinical Oncology reminded clinicians in educational materials about the provision it released Feb. 4.

The group is concerned, it said, because "the federal government has not yet issued regulations to guide implementation of the new law," and, at least so far, has characterized it as a "self-implementing" statute that insurers are "expected to implement ... using a good faith, reasonable interpretation of the law."

"While much of the statutory language is clear, in the absence of federal guidance, payers will likely vary on the legal interpretation of each element of the provision. It is likely that securing compliance with the law may require considerable negotiations with some insurers or health plans. There is no assurance that all parties will agree on the legal interpretation of each element of the provision," the group said.

To help, the American Society of Clinical Oncology (ASCO) issued a detailed explanation of the measure, plus educational materials for patients and a form investigators can fill out to demonstrate that a trial and potential subject meet the law’s requirements.

"ASCO and other groups fought long and hard for this law requiring insurers nationwide to cover the routine costs of care for individuals participating in clinical trials," ASCO president Dr. Clifford Hudis noted in a statement.

The hope is to counter poor study enrollment, the main reason that about 20% of cancer trials are never completed, according to a study reported at the 2014 Genitourinary Cancers Symposium earlier this year. Sometimes patients simply can’t afford to participate, because "some health plans have denied coverage ... of routine costs that are offered as part of the clinical trial." The new law might help patients afford clinical trial participation, the group said.

The law applies to plans newly issued or renewed after Jan. 1, 2014. Routine costs include all items and services that an insurance company would cover for a patient not enrolled in a clinical trial. Plans cannot prohibit participation in clinical trials; deny or limit coverage of routine patient costs for items and services furnished in connection with participation in a trial; or discriminate against an individual because they are enrolled in a trial.

The provision covers studies that are either federally funded, conducted under an Investigational New Drug Application, or exempt from an Investigational New Drug Application.

It does not apply to Medicaid plans, and payers are only required to cover routine costs delivered by out-of-network providers if out-of-network benefits are part of a patient’s insurance plan. "An insurer may attempt to deny coverage on the grounds that the service or item is ‘clearly inconsistent with the established standard of care.’ Providers may consider requesting that the insurers prove that the item or service is inconsistent with the standard of care," ASCO noted.

[email protected]

Laparoscopic sleeve gastrectomy not only fails to improve gastroesophageal reflux disease in most patients who undergo the weight-loss procedure, it actually worsens GERD symptoms in many of them and induces GERD in 9%, according to a report published online Feb. 5 in JAMA Surgery.

In addition, patients with preexisting GERD who undergo laparoscopic sleeve gastrectomy (LSG) have high rates of surgical complications; revision surgery; failure to achieve weight loss; and failure to resolve weight-related comorbidities such as diabetes, obstructive sleep apnea, and hypertension. In contrast, patients who undergo gastric bypass show significant improvement in all of these outcomes, said Dr. Cecily E. DuPree and her associates in the department of surgery, Madigan Army Medical Center, Fort Lewis, Wash.

Based on the findings from their study of a national database including 4,832 patients who had laparoscopic sleeve gastrectomy (LSG) and 33,867 who had gastric bypass (GB), "we believe that all patients should be evaluated for the presence and severity of GERD and counseled regarding the relative efficacy of LSG vs. GB or other bariatric operations before surgery. Although there is no definitive evidence to support the listing of GERD as an absolute contraindication to LSG, the available data suggest that the presence of preexisting severe GERD or esophageal dysmotility may be considered a relative contraindication," they said.

Dr. DuPree and her colleagues noted that until now, the sleeve procedure’s effect on GERD was unknown. Small, single-center series "have raised significant concerns," but no large study has examined the issue. So she and her associates used data from a large, nationwide database (the Bariatric Outcomes Longitudinal Database) to track the resolution, persistence, or development of GERD in 4,832 patients who underwent laparoscopic sleeve gastrectomy in 2007-2010, comparing their outcomes with those of 33,867 patients who underwent gastric bypass during the same period and served as controls.

The overall prevalence of GERD was 49.7% in the entire study population, and that of severe GERD was 25.7%, confirming that this disorder is very common in candidates for bariatric surgery.

The prevalence of GERD was 44.5% among patients undergoing the sleeve procedure. "This highlights the concern that there is a large population at risk of adverse outcomes after LSG if the procedure is associated with anatomical or physiologic changes that increase the risk of postoperative GERD," the investigators noted.

Most LSG patients (84.1%) had persistent GERD symptoms after the procedure; only 15.9% reported resolution of symptoms. An additional 9.0% of LSG patients reported postoperative worsening of GERD symptoms. And 8.6% of patients who didn’t have GERD before undergoing sleeve gastrectomy developed the disorder afterward.

In contrast, most patients who underwent gastric bypass showed complete resolution (62.8%) or stabilization (17.6%) of GERD symptoms. Only 2.2% reported worsening GERD symptoms, and none developed de novo symptoms.

Among the LSG patients, the complication rate was significantly higher in those with preexisting GERD (15.1%) or preexisting severe GERD (16.3%) than in those without GERD (10.6%). "There was also a small but statistically significant increase in the need for revisional surgery between LSG patients with and without preoperative GERD symptoms (0.6% vs. 0.3%)," the investigators wrote (JAMA Surg. 2014 [doi:10.1001/jamasurg.2013.4323]).

