Eosinophilic gastrointestinal disorders

Eosinophilic
Gastrointestinal
Disorders
5th June 2020
Nattasasi Suchamalawong, MD.
Pediatric Allergy and Immunology Unit,
King Chulalongkorn Memorial Hospital

Outline
Definition
Epidemiology
Pathogenesis and pathology
Eosinophilic gastroenteritis disorder : EoE , EG , EGE , EC
Clinical manifestation
Treatment
Prognosis

Eosinophilic gastrointestinal disorders (EGID)
• Disorders selectively affect the GI tract with eosinophil-rich inflammation in the absence of
known causes for eosinophilia
• Include : Eosinophilic esophagitis (EoE), eosinophilic gastritis, eosinophilic gastroenteritis,
eosinophilic enteritis, and eosinophilic colitis
• primarily polygenic eosinophilic inflammatory disorders involving mechanisms that fall
between pure IgE–mediated and T helper cell type 2 (Th2) responses.
• Eosinophil accumulation in the GI tract
• IgE-mediated food allergy, eosinophilic gastroenteritis, allergic colitis, EoE,
inflammatory bowel disease (IBD), and gastroesophageal reflux disease (GERD).
Chen E. Rosenberg ,Marc E. Rothenberg. Middleton. Edition 9th.2020

Spectrum of gastrointestinal inflammatory
disease involving eosinophils
Rothenberg et al. Eosinophilic gastrointestinal disorders (EGID) Journal of Allergy and Clinical Immunology January 2004, Pages 11-28

EoE
EG, EGE EC

Differential diagnosis
Licari et al. Eosinophilic Gastrointestinal Diseases in Children: A Practical Review. Current Pediatric Reviews, 2019
• Food and drug allergy
• Parasite infections (ascariasis, toxocariasis, trichinosis, schistosomiasis, teniasis,
ankylostomiasis, trichuriasis, strongyloidiasis)
• Malignancies (leukemia, lymphoma)
• Inflammatory bowel diseases (Crohn disease, ulcerative colitis)
• Chronic graft-versus-host disease
• Autoimmune disease (eosinophilic granulomatosis with polyangiitis or Churg-
Strauss syndrome)
• Hypereosinophilic Syndrome (HES)

Epidemiology
Prevalence EoE : 57 case per 100,000 person in US (most common in EGID)
Prevalence of EG and EGE ranging 1.5 – 6.4/100.000 and 2.7 – 8.3/100.000
Prevalence of EC ranges from 1.7 – 3.5/100.000 subjects.

REGULATION OF EOSINOPHIL
TISSUE ACCUMULATION
• IL3, IL5, GMCSF, eotaxin 1-3 → enhance
eosinophil development, migration ,effector
function
• IL1, IL4, IL13, TNF-a → eosinophil trafficking
• IL5, LTC4 → eosinophil trafficking by promote
chemoattraction
Marc E. Rothenberg. Allergy Clin Immunol 2004;113:11-28
Eotaxin 1 : eosinophil accumulation in GI tract
IL5 : eosinophil growth factor

eosinophil recruitment
into the tissue
• Selectin → reverse interaction between
eosinophil and endothelial cell
• Integrin
• ẞ1 (VCA4)
• ẞ2 (CD18 family)
• ɑ4ẞ7 (B7) binding MAdCAM at laminar
propria, lymph nodes and payer’s patch
Eotaxin 1 : chemoattraction dependent on VLA-4 (α4β1)
Eotaxin, a selective chemokine regulating eosinophil migration,
Binds to the eosinophilic chemokine receptor CCR3
Which leads to further upregulation of cytokines
Including interleukins (ILs) IL-3, IL-5, and IL-13
Sara Naramore. JPGN Volume 67, Number 3, September 2018

Proinflammatory role of
eosinophils
Eosinophil : pleiotropic cells that respond to a
variety of triggers. eosinophil granule
constituents are toxic to a variety of tissues
major basic proteins MBP-1and MBP-2 and
matrix composed of eosinophil cationic
protein (ECP),eosinophil-derived neurotoxin
(EDN), and eosinophil peroxidase (EPO).
extracellular deposition of MBP and ECP in the
small bowel : correlation between the level of
eosinophils and disease severity.

