Editorials The Skinny on Eosinophilic Esophagitis See “Delay in diagnosis of eosinophilic esophagitis increases risk for stricture formation in a time-dependent manner,” by Schoepfer AM, Safroneeva E, Bussmann C, et al, on page 1230.
C
onsensus guidelines define eosinophilic esophagitis (EoE) as “a chronic, immune/antigen-mediated, esophageal disease characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil-predominant inflammation.”1 Because this is a relatively new disease, it is understandable that most therapeutic interventions that have been investigated to date have focused on acute treatment of this chronic disease. Thus, treatments such as topical steroids or diet elimination therapy with or without dilation may yield effective symptomatic and endoscopic results when used over a 4- to 8-week period.1 The effort surrounding these advancements has been formidable by multiple teams of superb investigators. The problem has been that the need to understand and potentially treat the chronic aspect of this disease has only preliminarily been studied. There are several types of data that raise the importance of this need. First, the prevalence of strictures and dysphagia attributed to these strictures is remarkably high in patients with EoE.2 This is particularly true in patients once they enter late adolescence and adulthood, where the prevalence of dysphagia is nearly uniform.3 Second, careful analysis of tissue and inflammatory mediators in EoE have demonstrated the profibrotic process that results from the eosinophil mediated inflammation in these patients.4,5 For example, subepithelial collagen deposition is a common finding in these patients. Also, many of the inflammatory mediators released from eosinophils are profibrotic. Third are the much needed data from the study by Schoepfer et al.6 Through the unique, comprehensive, and long-term data available in this database of Swiss EoE patients, we have learned that, with increasing duration of delay in diagnosis, the chance of incident esophageal stricture increases markedly. It is a study such as this one that begs the question, should patients with EoE be on maintenance therapy? What has stopped us so far from endorsing maintenance therapy? When the first proton pump inhibitor, omeprazole, was released, strong warnings were given to not use this medication beyond a finite number of weeks. At the time, this made intuitive sense without knowledge of the potential side effects of long-term treatment. In retrospect, however, this seems to be unfortunate, because we left patients with high-grade, erosive esophagitis GASTROENTEROLOGY 2013;145:1186–1202
without maintenance treatment. Indeed, many of these patients likely developed strictures as well. Although it is not clear that all patients with high-grade erosive esophagitis will progress to stricture formation, we treat all these patients chronically with proton pump inhibitors, and if not with fundoplication. Should this apply to EoE, particularly because the fibrotic consequences are more severe, such as small-caliber esophagus, an entity rarely described as a complication of gastroesophageal reflux disease? Furthermore, the study by Schoepfer3 demonstrates that, after decades of untreated disease, stricture formation will have occurred in most if not all patients. Granted, the risks of chronic topical steroid use seem to be more concerning than chronic proton pump inhibitor use, but with the documented safety of steroid inhaler use in patients with asthma and the growing concerns over bone loss, vitamin deficiency, and enteric infection with proton pump inhibitors, the risk gap might be smaller than we anticipate between these 2 drug classes. One of the main issues is whether, as in gastroesophageal reflux disease, all patients with gross inflammatory lesions will progress to stricture formation, or as in Crohn’s disease, can we target subsets of patients predicted to have more severe disease. A classic study by Lichtenstein et al performed almost 20 years ago described a phenotype of Crohn’s disease: Those patients who present with perforation which predicts likelihood of repeated surgery.7 Since this study, further characterization of patients with Crohn’s disease has led to potential genotypic and serum marker differences in disease presentation and prognosis, which may perhaps serve as a guide to therapy. Do such different phenotypes exist in EoE that are more or less likely to progress to severe fibrotic disease? The study by Schoepfer3 did not identify any factors other than disease duration, suggesting that all patients with EoE have similar risk and therefore should be treated. Information that was not discussed in their study that might have been helpful is further characterization of the strictures found. Specifically, was diffuse small-caliber esophagus, one stricture of great length, considered equivalent to a single esophageal stricture 1 cm in length? Similarly, did they see patients with lesser changes of fibrosis such as focal stricture or ringed esophagus, progress to more severe forms of disease? More specifically, the concern is will all patients progress to small caliber esophagus if left untreated, albeit, over varying amounts of time or will some strictures be milder than others? On the other hand, it should be noted that the proportion of younger patients with long duration of untreated disease seems to be greater than that proportion
