Uncover the signs of chronic inflammation across the 3 domains
of EoE: symptoms, endoscopy, and histopathology.1-4
SEE EoE BEYOND
Symptoms
~50% of dysphagia cases may not be reported to a clinician, and it is the most common symptom of EoE.*1,3-5 Patients may develop adaptive behaviors that mask symptoms, making EoE difficult to diagnose by symptoms alone.3,4,6,7
*In an online April 2018 Takeda-sponsored
SEE EoE BEYOND
Endoscopy
Because nearly 1 in 4 patients with EoE had normal endoscopic findings,† EoE should not be ruled out based on endoscopic findings alone.8
†In a retrospective study of 117 patients with EoE, the esophageal mucosa was regarded as normal in 24.8% of the patients.8
SEE EoE BEYOND
Histopathology
Without investigating symptoms and endoscopic findings, the histological presence of esophageal eosinophilia alone does not establish an EoE diagnosis.3
EoE is a chronic, immune-mediated, inflammatory disease localized in the esophagus9
In this relatively newly characterized disease, chronic esophageal inflammation due to an immune response to food allergens or aeroallergens is the key driver of EoE severity.10-12 Untreated, persistent inflammation can cause symptoms, such as dysphagia, that can induce fear and anxiety for patients.13 Some patients cope with these symptoms by developing adaptive behaviors which can minimize awareness and reporting of symptoms, potentially leading to the diagnostic delays and possible complications as a result of unmanaged persistent inflammation.1,6,7,14-17
In EoE, chronic inflammation can manifest in different ways13,14,18
In addition to symptoms like dysphagia, untreated chronic inflammation can manifest in endoscopic complications like strictures, and in the histological presence of elevated eosinophils and other markers of inflammation.14-16 Some patients with EoE may also present with psychiatric comorbidities.18 One retrospective study found that up to 28% of patients with EoE experienced psychiatric comorbidities such as anxiety (23%) and depression (17%).‡18
EoE involves the complex interplay of genetics, environmental factors, immune system dysfunction and atopy10
EoE can be characterized as a localized adaptive immune response triggered by antigens in the esophagus, involving increased levels of immunoglobulin G4 (IgG4) and recruitment of other cells known to contribute to that chronic esophageal inflammation.3,10,19-23 Many patients with EoE have a history of IgE-mediated allergic comorbidities, with sensitivity to food or other allergens in the esophagus.3,19,21,24,25 Esophageal inflammation and remodeling in EoE may be a result of repeated exposure to food and environmental allergens that can eventually lead to impaction of solid or coarse foods which may not necessarily contain those inflammation triggering allergens.19,21 Educating your patients about the consequences of this ongoing inflammatory process is important.
‡In a study using the University of North Carolina EoE Clinicopathologic Database from 2002 to 2018. Of 883 patients diagnosed with EoE (per consensus guidelines), 241 (28%) had a psychiatric comorbidity. Study limitations include this is one, single center, retrospective study where a comparison to the national representative figures was done through nonstatistical analyses.18
The mechanism of disease in EoE
The prevalence
of EoE is rising9,26,27
Approximately 1 in 2000 people in the US live with EoE19,26-29
The majority of EoE cases are in children, adolescents, and adults ages 50 or younger, but it can affect all ages.1,3,28,30,31
EoE is approximately twice as common in men vs women and more common among Caucasians, but can affect all sexes and races28,30,31
EoE is a leading cause of dysphagia and food impaction for children and young adults3
Emerging evidence suggests environmental factors such as microbes, early-life events affecting the microbiome, and other factors may be contributing to the rise in prevalence of EoE9,12,19,32-34
One study reported that one third of adults and 1 in 7 children with EoE have received a diagnosis of a psychiatric condition§18
§In a study using the University of North Carolina EoE Clinicopathologic Database from 2002 to 2018. Of 883 patients diagnosed with EoE (per consensus guidelines), 241 (28%) had a psychiatric comorbidity. Study limitations include this is one, single center, retrospective study where a comparison to the national representative figures was done through nonstatistical analyses.18
Adaptive behaviors can contribute to disconnects in what
patients
say and what their endoscopies show1,3,12,33
For patients with EoE, inflammation can lead to symptoms such as dysphagia and food impaction, which may produce a certain amount of fear and interfere with everyday life.13 Without realizing, some patients develop adaptive behaviors to cope with these symptoms.6,33 But adaptive behaviors can minimize awareness and symptom reporting, so symptoms of EoE should always be assessed in conjunction with endoscopies and biopsies.3,4,6,33
Identify adaptive behaviors to help reveal EoE||
Chewing food excessively3,33,35
Eating slowly7,33,35
Cutting food into small pieces1,12
||Illustrative only. Adaptive behaviors will vary by patient.
