Abstract
Background:
Esophageal food impaction (EFI) commonly occurs in eosinophilic esophagitis (EoE), but its spectrum of severity remains incompletely described.
Aims:
To determine whether presentation and outcomes of EoE differ based on type of EFI.
Methods:
Patients with newly diagnosed EoE were categorized by EFI type: those with transient symptoms, those with an emergency department (ED) visit but no esophagogastroduodenoscopy (EGD), and those with an ED visit and EGD. Patient, EoE, and treatment data were collected. We compared characteristics and treatment responses and used multinominal logistic regression to adjust for confounders.
Results:
Of 814 EFI patients with EoE, 485 had transient symptoms (symptoms-only), 76 required only an ED visit (ED-only), and 253 required an ED visit and EGD (ED+EGD). Compared to symptoms-only, ED-only and ED+EGD were more likely to have rings (67% and 70% vs 57%; p<0.001) and stricture (41% and 44% vs 35%; p=0.04). Topical corticosteroid (tCS) therapy led to histologic response (<15 eos/hpf) more commonly in the symptoms-only group, followed by ED+EGD and ED-only (61% vs 52% vs 34%; p=0.009). After tCS therapy, patients with only symptoms were less likely to have narrowing or require dilation. All EFI groups had similar responses to dietary therapy.
Conclusions:
In EoE patients, most EFI symptoms self-resolved. Patients requiring at least an ED visit had more fibrostenosis at baseline, less histologic response with tCS therapy, and more persistent fibrostenosis after tCS therapy. Patients with more severe EFI presentations warrant close monitoring and endoscopic management of fibrostenotic disease.
Keywords: Eosinophilic esophagitis, esophageal food impaction, topical corticosteroids, dietary therapy, fibrostenosis
Introduction
Eosinophilic esophagitis (EoE) is a chronic immune-mediated inflammatory disease of the esophagus that often presents with dysphagia and esophageal food impaction (EFI) [1,2]. EoE is now recognized as a leading cause of EFI, with approximately 50% of patients presenting for EFI emergency care receiving a subsequent EoE diagnosis [2–7]. The prevalence of EoE and frequency of EoE-associated emergency department (ED) visits have been increasing [8–10]. EFI events often require endoscopic removal, and adverse events such as esophageal injury and perforation can rarely occur [11–15]. EoE and associated EFI also impact patients’ mental health by contributing to maladaptive lifestyle and social changes such as hypervigilance when eating, anxiety, and reduced quality-of-life, and are correlated with increased rates of psychiatric comorbidity [16,17].
Despite this well-recognized burden and impact of EFI among patients with EoE, the spectrum of EoE-associated EFI presentation is unknown. Prior studies on EFI in EoE patients have not extensively described the severity of EoE-related food impactions or what proportion of patients who present for emergency care with EoE-attributable EFI require endoscopy [3,18,19]. Additionally, whether the EFI type and severity are related to demographics of affected patients, EoE disease characteristics, or efficacy of eventual EoE therapy is not known. A more thorough understanding of how patients with EFI due to EoE present and respond to therapy would inform how their management could be optimized.
The aims of this study were to determine the spectrum of EFI severity in EoE patients, the treatment these patients received, and whether presentation and outcomes of EoE differ based on the type and severity of EFI symptoms.
Methods
We identified a retrospective cohort of EoE patients who experienced EFI from the UNC EoE Clinicopathologic Database (spanning 2001 to 2024 for this analysis), which has been described previously [20–24]. Participants included patients of any age who were newly diagnosed with EoE by consensus guidelines at UNC, and who experienced an EFI as notated in their medical chart [25]. Patients diagnosed prior to 2018 were PPI non-responsive, but patients diagnosed in 2018 or thereafter did not require a trial of PPI for diagnosis. Data relating to patient demographics, EoE symptoms, medical and procedural treatments, endoscopic findings, pathologic data, and treatment response were collected. Symptom length prior to diagnosis was calculated as the time difference between when a patient reported first experiencing symptoms and when EoE was diagnosed on endoscopy. Specific data related to any EFI-related symptoms, ED visits attributable to EFI, or esophagogastroduodenoscopy (EGD) performed for EFI were also collected. For patients treated with topical corticosteroids (tCS) or dietary therapy, histologic response (<15 eos/hpf) [26–28], global symptomatic response (as reported by the patient in the chart), endoscopic response (as reported by the endoscopist), EoE Endoscopic Reference Score (EREFS; range 0–9; available for patients after its initial description in 2013) [29], and an endoscopic severity score (ESS; range 0–5, calculated as present/absent for exudates, rings, edema, furrows, and stricture; available for all patients) were obtained [30,31].