Editorials, continued seen in older patients. As in Crohn’s disease, does earlier age of onset of disease portend more severe progression of disease?7 One thing we cannot know by these studies is when EoE begins in individual patients. Although onset of symptoms is the best we can go by, there may be variably long periods of quiescent inflammation and fibrogenesis that precede the first symptom, particularly dysphagia. This is suggested in recent studies by Hirano et al,8 in which patients with a normal caliber esophagus are demonstrated to have decreased esophageal compliance in areas not thought to be diseased. As a result, one must wonder if adults with onset of EoE symptoms have had a slower, smoldering course beginning in childhood similar too but less severe than adolescents with earlier onset of dysphagia and stricture formation. On a more basic level, we do not know if EoE is the same disease in childhood as it is in adults? Unfortunately, without regular endoscopy of an asymptomatic population (something unlikely to occur!) or identification of a noninvasive marker of EoE, answering this question will be difficult. If maintenance therapy is indicated in patients with EoE, what should that therapy be? Steroids seem to be a logical choice for several reasons. First, there are clear data demonstrating excellent control of inflammatory change and reduction of tissue eosinophilia.9 Second, there are data from tissue remodeling studies in EoE showing reversal with steroids10 through gene down regulation.11 Furthermore, there are some clinical data suggesting an increase in stricture diameter with steroids based on endoscopic and/or radiologic assessment.12,13 Third, we know that in other diseases, such as asthma, chronic steroid use seems to be safe and well-tolerated. Unfortunately, limited data are available on what dose is needed to maintain remission in EoE and whether systemic absorption is clinically important. The only controlled trial performed, also from the Swiss group, demonstrates suboptimal efficacy at a quarter (0.5 mg budesonide) of the adult dose used for acute treatment.14 We may, thus, be faced with the prospect of using the dosage needed to eliminate inflammation as that needed to control inflammation, similar to the strategy in inflammatory bowel disease. At a dose of 2 mg of budesonide or 1760 mg of fluticasone daily, there will be greater long-term concern over bone and adrenal effects. Elimination diets, on the other hand, do not seem to pose long-term risks as long as proper nutrition and potential supplementation is used. Although elemental diets will be neither tolerable nor practical for long-term treatment, elimination diets based on empiric evidence (such as the 6food elimination diet) or food challenge and withdrawal based on esophageal biopsy, have great theoretical appeal and proven efficacy.15,16 This may be achievable in some, particularly when a small number of easily avoidable foods can be identified; for many, however, the list will be
too long, the social compromises too great, and the endoscopic monitoring too cumbersome and expensive to use. With less invasive esophageal testing, however, such as the string test, this last issue may be improved. Even so, there are few data yet on the ability of food elimination to reverse fibrosis and maintain remission, although it is likely to come. Finally, dilation will likely hold a place in maintenance. If these therapies are used to reverse fibrotic disease, this will take time when the patient remains at risk for repeated food impaction and ongoing symptoms. Furthermore, we do not have the clinical data to know whether all fibrosis is potentially reversible or as in clinically advanced hepatic cirrhosis or Crohn’s disease, there will be a point beyond which significant improvement is not achievable with medical therapy. This may be true in patients with marked luminal compromise with small-caliber esophagus. Finally, given the relatively young age at which this disease occurs, a lifetime of therapy may require combinations of all these therapies based on lifestyle and choice. Finally, without clear identification of more aggressive EoE phenotypes nor randomized controlled trials demonstrating that steroids help prevent stricture formation, are there patients to whom we should offer maintenance therapy at this point? Patients with more severe forms of this disease such as those who rapidly relapse off therapy, with repeated food impactions, with small caliber esophagus or documented progression might be considered. We are not at a point yet where we can recommend maintenance therapy to all patients with