Asking the right questions can identify adaptive behaviors
and potentially reveal masked symptoms of EoE1
SEE EoE THROUGH 3 DOMAINS:
Symptoms, Endoscopy, Histopathology
Diagnosis and monitoring of EoE requires the holistic approach
of assessing the 3 domains together2-4,33
There are several limitations associated with each of the 3 domains so no single domain alone should be relied on to draw conclusions about diagnosis, or how to manage ongoing disease activity.2-4,33 EoE is heterogeneous and can have overlapping signs and symptoms with other eosinophilic conditions, reinforcing the need for a differential diagnosis through the 3 domains.2
SEEING EoE BEYOND
Symptoms
In adults with EoE, dysphagia is the most frequently reported symptom, and in the US, 1 in 6 adults reported experiencing difficulty swallowing.¶1,5,7 Symptoms like dysphagia can create a certain amount of fear for patients.13 Beyond dysphagia, EoE presents with a variety of symptoms across all ages.1,30 Understanding how symptoms may vary between age groups can be helpful when assessing clinical manifestations of EoE.1,28 Family history of EoE or dysphagia should increase the clinical index of suspicion.2
¶In an online April 2018 Takeda-sponsored
Common symptoms of EoE#33,38
Toddlers & Infants
- Feeding aversion/
intolerance - Vomiting
- Food refusal
- Choking with meals
- Sleep disturbance
Children
- Dysphagia
- Choking/gagging with coarse textures
- Food impactions
- Abdominal/chest pain
- Throat pain
- Vomiting/regurgitation
- Nausea
- Sleep disturbance
- Decreased appetite
Adults
- Dysphagia
- Food impactions
- Food avoidance
- Intractable heartburn
- Regurgitation
- Chest pain
#Individual symptoms will vary by patient.
Limitations of symptoms alone
Symptoms may not correlate with endoscopic and histologic findings because they can be masked by adaptive behaviors that vary by patient.1-4 Some patients may present with symptoms of EoE that can overlap with other conditions.1-3 Endoscopies with biopsies must be performed where EoE is a clinical possibility.1-3 Learn more about adaptive behaviors, or scroll to see EoE beyond endoscopy.
SEEING EoE BEYOND
Endoscopy
Esophageal remodeling driven by inflammation can manifest as endoscopic features that can vary
by age.3,39
Data in adults suggest that there's potential for inflammation to progress into strictures in some EoE patients with untreated disease.21,40
Illustration adapted from Dellon ES, Hirano I. Gastroenterology. 2018;154(2):319-332.e3.
