Abstract
Background:
Eosinophilic esophagitis (EoE) guidelines suggest that nasal or inhaled steroids for rhinitis, sinusitis, or asthma may obscure EoE treatment outcomes. Few data support this assertion.
Objective:
To assess whether EoE treatment outcomes vary by nasal/inhaled steroid use or concomitant allergic rhinitis.
Methods:
We conducted a retrospective cohort study of newly diagnosed EoE patients treated with a topical corticosteroid (tCS), with follow-up endoscopy and biopsy. Extracted variables included diagnosis of allergic rhinitis, treatment with nasal and/or inhaled steroids, and post-treatment symptoms, endoscopic data, and pathology results. Patients with/without treatment with nasal and/or inhaled steroids were compared. We also compared outcomes by diagnosis of allergic rhinitis and season at follow-up.
Results:
Of 473 patients, 185 (39%) had allergic rhinitis. Post-treatment symptom response (83% vs. 77%; p = 0.37), EREFS (1.9 ± 1.9 vs. 2.3 ± 1.9; p=0.07), and eosinophil counts (25.5 ± 41.8 vs. 23.0 ± 32.4; p = 0.38) did not differ by allergic rhinitis status. No differences in histologic responses were found by nasal/inhaled steroid use (aOR for <15 eos/hpf: 0.96; 95% CI: 0.53–1.74) or in asthma patients on inhaled steroids. Patients with allergic rhinitis had higher post-treatment eosinophil counts in spring (41.3 ± 7.4 spring vs. 20.5 ± 3.3 other seasons; p=0.01).
Conclusion:
Treatment responses did not differ by nasal/inhaled steroid use or by concurrent allergic rhinitis. Patients with allergic rhinitis had a higher post-treatment eosinophil count in spring. These data support use of nasal/inhaled steroid in EoE patients but suggest caution when assessing responses in spring months.
Keywords: eosinophilic esophagitis, aeroallergens, nasal and inhaled corticosteroids, allergic rhinitis, histologic response
Introduction
Eosinophilic esophagitis (EoE) is an immune-mediated esophageal condition induced by allergen exposure, most typically food allergens. In adults, EoE is characterized by symptoms of dysphagia, food impaction, heartburn, and chest pain while in children poor growth and feeding intolerance are seen.1 It is diagnosed by the presence of consistent symptoms and esophageal biopsies showing at least 15 eosinophils per high-power field (eos/hpf) following the elimination of other etiologies of esophageal eosinophilia.1 EoE diagnoses have been steadily increasing over the past four decades as the condition affects more individuals of all ages.2,3 Treatment strategies for EoE include esophageal dilation, elimination diets, and pharmacologic agents. For greater than two decades, topical corticosteroids, including swallowed fluticasone and budesonide, have been adapted for off-label use from asthma preparations and remain among the first-line treatments for EoE.1,4,5 Given the limitations of using off label non-esophageal steroid formulations for EoE, the US Food and Drug Administration (FDA) approved budesonide oral suspension (BOS) in 2024, which became the second FDA approved medication following dupilumab’s approval in 2022.6,7
Multiple lines of data link the pathogenesis of EoE with atopy. For instance, EoE patients frequently demonstrate sensitivity to aeroallergens, such as pollen, mold, and dust mites,8 and aeroallergens may trigger disease activity.9,10 Additionally, EoE is more frequently diagnosed in the spring11 and summer12 months, esophageal eosinophilia differs by climate zone,13 and the disease is strongly associated with additional comorbid atopic conditions such as atopic dermatitis, asthma, IgE-mediated food allergy, and allergic rhinitis (AR).14–16 AR is the most frequently reported comorbid atopic diagnosis, and symptoms of AR often precede those of EoE.14 Given comorbid allergic conditions, including AR and/or asthma, EoE patients may concurrently be treated with intranasal and/or inhaled corticosteroids. Within the current guidelines, a key concept suggests holding intranasal and/or inhaled corticosteroids prior to assessment of EoE disease activity given that these medications could be swallowed and have a topical effect in the esophagus, thus confounding EoE assessments.1 However, there is limited evidence to support this assertion. To our knowledge, there are no papers specifically looking at the impact of intranasal and/or inhaled steroids on EoE-related disease activity. As such, equipoise remains in the extent to which EoE-related disease activity may or may not be masked by intranasal and/or inhaled corticosteroids.