Cytotoxic granules in eosinophil
function major basic
proteins (MBP)
eosinophil cationic
protein (ECP)
eosinophil
peroxidase (EPO)
eosinophil-derived
neurotoxin (EDN),
Cytotoxic effect
on epithelium
   -
Antiviral and
ribonucleus activity
-  - 
Toxic pores  - - -
Increase smooth
muscle activity
 - - -
Severity of EGID   - -

non-IgE mediated responses to environmental factors
STAT6 signaling leads to the production
of IL-4 and IL-13 by Th-2 cells
mast cell release of leukotrienes has been
debated in EoE and requires further
investigation in neEGIDs too
Allergens bind IgE receptor on mast cells
and basophils leading to cell activation
and release of inflammatory mediators,
including IL-13 which is involved with
eosinophil recruitment.
1
2

Pathogenesis
SPERGEL AND ACEVES et al . J Allergy Clin Immunol 2018;142:1-

Key-mediators involved in eosinophilic
gastrointestinal inflammation.

Etiology
Disease Etiology
EOSINOPHILIC ESOPHAGITIS
(EoE)
• involves genetic, host immune system, and
environmental factors
• genetically susceptible predominantly non–IgEmediated
responses
EOSINOPHILIC GASTRITIS AND
GASTROENTERITIS (EG , EGE)
•Idiopathic
•Increased total IgE and food-specific IgE levels
•Increased rate of atopy and sensitization to multiple food
, GI infection
EOSINOPHILIC COLITIS (EC) •Non-IgE–associated disease
•T cell–mediated process
•Mice model: STAT6-dependent mechanism
•Infant : FPIES , Protein-induced enteropathy
•Elderly : helminthic infection , IBD ,Vasculitis (EGPA)

Symptoms of eosinophilic esophagitis
eosinophilic esophagitis (EoE) vary according to age
Typical presentation : feeding problem , vomiting, dysphagia
, food impaction
Child : vomit , feeding disorder
Adult : dysphagia , food impaction
Chronic : chronic reflux , heartburn , regurgitation
The column on the right side of the chart specifies the fractional
representation of each presenting symptom within the population.

Clinical : EGE, and EC
Sunkara et al. Clinical and Experimental Gastroenterology 2019:12.
Disease Clinical
•Vary depend on site and layer of GI wall infiltrated by eosinophil
•nausea, vomiting, abdominal pain , bloating , diarrhea, bloody stool,
iron deficiency anemia, malabsorption, protein-losing enteropathy,
ascites and failure to thrive.
• gastric ulcer disease is not common
EOSINOPHILIC COLITIS (EC) • bloody diarrhea , abdominal pain , vomiting , anemia ,
hypoalbuminemia , ascites, bowel obstruction , malabsorption
• Mucosal predominated
Gabriele GIUDICI. Et al . Eosinophilic colitis: clinical review and update 2020.pubmed.nubi.gov

Nonesophageal Eosinophilic Gastrointestinal Disorder
Naramore and Gupta. JPGN Volume 67, Number 3, September 2018

EGID : clinical manifestation
EoE EE = EGE EC
Guillaume Pineton de Chambrun et. al.Curr Gastroenterol Rep (2018) 20: 37

Diagnosis
There is debate as to the eosinophil threshold for diagnosis, and this level
depends on the area of the GI tract examined
Eosinophils are normally present in the stomach, small bowel, and colon, which
is in contrast to the esophagus where they are not normally seen
Experts suggest
At least 15 eos/hpf in the esophagus establishes EoE
At least 30 eos/hpf in the stomach designates EG
at least 50 eos/hpf in the duodenum establishes EGE
and even higher levels in the colon, particularly on the right side, suggest EC
Erin C. Steinbach. et. al. JACI. 2018

Naramore and Gupta. JPGN Volume 67, Number 3, September 2018

Diagnostic Workup for
Eosinophilic Gastrointestinal Disorders
General
-CBC
-Serum electrolytes, albumin, iron study
-ESR or CRP
-Serum total IgE level
-Infectious workup (stool and colonic aspirate
analysis) and serologic studies to exclude a parasitic
infection
- Upper and lower gastrointestinal endoscopy with
biopsies
- pH monitoring or pH-impedance study
(if clinically indicated)
No pathognomonic symptoms or blood
tests for diagnosing EGIDs
A diagnostic evaluation should be
performed on all patients with these
refractory problems
Individuals with a
◦ Strong history of allergic diseases,
◦ Peripheral blood eosinophilia,
◦ Family history of EGIDs