Patients were categorized into three groups based on type and severity of EFI: those with transient symptoms who cleared the EFI without ED visit (“symptoms-only”), those with an ED visit but no EGD who cleared the EFI without endoscopic procedural intervention (“ED-only”), and those with an ED visit and EGD for endoscopic removal of food bolus impaction performed during that same ED visit (“ED+EGD”). Since it is likely that most patients with the more severe presentations (ED-only or ED+EGD) had previously experienced less severe transient symptoms (symptoms-only), patients were classified based on their most severe EFI-related presentation with the understanding they may have had prior symptoms or presentations that were less severe, though these data were not extracted. Outcomes of interest included proportional breakdown of EFI types in EoE patients, the baseline clinical characteristics by EFI type, and treatment response to tCS or dietary therapy by EFI type. For treatment at our center, patients decide on medications or diet using a shared decision-making approach [32]. Patients opting for topical steroids are treated with either oral viscous budesonide 1–2mg/day or fluticasone swallowed from an inhaler 440–1760mcg/day, with dose determined by the provider based on patient age and size; no patients in this study had received budesonide oral suspension [23,24,30]. Diet therapy is generally with an empiric elimination diet, with the level of restriction based on patient preference, though some patients did have prior targeted (allergy test-directed) diet elimination [33]. Post-treatment endoscopy with biopsy was typically performed after 8–12 weeks of tCS, and after 6–8 weeks of diet elimination [25].
After stratifying patients into the three groups noted above (symptoms-only, ED-only, and ED+EGD), we compared demographics, EoE characteristics, and treatment responses between EFI groups in a bivariate analysis. Proportions were compared with chi squared. Means were compared with one-way ANOVA. We then used multinominal logistic regression to adjust for potential confounders and assess for independent predictors of EFI type, using the symptoms-only group as the referent. Data on treatment outcomes following tCS and diet therapy were analyzed separately. Stata version 12 (College Station, TX) was used to perform all statistical analyses. The University of North Carolina Institutional Review Board approved this study.
Results
Baseline characteristics by EFI type
Of 1460 patients in the database, we identified 814 patients with EoE who experienced EFI. Of those, 485 (60%) had transient symptoms (symptoms-only), 76 (9%) required an ED visit only (ED-only), and 253 (31%) required an ED visit and EGD (ED+EGD) (Table 1). In the overall EFI cohort, 67% were male, 90% were white, and 24% were under the age of 18 years old.
Table 1:
Baseline characteristics by EFI type (symptoms only, ED only, ED + EGD)
| EFI symptoms only (n = 485) |
EFI with ED visit only (n = 76) |
EFI with ED visit and EGD (n = 253) |
p | |
|---|---|---|---|---|
| Age at diagnosis (mean yrs ± SD) | 33.1 ± 18.2 | 31.7 ± 18.0 | 35.1 ± 16.3 | 0.21 |
| Children <18 years (n, %) | 122 (25) | 21 (28) | 53 (21) | 0.34 |
| Male (n, %) | 306 (63) | 54 (71) | 184 (73) | 0.02 |
| White (n, %) | 434 (90) | 68 (89) | 231 (93) | 0.44 |
| BMI (mean kg/m2 ± SD) | 25.2 ± 6.6 | 24.9 ± 5.5 | 27.5 ± 7.2 | < 0.001 |