While research indicates a strong relationship between EoE and AR, we lack clarification as to how this comorbid diagnosis affects treatment response. We also lack knowledge regarding the impact of concurrent non-esophageal corticosteroid use, whether intranasal and/or inhaled, on EoE-related outcomes. As such, we aimed to assess both if AR is associated with the probability of obtaining a histologic response to tCS, as well as whether concurrent use of intranasal and/or inhaled corticosteroids impacts treatment outcomes in patients with EoE. Lastly, we also assessed if there is an association between histologic response to tCS and season of treatment.
Methods
We conducted a retrospective cohort study at the University of North Carolina (UNC) using the UNC EoE Clinicopathologic database. The UNC EoE Clinicopathologic database has been well-described17–20 and consists of patients of any age diagnosed with EoE according to consensus guidelines1,21 and seen between 2002 to 2024. The UNC Institutional Review Board provided approval for this study.
We utilized the UNC EoE Clinicopathologic database to identify all patients who were treated with tCS and completed a post-treatment endoscopy with biopsies. These criteria were utilized to assess baseline and post-treatment follow-up data. At our institution, patients have historically been treated with either oral viscous budesonide or fluticasone from a multi-dose inhaler (all patients in this study were included prior to the approval and use of budesonide oral suspension).6 Though dependent on provider choice, dose of tCS typically ranged between 1–2 mg/day for oral viscous budesonide and 440–1760 mcg/day for fluticasone.22,23 At UNC, we typically repeat an upper endoscopy for assessment of endoscopic and histologic response following an 8–12 week course of treatment.
Following cohort assembly, we extracted medical record data with a standardized data collection form to obtain baseline and follow-up data before and following the initial treatment course with tCS. Extracted data included patient demographics and comorbidities, symptoms, endoscopic findings, and histologic findings. The months and season of the follow-up endoscopy was recorded (spring: March 20 - June 19, summer: June 20 - September 21, fall: September 22 - December 20, winter: December 21 - March 19). For all patients, we extracted prior relevant medication use including any history of oral histamine 1 receptor antagonist, intranasal histamine 1 receptor antagonist, subcutaneous immunotherapy, sublingual immunotherapy, intranasal corticosteroids, and inhaled corticosteroids. AR was defined as a diagnosis of AR, seasonal allergies, and/or hay fever at any point within the medical record with one of the following: confirmed diagnosis by an ENT provider or by an allergist, or self-report of AR, seasonal allergies, and/or hay fever in addition to a history of use of intranasal steroids, histamine 1 receptor antagonist orally, histamine 1 receptor antagonist nasal spray, history of subcutaneous immunotherapy for AR, or history of subcutaneous immunotherapy for AR.
For outcome assessment, patients were considered to have concurrent intranasal or inhaled corticosteroid use if a provider documented use of these medications in the three months leading up to the follow-up endoscopy. We extracted baseline and post-treatment endoscopic findings as documented at these time points (yes/no as per endoscopist’s assessment of the appearance of the esophagus), as well as the EoE Endoscopic Reference Score (EREFS) at both time points (for cases after 2014; 0–9 scale for worst findings overall). An endoscopic severity score was also utilized (ESS, score 0–5 with 0/1 assigned for the presence/absence of each individual EREFS finding) for all included cases.20,24 For histologic findings, we collected baseline and post-treatment peak eos/hpf and determined histologic response for all patients (thresholds of < 15, ≤ 6 and < 1 eos/hpf) following tCS treatment.25 At UNC, validated patient-reported outcomes are not routinely utilized, so we extracted a global symptom response from the chart, which we have successfully used in other studies.26,27 The global symptom response is a dichotomous outcome of patients’ perceived disease severity assessed at any individual time point by a UNC gastroenterologist.