Diagnostic Workup for
Eosinophilic Gastrointestinal Disorders
In the Presence of Hypereosinophilia
Review of the peripheral blood smear (evaluate for dysplastic features ) and Bone marrow analysis
Flow cytometry for lymphocyte subsets
Serum tryptase (elevated in systemic mastocytosis and some neoplastic forms of hypereosinophilia)
Serum immunoglobulins (screen for immune deficiency)
Serum vitamin B12 (elevated in myeloproliferative neoplasms)
Anti-neutrophil cytoplasmic antibodies (ANCAs), anti-nuclear antibody (ANA) and HIV serologies
As the presence of other organ involvement excludes the diagnosis of eosinophilic gastrointestinal disorder, the following testing to
screen for end-organ involvement is also recommended:
Renal function tests (serum chemistries, creatinine, urinalysis) Hepatic function tests (liver enzymes)
Cardiac function (troponin, electrocardiogram, echocardiogram) Pulmonary function tests and chest radiograph
Genetic analysis for FIP1L1-PDGFRA fusion gene biopsy of any other potentially involved tissue (ascites)

Investigation
Stool exam
Common dog hookworm Ancylostoma caninum
Before using systemic immunosuppression for EGIDs, infection with
Strongyloides stercoralis should be ruled out
Skin prick testing with a panel of food and aeroallergens helps to
identify sensitizations to specific allergens

Limited role of allergy testing in EGID
Norihisa Ishimura et. al. Journal of Gastroenterology and Hepatology 28 (2013) 1306–1313
- Patients with EoE and EGE were found to be frequently sensitized to multiple allergens, especially aeroallergens
- Our results showed that the sensitivities to foods and aeroallergens tended to be higher in patients with EGE
than those with EoE
- Measuring serum allergen specific IgE antibodies to determine the target antigen for patients with EGID was
easy to perform and had a low level of invasiveness

milk is the most common food that causes EoE.
milk elimination–only studies, the rate of success has been around 65%

Aeroallergens as antigens in patients with EoE
•Animal models: Intranasal instillation of aeroallergen antigens,
including
•Dust mite •Aspergillus fumigatus •Cockroach
•20% of EoE exacerbations with recurrent food bolus impactions can
also be linked to the pollen season
•Sublingual immunotherapy (SLIT) for aeroallergens and oral
immunotherapy can drive esophageal eosinophilia

Specific IgG4 antibodies to cow's milk proteins in
pediatric patients with eosinophilic esophagitis
sIgG4 to CM proteins are common and high titer in children with EoE.
Although it is not clear that this response is pathogenic, sIgG4 levels imply that these antibodies are
an important feature of the local immune response that gives rise to EoE
Alexander J. Schuyler et. al. JACI. 2018
2-9 year 10-18 year

Alexander J. Schuyler et. al. JACI. 2018

Journal of Clinical Gastroenterology54(1):43-49, January 2020
- EoE patients elevated systemic IgG4 serum levels compared with GERD patients can
be seen and decrease under topical steroid therapy.
- local IgG4 plasma cells expression is high in EoE, but not in GERD patients

Updated international consensus diagnostic criteria for eosinophilic esophagitis:
Proceedings of the AGREE conference
Dellon ES, Liacouras CA, et al.Gastroenterology . 2018 October ; 155(4): 1022–
1033.e10.
ESPGHAN EoE Working Group/GI Committee JPGN .Volume 58, Number 1, January 2014

Updated international consensus diagnostic criteria
for eosinophilic esophagitis: Proceedings of the
AGREE conference
Dellon ES, Liacouras CA, et al.Gastroenterology . 2018 October ; 155(4): 1022–1033.e10.

Antoine Abou Rached. Et. al. World J Gastrointest Pharmacol Ther 2016 November 6; 7(4):
Algorithm for eosinophilic gastroenteritis diagnosis.