In adults, esophageal remodeling can manifest as fibrostenotic complications, such as strictures, which can lead to food impactions.14,39,41 For infants and toddlers, remodeling can lead to food avoidance and failure to thrive.1,3 In children, endoscopic features like edema and exudates are more commonly seen.14,39,41 Diagnostic delays may increase the risk of fibrostenotic complications.14,16
Assessing endoscopic severity of EoE through 5 key features
There are 5 key endoscopic features, edema, rings, exudates, furrows, and strictures, that have been well-studied and validated to help assess the endoscopic severity of inflammation and fibrostenotic remodeling in EoE across all ages.3,14,33,42,43 Though endoscopic findings are well-documented in EoE, they cannot reliably establish a diagnosis on their own.3,42
Edema
- Swelling of the esophageal mucosa3,33,44
- Thick and whitish appearance33,44
- Decreased vascularity3,44
- May be more common in children39,41
Horizontal Rings
- Formation of multiple rings33
- Can appear fine, web-like, or thickened33
- Also termed trachealization or the "corrugated/ringed" esophagus33
- May be more common in adults39,41
Exudates
- Patches of whitish papules33
- Often 1-2 mm in diameter33
- Resembles esophageal candidiasis33
- May be more common in children39,41
Furrows
- Vertical esophageal lines or ridges in the esophageal wall33
- May be more common in children39,41
Strictures
- Narrowed esophagus, usually <13 mm diameter3,33
-
- Featureless, unchanging column33
- Poor expansion on air insufflation33
- Proximal and/or distal stenosis33
- Can cause food impactions and block endoscope45
- May be more common in adults39,41
- Edema
- Horizontal Rings
- Exudates
- Furrows
- Strictures
Edema
- Swelling of the esophageal mucosa3,33,44
- Thick and whitish appearance33,44
- Decreased vascularity3,44
- May be more common in children39,41
Horizontal Rings
- Formation of multiple rings33
- Can appear fine, web-like, or thickened33
- Also termed trachealization or the "corrugated/ringed" esophagus33
- May be more common in adults39,41
Exudates
- Patches of whitish papules33
- Often 1-2 mm in diameter33
- Resembles esophageal candidiasis33
- May be more common in children39,41
Furrows
- Vertical esophageal lines or ridges in the esophageal wall33
- May be more common in children39,41
Strictures
- Narrowed esophagus, usually <13 mm diameter3,33
-
- Featureless, unchanging column33
- Poor expansion on air insufflation33
- Proximal and/or distal stenosis33
- Can cause food impactions and block endoscope45
- May be more common in adults39,41
Internal images of the body are artistic representations. Endoscopic features will vary by patient.
Limitations of endoscopy alone
Due to the patchy nature of the disease, some patients with EoE can present with normal endoscopic findings.1-4 Endoscopies can miss complications, such as strictures, caused by chronic inflammation in EoE.46 Endoscopic findings should be assessed in conjunction with symptoms and histopathology.1-4 Scroll on to see EoE beyond histopathology.
SEEING EoE BEYOND
Histopathology
Chronic inflammation in EoE can be found inside the esophageal tissue, where eosinophils and other cells can cause recruitment of additional inflammatory immune cells.12,21 Guidelines suggest that an eosinophil count of ≥15/hpf (high-power field) in at least one of multiple esophageal biopsy samples taken from different locations is clinically indicative of EoE.2,3 The presence of esophageal eosinophilia alone, however, cannot establish an EoE diagnosis without further investigation of symptoms and endoscopy.2-4
See inflammation beyond eosinophils2,3,47
Other histologic features can help assess the severity and extent of esophageal inflammation. The interactive tissue below can help reveal other markers of inflammation.
Basal zone hyperplasia (BZH):
>15% of the epithelial thickness3,12,47
Papillary elongation:
Papillae extend above the mid portion of the squamous mucosa.3,12,48 Also observed in GERD.48
Lamina propria fibers (LPF):
Thickened connective tissue fibers in the lamina propria3,47
Dilated intercellular spaces (DIS):
Spaces around squamous epithelial cells that exhibit intercellular bridges3,12,47
Eosinophil inflammation (EI):
Eosinophil count within the most densely populated HPF (high-power field)3,12,47
Internal images of the body are artistic representations. Histologic features will vary by patient.
Internal images of the body are artistic representations. Histologic features will vary by patient.