For analysis, descriptive statistics including the mean, standard deviation, and the shape of the distribution were determined for continuous variables. Frequencies were tabulated for categorical variables. All analyses were completed with Stata 14.2. Patients with and without AR were compared at baseline and following tCS treatment. We conducted bivariate analyses using chi-squared test for categorical variables and the 2-sample t test for continuous variables. Following bivariate analysis, we performed ANCOVA modeling to assess the relationship between AR, dichotomously recorded, and probability of histologic response, adjusted for confounders. Variables that changed the beta coefficient of AR in the multivariate model by >10% were kept.
We next compared the probability of obtaining a histologic response to swallowed steroids between patients treated with inhaled and/or intranasal corticosteroids with patients who did not receive treatment with the aforementioned medications prior to follow-up endoscopy with biopsies. ANCOVA modeling assessed whether there was an association between inhaled and/or intranasal corticosteroids use and histologic response, adjusted for covariates. Lastly, we assessed the probability of histologic response, defined above, versus the season at which the follow-up endoscopy was completed. Following bivariate analyses, ANCOVA modeling was again utilized to assess the probability of histologic response adjusted for confounders. We conducted the same analyses for the entire cohort, as well as for patients with and without AR.
Results
Baseline characteristics of all included patients
Of 1459 EoE patients within the UNC EoE Clinicopathologic database, 473 (32%) met inclusion criteria for this study. Among the 473 patients, 315 (67%) of the included patients were male, 419 (89%) were white, and 159 (34%) were children at time of diagnosis. The mean age at diagnosis was 29.0 ± 18.4 years with a mean symptom length prior to diagnosis of 8.5 ± 9.5 years. An atopic condition was present in 302 (64%) patients with AR being the most prevalent (n=185; 39%). Other comorbid allergic diagnoses present included asthma (28%), eczema (16%), and food allergy (32%).
The most common symptoms present in included patents were dysphagia (76%), food impaction (33%), and vomiting (25%). On baseline endoscopy, findings included furrows (75%), rings (58%), edema (57%), exudates (55%), and stricture (34%). Total EREFS at baseline was 4.2 ± 1.5, and the baseline peak eosinophil count was 74.1 ± 52.0 eos/hpf.
Comparison of patients with and without allergic rhinitis at baseline
EoE patients with AR (39%) and without AR (61%) did not differ by age at diagnosis (27.7 years vs. 29.9 years; p=0.22), sex (63% male vs. 69% male; p=0.22), race (91% white vs. 89% white; p=0.57), or BMI (23.7 vs. 24.5; p=0.17) (Table 1). The groups also did not differ in symptom length prior to diagnosis (7.7 years vs. 9.0 years; p=0.17), nor in their baseline presenting symptoms or baseline peak eosinophil count (79.2 ± 56.4 eos/hpf vs. 70.9 ± 48.7 eos/hpf; p=0.09).
Table 1:
