INTRODUCTION — Eosinophilic esophagitis (EoE) has been defined by a panel of experts as "a chronic, immune/antigen-mediated, esophageal disease characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil-predominant inflammation" with other causes excluded [1]. The management of EoE includes dietary, pharmacologic, and endoscopic interventions. It is uncertain whether treatment of symptoms alone is sufficient or if complete resolution of eosinophilic inflammation is also required.
This topic reviews the clinical evidence for the role of food allergies in EoE and elimination and elemental diets for the treatment of EoE. The various types of allergy testing used in the diagnostic evaluation of EoE are reviewed separately. Other aspects of disease pathogenesis, clinical manifestations, general diagnostic evaluation, additional treatment options, and prognosis are also discussed elsewhere. (See "Eosinophilic esophagitis (EoE): Genetics and immunopathogenesis" and "Allergy testing in eosinophilic esophagitis" and "Clinical manifestations and diagnosis of eosinophilic esophagitis (EoE)" and "Treatment of eosinophilic esophagitis (EoE)" and "Patient education: Eosinophilic esophagitis (The Basics)".)
ROLE OF FOOD ALLERGY IN EoE — Food allergy is defined by a recurrent and predictable immune response upon ingestion of a food antigen. The mechanism of food allergy can vary from immediate immunoglobulin E (IgE) mediated hypersensitivity to chronic autoimmune reactions driven by antigen-specific T cells. (See "Pathogenesis of food allergy", section on 'Types of reactions' and "Clinical manifestations of food allergy: An overview".)
The pathogenesis of EoE appears to depend largely upon delayed cell-mediated hypersensitivity. Evidence for this is based upon clinical reactions in human subjects, data that show the presence of food reactive pathogenic effector CD4+/G protein-coupled receptor 15 (GPR15)+/interleukin (IL) 5/IL-13 producing T cells [2], and animal models that rely on the presence of T cells for disease induction [3,4]. Disease induction and/or propagation have not been shown to rely on IgE-mediated mechanisms, even though IgE sensitization to foods is common in EoE and the prevalence of food-induced anaphylaxis is higher in children with EoE [5-9]. In addition, EoE triggered by a specific food can develop after resolution of IgE-mediated allergy to the same food [10,11].
The relationship among gastric acid/gastroesophageal reflux disease (GERD), esophageal eosinophilia, and food allergies still requires clarification. As an example, whether acid can induce epithelial barrier damage that predisposes to food sensitization or whether acid suppression allows for increased IgE sensitization remains to be systematically studied. Data indicate that proton pump inhibitors (PPIs) significantly alter gene expression in esophageal epithelial cells by promoting stress response and decreasing mitotic signal genes [12]. (See "Pathogenesis of food allergy".)
Clinical evidence for the role of food in EoE is reviewed below. The immunopathogenesis and murine models of EoE are reviewed in greater detail separately. (See "Eosinophilic esophagitis (EoE): Genetics and immunopathogenesis" and "Allergy testing in eosinophilic esophagitis".)
The evidence for the role of food allergies in the pathogenesis of EoE is based upon the clinical response when patients are placed on various elimination diets, with resolution of symptoms and normalization of esophageal biopsies. The use of elimination diets with serial endoscopies after food reintroduction has helped identify the most common food triggers. In addition, the onset of EoE during clinical oral immunotherapy (OIT) trials for peanut, hen's egg, and cow's milk supports the hypothesis that delayed-type hypersensitivity is the mechanism underlying EoE pathogenesis. For OIT, the rates of EoE onset can be up to 5 percent, but the rate of gastrointestinal symptoms is higher, up to 20 percent. The true rates of OIT-induced EoE may not be discovered due to OIT discontinuation and, at times, protein pump inhibitor (PPI) therapy, which results in EoE remission [13]. (See 'Implicated foods' below and "Oral immunotherapy for food allergy", section on 'Efficacy and adverse effects'.)