In contrast, the presence of GERD had no effect on complications in the control group.

Similarly, the rate of failure to lose weight was higher in LSG patients with preoperative GERD and in LSG patients with severe preoperative GERD than in those without GERD. Again, the presence of GERD had no such effect on weight loss in the gastric bypass patients.

In addition, the percentage of patients who showed resolution of comorbidities was significantly decreased among patients with preoperative GERD who underwent LSG, compared with all other groups.

"These data raise significant concerns about the effect of LSG on the obesity-related comorbidity of GERD and suggest that most patients with preexisting GERD will have either no improvement or possibly worsening of their symptoms after LSG," Dr. DuPree and her associates said.

The exact reason why the sleeve procedure could contribute to the worsening of reflux or the de novo development of GERD is not known, but there are several anatomical or physiologic factors that may play a role. Laparoscopic sleeve gastrectomy may decrease lower esophageal sphincter resting tone, and it may disrupt the antropyloric pump mechanism or narrow the pylorus.

It is also possible that an excessively large or dilated gastric sleeve may retain the capacity for increased acid production, causing reflux, or that it may decrease esophageal acid clearance. And a hiatal hernia that is unrecognized at the time of surgery or that develops afterward could also produce reflux symptoms.

Modifying surgical technique so that sleeve size and volume are attended to, narrowing of the gastric body or pylorus is avoided, and hiatal hernias are assiduously identified and repaired may reduce the risk of post-LSG GERD, the investigators said.

Laparoscopic sleeve gastrectomy not only fails to improve gastroesophageal reflux disease in most patients who undergo the weight-loss procedure, it actually worsens GERD symptoms in many of them and induces GERD in 9%, according to a report published online Feb. 5 in JAMA Surgery.

In addition, patients with preexisting GERD who undergo laparoscopic sleeve gastrectomy (LSG) have high rates of surgical complications; revision surgery; failure to achieve weight loss; and failure to resolve weight-related comorbidities such as diabetes, obstructive sleep apnea, and hypertension. In contrast, patients who undergo gastric bypass show significant improvement in all of these outcomes, said Dr. Cecily E. DuPree and her associates in the department of surgery, Madigan Army Medical Center, Fort Lewis, Wash.

Based on the findings from their study of a national database including 4,832 patients who had laparoscopic sleeve gastrectomy (LSG) and 33,867 who had gastric bypass (GB), "we believe that all patients should be evaluated for the presence and severity of GERD and counseled regarding the relative efficacy of LSG vs. GB or other bariatric operations before surgery. Although there is no definitive evidence to support the listing of GERD as an absolute contraindication to LSG, the available data suggest that the presence of preexisting severe GERD or esophageal dysmotility may be considered a relative contraindication," they said.

Dr. DuPree and her colleagues noted that until now, the sleeve procedure’s effect on GERD was unknown. Small, single-center series "have raised significant concerns," but no large study has examined the issue. So she and her associates used data from a large, nationwide database (the Bariatric Outcomes Longitudinal Database) to track the resolution, persistence, or development of GERD in 4,832 patients who underwent laparoscopic sleeve gastrectomy in 2007-2010, comparing their outcomes with those of 33,867 patients who underwent gastric bypass during the same period and served as controls.

The overall prevalence of GERD was 49.7% in the entire study population, and that of severe GERD was 25.7%, confirming that this disorder is very common in candidates for bariatric surgery.

The prevalence of GERD was 44.5% among patients undergoing the sleeve procedure. "This highlights the concern that there is a large population at risk of adverse outcomes after LSG if the procedure is associated with anatomical or physiologic changes that increase the risk of postoperative GERD," the investigators noted.

Most LSG patients (84.1%) had persistent GERD symptoms after the procedure; only 15.9% reported resolution of symptoms. An additional 9.0% of LSG patients reported postoperative worsening of GERD symptoms. And 8.6% of patients who didn’t have GERD before undergoing sleeve gastrectomy developed the disorder afterward.

In contrast, most patients who underwent gastric bypass showed complete resolution (62.8%) or stabilization (17.6%) of GERD symptoms. Only 2.2% reported worsening GERD symptoms, and none developed de novo symptoms.

Among the LSG patients, the complication rate was significantly higher in those with preexisting GERD (15.1%) or preexisting severe GERD (16.3%) than in those without GERD (10.6%). "There was also a small but statistically significant increase in the need for revisional surgery between LSG patients with and without preoperative GERD symptoms (0.6% vs. 0.3%)," the investigators wrote (JAMA Surg. 2014 [doi:10.1001/jamasurg.2013.4323]).

In contrast, the presence of GERD had no effect on complications in the control group.

Similarly, the rate of failure to lose weight was higher in LSG patients with preoperative GERD and in LSG patients with severe preoperative GERD than in those without GERD. Again, the presence of GERD had no such effect on weight loss in the gastric bypass patients.

In addition, the percentage of patients who showed resolution of comorbidities was significantly decreased among patients with preoperative GERD who underwent LSG, compared with all other groups.

"These data raise significant concerns about the effect of LSG on the obesity-related comorbidity of GERD and suggest that most patients with preexisting GERD will have either no improvement or possibly worsening of their symptoms after LSG," Dr. DuPree and her associates said.