Baseline characteristics by allergic rhinitis status
| Allergic rhinitis (n = 185) | No allergic rhinitis (n = 288) | P value | |
|---|---|---|---|
| Age at diagnosis (mean years ± SD) | 27.7 ± 18.6 | 29.9 ± 18.30 | 0.22 |
| Children <18 years (n, %) | 69 (37) | 90 (31) | 0.17 |
| Male (n, %) | 117 (63) | 198 (69) | 0.22 |
| White (n, %) | 166 (91) | 253 (89) | 0.57 |
| BMI (mean kg/m2 ± SD) | 23.7 ± 8.0 | 24.5 ± 6.3 | 0.29 |
| Symptom length pre diagnosis (mean years ± SD) | 7.7 ± 8.2 | 9.0 ± 10.2 | 0.17 |
| Symptoms (n, %) | |||
| Dysphagia | 134 (73) | 225 (80) | 0.09 |
| Food impaction | 57 (31) | 97 (34) | 0.44 |
| Heartburn | 32 (17) | 55 (19) | 0.58 |
| Chest pain | 13 (7) | 17 (6) | 0.66 |
| Vomiting | 54 (29) | 63 (22) | 0.09 |
| Failure to thrive | 16 (9) | 12 (4) | 0.05 |
| Endoscopic findings (n, %) | |||
| Exudates | 105 (57) | 154 (55) | 0.61 |
| Rings | 97 (53) | 175 (62) | 0.07 |
| Edema | 100 (55) | 168 (59) | 0.37 |
| Furrows | 136 (74) | 219 (77) | 0.39 |
| Stricture | 56 (30) | 103 (36) | 0.19 |
| Narrowing | 23 (13) | 40 (14) | 0.23 |
| Crepe-paper mucosa | 9 (5) | 8 (3) | 0.24 |
| Dilation | 52 (28) | 108 (38) | 0.03 |
| Stricture diameter (before dilation) (mean mm ± SD) | 4.8 ± 6.4 | 4.8 ± 6.2 | 0.95 |
| EREFS findings (mean ± SD) | |||
| Exudates | 0.76 ± 0.56 | 0.90 ± 0.69 | 0.10 |
| Rings | 0.94 ± 0.85 | 1.08 ± 0.91 | 0.20 |
| Edema | 0.80 ± 0.45 | 0.79 ± 0.45 | 0.88 |
| Furrows | 1.02 ± 0.48 | 1.13 ± 0.49 | 0.07 |
| Stricture | 0.42 ± 0.50 | 0.47 ± 0.50 | 0.44 |
| Total EREFS (mean ± SD) | 3.88 ± 1.76 | 4.37 ± 1.97 | 0.04 |
| Total ESS (mean ± SD) | 2.68 ± 1.53 | 2.86 ± 1.51 | 0.19 |
| Peak eosinophil count (mean eos/hpf ± SD) | 79.2 ± 56.4 | 70.9 ± 48.7 | 0.09 |
| Oral anti-histamine prior to follow-up endoscopy | 83 (45) | 62 (22) | <0.001 |
| Nasal anti-histamine prior to follow-up endoscopy | 8 (4) | 2 (1) | 0.008 |
| Nasal corticosteroids prior to follow-up endoscopy | 34 (18) | 14 (5) | <0.001 |
| Inhaled steroid prior to follow-up endoscopy | 30 (16) | 14 (5) | <0.001 |
Endoscopic findings at baseline did not differ by groups. However, patients with a diagnosis of AR had a lower total EREFS score at baseline when compared to EoE patients without an AR diagnosis (3.88 ± 1.76 vs. 4.37 ± 1.97; p=0.04). Patients with AR were also less likely to undergo dilation at baseline (28% vs 38%; p=0.03). No differences were found in individual endoscopic findings including exudates, rings, edema, furrows, structure, and narrowing.
As expected, at baseline, EoE patients with AR were significantly more likely to be treated with oral antihistamines (45% vs. 22%; p < 0.001), nasal antihistamines (4% vs 1%, p=0.008), nasal corticosteroids (18% vs 5%; p < 0.001), inhaled corticosteroids (16% vs 5%; p < 0.001), and to have a history of treatment with subcutaneous immunotherapy (3% vs. 0%; p=0.006).
Treatment response by allergic rhinitis status
The type of tCS did not differ between groups, with swallowed budesonide being the most frequently used for both groups (69% vs 73%, p=0.49) (Table 2). Mean tCS dose also did not differ between groups (1694 ± 768 mcg vs. 1753 ± 681 mcg; p=0.38).