Limitations of histopathology alone
Histopathology may help confirm a suspected diagnosis, but esophageal eosinophilia can be a sign of various esophageal-related diseases besides EoE, like eosinophilic gastritis and GERD.2 Moreover, due to patchy infiltration of eosinophils along the esophagus in EoE, multiple biopsies should be taken from distal, mid, and proximal locations.2,3,49
Investigate all 3 domains of EoE to reduce delays
in diagnosis and help manage EoE over time2,3
According to the latest guidelines, PPIs are no longer
a tool to diagnose EoE.2
Rationale for changing the EoE diagnostic criteria and removing the PPI trial2:
- Similarities between EoE and PPI-REE
- EoE and GERD are not necessarily mutually exclusive
- Lack of a criterion standard for GERD diagnosis
- Novel mechanisms of action of PPIs to explain response of eosinophilia
- Observation that PPI-REE could also respond to classic EoE treatments
- Concern about using a treatment response to define a disease
There is a multidisciplinary path to EoE diagnosis3,11,46
Diagnosing, managing, and monitoring EoE can require collaboration across disciplines like gastroenterologists, allergists, pathologists, primary care clinicians, and dietitians.3,11,46 Many patients with EoE may see a variety of these clinicians before receiving a confirmed diagnosis for their condition.3,11,46 But a gastroenterologist will likely be involved when making a diagnosis because endoscopies and biopsies are required to reveal EoE.1,3,11
Help reduce the risk of complications by uncovering inflammation in EoE early14,16
Diagnostic delays may increase the risk of complications14,16
- Mean diagnostic delay is up to 3.5 years in children and 8 years in adults based on a systematic review30
- For every decade of living with EoE, the likelihood of esophageal fibrosis doubles**3,14
- Mean diagnostic delays of up to 8 years in symptomatic adults may translate to a 40% increase in risk of fibrostenosis**14
- Fibrostenosis was seen in 46% of symptomatic adult patients with a
2-year diagnostic delay, and in 87% of symptomatic patients with a delay of 20 years or more††16 - A psychiatric diagnosis in patients with EoE was more likely in adult patients with a longer duration of symptoms preceding diagnosis‡‡18
- According to one study, US adult patients with EoE had a higher prevalence of a psychiatric diagnosis when compared to the general adult population in the US (36% compared to 18.9%, respectively)‡‡18
**Retrospective study from 2001–2011, N=379.
††Retrospective study from 1989–2007 using Swiss EoE Database, N=200.
‡‡In a study using the University of North Carolina EoE Clinicopathologic Database from 2002 to 2018. Of 883 patients diagnosed with EoE (per consensus guidelines), 241 (28%) had a psychiatric comorbidity. Study limitations include this is one, single center, retrospective study where a comparison to the national representative figures was done through nonstatistical analyses.18
Strictures may be more likely when diagnosis is delayed16
Other factors can contribute
to diagnostic delays in EoE
PPI-REE
Up until 2018, experts believed that evaluating the response to a proton-pump inhibitor (PPI) was the best way to rule out inflammation related to gastroesophageal reflux disease (GERD) in patients with EoE.2 This led to the term PPI-responsive EoE (PPI-REE), which was initially considered a separate disease.2 Current guidelines no longer support using PPIs as a diagnostic tool.2 Therefore, rather than being considered a separate disease, PPI-REE is now considered a type of EoE.2 In all cases, EoE should be diagnosed through a holistic assessment of symptoms, endoscopy, and histopathology.2-4
Differential diagnosis
Patients with EoE can exhibit signs and symptoms that can also present in other eosinophilic gastrointestinal diseases.§§1-3 These other diseases should be ruled out to confirm an EoE diagnosis.1-3 However, EoE can coexist with other eosinophilic conditions as well, which can make diagnosing EoE a challenge.1-3 To differentially diagnose EoE from other eosinophilic conditions, there should be holistic consideration of symptoms, endoscopy, and histopathology.2
§§Such as gastroesophageal reflux disease (GERD), other eosinophilic gastrointestinal diseases such as eosinophilic gastroenteritis, hypereosinophilic syndrome, Crohn’s disease, infection (candida or parasites), achalasia, drug hypersensitivity, connective tissue diseases, and others.
Comorbidities
Patients frequently present with atopic comorbidities that can lead to delayed diagnosis of EoE. In one study, ~78% of patients had ≥1 atopic disease.||||25 A family or personal history of pre-existing allergic diseases should increase the suspicion for EoE and should be considered.2,25 Consider investigating EoE further with endoscopies and biopsies when patients present with symptoms of esophageal dysfunction along with any of the following:
- Allergic rhinitis1,25
- Asthma1,25
- Atopic dermatitis1,25
- Food allergy1,25
- GERD3,38
||||In a retrospective study of 449 patients who presented with clinical and pathological features of EoE and received an esophageal biopsy between
A more standardized approach
to EoE management needs to be established50
Finding the appropriate way to manage EoE starts with a patient-centric approach and shared decision-making that suits the patient's lifestyle.3 The
New guidelines have been developed to help standardize EoE management in practice35,40
There is significant variation in EoE treatment patterns, with physicians using diet (7%), topical steroids (32%), twice-a-day PPIs (33%), and daily PPIs (28%) according to a study from 2018.¶¶50 Only 12% of physicians said they use all three EoE diagnostic criteria listed in evidence-based guidelines from 2011.¶¶50 This highlights the need for better standardization in practice.