The exact reason why the sleeve procedure could contribute to the worsening of reflux or the de novo development of GERD is not known, but there are several anatomical or physiologic factors that may play a role. Laparoscopic sleeve gastrectomy may decrease lower esophageal sphincter resting tone, and it may disrupt the antropyloric pump mechanism or narrow the pylorus.

It is also possible that an excessively large or dilated gastric sleeve may retain the capacity for increased acid production, causing reflux, or that it may decrease esophageal acid clearance. And a hiatal hernia that is unrecognized at the time of surgery or that develops afterward could also produce reflux symptoms.

Modifying surgical technique so that sleeve size and volume are attended to, narrowing of the gastric body or pylorus is avoided, and hiatal hernias are assiduously identified and repaired may reduce the risk of post-LSG GERD, the investigators said.

Laparoscopic sleeve gastrectomy not only fails to improve gastroesophageal reflux disease in most patients who undergo the weight-loss procedure, it actually worsens GERD symptoms in many of them and induces GERD in 9%, according to a report published online Feb. 5 in JAMA Surgery.

In addition, patients with preexisting GERD who undergo laparoscopic sleeve gastrectomy (LSG) have high rates of surgical complications; revision surgery; failure to achieve weight loss; and failure to resolve weight-related comorbidities such as diabetes, obstructive sleep apnea, and hypertension. In contrast, patients who undergo gastric bypass show significant improvement in all of these outcomes, said Dr. Cecily E. DuPree and her associates in the department of surgery, Madigan Army Medical Center, Fort Lewis, Wash.

Based on the findings from their study of a national database including 4,832 patients who had laparoscopic sleeve gastrectomy (LSG) and 33,867 who had gastric bypass (GB), "we believe that all patients should be evaluated for the presence and severity of GERD and counseled regarding the relative efficacy of LSG vs. GB or other bariatric operations before surgery. Although there is no definitive evidence to support the listing of GERD as an absolute contraindication to LSG, the available data suggest that the presence of preexisting severe GERD or esophageal dysmotility may be considered a relative contraindication," they said.

Dr. DuPree and her colleagues noted that until now, the sleeve procedure’s effect on GERD was unknown. Small, single-center series "have raised significant concerns," but no large study has examined the issue. So she and her associates used data from a large, nationwide database (the Bariatric Outcomes Longitudinal Database) to track the resolution, persistence, or development of GERD in 4,832 patients who underwent laparoscopic sleeve gastrectomy in 2007-2010, comparing their outcomes with those of 33,867 patients who underwent gastric bypass during the same period and served as controls.

The overall prevalence of GERD was 49.7% in the entire study population, and that of severe GERD was 25.7%, confirming that this disorder is very common in candidates for bariatric surgery.

The prevalence of GERD was 44.5% among patients undergoing the sleeve procedure. "This highlights the concern that there is a large population at risk of adverse outcomes after LSG if the procedure is associated with anatomical or physiologic changes that increase the risk of postoperative GERD," the investigators noted.

Most LSG patients (84.1%) had persistent GERD symptoms after the procedure; only 15.9% reported resolution of symptoms. An additional 9.0% of LSG patients reported postoperative worsening of GERD symptoms. And 8.6% of patients who didn’t have GERD before undergoing sleeve gastrectomy developed the disorder afterward.

In contrast, most patients who underwent gastric bypass showed complete resolution (62.8%) or stabilization (17.6%) of GERD symptoms. Only 2.2% reported worsening GERD symptoms, and none developed de novo symptoms.

Among the LSG patients, the complication rate was significantly higher in those with preexisting GERD (15.1%) or preexisting severe GERD (16.3%) than in those without GERD (10.6%). "There was also a small but statistically significant increase in the need for revisional surgery between LSG patients with and without preoperative GERD symptoms (0.6% vs. 0.3%)," the investigators wrote (JAMA Surg. 2014 [doi:10.1001/jamasurg.2013.4323]).

In contrast, the presence of GERD had no effect on complications in the control group.

Similarly, the rate of failure to lose weight was higher in LSG patients with preoperative GERD and in LSG patients with severe preoperative GERD than in those without GERD. Again, the presence of GERD had no such effect on weight loss in the gastric bypass patients.

In addition, the percentage of patients who showed resolution of comorbidities was significantly decreased among patients with preoperative GERD who underwent LSG, compared with all other groups.

"These data raise significant concerns about the effect of LSG on the obesity-related comorbidity of GERD and suggest that most patients with preexisting GERD will have either no improvement or possibly worsening of their symptoms after LSG," Dr. DuPree and her associates said.

The exact reason why the sleeve procedure could contribute to the worsening of reflux or the de novo development of GERD is not known, but there are several anatomical or physiologic factors that may play a role. Laparoscopic sleeve gastrectomy may decrease lower esophageal sphincter resting tone, and it may disrupt the antropyloric pump mechanism or narrow the pylorus.

It is also possible that an excessively large or dilated gastric sleeve may retain the capacity for increased acid production, causing reflux, or that it may decrease esophageal acid clearance. And a hiatal hernia that is unrecognized at the time of surgery or that develops afterward could also produce reflux symptoms.