eosinophilic esophagitis, particularly when steroids are the preferred therapy by the patient. What can we take from this landmark study to our current treatment of patients with EoE? First, we need to caution patients, and at least adults, that this is a chronic and perhaps lifelong disease in many commonly leads to stricture formation if untreated. Second, until we can better distinguish disease phenotypes or perhaps genotypes of EoE, we have no choice but to count the majority of patients at risk for progressive fibrosis and stricture formation. Third, when contemplating maintenance therapy, we have to be particularly cognizant not only of treatment side effects but also of the effects of this disease on quality of life, as well as the potential morbid complications including food impaction and iatrogenic or spontaneous esophageal perforation even though this is a “benign” disease. Fourth, I think that patients at high risk for disease complications, particularly those with rapid relapse, severe strictures, or repeated food impactions, should be offered long-term maintenance therapy. What recommended form this therapy will take and what its risks will be are the needs that landmark trials such as this inspire. Nevertheless, our long-term goal for EoE, in contrast with most medical conditions, is to maintain the fat and avoid the skinny esophagus. 1187
Editorials, continued DAVID A. KATZKA Division of Gastroenterology and Hepatology Mayo Clinic Rochester, Minnesota References 1. Liacouras CA, Furuta GT, Hirano I, et al. Eosinophilic esophagitis: Updated consensus recommendations for children and adults. J Allergy Clin Immunol 2011;128:3–20.e6. 2. Hirano I. Dilation in eosinophilic esophagitis: to do or not to do? Gastrointest Endosc 2010;71:713–714. 3. Schoepfer AM, Gonsalves N, Bussmann C, et al. Esophageal dilation in eosinophilic esophagitis: effectiveness, safety, and impact on the underlying inflammation. Am J Gastroenterol 2010;105:1062–1070. 4. Aceves SS, Newbury RO, Dohil R, et al. Esophageal remodeling in pediatric eosinophilic esophagitis. J Allergy Clin Immunol 2007; 119:206–212. 5. Aceves SS. Tissue remodeling in patients with eosinophilic esophagitis: what lies beneath the surface? J Allergy Clin Immunol 2011; 128:1047–1049. 6. Schoepfer AM, Safroneeva E, Bussmann C, et al. Delay in diagnosis of eosinophilic esophagitis increases risk for stricture formation in a time-dependent manner. Gastroenterology 2013;145:1230–1236. 7. Lautenbach E, Berlin JA, Lichtenstein GR. Risk factors for early postoperative recurrence of Crohn’s disease. Gastroenterology 1998; 115:259–267. 8. Kwiatek MA, Hirano I, Kahrilas PJ, et al. Mechanical properties of the esophagus in eosinophilic esophagitis. Gastroenterology 2011; 140:82–90. 9. Dellon ES, Gonsalves N, Hirano I, et al. American College of Gastroenterology. ACG clinical guideline: Evidenced based approach to the diagnosis and management of esophageal eosinophilia and eosinophilic esophagitis (EoE). Am J Gastroenterol 2013;108:679–692.
10. Kagalwalla AF, Akhtar N, Woodruff SA, et al. Eosinophilic esophagitis: epithelial mesenchymal transition contributes to esophageal remodeling and reverses with treatment. J Allergy Clin Immunol 2012; 129:1387–1396.e7. 11. Aceves SS, Newbury RO, Chen D, et al. Resolution of remodeling in eosinophilic esophagitis correlates with epithelial response to topical corticosteroids. Allergy 2010;65:109–116. 12. Lee J, Huprich J, Kujath C, et al. Esophageal diameter is decreased in some patients with eosinophilic esophagitis and might increase with topical corticosteroid therapy. Clin Gastroenterol Hepatol 2012; 10:481–486. 13. Lucendo AJ, Pascual-Turrion JM, Navarro M, et al. Endoscopic, bioptic, and manometric findings in eosinophilic esophagitis before and after steroid therapy: a case series. Endoscopy 2007; 39:765–771. 14. Straumann A, Conus S, Degen L, et al. Long-term budesonide maintenance treatment is partially effective for patients with eosinophilic esophagitis. Clin Gastroenterol Hepatol 2011;9:400–409.e1. 15. Gonsalves N, Yang GY, Doerfler B, et al. Elimination diet effectively treats eosinophilic esophagitis in adults; food reintroduction identifies causative factors. Gastroenterology 2012;142:1451–1457. 16. Kagalwalla AF, Sentongo TA, Ritz S, et al. Effect of six-food elimination diet on clinical and histologic outcomes in eosinophilic esophagitis. Clin Gastroenterol Hepatol 2006;4:1097–1102. Reprint requests Address requests for reprints to: David A. Katzka, MD, Division of Gastroenterology and Hepatology, Mayo Clinic, 200 First St., S.W., Rochester, Minnesota 55905. e-mail: [email protected]. Conflicts of interest The author discloses no conflicts. © 2013 by the AGA Institute 0016-5085/$36.00 http://dx.doi.org/10.1053/j.gastro.2013.10.037
Could Aspiration Therapy for Obesity Be an Effective and Safe Alternative to Traditional Bariatric Surgery? See, “Aspiration therapy leads to weight loss in obese subjects: a pilot study,” by Sullivan S, Stein R, Jonnalagadda S, et al on page 1245.