DIETARY THERAPY — The three main modes of treatment for EoE are pharmacologic therapy (ie, topical glucocorticoids, proton pump inhibitor [PPI]), dietary therapy, and dilatation of esophageal strictures [14]. The choice of first-line therapy is patient dependent. Dietary changes, PPIs, or topical glucocorticoids are first-line options for initial treatment of EoE. Dietary avoidance is a common primary approach, particularly in children, and is also a good initial treatment option in motivated adults. It can also be used as a secondary approach if pharmacologic treatments fail. Dietary elimination is associated with resolution of symptoms, esophageal eosinophilia, and, in some cases, esophageal subepithelial fibrosis [15,16]. Food elimination coupled with topical glucocorticoids can improve symptoms and histology [17,18] and reverse fibrotic complications [19] in children with EoE. Dietary therapy is presented here. The general approach to the treatment of EoE and detailed discussions on the use of topical glucocorticoids, PPIs, and esophageal dilatation are presented separately. (See "Treatment of eosinophilic esophagitis (EoE)".)
The appeal of the dietary approach is that it potentially offers an effective nonpharmacologic treatment, with continued food avoidance functioning as a long-term disease control option. On the other hand, allergen avoidance with elimination and elemental diets poses a risk of nutritional deprivation, can be difficult for patients and their caregivers (particularly if nasogastric feedings are required), can lead to psychological problems, can be expensive [20], and may lead to food aversion in children [21,22]. Relapse upon discontinuation of the diet is common [7], and long-term EoE recurrence rates while on the same diet remain to be clearly elucidated. This point is salient since adherence to the diet is difficult and can impact quality of life [23]. In one survey, adult patients with EoE deemed diet to be the most inconvenient therapeutic option [24]. On the other hand, once a "safe" diet is determined, further elimination of foods is usually unnecessary.
Types of dietary therapy — The three primary choices for initial dietary avoidance of potential food allergen triggers in patients with EoE are an empiric elimination diet, a testing-directed diet, or an elemental diet. (See "Allergy testing in eosinophilic esophagitis" and 'Choosing an elimination diet' below.)
Empiric elimination diet — The most commonly used dietary therapy for EoE is the empiric elimination diet. This diet is based upon the concept that the empiric avoidance of those foods that most commonly cause immediate hypersensitivity in a population would also resolve EoE. The initial form of this diet empirically eliminated the six foods/food groups (six-food elimination diet [SFED]) that account for the majority of IgE-mediated food reactions (ie, cow's milk, hen's egg, soy, wheat, peanuts/tree nuts, fish/shellfish). However, adherence to dietary therapy that involves elimination of multiple foods is difficult, raising the question of whether less restrictive diets were an option as the initial approach. Subsequent data have shown that fish/shellfish and peanuts/tree nuts are rare triggers for EoE, and foods such as grains, legumes, and meats are more common triggers. Thus, four-food group elimination (4FED; cow's milk, hen's egg, soy +/- other legumes, and wheat) has become the most common empiric elimination diet, followed by cow's milk elimination only. Sequentially increasing the number of eliminated foods is another option and could decrease the number of endoscopies required in some patients [25]. (See 'Implicated foods' below and 'Efficacy of different dietary approaches' below and 'Choosing an elimination diet' below.)
Testing-directed elimination diet — This diet is also called the directed elimination diet or testing-based elimination diet. It has become an increasingly uncommon approach due to limited utility, labor intensity, and greater success of empiric elimination diets. Skin prick testing (SPT), which examines immediate hypersensitivity to food antigens, and atopy patch testing (APT), which attempts to elucidate delayed-type, cell-mediated reactions to foods, are performed to test for food allergies, with subsequent elimination of foods with positive test results (plus cow's milk because of its poor negative predictive value on testing). SPT is standardized and validated for immediate food hypersensitivity. However, APT is not standardized or validated for EoE and now is rarely used clinically or in research. This testing-directed approach met with some success in children [9,26] but has had more mixed results in adults [27-29]. Studies in adults and children have shown that directed diets based upon in vitro specific IgE testing in isolation or in addition to skin prick/patch testing can be successful to varying extents, although further study is needed before routine use of serum-based testing is recommended [17,28,30,31]. In vitro T cell proliferation to food antigens such as milk may provide an approach for determining EoE-triggering foods in the future. (See "Allergy testing in eosinophilic esophagitis" and 'Efficacy of different dietary approaches' below and 'Choosing an elimination diet' below.)
Elemental diet — The patient is placed on an amino acid-based (elemental) formula (table 1 and table 2), which eliminates all potential food allergens. This approach is the most effective, but is challenging to follow, particularly for adults, and therefore is used rarely. (See 'Efficacy of different dietary approaches' below and 'Choosing an elimination diet' below.)