Algorithm for eosinophilic enteritis

Endoscopic feature in EoE
GONSALVES AND ACEVES et al. J Allergy Clin Immunol 2020;145:1-

Histologic finding in EoE
Hiroki Sato et.al. European Journal of Gastroenterology & Hepatology. 2018

Hiroki Sato et.al. European Journal of Gastroenterology & Hepatology. 2018
Endoscopic, radiographic, and histological findings of
muscular type of eosinophilic gastroenteritis
Gross endoscopic appearance
- normal aspect
- erythematous
- nodular , friable
- ulcerated mucosa
- pseudopolyps or polyps

Jennifer M. Hurrell et. al. Adv Anat Pathol Volume 18, Number 5, September 2011

Eosinophilic enteritis Inflammatory Bowel Disease
Jennifer M. Hurrell et. al. Adv Anat Pathol Volume 18, Number 5, September 2011
Epithelial hyperplasia

Eosinophilic
Esophagitis
Evan S. Dellon et al. Pharmacotherapies for Eosinophilic Esophagitis.Drugs .2019 :79;1419-1434

Empiricic elimination diet in EoE

Dietary reintroduction
- Reintroduction of foods after achieving
histologic remission approximately 6 weeks
- Common method is to introduce 2 or more foods
sequentially at 2-week intervals, depending on how
many foods were initially eliminated

Topical steroids
Proton pump inhibitor

Algorithm for EoE management
GONSALVES AND ACEVES et al. J Allergy Clin Immunol 2020;145:1-

Ikuo Hirano et al. Annals of Allergy, Asthma & Immunology, 2020-05-01, Volume 124, Issue 5, Pages 416-423,
Practice Parameters : Guideline Recommendations on the Management of Eosinophilic Esophagitis
Recommendation Strength of
recommendation
- In patients with EoE, : recommends topical glucocorticosteroids Strong
- In patients with symptomatic EoE, suggests using proton pump inhibition
- Suggests topical steroids rather than oral steroids.
- Suggests using elemental diet , an empiric, 6-food elimination diet
- Suggests using an allergy testing-based elimination diet
- In patient with EoE in remission after short-term use of topical steroids, suggests
continuation of topical steroids over discontinuation of treatment.
jhk
- In adult patients with dysphagia from a stricture associated with EoE, suggests
endoscopic dilation
Conditional

Ikuo Hirano et al. Annals of Allergy, Asthma & Immunology, 2020-05-01, Volume 124, Issue 5, Pages 416-423,
Practice Parameters : Guideline
Recommendations on the Management
of Eosinophilic Esophagitis
Recommendation Strength of
recommendation
- In patients with EoE, the AGA/JTF recommends topical glucocorticosteroids Strong
- In patients with EoE, : suggests against the use of anti-IgE therapy for EoE. Conditional
In patients with EoE, :
- recommends using anti–IL-5 therapy for EoE only in the context of a clinical
trial.
- recommends using anti–IL-13 or anti–IL-4 receptor α therapy for EoE only in
the context of a clinical trial.
- suggest using montelukast, cromolyn sodium, immunomodulators, and
anti-TNF for EoE only in the context of a clinical trial.
No recommendation

Eosinophilic gastroenteritis
 Eliminating the dietary intake of the foods implicated by skin prick testing has variable
effects
•Complete resolution is generally achieved with amino acid–based elemental diets , Six
food elimination diet (effective in mucosal EGE).
•Drugs
•Corticosteroid : Prednisolone (effective > 90% of serosal type ) 30-40 mg/day 6-8 wks
Budesonide CIR (controlled lieal release) 9 mg/day*2 wk then 6 mg/day
•Steroid sparing : montelukast , Cromoglycate,ketotifen, immunomodulator (AZA,6MP) ,
PPI , Biological agent (Reslizumab , infliximab , Omalizumab ,suplatast tosilate)
Tagore Sunkara et al. Clinical and Experimental Gastroenterology.2019 Jun 5;12:239-253

Alfredo J. Lucendo et. al. JPGN Volume 61, Number 1, July 201
Clinical and Histological Response
Overall effectiveness in inducing clinical remission/clinical improvement was
reported for 68 patients (87.2% of children and 88% of adults)
Histological assessments after dietary treatment were made in 20 individual
cases (22.5%), all of them being children.
Resolution or decrease in eosinophilic infiltration was documented in 16
cases (80%), and changes were not noted in the 4 remaining patients

Efficacy of Dietary Treatment for Inducing Disease
Remission in Eosinophilic Gastroenteritis
Alfredo J. Lucendo et. al. JPGN Volume 61, Number 1, July 201
Exclusive feeding with an amino acid–based elemental formula
◦ Clinical remission was reported in 75.8% (22 patients);
◦ Histological remission was only assessed for only 1 patient with small bowel
involvement and in a further 5 patients with eosinophilic gastritis in a single
research , 5 of these 6 (83%) had normalized mucosal biopsies
6 food and 7 food elimination
◦ 34 patients with EGE or colitis have been given this dietary treatment
◦ Symptomatic improvement has been reported in 29 (85.3%)
◦ Histological assessments, however, have rarely been reported