O
besity is a major public health challenge in the 21st century. It is present in >30% of adult Americans and has wide geographical variation.1 It is associated with multiple medical problems, including heart disease, diabetes, cancer, gallstones, and musculoskeletal disability leading to not only morbidity, but also increased mortality with an estimated decrease in life expectancy between 6 and 20 years.2 The US Preventative Services Task Force has suggested screening all adults for obesity and aggressively treating those with a body mass index (BMI) of >30.3 Despite these suggestions, many practitioners have a nihilistic opinion of the possibility of patients controlling their weight. Dietary and medical therapy have limited efficacy and surgical therapies, although more effective, 1188
have substantial morbidity and a small, but real mortality. In this issue of GASTROENTEROLOGY, a novel, less invasive approach to weight control is presented: aspiration of gastric contents via a gastrostomy tube.4 The 10 subjects who completed the 12-month trial of aspiration therapy lost 18% of their body weight compared with 5.9% in the small control group (4 patients). Obesity is directly related to an overall increase in caloric intake and a decrease in activity-induced caloric expenditure in the modern environment. Attempts to control calorie intake through dietary manipulation and to increase expenditure via increased exercise have been only moderately successful. A meta-analysis of 46 studies using a variety of diet programs found an average 6% loss of weight after 12 months,5 which is similar to the weight loss seen in the control group in the paper presented in this issue. Although a 5%–10% weight loss is much better than none, most patients with substantial degrees of obesity would consider success to require between a
C
onsensus guidelines define eosinophilic esophagitis (EoE) as “a chronic, immune/antigen-mediated, esophageal disease characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil-predominant inflammation.”1 Because this is a relatively new disease, it is understandable that most therapeutic interventions that have been investigated to date have focused on acute treatment of this chronic disease. Thus, treatments such as topical steroids or diet elimination therapy with or without dilation may yield effective symptomatic and endoscopic results when used over a 4- to 8-week period.1 The effort surrounding these advancements has been formidable by multiple teams of superb investigators. The problem has been that the need to understand and potentially treat the chronic aspect of this disease has only preliminarily been studied. There are several types of data that raise the importance of this need. First, the prevalence of strictures and dysphagia attributed to these strictures is remarkably high in patients with EoE.2 This is particularly true in patients once they enter late adolescence and adulthood, where the prevalence of dysphagia is nearly uniform.3 Second, careful analysis of tissue and inflammatory mediators in EoE have demonstrated the profibrotic process that results from the eosinophil mediated inflammation in these patients.4,5 For example, subepithelial collagen deposition is a common finding in these patients. Also, many of the inflammatory mediators released from eosinophils are profibrotic. Third are the much needed data from the study by Schoepfer et al.6 Through the unique, comprehensive, and long-term data available in this database of Swiss EoE patients, we have learned that, with increasing duration of delay in diagnosis, the chance of incident esophageal stricture increases markedly. It is a study such as this one that begs the question, should patients with EoE be on maintenance therapy? What has stopped us so far from endorsing maintenance therapy? When the first proton pump inhibitor, omeprazole, was released, strong warnings were given to not use this medication beyond a finite number of weeks. At the time, this made intuitive sense without knowledge of the potential side effects of long-term treatment. In retrospect, however, this seems to be unfortunate, because we left patients with high-grade, erosive esophagitis GASTROENTEROLOGY 2013;145:1186–1202