These diets are used both as therapy and as a diagnostic tool to identify specific food triggers. As such, the initial diets are not permanent but rather a starting point. The exact timeframe for foods to induce EoE and for the disease findings to resolve upon food trigger removal is not clear. Data in adult patients show that EoE can recrudesce endoscopically and histologically in as little as 7 to 14 days, while symptoms and esophageal eosinophilia can recur in approximately three days after food reintroduction [4,32]. However, one study showed that more than six weeks of dietary elimination was required for maximal effectiveness [33]. Thus, the initial diet is typically followed for four to eight weeks. Symptoms are assessed, and a repeat upper endoscopy with esophageal biopsies is performed at the end of the initial avoidance period.
Implicated foods — The most common food triggers are reviewed in the table (table 3). Both empiric and directed methods for antigen elimination show that cow's milk is the most common food trigger for EoE in children, and it is also a common trigger in adults [9,30,34-37]. However, some patients with EoE triggered by cow's milk are able to tolerate more processed forms of dairy, such as baked milk or extensively hydrolyzed cow's milk-based formula [38,39]. Among adults, 43 percent respond to cow's milk and wheat/gluten elimination (of these, 52 percent had only milk as a trigger, 16 percent had only wheat/gluten, and, for 28 percent, both milk and wheat/gluten were triggers) [25]. While peanuts, tree nuts, fish, and shellfish are common triggers in food-induced anaphylaxis, they do not commonly trigger EoE in either children or adults [4,9,28,34].
Empiric diet followed by single-food antigen reintroduction implicates wheat as the second most common trigger in children (26 percent), while directed diets demonstrate hen's egg as the second most common food trigger in children [9]. In another pediatric study of 78 children with EoE who underwent empiric four-food elimination and single-food antigen reintroduction, histologic inflammation was triggered by cow's milk in 85 percent, hen's egg in 35 percent, wheat in 33 percent, and soy in 19 percent [40]. In adults in the United States, wheat was the most common antigenic trigger identified (60 percent), followed by cow's milk (50 percent), in a study of prospective empiric elimination and single-food reintroduction [4]. In another United States study that included nine patients who underwent food reintroduction after an empiric or directed elimination diet, cow's milk was identified as a trigger in four, hen's egg in four, wheat in two, shellfish in one, legumes in one, and tree nuts in one [28]. Cow's milk was the most common (62 percent), followed by wheat (29 percent), hen's egg (26 percent), and legumes (24 percent), in a similar study in Spanish adults [35].
Population differences in EoE-triggering foods are probably related to which foods are most frequently ingested. The positive and negative predictive values for the most common EoE food triggers are discussed separately. (See "Allergy testing in eosinophilic esophagitis", section on 'Food allergy testing in EoE'.)
Efficacy of different dietary approaches — A number of pediatric studies have documented that amino acid-based (elemental) formula (table 1 and table 2), which results in removal of all allergenic food peptides, is the most effective dietary treatment of EoE [7,15,26,41-43]. Elemental formula has not been extensively studied in adults with EoE, primarily because it is a difficult approach for adults to follow. The response rate on an elemental diet is approximately 95 percent compared with 50 to 70 percent on an elimination diet and 50 to 60 percent on a testing-directed diet [44].
All available data on dietary management of EoE come from a mix of observational studies and randomized trials without placebo controls. The primary outcome assessed in a 2020 systematic review and meta-analysis of treatment for EoE was histologic findings on esophageal biopsies. It is important to note that symptoms and histologic findings do not always correlate.
The 2020 systematic review and meta-analysis reported the following findings for dietary therapy [45]:
●Empiric elimination diet – Nine observational studies with 633 patients were included in the meta-analysis of the SFED, which found that 32.1 percent failed to attain histologic remission compared with 86.7 percent in pooled contemporaneous placebo controls from topical glucocorticoid trials, resulting in a relative risk (RR) of 0.38 (95% CI 0.32-0.43). A modestly higher failure rate (43.1 percent) was seen with the 4FED, with a RR of 0.46 (95% CI 0.42-0.57) in three observational studies (426 patients). The failure rate was 57.9 percent (RR 0.66, 95% CI 0.57-077) for two-food elimination (cow's milk and wheat or cow's milk and soy; two studies with 311 patients), whereas the failure rate for elimination of a single food (cow's milk; two studies with 203 patients) was 45.9 percent (RR 0.52, 95% CI 0.37-0.74). A subsequent randomized trial in 63 children with EoE showed that isolated cow's milk elimination compared with 4FED resulted in a similar rate of histologic remission, somewhat lower improvement in symptoms, but greater increase in quality of life [46].
