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1 increasingly prescribed for the treatment of eosinophilic esophagitis.
2 without GERD, 18 with achalasia, and 15 with eosinophilic esophagitis.
3 roles of IgE and IgG4 in the development of eosinophilic esophagitis.
4 search contributions in our understanding of eosinophilic esophagitis.
5 nts showed esophageal candidiasis, and 2 had eosinophilic esophagitis.
6 ainst IL-5, in children and adolescents with eosinophilic esophagitis.
7 phil counts in children and adolescents with eosinophilic esophagitis.
8 implicated a role for periostin in allergic eosinophilic esophagitis.
9 ost often encountered and well studied EGID, eosinophilic esophagitis.
10 uld be aware of the clinical presentation of eosinophilic esophagitis.
11 knowledge of the evaluation and treatment of eosinophilic esophagitis.
12 l presentation, diagnosis, and management of eosinophilic esophagitis.
13 e role of food allergy in many patients with eosinophilic esophagitis.
14 ticasone propionate (FP) in the treatment of eosinophilic esophagitis.
15 allowed FP in pediatric patients with active eosinophilic esophagitis.
16 aphy is useful but will miss subtle signs of eosinophilic esophagitis.
17 that specifically homes to the esophagus in eosinophilic esophagitis.
18 tions for the clinical care of patients with eosinophilic esophagitis.
19 antly, IL-5-deficient mice were resistant to eosinophilic esophagitis.
20 reflux management may need to be treated for eosinophilic esophagitis.
21 esonide tablet licensed for the treatment of eosinophilic esophagitis.
22 s, chronic rhinosinusitis, food allergy, and eosinophilic esophagitis.
23 llected in 2020 from US and EU patients with eosinophilic esophagitis.
24 onditions, such as systemic mastocytosis and eosinophilic esophagitis.
25 usceptibility and pathogenesis, most notably eosinophilic esophagitis.
26 leukin-13 signaling, which have key roles in eosinophilic esophagitis.
27 and were currently prescribed treatment for eosinophilic esophagitis.
28 f other eosinophilic disorders, most notably eosinophilic esophagitis.
29 e dysregulated in atopic disorders including eosinophilic esophagitis.
30 ophageal biopsy specimens from patients with eosinophilic esophagitis.
31 ng asthma, chronic rhinosinusitis (CRS), and eosinophilic esophagitis.
33 n an allergic inflammatory tissue focused on eosinophilic esophagitis, a prototypic, chronic, allergi
34 gic inflammatory diseases, including asthma, eosinophilic esophagitis, allergic rhinitis, and atopic
35 ageal biopsy specimens from 11 subjects with eosinophilic esophagitis and 8 without (controls) were a
37 ologies to understand the pathophysiology of eosinophilic esophagitis and development of novel therap
39 ffective and novel strategy in patients with eosinophilic esophagitis and esophago-pleural fistula as
40 y, sera were collected from 15 subjects with eosinophilic esophagitis and from 41 without (controls),
41 gion, rs3806932 (G allele protective against eosinophilic esophagitis) and rs2416257 (A allele associ
42 elial dysregulation in asthma, food allergy, eosinophilic esophagitis, and allergic rhinosinusitis.
43 allergic rhinoconjunctivitis, food allergy, eosinophilic esophagitis, and asthma is a widely prevale
47 icant increase in the literature surrounding eosinophilic esophagitis as more than two-thirds of the
48 mbling immune complexes were found in 2 of 5 eosinophilic esophagitis biopsy specimens based on ultra
49 o be able to properly identify patients with eosinophilic esophagitis but also be informed about the
50 biopsy specimens from 21 of 24 patients with eosinophilic esophagitis, but in none of the specimens f
54 Esophagectomy samples from 2 patients with eosinophilic esophagitis contained 180 and 300 IgG4 plas
55 herapy) and 20 controls, stored in the Swiss Eosinophilic Esophagitis Database (SEED) and Biobank, we
56 s recapitulated the majority of the clinical Eosinophilic Esophagitis Diagnostic Profile (EDP) on flu
63 previously proposed that the pathogenesis of eosinophilic esophagitis (EE) is mediated by an IL-13-dr
69 ate (FP) and dose reduction in patients with eosinophilic esophagitis (EoE) and analyzed esophageal t
70 ely mimic the Th2 and inflammatory milieu of eosinophilic esophagitis (EoE) and assessed alterations
73 us removal occur frequently in patients with eosinophilic esophagitis (EoE) and harbor a risk for sev
75 responsive, representing 2 entities known as eosinophilic esophagitis (EoE) and PPI-responsive esopha
76 for a long time an option for patients with eosinophilic esophagitis (EoE) and remains the only ther
77 ruments are needed to assess the activity of eosinophilic esophagitis (EoE) and to provide end points
78 l biopsy tissue from individuals with active eosinophilic esophagitis (EoE) and were present at marke
83 of interleukin (IL)-5 in the pathogenesis of eosinophilic esophagitis (EoE) has been established in a
86 expression and translation, in patients with eosinophilic esophagitis (EoE) has not been explored.
89 ints used to determine treatment efficacy in eosinophilic esophagitis (EoE) have evolved over time.
90 with subepithelial fibrosis in subjects with eosinophilic esophagitis (EoE) have not been delineated.