¶¶In an online survey that was
##Secondary causes of esophageal eosinophilia: gastroesophageal reflux disease, eosinophilic gastrointestinal disease, achalasia, hypereosinophilic syndrome, esophageal Crohn’s disease, infections (fungal, viral), connective tissue disorders, autoimmune disorders, vasculitis, drug hypersensitivity reactions, pill esophagitis, stasis esophagitis, graft versus host disease, Marfan syndrome type II, hyper-IgE syndrome, PTEN hamartoma tumor syndrome, Netherton’s syndrome, severe atopy metabolic wasting syndrome.
***Recommendation in favor of empiric elimination diets is based on the published experience with the six food elimination diet (SFED). Patients who put a higher value on avoiding the challenges of adherence to diet involving elimination of multiple common food staples and the prolonged process of dietary reintroduction may reasonably decline this treatment option. Emerging data on less restrictive diets (4 food, milk elimination, 2-4-6 step up diet) may increase both provider and patient preference for diet therapy.
†††Patients who put a higher value on avoiding the challenges of adherence to an elemental diet and the prolonged process of dietary reintroduction may reasonably decline this treatment option.
‡‡‡Due to the potential limited accuracy of the currently available, allergy-based testing for the identification of specific food triggers for EoE, patients may prefer alternative medical or dietary therapies to an exclusively testing-based elimination diet.
§§§Esophageal dilation does not address the esophageal inflammation associated with eosinophilic esophagitis.
Chronic inflammation in EoE can be managed by either medical or dietary therapy40
As outlined in the 2020 AGA and the JTF Clinical Guidelines for the Management of Eosinophilic Esophagitis.
Learn more about the "strength of recommendation" and the "quality of evidence."
Therapeutic approach
Strength of Recommendation||||||
Quality of Evidence||||||
Proton Pump Inhibitors
(vs no treatment)
Strength of Recommendation||||||: Conditional
Quality of Evidence||||||: Very Low
Topical Glucocorticosteroids
(vs no treatment)
Strength of Recommendation||||||: Strong
Quality of Evidence||||||: Moderate
Topical Glucocorticoids
(vs Systemic [Oral] Glucocorticosteroids)
Strength of Recommendation||||||: Conditional
Quality of Evidence||||||: Moderate
Esophageal Dilation
(vs no dilation)
Strength of Recommendation||||||: Conditional
- Recommended for adult patients with dysphagia from a stricture associated with EoE
Esophageal dilation does not address the esophageal inflammation associated with eosinophilic esophagitis.
Quality of Evidence||||||: Very Low
Anti-Interleukin-13, Anti-Interleukin-5, and Anti-Interleukin-4 receptor α
(only in clinical trials)
Strength of Recommendation||||||: No Recommendations
Quality of Evidence||||||: Knowledge Gap
Anti-IgE Therapy
Strength of Recommendation||||||: Conditional recommendation against the use of anti-IgE therapy for EoE
Quality of Evidence||||||: Very Low
Montelukast, Cromolyn Sodium, Immunomodulators, or
(only in clinical trials)
Strength of Recommendation||||||: No Recommendations
Quality of Evidence||||||: Knowledge Gap
Dietary approach
Strength of Recommendation||||||
Quality of Evidence||||||
Elemental Diet
(vs no treatment)
Strength of Recommendation||||||: Conditional
- Patients who put a higher value on avoiding the challenges of adherence to an elemental diet and the prolonged process of dietary reintroduction may reasonably decline this treatment option
Quality of Evidence||||||: Moderate
Empiric 6-Food Elimination Diet
(vs no treatment)
Strength of Recommendation||||||: Conditional
- Patients who put a higher value on avoiding the challenges of adherence to diet involving elimination of multiple common food staples and the prolonged process of dietary reintroduction may reasonably decline this treatment option
Quality of Evidence||||||: Low