●Testing-directed elimination diet – Eleven observational studies (830 patients) were included in the meta-analysis of allergy testing based-elimination diets, which found that 49.2 percent failed to achieve histologic remission compared with 86.7 percent in the same historical controls noted above (RR 0.52, 95% CI 0.37-0.74).
●Elemental diet – Six observational studies (431 patients, mostly children) were included in the meta-analysis of elemental diet for EoE, which found that 6.4 percent failed to attain histologic remission (<15 eosinophils/high-powered field) compared with 86.7 percent in the same historical controls noted above (RR 0.08, 95% CI 0.01-0.14).
Choosing an elimination diet — Efficacy alone does not drive the dietary treatment choice for EoE. Other important factors that may influence the decision include costs (often not borne by insurance providers), convenience, ease of adherence, and patient/caregiver preferences. When choosing a diet for any given person with EoE, it is important to have a discussion with the patient and their caregiver(s) regarding the advantages and disadvantages of dietary manipulation, as well as the importance of adherence to the chosen food restrictions. Approximately one-third of pediatric patients with EoE who go on an elimination diet are nonadherent, similar to the rates seen with pharmacologic therapy for EoE [47]. It is also important to consider the resources of the treating center (eg, APT, nutritional counseling). Alternatives to dietary therapy are also discussed. (See "Allergy testing in eosinophilic esophagitis" and "Management of food allergy: Nutritional issues" and "Treatment of eosinophilic esophagitis (EoE)".)
The empiric elimination diet is the preferred approach at the author's center. The most commonly used empiric elimination diet is the 4FED, which removes cow's milk, hen's egg, soy, and wheat [14,48,49]. In young children, isolated cow's milk elimination can also be used. Success rates associated with the 4FED and cow's milk-only empiric diets are similar to that seen for the testing-based diet, particularly in children (see 'Efficacy of different dietary approaches' above). There is a paucity of data on directed diets in adults, but it seems that there is greater success with empiric diets in adults. The empiric diet does not require APT, although SPT to the common food allergens should still be performed because of the risk of unmasking an IgE-mediated allergy after elimination and reintroduction of a food in the diet (see 'Reintroduction of foods' below). This approach is particularly useful in the patient who is negative to all foods on testing and in adults who tend to have fewer "positive" tests to foods that are often not clinically relevant. The primary issue with this diet is compliance and potential nutritional deficiencies because it requires removal of many of the staples in the diet. Thus, the cow's milk-only empiric elimination diet may be preferred in some patients. (See 'Empiric elimination diet' above and 'Testing-directed elimination diet' above and "Allergy testing in eosinophilic esophagitis", section on 'Food allergy testing in EoE' and "Management of food allergy: Nutritional issues".)
The use of the empiric elimination diet has brought up a number of issues regarding avoidance of specific foods versus food groups. Initial studies did wheat elimination only, a practice follow by most US practitioners who were polled (17 of 21). In contrast, international practitioners were more likely to eliminate all gluten-containing grains (wheat, rye, barley) [50]. These clinical practices may reflect the required allergen labeling that is different in the US and Europe. In addition, while most US clinicians recommend avoidance of only soy, Spanish investigators tend to recommend avoidance of all legumes [48].
Testing-directed diets are used less commonly due to limited accuracy of available testing in identifying EoE triggers. If used, a testing-directed elimination diet should include the elimination of cow's milk regardless of the testing results because of the poor negative predictive values for cow's milk (see "Allergy testing in eosinophilic esophagitis"). One potential advantage of a testing-based diet is the avoidance of fewer foods if there are a limited number of foods identified by testing. This can lower the cost of the elimination diet and also make the diet easier to follow. In addition, less common food triggers may be identified and removed from the diet with this approach that would have been missed and continued in the diet with the empiric elimination approach. However, these advantages must be weighed against the ability of the clinical practice to do patch testing, a process that is time consuming for both the practice and the patient. In addition, there may be greater issues with compliance in patients who fail this dietary approach and then attempt an even more restrictive diet if they become discouraged or overwhelmed by the effort (table 4). (See 'Testing-directed elimination diet' above.)