Antoine Abou Rached. Et. al. World J Gastrointest Pharmacol Ther 2016 November 6; 7(4):

Treatments used in Esophageal enteritis
Drugs Mechanisms of action Treatment indication
Dietary strategies Targeted elimination diet or
elemental diet
First-line treatment based on food allergy tests
Prednisone Systemic corticosteroid First-line treatment for induction of remission
and Maintenance for steroid dependent disease (low
dose)
Budesonide Corticosteroid with low absorption First-line treatment for induction of remission
and Maintenance for steroid dependent disease (low
dose)
Montelukast Selective leukotriene inhibitor First-line treatment or
Steroid sparing agent
Sodium cromoglycate Mast cell stabilizer First-line treatment or
Ketotifen 2nd-generation H1-antihistamine
agent
First-line treatment or
Azathioprine Apoptosis of T and B cells Steroid sparing agent
Mepolizumab Anti-IL5 monoclonal antibody In case of refractory disease
Omalizumab Anti-IgE monoclonal antibody In case of refractory disease
Infliximab/adalimumab Anti-TNF monoclonal antibodies In case of refractory disease

Eosinophilic colitis
•Eosinophilic colitis of infancy is generally a benign disease.
•Elimination food , Elemental diet shown to be effective 75% in infant , but no clear
evidence in adults.
•Eosinophilic colitis in elderly
•Requires medical management because IgE-associated triggers are rarely identified
•Anti-inflammatory drugs : Corticosteriods (Prednisolone , budesonide)
• Steroid sparing agent : Mast cell stabilizer (Cromoglycate, Ketotifen), montelukast,
are generally not successful
•Severe or steroid refractory : Immunosuppressive drug IV (AZA, 6MP) , anti-TNF agents
Eosinophilic colitis: clinical review and update 2020 .Minerva Gastroenterologica e Dietologica ,2020 Jan
Impellizzeri G, et al . Dig Liver Dis. 2019 Jun;51(6):769

Emerging therapies for EGIDs
•Topical corticosteroid
•Anti-IL-5 agents : mepolizumab and reslizumab
•Anti-IL-4 receptor alpha antagonist : dupilumab
•Anti-thymic stromal lymphopoietin (TSLP) agent
•Omalizumab and infliximab have not shown efficacy in EoE

Joshua B. Wechsler et al. Biological therapies for EGID. JACI. 2
Therapeutic targets for current and future biologics in EoE

Joshua B. Wechsler et al. Biological therapies for EGID. JACI. 2

Corticosteroids
• Prednisone : induce Eosinophil apoptosis and
inhibiting chemotaxis
•remains the mainstay for induction of remission of
EGE.
•response rate up to 90%
•Dose
• 0.5 to 1 mg/kg usually induces remission within
a 2-3 wks period (30-40 mg/day) tapering dosage
over a 6 to 8 wks period.
• MT : low dose (1-10 mg/day)
•Re-evaluation of the EGE diagnosis (and type) must
be considered in cases of initial unresponsiveness
Budesonide: reduce inflammation & capillary
permeability
•High affinity for steroid receptors and produces
fewer side effects
•dose 9 mg/d, can be tapered to 6 mg/d for use
as prolonged maintenance therapy
• The better safety profile of budesonide,
compared to other steroid drugs, is of particular
benefit for management of EGE cases over the
long term, setting of steroid dependent disease

Leukotriene-receptor antagonist :
Montelukast sodium
Selective leukotriene (LTD4) inhibitor with demonstrated efficacy for
various eosinophilic disorders, including EGE
Significant clinical response in patients, either when the drug is used
alone or in combination with steroids for induction and maintenance
of remission in steroid dependent or refractory disease.
The usual dose is 5-10 mg/day.
Clinical and histological response with in 2-4 weeks, remission of at
least 12 months.