Modifying surgical technique so that sleeve size and volume are attended to, narrowing of the gastric body or pylorus is avoided, and hiatal hernias are assiduously identified and repaired may reduce the risk of post-LSG GERD, the investigators said.

SAN DIEGO – Electrical stimulation therapy of the lower esophageal sphincter is effective for treating refractory gastroesophageal reflux disease, according to interim results from a trial presented at the annual meeting of the American College of Gastroenterology.

A total of 32 patients underwent implantation of a pair of electrodes in the muscular layer of the gastroesophageal junction. The electrodes were connected to a pulse generator in the abdomen that delivered intermittent stimulation.

Six months later, the patients had a sustained, more than one-half reduction from baseline in exposure of the esophagus to acid and a two-thirds reduction in symptoms, reported first author Dr. Edy E. Soffer at the meeting.

Additionally, whereas most of the patients had been taking proton pump inhibitors (PPIs) at baseline, only about 1 in 10 were doing so at 6 months. None experienced any device-related adverse events.

The findings support the effectiveness and safety of electrical stimulation therapy in this population, according to Dr. Soffer, who is a professor in the gastroenterology division, Keck School of Medicine, University of Southern California, Los Angeles.

"Currently, there are ongoing studies, and there will be future sham-controlled studies that should clarify further the role of this intervention in the treatment of GERD [gastroesophageal reflux disease] and its mechanism of action," he noted.

Session attendee Dr. Marcelo Vela of the Baylor Clinic, Houston, noted that earlier studies have shown that this therapy increases basal pressure of the lower esophageal sphincter (LES). "Because the main mechanism for reflux is transient LES relaxations [TLESRs], particularly with small hernias as in your patients, do you have any data on TLESRs?" he asked.

"No, LES pressure was not an endpoint in these studies," Dr. Soffer replied. "Initially, we thought that this [basal pressure] is the main mechanism; as we are learning more, it is probably not going to be the main mechanism. We are looking at others, including TLESRs. ... We don’t have data yet."

Dr. Joel Richter, of the University of South Florida, Tampa, wondered whether patients experienced any of the oft-feared complications of antireflux surgery, such as bloating, diarrhea, and dysphagia.

"There were only two cases of dysphagia, and they basically resolved on their own," Dr. Soffer replied. "We didn’t see any of the symptoms that you see with postsurgical therapy. ... The intervention really should not result in the symptoms that come after standard surgical care."

Dr. Richter also requested more information on hiatal hernia repairs undertaken in some patients. "If you had a hernia repair, how do you know what part of the success was related to the hernia repair versus the stimulation?" he asked.

Thirteen patients had a hernia repair, with technique left up to the treating physician, Dr. Soffer replied. "We will look separately, when we complete that phase, at those that had the hernia repair versus those that did not."

"Was there a bit of a trend toward any improvement depending on your hernia size?" Dr. Richard McCallam of Texas Tech University in El Paso asked, while also noting that patients with hernias measuring 3 cm or more were excluded.

There were too few patients to assess trends, according to Dr. Soffer. "We tried not to take patients who had particularly severe disease at the beginning," he added. "The 3-cm hernia repair will be the one perhaps that will need to be looked at more carefully. This is a more sustained hernia situation as compared to the 1- and 2-cm [ones]."

The investigators enrolled GERD patients in the study who had a GERD health-related quality of life score of 20 or higher when not taking PPIs, and who had at least a partial response to these agents. They were required to have a basal LES end-expiratory pressure of at least 5 mm Hg, and to have a pH below 4.0 for more than 5% of the time on 24-hour esophageal pH monitoring.

The patients’ mean age was 50 years, and 18 of them were male, according to Dr. Soffer.

The main results showed a sustained reduction in esophageal acid exposure; the percentage of time at pH less than 4.0 was 10.3% at baseline, compared with 3.7% at 3 months (P less than .01), and 4.6% at 6 months (P less than .01).

There was also a sustained improvement in symptoms as assessed from GERD health-related quality of life; the score was 15 at baseline on PPIs and 31 at baseline off PPIs. These figures compared with a score of 4 at 3 months and 5 at 6 months.

Large proportions of patients met criteria for successful treatment at 6 months: 65% had control of esophageal acid exposure (either normalization or a greater than one-half reduction), 86% had control of GERD symptoms compared with level without medical therapy (a greater than 50% improvement versus baseline level not on PPIs), and 76% had control of GERD symptoms compared with level with medical therapy (any improvement of symptoms versus baseline level on PPIs).

Quality of life as assessed with the Short Form-12 showed improvement at 6 months in physical health scores compared with those measured at baseline while off PPIs.

Patients also had significant reductions from the level at baseline off PPIs at both 3 and 6 months in the median percentages of daily diary days with heartburn and with regurgitation symptoms.

Analyses of daytime versus nighttime symptoms are still ongoing, according to Dr. Soffer.

Stimulation therapy was also associated with a dramatic reduction in PPI use. Whereas only 10% of patients did not use any of these agents at baseline, 89% were not using any at 6 months.

There were just two serious adverse events: a procedure-related trocar perforation of the small bowel during laparoscopy (the stimulation device was prophylactically removed and there was resolution after surgical repair) and atrioventricular nodal reentrant tachycardia unrelated to the device or procedure.