Table 2:
Treatment response data by allergic rhinitis status
| Allergic rhinitis (n=185) | No allergic rhinitis (n=288) | P value | |
|---|---|---|---|
| Type of steroid used (n, %) | |||
| Fluticasone | 57 (31) | 78 (27) | 0.49 |
| Budesonide | 127 (69) | 209 (73) | 0.49 |
| Mean steroid dose (mcg ± SD) | 1694 ± 768 | 1753 ± 681 | 0.38 |
| Post-treatment peak eosinophil count (mean eos/hpf ± SD) | 25.5 ± 41.8 | 23.0 ± 32.4 | 0.47 |
| p value vs baseline | <0.001 | <0.001 | |
| Histologic response (n, %) | |||
| <15 eos/hpf | 110 (59) | 160 (56) | 0.40 |
| ≤6 eos/hpf | 98 (53) | 142 (49) | 0.44 |
| <1 eos/hpf | 66 (36) | 80 (28) | 0.07 |
| Global symptom response (n, %)* (n = 58, 77) | 48 (83) | 72 (77) | 0.37 |
| If no dilation performed (n=43, 63) | 34 (79) | 49 (77) | 0.76 |
| If dilation performed (n=14, 30) | 13 (93) | 23 (77) | 0.20 |
| Post-treatment endoscopic findings (n, %) | |||
| Normal | 45 (24) | 53 (18) | 0.12 |
| Exudates | 39 (21) | 75 (26) | 0.23 |
| Rings | 75 (41) | 132 (46) | 0.31 |
| Edema | 47 (25) | 91 (32) | 0.16 |
| Furrows | 73 (40) | 136 (47) | 0.11 |
| Stricture | 50 (27) | 108 (38) | 0.02 |
| Narrowing | 27 (15) | 58 (20) | 0.14 |
| Crepe-paper mucosa | 2 (1) | 3 (1) | 0.96 |
| Dilation | 50 (27) | 102 (35) | 0.07 |
| Candida | 13 (7) | 17 (6) | 0.61 |
| Post-treatment EREFS total (mean scores ± SD) | 1.9 ± 1.9 | 2.3 ± 1.9 | 0.07 |
| Post-treatment ESS total (mean scores ± SD) | 1.5 ± 1.4 | 1.8 ± 1.5 | 0.03 |
| Season of treatment and post-treatment peak eosinophil count (mean eos/hpf ± SD) | |||
| Spring | 39.4 ± 65.8 | 24.0 ± 34.4 | 0.13 |
| Summer | 18.5 ± 30.0 | 17.9 ± 27.5 | 0.89 |
| Fall | 25.6 ± 40.2 | 24.9 ± 30.2 | 0.90 |
| Winter | 24.0 ± 34.6 | 25.5 ± 37.28 | 0.83 |
Global symptom response did not differ between patients with and without AR, and post treatment endoscopic data was similar. However, patients with AR were less likely to have strictures (27% vs 38%; p = 0.02). The mean post-treatment total EREFS score trended lower in patients with AR (1.9 ± 1.9 vs. 2.3 ± 1.0; p=0.07), and the mean post-treatment ESS score was significantly lower (1.5 ± 1.4 vs. 1.8 ± 1.5, p=0.03). We found no differences in the aforementioned outcomes when comparing white and non-white patients.
Both groups achieved significant reductions in peak eosinophil count post-treatment (both p<0.001), with no significant difference in post treatment peak eosinophil counts between groups (25.5 vs. 23.0; p=0.47). In unadjusted analyses, histologic responses did not differ by group at any threshold: <15 eos/hpf (59% vs. 56%; p=0.40), ≤6 eos/hpf (53% vs. 49%; p=0.44), or <1 eos/hpf (36% vs. 28%; p=0.07). On multivariate modeling, there was no significant difference in post treatment peak eosinophil counts (24.2 eos/hpf vs. 23.5 eos/hpf; p = 0.85) or probability of histologic response (62% vs. 55% probability of <15 eos/hpf; p = 0.17).
Impact of concurrent intranasal and/or inhaled corticosteroids on treatment response
In the entire cohort of patients, concurrent use of intranasal and/or inhaled corticosteroids did not affect post-treatment eosinophil counts on bivariate analysis (28.5 ± 42.7 vs. 23.1 ± 35.0 eos/hpf; p = 0.23). In multivariate models, concurrent use of intranasal and/or inhaled corticosteroids was not associated with histologic response at <15 eos/hpf (aOR 0.96, 95% CI: 0.53–1.74), nor at ≤6 or <1 eos/hpf.
When separated by AR status, concurrent use of intranasal and/or inhaled corticosteroids during treatment of EoE in patients with AR alone did not impact histologic response on bivariate (p=0.94) or multivariate (p=0.97) analysis. In patients without AR, concurrent use of corticosteroids during treatment of EoE also did not impact histologic response on bivariate (p=0.43) or multivariate (p=0.50) analysis.
We also assessed outcomes by asthma diagnosis. There were 133 (28%) patients diagnosed with asthma. On bivariate analysis, asthma was significantly associated with higher post-treatment histologic outcomes (31.8 vs. 20.7; p = 0.003). Similar findings were appreciated after controlling for the same covariates assessed for AR patients (30.6 vs. 21.0; p = 0.01). However, no differences were found in multivariate analyses when assessing the impact of inhaled steroids on post-treatment outcomes (32.0 vs. 28.9; p = 0.76).