without maintenance treatment. Indeed, many of these patients likely developed strictures as well. Although it is not clear that all patients with high-grade erosive esophagitis will progress to stricture formation, we treat all these patients chronically with proton pump inhibitors, and if not with fundoplication. Should this apply to EoE, particularly because the fibrotic consequences are more severe, such as small-caliber esophagus, an entity rarely described as a complication of gastroesophageal reflux disease? Furthermore, the study by Schoepfer3 demonstrates that, after decades of untreated disease, stricture formation will have occurred in most if not all patients. Granted, the risks of chronic topical steroid use seem to be more concerning than chronic proton pump inhibitor use, but with the documented safety of steroid inhaler use in patients with asthma and the growing concerns over bone loss, vitamin deficiency, and enteric infection with proton pump inhibitors, the risk gap might be smaller than we anticipate between these 2 drug classes. One of the main issues is whether, as in gastroesophageal reflux disease, all patients with gross inflammatory lesions will progress to stricture formation, or as in Crohn’s disease, can we target subsets of patients predicted to have more severe disease. A classic study by Lichtenstein et al performed almost 20 years ago described a phenotype of Crohn’s disease: Those patients who present with perforation which predicts likelihood of repeated surgery.7 Since this study, further characterization of patients with Crohn’s disease has led to potential genotypic and serum marker differences in disease presentation and prognosis, which may perhaps serve as a guide to therapy. Do such different phenotypes exist in EoE that are more or less likely to progress to severe fibrotic disease? The study by Schoepfer3 did not identify any factors other than disease duration, suggesting that all patients with EoE have similar risk and therefore should be treated. Information that was not discussed in their study that might have been helpful is further characterization of the strictures found. Specifically, was diffuse small-caliber esophagus, one stricture of great length, considered equivalent to a single esophageal stricture 1 cm in length? Similarly, did they see patients with lesser changes of fibrosis such as focal stricture or ringed esophagus, progress to more severe forms of disease? More specifically, the concern is will all patients progress to small caliber esophagus if left untreated, albeit, over varying amounts of time or will some strictures be milder than others? On the other hand, it should be noted that the proportion of younger patients with long duration of untreated disease seems to be greater than that proportion
Editorials, continued seen in older patients. As in Crohn’s disease, does earlier age of onset of disease portend more severe progression of disease?7 One thing we cannot know by these studies is when EoE begins in individual patients. Although onset of symptoms is the best we can go by, there may be variably long periods of quiescent inflammation and fibrogenesis that precede the first symptom, particularly dysphagia. This is suggested in recent studies by Hirano et al,8 in which patients with a normal caliber esophagus are demonstrated to have decreased esophageal compliance in areas not thought to be diseased. As a result, one must wonder if adults with onset of EoE symptoms have had a slower, smoldering course beginning in childhood similar too but less severe than adolescents with earlier onset of dysphagia and stricture formation. On a more basic level, we do not know if EoE is the same disease in childhood as it is in adults? Unfortunately, without regular endoscopy of an asymptomatic population (something unlikely to occur!) or identification of a noninvasive marker of EoE, answering this question will be difficult. If maintenance therapy is indicated in patients with EoE, what should that therapy be? Steroids seem to be a logical choice for several reasons. First, there are clear data demonstrating excellent control of inflammatory change and reduction of tissue eosinophilia.9 Second, there are data from tissue remodeling studies in EoE showing reversal with steroids10 through gene down regulation.11 Furthermore, there are some clinical data suggesting an increase in stricture diameter with steroids based on endoscopic and/or radiologic assessment.12,13 Third, we know that in other diseases, such as asthma, chronic steroid use seems to be safe and well-tolerated. Unfortunately, limited data are available on what dose is needed to maintain remission in EoE and whether systemic absorption is clinically important. The only controlled trial performed, also from the Swiss group, demonstrates suboptimal efficacy at a quarter (0.5 mg budesonide) of the adult dose used for acute treatment.14 We may, thus, be faced with the prospect of using the dosage needed to eliminate inflammation as that needed to control inflammation, similar to the strategy in inflammatory bowel disease. At a dose of 2 mg of budesonide or 1760 mg of fluticasone daily, there will be greater long-term concern over bone and adrenal effects. Elimination diets, on the other hand, do not seem to pose long-term risks as long as proper nutrition and potential supplementation is used. Although elemental diets will be neither tolerable nor practical for long-term treatment, elimination diets based on empiric evidence (such as the 6food elimination diet) or food challenge and withdrawal based on esophageal biopsy, have great theoretical appeal and proven efficacy.15,16 This may be achievable in some, particularly when a small number of easily avoidable foods can be identified; for many, however, the list will be