There were no device-related serious adverse events. There were 35 nonserious events possibly or probably related to the device or procedure.

Dr. Soffer is a consultant for and shareholder in EndoStim*. The study was supported by EndoStim.

*Correction, 2/4/2014: An earlier version of the story misstated Dr. Soffer's conflicts of interest.

SAN DIEGO – Electrical stimulation therapy of the lower esophageal sphincter is effective for treating refractory gastroesophageal reflux disease, according to interim results from a trial presented at the annual meeting of the American College of Gastroenterology.

A total of 32 patients underwent implantation of a pair of electrodes in the muscular layer of the gastroesophageal junction. The electrodes were connected to a pulse generator in the abdomen that delivered intermittent stimulation.

Six months later, the patients had a sustained, more than one-half reduction from baseline in exposure of the esophagus to acid and a two-thirds reduction in symptoms, reported first author Dr. Edy E. Soffer at the meeting.

Additionally, whereas most of the patients had been taking proton pump inhibitors (PPIs) at baseline, only about 1 in 10 were doing so at 6 months. None experienced any device-related adverse events.

The findings support the effectiveness and safety of electrical stimulation therapy in this population, according to Dr. Soffer, who is a professor in the gastroenterology division, Keck School of Medicine, University of Southern California, Los Angeles.

"Currently, there are ongoing studies, and there will be future sham-controlled studies that should clarify further the role of this intervention in the treatment of GERD [gastroesophageal reflux disease] and its mechanism of action," he noted.

Session attendee Dr. Marcelo Vela of the Baylor Clinic, Houston, noted that earlier studies have shown that this therapy increases basal pressure of the lower esophageal sphincter (LES). "Because the main mechanism for reflux is transient LES relaxations [TLESRs], particularly with small hernias as in your patients, do you have any data on TLESRs?" he asked.

"No, LES pressure was not an endpoint in these studies," Dr. Soffer replied. "Initially, we thought that this [basal pressure] is the main mechanism; as we are learning more, it is probably not going to be the main mechanism. We are looking at others, including TLESRs. ... We don’t have data yet."

Dr. Joel Richter, of the University of South Florida, Tampa, wondered whether patients experienced any of the oft-feared complications of antireflux surgery, such as bloating, diarrhea, and dysphagia.

"There were only two cases of dysphagia, and they basically resolved on their own," Dr. Soffer replied. "We didn’t see any of the symptoms that you see with postsurgical therapy. ... The intervention really should not result in the symptoms that come after standard surgical care."

Dr. Richter also requested more information on hiatal hernia repairs undertaken in some patients. "If you had a hernia repair, how do you know what part of the success was related to the hernia repair versus the stimulation?" he asked.

Thirteen patients had a hernia repair, with technique left up to the treating physician, Dr. Soffer replied. "We will look separately, when we complete that phase, at those that had the hernia repair versus those that did not."

"Was there a bit of a trend toward any improvement depending on your hernia size?" Dr. Richard McCallam of Texas Tech University in El Paso asked, while also noting that patients with hernias measuring 3 cm or more were excluded.

There were too few patients to assess trends, according to Dr. Soffer. "We tried not to take patients who had particularly severe disease at the beginning," he added. "The 3-cm hernia repair will be the one perhaps that will need to be looked at more carefully. This is a more sustained hernia situation as compared to the 1- and 2-cm [ones]."

The investigators enrolled GERD patients in the study who had a GERD health-related quality of life score of 20 or higher when not taking PPIs, and who had at least a partial response to these agents. They were required to have a basal LES end-expiratory pressure of at least 5 mm Hg, and to have a pH below 4.0 for more than 5% of the time on 24-hour esophageal pH monitoring.

The patients’ mean age was 50 years, and 18 of them were male, according to Dr. Soffer.

The main results showed a sustained reduction in esophageal acid exposure; the percentage of time at pH less than 4.0 was 10.3% at baseline, compared with 3.7% at 3 months (P less than .01), and 4.6% at 6 months (P less than .01).

There was also a sustained improvement in symptoms as assessed from GERD health-related quality of life; the score was 15 at baseline on PPIs and 31 at baseline off PPIs. These figures compared with a score of 4 at 3 months and 5 at 6 months.

Large proportions of patients met criteria for successful treatment at 6 months: 65% had control of esophageal acid exposure (either normalization or a greater than one-half reduction), 86% had control of GERD symptoms compared with level without medical therapy (a greater than 50% improvement versus baseline level not on PPIs), and 76% had control of GERD symptoms compared with level with medical therapy (any improvement of symptoms versus baseline level on PPIs).

Quality of life as assessed with the Short Form-12 showed improvement at 6 months in physical health scores compared with those measured at baseline while off PPIs.

Patients also had significant reductions from the level at baseline off PPIs at both 3 and 6 months in the median percentages of daily diary days with heartburn and with regurgitation symptoms.

Analyses of daytime versus nighttime symptoms are still ongoing, according to Dr. Soffer.

Stimulation therapy was also associated with a dramatic reduction in PPI use. Whereas only 10% of patients did not use any of these agents at baseline, 89% were not using any at 6 months.

There were just two serious adverse events: a procedure-related trocar perforation of the small bowel during laparoscopy (the stimulation device was prophylactically removed and there was resolution after surgical repair) and atrioventricular nodal reentrant tachycardia unrelated to the device or procedure.