Seasonal variation in treatment response
The distribution of follow-up endoscopies by season was relatively uniform: spring (21%), summer (28%), fall (27%), winter (24%). The season during which the follow-up endoscopy took place did not affect the probability of response at 15 eos/hpf (p=0.59), nor at 6 eos/hpf or 0 eos/hpf when considering the entire cohort. This lack of association persisted when evaluating patients with and without AR (Table 2).
However, when evaluating patients with AR specifically with multivariate modeling, endoscopies in the spring had a higher post-treatment mean eosinophil count than other seasons: spring 41.4 eos/hpf, summer 19.7, fall 25.6, winter 14.7; p=0.04. We also evaluated whether the same patients differed in outcomes when assessed by intranasal and/or inhaled corticosteroid use. There was no difference in either subgroup by season.
Discussion
Although the relationship between EoE and AR has been well documented, our current understanding as to how AR might affect EoE treatment response is limited.8,9,14 Similarly, current EoE guidelines recommend that patients with comorbid AR, allergic sinusitis, and/or asthma stop intranasal and/or inhaled corticosteroid treatments prior to attempting to diagnose EoE and/or assessing for EoE-related treatment responses; however, there is limited evidence to support this recommendation.1 This study evaluated these associations in a large cohort of both children and adults with EoE. We found that a diagnosis of AR did not affect histologic responses to tCS. Additionally, concurrent use of intranasal and/or inhaled corticosteroids during EoE treatment did not impact histologic response. Interestingly, in AR patients only, endoscopies performed in the spring months were associated with higher absolute post-treatment eosinophil counts. This suggests that seasonal aeroallergen exposure impacts the assessment of treatment response in EoE patients with AR, which is consistent with prior work.27 While there was not a difference in outcomes by intranasal and/or inhaled corticosteroid, this may be from reduced statistical power and confounding by indication.
Atopic conditions including AR, food allergies, eczema, and asthma are common among patients of any age diagnosed with EoE.23 Of possible comorbid atopic conditions, AR is the most frequent concurrent diagnosis.14 Moreover, aeroallergens have been implicated in the pathogenesis of EoE, as EoE patients are frequently sensitized to aeroallergens,28,29 esophageal eosinophilia may vary by season,9 and EoE disease activity may flare in different seasons.30 Few data exist looking at the impact of comorbid AR on EoE presentation and treatment outcomes.31 One paper evaluated the association of concurrent atopic disease and response to treatment in pediatric patients with EoE. As appreciated in this study, there were no significant differences between patients with additional or no additional atopic conditions regarding presenting demographics and symptoms, nor treatment outcomes with tCS.31 An additional study looked at the impact of multiple concurrent atopic conditions in adult and pediatric patients with EoE.23 As compared to the present study, patients were categorized by presence of any atopic condition. Similar findings were reported with no significant differences at baseline or following treatment.
As patients with EoE frequently have comorbid AR and/or asthma, they may be exposed to intranasal and/or inhaled corticosteroids while undergoing treatment specifically for EoE. Theoretically, if these medications were swallowed, they could provide a treatment of EoE obscuring a diagnosis of EoE or confounding assessment of treatment response. In our study, we found that a diagnosis of AR did not affect the probability of histologic response achieved by tCS. These findings, especially in light of prior work, indicate that an AR diagnosis does not likely impact treatment-related outcomes. In fact, patients with AR exhibited lower endoscopic severity scores, which could point to earlier disease recognition in this population or possibly a differing phenotype. We also found that concurrent use of intranasal and/or inhaled corticosteroid did not impact relevant outcomes in EoE patients receiving tCS. This held true for the entire cohort and when stratified by AR status. As opposed to current guidance advising the discontinuation of intranasal and/or inhaled corticosteroids while assessing EoE-related outcomes, our data suggest that this recommendation may not be necessary. This finding has important clinical indications as halting medication use can result in increased burden of disease and decreased quality of life. However, in cases where they may be a diagnostic dilemma (e.g. clinically suspected EoE but normal endoscopy/biopsy in a patient on an inhaled or intranasal steroid), repeat endoscopy with discontinuation of the medications could be considered. Lastly, within the AR cohort, follow-up endoscopies performed in the spring months showed higher absolute eosinophil counts as compared to the other seasons. Given that spring in North Carolina is the season in which pollen is most prevalent, this finding could suggest that the increased eosinophil count is due to inhaled or ingested aeroallergens.30 This has important clinical implications, as physicians should be aware that patients with AR may have spurious results in the spring and a consideration may be made to postpone or repeat the follow-up procedure, though exact timing should depend on local seasons and pollen exposures.