too long, the social compromises too great, and the endoscopic monitoring too cumbersome and expensive to use. With less invasive esophageal testing, however, such as the string test, this last issue may be improved. Even so, there are few data yet on the ability of food elimination to reverse fibrosis and maintain remission, although it is likely to come. Finally, dilation will likely hold a place in maintenance. If these therapies are used to reverse fibrotic disease, this will take time when the patient remains at risk for repeated food impaction and ongoing symptoms. Furthermore, we do not have the clinical data to know whether all fibrosis is potentially reversible or as in clinically advanced hepatic cirrhosis or Crohn’s disease, there will be a point beyond which significant improvement is not achievable with medical therapy. This may be true in patients with marked luminal compromise with small-caliber esophagus. Finally, given the relatively young age at which this disease occurs, a lifetime of therapy may require combinations of all these therapies based on lifestyle and choice. Finally, without clear identification of more aggressive EoE phenotypes nor randomized controlled trials demonstrating that steroids help prevent stricture formation, are there patients to whom we should offer maintenance therapy at this point? Patients with more severe forms of this disease such as those who rapidly relapse off therapy, with repeated food impactions, with small caliber esophagus or documented progression might be considered. We are not at a point yet where we can recommend maintenance therapy to all patients with eosinophilic esophagitis, particularly when steroids are the preferred therapy by the patient. What can we take from this landmark study to our current treatment of patients with EoE? First, we need to caution patients, and at least adults, that this is a chronic and perhaps lifelong disease in many commonly leads to stricture formation if untreated. Second, until we can better distinguish disease phenotypes or perhaps genotypes of EoE, we have no choice but to count the majority of patients at risk for progressive fibrosis and stricture formation. Third, when contemplating maintenance therapy, we have to be particularly cognizant not only of treatment side effects but also of the effects of this disease on quality of life, as well as the potential morbid complications including food impaction and iatrogenic or spontaneous esophageal perforation even though this is a “benign” disease. Fourth, I think that patients at high risk for disease complications, particularly those with rapid relapse, severe strictures, or repeated food impactions, should be offered long-term maintenance therapy. What recommended form this therapy will take and what its risks will be are the needs that landmark trials such as this inspire. Nevertheless, our long-term goal for EoE, in contrast with most medical conditions, is to maintain the fat and avoid the skinny esophagus. 1187
Editorials, continued DAVID A. KATZKA Division of Gastroenterology and Hepatology Mayo Clinic Rochester, Minnesota References 1. Liacouras CA, Furuta GT, Hirano I, et al. Eosinophilic esophagitis: Updated consensus recommendations for children and adults. J Allergy Clin Immunol 2011;128:3–20.e6. 2. Hirano I. Dilation in eosinophilic esophagitis: to do or not to do? Gastrointest Endosc 2010;71:713–714. 3. Schoepfer AM, Gonsalves N, Bussmann C, et al. Esophageal dilation in eosinophilic esophagitis: effectiveness, safety, and impact on the underlying inflammation. Am J Gastroenterol 2010;105:1062–1070. 4. Aceves SS, Newbury RO, Dohil R, et al. Esophageal remodeling in pediatric eosinophilic esophagitis. J Allergy Clin Immunol 2007; 119:206–212. 5. Aceves SS. Tissue remodeling in patients with eosinophilic esophagitis: what lies beneath the surface? J Allergy Clin Immunol 2011; 128:1047–1049. 6. Schoepfer AM, Safroneeva E, Bussmann C, et al. Delay in diagnosis of eosinophilic esophagitis increases risk for stricture formation in a time-dependent manner. Gastroenterology 2013;145:1230–1236. 7. Lautenbach E, Berlin JA, Lichtenstein GR. Risk factors for early postoperative recurrence of Crohn’s disease. Gastroenterology 1998; 115:259–267. 8. Kwiatek MA, Hirano I, Kahrilas PJ, et al. Mechanical properties of the esophagus in eosinophilic esophagitis. Gastroenterology 2011; 140:82–90. 9. Dellon ES, Gonsalves N, Hirano I, et al. American College of Gastroenterology. ACG clinical guideline: Evidenced based approach to the diagnosis and management of esophageal eosinophilia and eosinophilic esophagitis (EoE). Am J Gastroenterol 2013;108:679–692.