There were no device-related serious adverse events. There were 35 nonserious events possibly or probably related to the device or procedure.

Dr. Soffer is a consultant for and shareholder in EndoStim*. The study was supported by EndoStim.

*Correction, 2/4/2014: An earlier version of the story misstated Dr. Soffer's conflicts of interest.

SAN DIEGO – Electrical stimulation therapy of the lower esophageal sphincter is effective for treating refractory gastroesophageal reflux disease, according to interim results from a trial presented at the annual meeting of the American College of Gastroenterology.

A total of 32 patients underwent implantation of a pair of electrodes in the muscular layer of the gastroesophageal junction. The electrodes were connected to a pulse generator in the abdomen that delivered intermittent stimulation.

Six months later, the patients had a sustained, more than one-half reduction from baseline in exposure of the esophagus to acid and a two-thirds reduction in symptoms, reported first author Dr. Edy E. Soffer at the meeting.

Additionally, whereas most of the patients had been taking proton pump inhibitors (PPIs) at baseline, only about 1 in 10 were doing so at 6 months. None experienced any device-related adverse events.

The findings support the effectiveness and safety of electrical stimulation therapy in this population, according to Dr. Soffer, who is a professor in the gastroenterology division, Keck School of Medicine, University of Southern California, Los Angeles.

"Currently, there are ongoing studies, and there will be future sham-controlled studies that should clarify further the role of this intervention in the treatment of GERD [gastroesophageal reflux disease] and its mechanism of action," he noted.

Session attendee Dr. Marcelo Vela of the Baylor Clinic, Houston, noted that earlier studies have shown that this therapy increases basal pressure of the lower esophageal sphincter (LES). "Because the main mechanism for reflux is transient LES relaxations [TLESRs], particularly with small hernias as in your patients, do you have any data on TLESRs?" he asked.

"No, LES pressure was not an endpoint in these studies," Dr. Soffer replied. "Initially, we thought that this [basal pressure] is the main mechanism; as we are learning more, it is probably not going to be the main mechanism. We are looking at others, including TLESRs. ... We don’t have data yet."

Dr. Joel Richter, of the University of South Florida, Tampa, wondered whether patients experienced any of the oft-feared complications of antireflux surgery, such as bloating, diarrhea, and dysphagia.

"There were only two cases of dysphagia, and they basically resolved on their own," Dr. Soffer replied. "We didn’t see any of the symptoms that you see with postsurgical therapy. ... The intervention really should not result in the symptoms that come after standard surgical care."

Dr. Richter also requested more information on hiatal hernia repairs undertaken in some patients. "If you had a hernia repair, how do you know what part of the success was related to the hernia repair versus the stimulation?" he asked.

Thirteen patients had a hernia repair, with technique left up to the treating physician, Dr. Soffer replied. "We will look separately, when we complete that phase, at those that had the hernia repair versus those that did not."

"Was there a bit of a trend toward any improvement depending on your hernia size?" Dr. Richard McCallam of Texas Tech University in El Paso asked, while also noting that patients with hernias measuring 3 cm or more were excluded.

There were too few patients to assess trends, according to Dr. Soffer. "We tried not to take patients who had particularly severe disease at the beginning," he added. "The 3-cm hernia repair will be the one perhaps that will need to be looked at more carefully. This is a more sustained hernia situation as compared to the 1- and 2-cm [ones]."

The investigators enrolled GERD patients in the study who had a GERD health-related quality of life score of 20 or higher when not taking PPIs, and who had at least a partial response to these agents. They were required to have a basal LES end-expiratory pressure of at least 5 mm Hg, and to have a pH below 4.0 for more than 5% of the time on 24-hour esophageal pH monitoring.

The patients’ mean age was 50 years, and 18 of them were male, according to Dr. Soffer.

The main results showed a sustained reduction in esophageal acid exposure; the percentage of time at pH less than 4.0 was 10.3% at baseline, compared with 3.7% at 3 months (P less than .01), and 4.6% at 6 months (P less than .01).

There was also a sustained improvement in symptoms as assessed from GERD health-related quality of life; the score was 15 at baseline on PPIs and 31 at baseline off PPIs. These figures compared with a score of 4 at 3 months and 5 at 6 months.

Large proportions of patients met criteria for successful treatment at 6 months: 65% had control of esophageal acid exposure (either normalization or a greater than one-half reduction), 86% had control of GERD symptoms compared with level without medical therapy (a greater than 50% improvement versus baseline level not on PPIs), and 76% had control of GERD symptoms compared with level with medical therapy (any improvement of symptoms versus baseline level on PPIs).

Quality of life as assessed with the Short Form-12 showed improvement at 6 months in physical health scores compared with those measured at baseline while off PPIs.

Patients also had significant reductions from the level at baseline off PPIs at both 3 and 6 months in the median percentages of daily diary days with heartburn and with regurgitation symptoms.

Analyses of daytime versus nighttime symptoms are still ongoing, according to Dr. Soffer.

Stimulation therapy was also associated with a dramatic reduction in PPI use. Whereas only 10% of patients did not use any of these agents at baseline, 89% were not using any at 6 months.