Mast cell stabilizer
Oral sodium cromoglycate (cromolyn)
Mast cell stabilizer : blocks the release
of immune mediators and the
subsequent activation of eosinophils.
shown to have significant efficacy in
many of the reported cases of EGE
(muscular type), for unknown reasons
Usual dose 100-300 mg tid or qid.
*10 wks
Ketotifen
1stgeneration H1-antihistamine
agent and mast cell stabilizer
Modulates the release of mast cell
mediators
This agent has been proposed as an
adjunct to steroids and montelukast
for treating refractory EGE
Usual dose is 1-2 mg twice daily.

Immunomodulators
Azathioprine
An immunomodulator that induces
apoptosis of T and B cells
The efficacy of this steroid-sparing agent
has been demonstrated in patients with
steroid dependent and refractory EGE
disease
The usual dose for EGE patients is similar to
that used in patients with IBD (2-2.5 mg/kg)
Prefer AZA and prednisolone was more
effective than Aza alone
6-Mercaptopurine
 ribonucleotide inhibiting an enzyme
phosphoribosyl pyrophosphate
amidotransferase, (PRPP amidotransferase)
involved in the synthesis RNA & DNA.
 Effective in EoE achieved clinical and
histological remission that was maintained
for >3 years.

Monoclonal antibodies
Anti IgE
• Its function in EoE or EGIDs is less clear
•Omalizumab was reported to similarly
result in a significant histologic response
but to be unlikely to efficiently treat EGE
patients with a serum IgE level > 700 kIU/L
•Treatment may be more effective for
patients with EGID than for those with
EoE
Anti IL-5
•High efficacy in hypereosinophilic syndromes
and eosinophilic asthma
•Mepolizumab (anti-IL5) was reported to have
improved tissue and peripheral eosinophilia
but without relieving symptoms
•Improve clinical and histologic efficacy in a
small series of patients with EGID and
hypereosinophilicsyndrome
•EoE: open label, phase 1-2 study of 4 adults

monoclonal antibodies
for the treatment of
eosinophilic esophagitis
Anti IL-5
anti-IgE monoclonal
antibody
Evan S. Dellon et al. Pharmacotherapies for
Eosinophilic Esophagitis.Drugs .2019 :79;1419-1434

Treatment of EGID
Treatment EoE EG EE EC
Diet elimination SFED , AA SFED, generally achieved
with AA
SFED , elemental diet SFED , elemental diet
Topical steroid Initial treatment
(MDI with puff
and swallow
teechnique)
Initial treatment
(Prednisolone)
response in serosal type
budesonide tablets
(budesonide
controlled ileal
release)
Effective in distal
colon (prednisolone ,
budesonide)
Systemic steroid Severe dysphagia,
acute weight lose,
acute exacerbate
Severe case, long term
treatment
Severe case Effective
Sodium cromoglycate
(cromolyn)
Not recommend Effect in muscular EGE Not recommend Not recommend
Ketotifen - adjunct to steroids and
montelukast
adjunct to steroids
and montelukast
No report efficacy

Treatment of EGID
Treatment EoE EG EE EC
montelukast - Limit data , mild
symptom
Not recommend Not recommend
Anti IgE Not recommend for
routine
Limit data Limit data Limit data
Anti IL5 Not recommend for
routine (Clinical trial)
Refractory disease Refractory disease Refractory disease
Imatinib - Limit data Limit data Limit data
other Dilatation : High grade stricture
Fecal microbiota transplantation : refractory disease
Surgery : severe disease with complication ; bowel obstruction ,
volvulus intussusception
AZA IV, 6MP IV in
severe case

Prognosis
disease prognosis
EOSINOPHILIC ESOPHAGITIS
(EoE)
• requires prolonged treatment, recurrent in most patients after
cessation of therapy
• long-term sequelae (untreated) including fibrostenotic complications
Chronic EoE : progressive esophageal scarring and dysfunction. (Barrett
esophagus)
•diseases wax and wane chronically
 regular endoscopic evaluation and symptom monitoring
 CBC : AEC often marker for tissue involvement
EOSINOPHILIC COLITIS (EC) • natural history for eosinophilic colitis has not been documented
 chronic waxing-and-waning disorder
 manifestation of other primary disease processes, routine
surveillance of other organ systems

- We were eventually able to identify 3 different courses of
EGE: single flare, recurring course, and continuous
course in
42%, 37%, and 21%, respectively.
- The disease course was different between the 3
anatomical patterns of EGE N J Shaheen et al .Disease esophagus . 2018 Aug 1;31(8):doy015

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