The highest success rates in symptomatic and histologic improvement are seen with the elemental diet. However, even in children, this diet is the most difficult to follow. Thus, we typically reserve the elemental diet for patients who fail other therapies, break through a therapy that initially appeared effective, need a safe source of calories during an elimination diet, or prefer this method as the initial approach. (See 'Elemental diet' above.)
Instituting an elimination diet — Generally, an approach that involves allergy/immunology, gastroenterology, and a dietitian may be the most successful. However, this model may be difficult in the private practice or community health care setting. When available, a dietitian who is familiar with food allergies is a valuable part of the patient's care team when instituting an elimination diet. The role of the dietitian can include help with information on the use of antigen-free foods, particularly ideas for substitutes of favorite foods and ways to ensure a nutritionally adequate diet, recipe suggestions, and review of allergen avoidance. Growth should be monitored, and supplements may be necessary depending upon the foods avoided. A working group report has practical suggestions for implementing and managing an elimination diet in EoE [51]. (See "Management of food allergy: Nutritional issues" and "Management of food allergy: Avoidance".)
Patients can start the diet as soon as they are ready. Some advance preparation may be required as far as grocery shopping for specialty items and exploring meal options with the foods available to increase the chances of adherence to the diet. Additionally, some patients without significant symptoms may prefer to wait until after a major holiday to start the diet. Patients also need to be honest about any cheating or accidental exposures while on the diet so that they do not undergo an endoscopy unnecessarily. Depending upon the size of the exposure, the proximity to the scheduled follow-up endoscopy, and the particular food, the endoscopy may be delayed.
Autoinjectable epinephrine is often prescribed for patients who are eliminating a food to which they have tested positive (serum IgE or SPT), especially if the food is a nut (peanut or tree nut) or cow's milk and/or the patient has a history of asthma, since there is a risk of an allergic reaction with accidental exposure or reintroduction after a period of avoidance. (See "Prescribing epinephrine for anaphylaxis self-treatment".)
Reintroduction of foods — If symptoms and histology have improved, foods are then reintroduced one at a time. If symptoms and histology have not improved after the initial dietary eliminations, pharmacologic therapy may be started or a more stringent elimination or elemental diet (if not the initial approach) may be undertaken.
There are several possible reasons for failure of the initial diet that should be explored before the therapy is adjusted. The initial diet may not have eliminated any of the food triggers for the patient; the initial diet may have eliminated some, but not all, of the food triggers; adherence to the diet may have been poor; allergies to inhalant allergens may be contributing to the disease process in addition to food allergies; or there may be an unidentified trigger. Additional etiologies should be considered in the patient with histologic improvement but persistence of symptoms. Pharmacologic therapy is probably the best option if adherence to the initial dietary elimination approach was an issue or if a patient fails elemental therapy despite good adherence. If a more stringent diet is chosen, foods to consider removing include corn, beef, chicken, pork, potato, and rice [9,26]. Further SPT and/or APT may be performed at this point if not done previously. (See "Treatment of eosinophilic esophagitis (EoE)" and "Allergy testing in eosinophilic esophagitis" and "Clinical manifestations and diagnosis of eosinophilic esophagitis (EoE)", section on 'Differential diagnosis'.)
In patients who have had histologic and symptomatic improvement, our usual approach to food reintroduction is as follows:
●We typically have patients consume the reintroduced food/food group in normal amounts for 8 to 12 weeks and then repeat the endoscopy if they are asymptomatic or symptoms are still significantly decreased from baseline. If the patient's endoscopy is normal, we then reintroduce another food and repeat the process. Adult data show that recurrence of esophageal eosinophilia can occur within a relatively rapid timeframe of three to seven days after food reintroduction [32]. Thus, a shorter timeframe of food reintroduction before endoscopy (eg, two to four weeks) is a reasonable alternative clinical approach.
●If a patient becomes symptomatic with a food reintroduction, the food is removed from the diet again, and an endoscopy is not performed. We proceed with reintroduction of the next food after symptoms have subsided (approximately two to four weeks). However, if the patient becomes symptomatic with reintroduction of several foods, then we will do an endoscopy to determine if it is normal. In patients with normal endoscopies at this stage, we consider concomitant diagnoses, such as irritable bowel syndrome and gastroesophageal reflux disease (GERD).