There were just two serious adverse events: a procedure-related trocar perforation of the small bowel during laparoscopy (the stimulation device was prophylactically removed and there was resolution after surgical repair) and atrioventricular nodal reentrant tachycardia unrelated to the device or procedure.

There were no device-related serious adverse events. There were 35 nonserious events possibly or probably related to the device or procedure.

Dr. Soffer is a consultant for and shareholder in EndoStim*. The study was supported by EndoStim.

*Correction, 2/4/2014: An earlier version of the story misstated Dr. Soffer's conflicts of interest.

The longer the interval between symptom onset and the diagnosis of eosinophilic esophagitis, the greater the chance that the patient will have developed esophageal strictures, according to a report in the December issue of Gastroenterology (doi:10.1053/j.gastro.2013.08.015).

In a retrospective study of 523 cases of eosinophilic esophagitis (EoE) recorded in a national Swiss database, patients "were likely to present with purely inflammatory endoscopic EoE features early in the disease course and then progress to develop fibrotic endoscopic features, in addition to inflammatory features," said Dr. Alain M. Schoepfer of the division of gastroenerology and hepatology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland, and his associates.

Moreover, an additional analysis of numerous potential disease-, environmental-, and patient-related risk factors demonstrated that the length of diagnostic delay is the single strongest risk factor for stricture formation, the investigators noted.

The natural history of untreated EoE has not been investigated extensively, and data regarding stricture formation are particularly lacking. In addition, eosinophilic esophagitis has long been associated with a substantial delay in diagnosis, with a median of 5 years elapsing between symptom onset and correct identification of the disorder.

Dr. Schoepfer and his colleagues examined the relationship between the duration of untreated disease (before EoE was diagnosed) and the prevalence of esophageal stricture using a database with detailed medical records of 323 patients they personally diagnosed and treated plus 200 others who were diagnosed and treated by other gastroenterologists throughout Switzerland. The database included the results from numerous biopsies of the proximal and distal esophagus for every patient, as well as information on 98 clinical factors that might influence stricture formation.

The median diagnostic delay was 6 years (range, 0 to more than 20 years).

Strictures were present at diagnosis in 75 patients (37.5%).

Features of active inflammation, such as edema, furrows, and whitish exudates, were present in 79.5% of patients while features of fibrotic activity, such as strictures, rings, and crepe-paper esophagus, were seen in 63.0%.

The prevalence of fibrotic features including strictures increased with increasing duration of diagnostic delay. This prevalence was 46.5% among patients who were diagnosed as having EoE within 0-2 years of symptom onset, rising to 87.5% among those diagnosed 20 years or more after symptom onset.

In contrast, the prevalence of inflammatory features alone decreased with increasing duration of diagnostic delay.

The prevalence of esophageal strictures likewise correlated with diagnostic delay. It was 17.2% among patients diagnosed within 0-2 years of symptom onset, compared with 70.8% among those diagnosed 20 years or more after symptom onset, the investigators said.

The prevalence of strictures did not differ by patient age at diagnosis. It was comparable between patients who were diagnosed before they reached 20 years of age and those diagnosed after age 20. The prevalence of strictures also did not differ between the 323 patients diagnosed and treated by Dr. Schoepfer and his associates, who were managed according to a strict standardized protocol, and the 200 other patients who were managed by numerous other gastroenterologists according to their own individual practice preferences.

In an analysis of nearly 100 potential risk factors for stricture formation, only the length of diagnostic delay was found to be significantly associated with the presence of strictures at diagnosis.

These findings demonstrate that a patient’s disease course "is a continuum – a march from a disease predominantly inflammatory in nature to a disease with endoscopic fibrotic features, including strictures, in addition to existing inflammation," the researchers said.

Clinicians should make every effort to reduce the delay in diagnosis of EoE, they added.

This study was supported by the Swiss National Science Foundation. No relevant financial conflicts of interest were reported.

The longer the interval between symptom onset and the diagnosis of eosinophilic esophagitis, the greater the chance that the patient will have developed esophageal strictures, according to a report in the December issue of Gastroenterology (doi:10.1053/j.gastro.2013.08.015).

In a retrospective study of 523 cases of eosinophilic esophagitis (EoE) recorded in a national Swiss database, patients "were likely to present with purely inflammatory endoscopic EoE features early in the disease course and then progress to develop fibrotic endoscopic features, in addition to inflammatory features," said Dr. Alain M. Schoepfer of the division of gastroenerology and hepatology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland, and his associates.

Moreover, an additional analysis of numerous potential disease-, environmental-, and patient-related risk factors demonstrated that the length of diagnostic delay is the single strongest risk factor for stricture formation, the investigators noted.

The natural history of untreated EoE has not been investigated extensively, and data regarding stricture formation are particularly lacking. In addition, eosinophilic esophagitis has long been associated with a substantial delay in diagnosis, with a median of 5 years elapsing between symptom onset and correct identification of the disorder.

Dr. Schoepfer and his colleagues examined the relationship between the duration of untreated disease (before EoE was diagnosed) and the prevalence of esophageal stricture using a database with detailed medical records of 323 patients they personally diagnosed and treated plus 200 others who were diagnosed and treated by other gastroenterologists throughout Switzerland. The database included the results from numerous biopsies of the proximal and distal esophagus for every patient, as well as information on 98 clinical factors that might influence stricture formation.