Allergy Testing-Based Elimination
Diet
(vs no treatment)
Strength of Recommendation||||||: Conditional
- Due to the potential limited accuracy of currently available, allergy-based testing for the identification of specific food triggers for EoE, patients may prefer alternative medical or dietary therapies to an exclusively testing-based elimination diet
Quality of Evidence||||||: Very Low
Current guidelines strongly recommend swallowed topical glucocorticosteroids in the management of EoE. Management approaches like PPI, diet therapy, and esophageal dilation were supported by evidence for conditional recommendations.||||||40
||||||An assessment/analysis was made of current treatment approaches and published by the AGA and the JTF using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE). Using the GRADE methodology, the AGA and JTF categorize the strength of their recommendations as either "strong" or "conditional." These recommendations are based on evidence that is categorized as "high," "moderate," "low," or "very low."40
Get the EoE Guidelines Pocket Guide
Ongoing monitoring of EoE requires clearly defined management goals
across the 3 domains35
In chronic inflammatory diseases, a treat-to-target approach involves monitoring specific and objective measures of inflammation.52 A treat-to-target approach in EoE can assess inflammation across the 3 domains and help identify discrepancies among them, like symptom persistence despite normalized histological findings.35 Management goals should be defined to help monitor each domain and achieve clinical, endoscopic, and histological response.35
Ongoing management and monitoring goals to consider in EoE:
- Resolution of dysphagia without modifying diet or avoiding specific food textures35
- Normalization of esophageal histopathology measured by eosinophils and other markers of esophageal inflammation and tissue injury35
- Reductions in endoscopic features of EoE combined with a maintained esophageal diameter of ≥16 mm35
A complete response in EoE management has been described as improvements in all 3 domains by minimizing symptoms, endoscopic findings, and histopathologic features of EoE.35
There are several challenges to treating patients with EoE. Despite the challenges, shared decision-making through a patient-centric approach may help keep patients engaged with long-term management plans.3,27
These challenges may include:
- Adherence challenges3,35,54
- Long-term impact on day-to-day life for patients3,53,54
- Muir AB, Brown-Whitehorn T, Godwin B, et al. Clin Exp Gastroenterol. 2019;12:391-399.
- Dellon ES, Liacouras CA, Molina-Infante J, et al. Gastroenterology. 2018;155(4):1022-1033.e10.
- Lucendo AJ, Molina-Infante J, Arias A, et al. United European Gastroenterol J. 2017;5(3):335-358.
- Safroneeva E, Straumann A, Coslovsky M, et al. Gastroenterology. 2016;150(3):581-590.e4.
- Adkins C, Takakura W, Spiegel BMR, et al. Clin Gastroenterol Hepatol. 2019; pii: S1542-3565(19)31182-6. doi: 10.1016/j.cgh.2019.10.029. [Epub ahead of print].
- Putnam PE. Gastrointest Endosc Clin N Am. 2008;18(1):11-23.
- Franciosi JP, Liacouras CA. Immunol Allergy Clin North Am. 2009;29(1):19-27.
- Müller S, Pühl S, Vieth M, et al. Endoscopy. 2007;39(4):339-344.
- Dellon ES, Hirano I. Gastroenterology. 2018;154(2):319-332.e3.
- Clayton F, Peterson K. Gastrointest Endosc Clin N Am. 2018;28(1):1-14.
- Dellon ES, Jones PD, Martin NB, et al. Dis Esophagus. 2013;26(1):7-13.
- Furuta GT, Katzka DA. N Engl J Med. 2015;373(17):1640-1648.
- Taft TH, Guadagnoli L, Edlynn E. J Asthma Allergy. 2019;12:389-399.
- Dellon ES, Kim HP, Sperry SL, et al. Gastrointest Endosc. 2014;79(4):577-585.e4.
- Rajan J, Newbury RO, Anilkumar A, et al. J Allergy Clin Immunol. 2016;137(1):147-156.e8.
- Schoepfer AM, Safroneeva E, Bussmann C, et al. Gastroenterology. 2013;145(6):1230-1236.e1-2.
- Steinbach EC, Hernandez M, Dellon ES. J Allergy Clin Immunol Pract. 2018;6(5):1483-1495.