168 ACKGROUND & AIMS: Pharmacologic treatment of eosinophilic esophagitis (EoE) is limited to off-label u
173 g studies have observed an increased risk of eosinophilic esophagitis (EoE) mostly among first-degree
178 nality and diagnosis and/or recrudescence of eosinophilic esophagitis (EoE) remains unclear, with som
179 ps most likely to trigger allergies achieves eosinophilic esophagitis (EoE) remission in children, da
181 he mechanical properties of the esophagus in eosinophilic esophagitis (EoE) using the functional lumi
184 toms and histological findings suggestive of eosinophilic esophagitis (EoE) who achieve complete remi
186 tain homeostasis, and disruption can lead to eosinophilic esophagitis (EoE), a chronic inflammatory d
187 ng eosinophilic tissue inflammation, such as eosinophilic esophagitis (EoE), a chronic inflammatory d
189 senger RNA in the esophagus of patients with eosinophilic esophagitis (EoE), a recently recognized al
190 ve been recognized as a primary treatment of eosinophilic esophagitis (EoE), an allergic inflammatory
192 L-22, and IL-23) of patients with achalasia, eosinophilic esophagitis (EoE), and gastroesophageal ref
193 advances in the pathologic understanding of eosinophilic esophagitis (EoE), as of yet, no single age
194 rs in the rapid increase in the incidence of eosinophilic esophagitis (EoE), but potential exposures
196 ated with pathological conditions, including eosinophilic esophagitis (EoE), in which basal progenito
197 orrelate with tissue pathology during active eosinophilic esophagitis (EoE), providing additional evi
198 ical, endoscopic, and histologic features of eosinophilic esophagitis (EoE), review the current diagn
199 plays an important role in the management of eosinophilic esophagitis (EoE), since it is involved in
200 vidence of epithelial barrier dysfunction in eosinophilic esophagitis (EoE), the lipid composition of
201 iagnosis of an emerging form of esophagitis, eosinophilic esophagitis (EoE), which is currently diagn
202 ntions have been used to treat patients with eosinophilic esophagitis (EoE), yielding varied results.
221 e of type 2 cytokines in the pathogenesis of eosinophilic esophagitis (EoE); however, heterogeneity i
222 contribute to the clinical manifestations of eosinophilic esophagitis (EoE); however, the molecular p
224 in asthma, rhinitis, chronic rhinosinusitis, eosinophilic esophagitis, food allergy, and atopic derma
225 verlap between symptoms of GERD and those of eosinophilic esophagitis, functional dyspepsia, and gast
226 ind, placebo-controlled trial of adults with eosinophilic esophagitis given an antibody against IgE (
227 tes of esophageal tissues from patients with eosinophilic esophagitis had a 45-fold increase in IgG4
229 ts were aged >= 12 years with a diagnosis of eosinophilic esophagitis, had an esophageal count of >=
234 ses marked by type 2 inflammation, including eosinophilic esophagitis in adults and adolescents.
235 ing on the pathophysiology, and treatment of eosinophilic esophagitis in both children and adults.
238 se in the number of publications relating to eosinophilic esophagitis in terms of case reports, cohor
239 ile the most commonly involved foods causing eosinophilic esophagitis include milk, eggs, nuts, beef,
240 diography may be useful for obvious signs of eosinophilic esophagitis including rings and strictures.
241 ied cytokines relevant toward development of eosinophilic esophagitis, including interleukin-5 and in
242 al or intragastric allergen does not promote eosinophilic esophagitis, indicating that hypersensitivi
259 to specific foods, indicate that, in adults, eosinophilic esophagitis is IgG4-associated, and not an
261 mechanism of persisting dysphagia in treated eosinophilic esophagitis is not apparent on high-quality
267 studies support the role of the allergist in eosinophilic esophagitis management, especially for food
270 ive instrument development phase, the PedsQL Eosinophilic Esophagitis Module is now undergoing multis
271 hods, the content validity of the new PedsQL Eosinophilic Esophagitis Module items was supported in t
274 trial, omalizumab did not reduce symptoms of eosinophilic esophagitis or tissue eosinophil counts com
275 5: Patients with known Barrett's esophagus, eosinophilic esophagitis, or idiopathic pulmonary fibros
279 at in patients without GERD or patients with eosinophilic esophagitis; patients with GERD had low MI
280 (1) anaphylactic sensitivity to peanut, (2) eosinophilic esophagitis related to cow's milk, and (3)
283 ented the unique epidemiologic parameters of eosinophilic esophagitis, some of its natural history, a
284 presentation, pathogenesis, and treatment of eosinophilic esophagitis, some of which will be summariz
285 During the last 5 years, the emergence of eosinophilic esophagitis stimulated many case series; th
288 ergic rhinitis, allergic conjunctivitis, and eosinophilic esophagitis), suggesting both cutaneous and
290 gitis or nonerosive but pH-abnormal GERD) or eosinophilic esophagitis than in patients without GERD o
294 in oral Ag-induced esophageal eosinophilia, eosinophilic esophagitis was induced by allergen exposur
295 bservational study was continued, a study of eosinophilic esophagitis was initiated, and new therapeu
296 patients with eosinophilic skin diseases or eosinophilic esophagitis were used for in vivo analyses.
297 ve, non-glucocorticoid-treated patients with eosinophilic esophagitis who had 2 consecutive endoscopi
298 ixed esophageal tissues from 2 patients with eosinophilic esophagitis who underwent esophagectomy and
299 s review covers the role of the allergist in eosinophilic esophagitis with a focus on the literature
300 ffective in inducing histologic remission in eosinophilic esophagitis, with a more pronounced effect