The median diagnostic delay was 6 years (range, 0 to more than 20 years).

Strictures were present at diagnosis in 75 patients (37.5%).

Features of active inflammation, such as edema, furrows, and whitish exudates, were present in 79.5% of patients while features of fibrotic activity, such as strictures, rings, and crepe-paper esophagus, were seen in 63.0%.

The prevalence of fibrotic features including strictures increased with increasing duration of diagnostic delay. This prevalence was 46.5% among patients who were diagnosed as having EoE within 0-2 years of symptom onset, rising to 87.5% among those diagnosed 20 years or more after symptom onset.

In contrast, the prevalence of inflammatory features alone decreased with increasing duration of diagnostic delay.

The prevalence of esophageal strictures likewise correlated with diagnostic delay. It was 17.2% among patients diagnosed within 0-2 years of symptom onset, compared with 70.8% among those diagnosed 20 years or more after symptom onset, the investigators said.

The prevalence of strictures did not differ by patient age at diagnosis. It was comparable between patients who were diagnosed before they reached 20 years of age and those diagnosed after age 20. The prevalence of strictures also did not differ between the 323 patients diagnosed and treated by Dr. Schoepfer and his associates, who were managed according to a strict standardized protocol, and the 200 other patients who were managed by numerous other gastroenterologists according to their own individual practice preferences.

In an analysis of nearly 100 potential risk factors for stricture formation, only the length of diagnostic delay was found to be significantly associated with the presence of strictures at diagnosis.

These findings demonstrate that a patient’s disease course "is a continuum – a march from a disease predominantly inflammatory in nature to a disease with endoscopic fibrotic features, including strictures, in addition to existing inflammation," the researchers said.

Clinicians should make every effort to reduce the delay in diagnosis of EoE, they added.

This study was supported by the Swiss National Science Foundation. No relevant financial conflicts of interest were reported.

The longer the interval between symptom onset and the diagnosis of eosinophilic esophagitis, the greater the chance that the patient will have developed esophageal strictures, according to a report in the December issue of Gastroenterology (doi:10.1053/j.gastro.2013.08.015).

In a retrospective study of 523 cases of eosinophilic esophagitis (EoE) recorded in a national Swiss database, patients "were likely to present with purely inflammatory endoscopic EoE features early in the disease course and then progress to develop fibrotic endoscopic features, in addition to inflammatory features," said Dr. Alain M. Schoepfer of the division of gastroenerology and hepatology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland, and his associates.

Moreover, an additional analysis of numerous potential disease-, environmental-, and patient-related risk factors demonstrated that the length of diagnostic delay is the single strongest risk factor for stricture formation, the investigators noted.

The natural history of untreated EoE has not been investigated extensively, and data regarding stricture formation are particularly lacking. In addition, eosinophilic esophagitis has long been associated with a substantial delay in diagnosis, with a median of 5 years elapsing between symptom onset and correct identification of the disorder.

Dr. Schoepfer and his colleagues examined the relationship between the duration of untreated disease (before EoE was diagnosed) and the prevalence of esophageal stricture using a database with detailed medical records of 323 patients they personally diagnosed and treated plus 200 others who were diagnosed and treated by other gastroenterologists throughout Switzerland. The database included the results from numerous biopsies of the proximal and distal esophagus for every patient, as well as information on 98 clinical factors that might influence stricture formation.

The median diagnostic delay was 6 years (range, 0 to more than 20 years).

Strictures were present at diagnosis in 75 patients (37.5%).

Features of active inflammation, such as edema, furrows, and whitish exudates, were present in 79.5% of patients while features of fibrotic activity, such as strictures, rings, and crepe-paper esophagus, were seen in 63.0%.

The prevalence of fibrotic features including strictures increased with increasing duration of diagnostic delay. This prevalence was 46.5% among patients who were diagnosed as having EoE within 0-2 years of symptom onset, rising to 87.5% among those diagnosed 20 years or more after symptom onset.

In contrast, the prevalence of inflammatory features alone decreased with increasing duration of diagnostic delay.

The prevalence of esophageal strictures likewise correlated with diagnostic delay. It was 17.2% among patients diagnosed within 0-2 years of symptom onset, compared with 70.8% among those diagnosed 20 years or more after symptom onset, the investigators said.

The prevalence of strictures did not differ by patient age at diagnosis. It was comparable between patients who were diagnosed before they reached 20 years of age and those diagnosed after age 20. The prevalence of strictures also did not differ between the 323 patients diagnosed and treated by Dr. Schoepfer and his associates, who were managed according to a strict standardized protocol, and the 200 other patients who were managed by numerous other gastroenterologists according to their own individual practice preferences.

In an analysis of nearly 100 potential risk factors for stricture formation, only the length of diagnostic delay was found to be significantly associated with the presence of strictures at diagnosis.

These findings demonstrate that a patient’s disease course "is a continuum – a march from a disease predominantly inflammatory in nature to a disease with endoscopic fibrotic features, including strictures, in addition to existing inflammation," the researchers said.

Clinicians should make every effort to reduce the delay in diagnosis of EoE, they added.

This study was supported by the Swiss National Science Foundation. No relevant 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.

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.