●If an endoscopy is abnormal after a food reintroduction but the patient is asymptomatic, the course depends upon the severity of the findings. We usually remove the food if there are significant findings, such as esophageal narrowing, linear furrows, fibrosis, and/or eosinophilia throughout the esophagus. In contrast, if the findings are minor, for example, mild eosinophilia in a single biopsy with a normal esophageal appearance, then we will leave the food in the diet and repeat the endoscopy after a few months. However, if it was one of the first foods added back, we would take it back out of the diet, even if histologic findings were minor, and try adding back in other foods first before retrying that food. In addition, other treatments are considered, for example, institution of a PPI for isolated distal eosinophilia.
An alternative to following each asymptomatic food reintroduction with an endoscopy is to have the patient reintroduce, one at a time, several of the foods that are lowest on the list of suspected triggers (usually nuts, seafood, and soy for the SFED, but this depends upon individual patient test results) and then perform the endoscopy. One possible benefit to this second approach is fewer endoscopies if the reintroductions are successful. However, if the endoscopy is abnormal, the patient will have to backtrack on the diet and undergo additional endoscopies to determine which of the foods are triggers. The best order and timing of food reintroduction still requires systematic evaluation.
Patients can have IgE sensitization to food antigens without clinical reactivity to the foods. Loss of tolerance can occur upon removal of these foods, particularly cow's milk and peanut, to which a person has IgE sensitization [52]. As such, subjects who have been counseled to avoid foods based upon IgE sensitization have the potential for IgE-mediated reactions (eg, anaphylaxis) upon food reintroduction. For this reason, the EoE consensus recommendation suggests dispensing an injectable epinephrine to patients who have significant levels of food-specific IgE if that food will be avoided during the course of EoE treatment [15].
We often prescribe autoinjectable epinephrine for patients who will be avoiding a food for which they demonstrated elevated serum IgE or that results in a large (>8 mm wheal) positive on SPT, especially if the food is a nut (peanut or tree nut) or cow's milk and/or if the patient has a history of asthma. In addition, we suggest that the practicing allergist perform a medically supervised oral food challenge if there is significant food-specific IgE to the antigen that will be reintroduced following dietary elimination, particularly if the patient has asthma [15]. The rates of loss of tolerance and subsequent IgE-mediated reactions with reintroduction in EoE patients treated with food avoidance have not been systematically evaluated. (See "Diagnostic evaluation of IgE-mediated food allergy" and "Oral food challenges for diagnosis and management of food allergies".)
NATURAL HISTORY OF FOOD ALLERGIES IN EoE — The natural history of food allergy in children with EoE appears to be distinct from the pattern seen in classic IgE-mediated food hypersensitivity, in which allergies to cow's milk, hen's egg, wheat, and soy are usually outgrown by approximately six to eight years of age [53]. In contrast, data in children with EoE suggest that food allergies associated with EoE usually persist [7].
Since adults can have new-onset EoE, this suggests that either food tolerance is not attained in childhood or is lost during adulthood, that older children/adults with EoE may have a proclivity to accumulate food reactions, or that these patients did not recognize symptoms or were able to adapt behavior changes to cope with their disease until they became highly symptomatic. As such, if reintroduction of a particular food fails, we suggest avoidance of that food for at least two years before attempting reintroduction again.
Although the mechanisms for the more persistent allergy are not clear, two potential theories that may overlap are immunoglobulin G4 (IgG4) and T cell response. IgG4 is sometimes found in immune complexes or as free granules in EoE esophageal biopsies and can associate with the severity of EoE histology [54]. Patients with active EoE to a food were found to have a T cell response in two separate independent studies [55,56]. However, the mounting data, including the failure of omalizumab to alter EoE, suggest that IgE has a less prominent and/or ancillary role in EoE, which may explain the differences in the natural disease history [57,58]. (See "Allergy testing in eosinophilic esophagitis", section on 'Specific IgG4 testing' and "Food allergy in children: Prevalence, natural history, and monitoring for resolution".)