- Reed CC, Corder SR, Kim E, et al. Am J Gastroenterol. 2020;115(6):853-858.
- O’Shea KM, Aceves SS, Dellon ES, et al. Gastroenterology. 2018;154(2):333-345.
- Clayton F, Fang JC, Gleich GJ, et al. Gastroenterology. 2014;147(3):602-609.
- Hill DA, Spergel JM. Curr Allergy Asthma Rep. 2016;16(2):9.
- Wright BL, Kulis M, Guo R, et al. J Allergy Clin Immunol. 2016;138(4):1190-1192.e3.
- O’Shea K, Hogan SP. Ann Esophagus. 2018;1:14.
- Simon D, Marti H, Heer P, et al. J Allergy Clin Immunol. 2005;115(5):1090-1092.
- Mohammad AA, Wu SZ, Ibrahim O, et al. J Am Acad Dermatol. 2017;76(3):559-560.
- Dellon ES, Jensen ET, Martin CF, et al. Clin Gastroenterol Hepatol. 2014;12(4):589-596.
- Dellon ES. Gastroenterol Clin North Am. 2013;42(1):133-153.
- Dellon ES. Gastroenterol Clin North Am. 2014;43(2):201-218.
- Spergel JM, Book WM, Mays E, et al. J Pediatr Gastroenterol Nutr. 2011;52(3):300-306.
- Shaheen NJ, Mukkada V, Eichinger CS, et al. Dis Esophagus. 2018;31(8):1-14.
- Mansoor E. Dig Dis Sci. 2016;61(10):2928-2934.
- Harris JK, Fang R, Wagner BD, et al. PLoS One. 2015;10(5):e0128346.
- Carr S, Chan ES, Watson W. Allergy Asthma Clin Immunol. 2018;14(Suppl 2):58.
- Alexander ES, Martin LJ, Collins MH, et al. J Allergy Clin Immunol. 2014;134(5):1084-1092.
- Hirano I, Furuta GT. Gastroenterology. 2020;158(4):840-851.
- Menard-Katcher C, Henry M, Furuta G, et al. World J Gastroenterol. 2014;20(31):11019-11022.
- Gonsalves N. Dig Dis. 2014;32(1-2):89-92.
- Wong S, Ruszkiewicz A, Holloway RH, et al. World J Gastrointest Pathophysiol. 2018;9(3):63-72.
- Straumann A, Aceves SS, Blanchard C, et al. Allergy. 2012;67(4):477-490.
- Hirano I, Chan ES, Rank MA, et al. Gastroenterology. 2020;158:1776-1786.
- Bystrom J, O’Shea NR. Postgrad Med J. 2014;90(1063):282-289.
- Hirano I. Dig Dis. 2014;32(1-2):78-83.
- van Rhijn BD, Verheij J, Smout AJ, et al. Neurogastroenterol Motil. 2016;28(11):1714-1722.
- Ahmed M. World J Gastrointest Pharmacol Ther. 2016;7(2):207-213.
- Eluri S, Runge TM, Cotton CC, et al. Gastrointest Endosc. 2016;83(6):1142-1148.
- Hirano I. Gastroenterology. 2018;155:601-606.
- Collins MH, Martin LJ, Alexander ES, et al. Dis Esophagus. 2017;30(3):1-8.
- Grin A, Streutker CJ. Arch Pathol Lab Med. 2015;139(6):723-729.
- Saffari H, Peterson KA, Fang JC, et al. J Allergy Clin Immunol. 2012;130(3):798-800.
- Eluri S, Iglesia EGA, Massaro M, et al. Dis Esophagus. 2020;doaa025. doi: 10.1093/dote/doaa025. Online ahead of print.
- Treatment of Eosinophilic Esophagitis (EoE): Clinical Decision Support Tool. Gastroenterology. 2020;158:1787.
- Drescher H, Lissoos T, Hajisafari E, et al. J Nurs Prac. 2019;15:676-681.
- Shah NA, Albert DM, Hall NM, et al. Clin Exp Gastroenterol. 2016;9:281-290.
- Philpott H, Dellon ES. J Gastroenterol. 2018;53(2):165-171.