10. Kagalwalla AF, Akhtar N, Woodruff SA, et al. Eosinophilic esophagitis: epithelial mesenchymal transition contributes to esophageal remodeling and reverses with treatment. J Allergy Clin Immunol 2012; 129:1387–1396.e7. 11. Aceves SS, Newbury RO, Chen D, et al. Resolution of remodeling in eosinophilic esophagitis correlates with epithelial response to topical corticosteroids. Allergy 2010;65:109–116. 12. Lee J, Huprich J, Kujath C, et al. Esophageal diameter is decreased in some patients with eosinophilic esophagitis and might increase with topical corticosteroid therapy. Clin Gastroenterol Hepatol 2012; 10:481–486. 13. Lucendo AJ, Pascual-Turrion JM, Navarro M, et al. Endoscopic, bioptic, and manometric findings in eosinophilic esophagitis before and after steroid therapy: a case series. Endoscopy 2007; 39:765–771. 14. Straumann A, Conus S, Degen L, et al. Long-term budesonide maintenance treatment is partially effective for patients with eosinophilic esophagitis. Clin Gastroenterol Hepatol 2011;9:400–409.e1. 15. Gonsalves N, Yang GY, Doerfler B, et al. Elimination diet effectively treats eosinophilic esophagitis in adults; food reintroduction identifies causative factors. Gastroenterology 2012;142:1451–1457. 16. Kagalwalla AF, Sentongo TA, Ritz S, et al. Effect of six-food elimination diet on clinical and histologic outcomes in eosinophilic esophagitis. Clin Gastroenterol Hepatol 2006;4:1097–1102. Reprint requests Address requests for reprints to: David A. Katzka, MD, Division of Gastroenterology and Hepatology, Mayo Clinic, 200 First St., S.W., Rochester, Minnesota 55905. e-mail: [email protected]. Conflicts of interest The author discloses no conflicts. © 2013 by the AGA Institute 0016-5085/$36.00 http://dx.doi.org/10.1053/j.gastro.2013.10.037
Could Aspiration Therapy for Obesity Be an Effective and Safe Alternative to Traditional Bariatric Surgery? See, “Aspiration therapy leads to weight loss in obese subjects: a pilot study,” by Sullivan S, Stein R, Jonnalagadda S, et al on page 1245.
O
besity is a major public health challenge in the 21st century. It is present in >30% of adult Americans and has wide geographical variation.1 It is associated with multiple medical problems, including heart disease, diabetes, cancer, gallstones, and musculoskeletal disability leading to not only morbidity, but also increased mortality with an estimated decrease in life expectancy between 6 and 20 years.2 The US Preventative Services Task Force has suggested screening all adults for obesity and aggressively treating those with a body mass index (BMI) of >30.3 Despite these suggestions, many practitioners have a nihilistic opinion of the possibility of patients controlling their weight. Dietary and medical therapy have limited efficacy and surgical therapies, although more effective, 1188
have substantial morbidity and a small, but real mortality. In this issue of GASTROENTEROLOGY, a novel, less invasive approach to weight control is presented: aspiration of gastric contents via a gastrostomy tube.4 The 10 subjects who completed the 12-month trial of aspiration therapy lost 18% of their body weight compared with 5.9% in the small control group (4 patients). Obesity is directly related to an overall increase in caloric intake and a decrease in activity-induced caloric expenditure in the modern environment. Attempts to control calorie intake through dietary manipulation and to increase expenditure via increased exercise have been only moderately successful. A meta-analysis of 46 studies using a variety of diet programs found an average 6% loss of weight after 12 months,5 which is similar to the weight loss seen in the control group in the paper presented in this issue. Although a 5%–10% weight loss is much better than none, most patients with substantial degrees of obesity would consider success to require between a