RESOURCES — Resources for patients/caregivers and clinicians include:
●American Academy of Allergy, Asthma, and Immunology (AAAAI)
●American College of Allergy, Asthma and Immunology (ACAAI)
●American Partnership for Eosinophilic Disorders (APFED)
●National Institutes of Health (NIH)/National Institute of Allergy and Infectious Diseases (NIAID)
●American College of Gastroenterology (ACG)
●American Gastroenterological Association (AGA)
●North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN)
The 2011 consensus recommendation [15] is available as an open access document on PubMed, and a two-page summary of the consensus report is available at the APFED website.
In addition, manufacturers of elemental formulas have template letters for medical necessity of amino acid diets available on their websites.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Eosinophilic esophagitis".)
SUMMARY AND RECOMMENDATIONS
●Definition – Eosinophilic esophagitis (EoE) is a chronic, immune-mediated disorder that involves the esophagus. The hallmarks of the disease are symptoms associated with esophageal dysfunction and eosinophil-predominant inflammation on histology. (See 'Introduction' above.)
●Pathogenesis – The pathogenesis of EoE appears to depend largely upon delayed, cell-mediated hypersensitivity. The evidence for the role of food allergies in the pathogenesis of EoE is in part based upon the clinical response when patients are placed on various elimination diets, with resolution of symptoms and normalization of esophageal biopsies. The presence of food-reactive CD4+ T cells has been demonstrated in EoE patients. (See 'Role of food allergy in EoE' above and "Allergy testing in eosinophilic esophagitis", section on 'Evidence for role of allergies in EoE'.)
●Modes of treatment – The three main modes of treatment for EoE are dietary therapy, pharmacologic therapy, dilatation of esophageal strictures, and combinations of these interventions as clinically indicated. (See 'Dietary therapy' above and "Treatment of eosinophilic esophagitis (EoE)".)
●Types of elimination diets – The primary choices for initial dietary avoidance of potential food allergen triggers in patients with EoE are (see 'Choosing an elimination diet' above):
•Empiric elimination diet – Empirically eliminate foods to which patients are most likely to be allergic.
•Testing-directed elimination diet – Perform skin prick testing (SPT) and atopy patch testing (APT) for food allergies, with subsequent elimination of foods with positive test results (plus cow's milk because of its poor negative predictive value on testing).
•Elemental diet – Place the patient on an amino acid-based (elemental) formula with exclusion of all solid foods, which eliminates all potential food allergens.
●Choosing an elimination diet – In patients who opt for a dietary approach to treatment (see 'Choosing an elimination diet' above):
•We discuss the available options with the patient/caregiver(s) and take into consideration a number of factors when choosing a diet, including age, dietary preferences, current diet (ie, what foods are staples in the diet versus rarely eaten and therefore unlikely to be triggers), growth and nutritional status, severity of EoE, need for repeat endoscopy with biopsies after food reintroduction, and the patient/caregiver(s) general preference for a simpler diet with less chance of initial success versus a complex diet with a higher chance of success.
•For most patients, we suggest a four-food (typically cow's milk, hen's egg, wheat, and soy) empiric elimination diet (Grade 2C). A reasonable alternative is cow's milk-only elimination, especially in patients who may find it difficult to adhere to more extensive elimination diets. The testing-directed elimination diet that includes the elimination of cow's milk regardless of the testing results because of the poor negative predictive values for cow's milk is also an option, particularly in children.
•We reserve the elemental diet for patients who fail other therapies, break through a therapy that was initially effective, or prefer this method as the initial approach because this type of diet is difficult to follow.
●Consulting a dietitian – When available, a dietitian who is familiar with food allergies is a valuable part of the patient's care team when instituting an elimination diet. (See 'Instituting an elimination diet' above.)
●When to prescribe autoinjectable epinephrine – Autoinjectable epinephrine is often prescribed for patients who are eliminating a food to which they have tested positive (serum IgE or SPT), especially if the food is a nut (peanut or tree nut) or cow's milk and/or the patient has a history of asthma, since there is a risk of an allergic reaction with accidental exposure or reintroduction after a period of avoidance. (See 'Instituting an elimination diet' above.)
●Reassessment and food reintroduction – The initial elimination diet is typically followed for eight weeks. Symptoms are assessed, and a repeat upper endoscopy with esophageal biopsies is performed at the end of the initial avoidance period. Foods are then reintroduced one at a time, with periodic evaluation to determine if each food is tolerated. Pharmacologic therapy or alternative dietary elimination approaches are options in the patient who fails an initial elimination diet. (See 'Reintroduction of foods' above.)