This study has several strengths. We used a large, well-described cohort of both adults and children with EoE and established strict and uniform criteria for inclusion. We evaluated histologic, endoscopic, and symptomatic data as well as medication use and seasonal variation, which are currently lacking in the literature. There are also limitations. We utilized a retrospective design and therefore had to rely on preexisting records that were occasionally incomplete. We had to rely on the diagnosis of AR based on medical record documentation and could not administer allergen testing ourselves. Similarly, we did not always have specific aeroallergen information for those with AR and therefore could not correlate specific exposures to outcomes. Patient reported outcomes are not frequently measured at our institution. Adherence to treatment was not strictly assessed, though we expect that non-adherence affected all groups similarly. We also only included patients treated with tCS, which could reduce generalizability or lead to selection bias. Lastly, we were not able to assess outcomes by dose of intranasal and/or inhaled corticosteroid.
In conclusion, we found that EoE patients with concurrent AR did not differ at baseline nor following treatment with tCS compared to EoE patients without AR. Moreover, we found that concurrent intranasal and/or inhaled corticosteroid treatment did not impact treatment outcomes in patients with EoE treated with tCS. Of interest, patients with AR did have a higher absolute eosinophil count when assessed for treatment response in the spring, suggesting the impact of aeroallergens on outcomes. These data support that intranasal and/or inhaled corticosteroids should not be withheld during assessment of EoE-related disease activity. Moreover, at least for our area, some consideration should be given to postponing disease activity assessment during the spring season in EoE patients with AR.
Funding support:
This project was supported in part by a summer research grant (NIH T35 DK007386) for medical students presented by the University of North Carolina Medical Student Summer Research Program (CMSRP).
Disclosures/Conflict of Interest:
Dr. Dellon reports research funding from: Adare/Ellodi, Allakos, Arena/Pfizer, AstraZeneca, Celldex, Dr. Falk Pharma, Eupraxia, Ferring, GSK, Meritage, Miraca, Nutricia, Celgene/Receptos/BMS, Phantom, Regeneron, Revolo, Sanofi, Shire/Takeda, Uniquity; consulting fees from: Abbvie, Adare/Ellodi, Alfasigma, ALK, Allakos, Amgen, Anaptysbio, Apogee, Apollo, Aqilion, Arena/Pfizer, AstraZeneca, Bethanamist, Biocryst, Bryn, Calypso, Celgene/Receptos/BMS, Celldex, Cyted, Domain, EsoCap, Eupraxia, Dr. Falk Pharma, Ferring, GI Reviewers, GSK, Holoclara, Invea, Knightpoint, LucidDx, Nexstone Immunology/Uniquity, Nutricia, Parexel/Calyx, Phathom, Regeneron, Revolo, Robarts/Alimentiv, Roivant, Sanofi, Shire/Takeda, Target RWE, Third Harmonic Bio, Upstream Bio; and educational grants from: Allakos, Aqilion, Holoclara, Invea. Dr. Reed reports consulting fees from AstraZeneca and GI Reviewers. Ms. Barnes has no disclosures.
Abbreviations/Acronyms:
- EoE
eosinophilic esophagitis
- eos/hpf
eosinophils per high-power field
- tCS
topical corticosteroids
- AR
allergic rhinitis
- UNC
University of North Carolina
- EREFS
eosinophilic esophagitis endoscopic reference score
- ESS
endoscopic severity score
Footnotes
Clinical trial registration: not applicable
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