| Any atopic condition (n, %) | 282 (60) | 40 (56) | 141 (54) | 0.30 |
| Allergic rhinitis | 206 (43) | 31 (42) | 98 (40) | 0.74 |
| Asthma | 119 (25) | 19 (26) | 62 (25) | 0.97 |
| Eczema | 57 (12) | 9 (12) | 22 (9) | 0.42 |
| Food allergy | 130 (28) | 15 (21) | 52 (22) | 0.15 |
| Family history of EoE or EGID* | 14 (3) | 1 (1) | 4 (2) | 0.46 |
| Any psychiatric diagnosis* | 150 (34) | 23 (34) | 62 (27) | 0.18 |
| Symptom length prior to diagnosis (mean years ± SD) | 8.0 ± 8.7 | 8.7 ± 8.8 | 8.1 ± 9.7 | 0.85 |
| Symptoms (n, %) | ||||
| Dysphagia | 438 (91) | 71 (95) | 222 (88) | 0.21 |
| Heartburn | 189 (40) | 24 (33) | 51 (21) | < 0.001 |
| Chest pain | 61 (13) | 11 (15) | 25 (10) | 0.45 |
| Abdominal pain | 73 (15) | 8 (11) | 12 (5) | < 0.001 |
| Nausea | 35 (7) | 6 (8) | 14 (6) | 0.64 |
| Vomiting | 101 (21) | 12 (16) | 37 (15) | 0.11 |
| Failure to thrive | 17 (4) | 1 (1) | 3 (1) | 0.13 |
| Endoscopic findings (n, %) | ||||
| Exudates | 233 (48) | 37 (49) | 104 (42) | 0.21 |
| Rings | 275 (57) | 50 (67) | 175 (70) | 0.001 |
| Edema | 218 (45) | 38 (51) | 121 (48) | 0.51 |
| Furrows | 349 (72) | 58 (77) | 184 (74) | 0.60 |
| Stricture | 168 (35) | 31 (41) | 110 (44) | 0.04 |
| Narrowing | 97 (20) | 19 (25) | 66 (26) | 0.12 |
| Crepe-paper mucosa | 10 (20) | 4 (5) | 15 (6) | 0.02 |
| Dilation | 182 (38) | 33 (44) | 89 (36) | 0.45 |
| Total EREFS (mean ± SD)** | 3.9 ± 1.9 | 4.0 ± 2.2 | 4.2 ± 1.7 | 0.43 |
| Total ESS (mean ± SD)** | 2.6 ± 1.6 | 2.9 ± 1.5 | 2.8 ± 1.4 | 0.10 |
| Peak eosinophil count (mean eos/hpf ± SD) | 64.7 ± 42.8 | 69.9 ± 48.3 | 63.0 ± 44.4 | 0.49 |
data available for family history for n=441, 68, 228; for psychiatric diagnosis, n=439, 68, 228
EREFS data available for n=272, 42, 137; ESS = endoscopic severity score, for which all data available
On comparison to symptoms only and ED only groups, patients with ED+EGD were more likely to be male (73% vs 63% and 71%; p=0.02) and higher BMI (27.5 vs 25.2 and 24.9; p<0.001) (Table 1). However, the three groups of EFI type were otherwise largely similar at baseline, with no major differences in clinical characteristics such as age at diagnosis, atopic conditions, family history of eosinophilic gastrointestinal disease, or symptom length prior to diagnosis.
When EoE symptoms were compared, patients in the ED+EGD group were less likely to report heartburn when compared to the symptoms-only and ED-only groups (21% vs 40% and 33%; p<0.001) or abdominal pain (5% vs 15% and 11%; p<0.001) (Table 1). Other symptoms were similar across groups. Endoscopically, the ED-only and ED+EGD groups were more likely to have rings (67% and 70% vs 50%; p<0.001) and stricture (41% and 44% vs 35%; p=0.04) when compared to the symptoms-only group. There was also a trend in the ED-only and ED+EGD towards higher EREFS and ESS that did not reach statistical significance.
On multinomial logistic regression, higher BMI (B=0.05; 95% CI: 0.03–0.08), less heartburn (B=−0.73; 95% CI: −1.12, −0.34) and less abdominal pain (B=−1.07; 95% CI: −1.79, −0.34) were independently associated with ED+EGD as compared to symptoms-only; there were no independent predictors of ED only compared to symptoms only.
Treatment response to topical steroids by EFI type
A total of 358 (44%) patients identified with EFI had data on tCS use and endoscopic follow-up of tCS treatment response (Table 2). After tCS therapy, histologic response (<15 eos/hpf) was most common in the symptoms-only group, followed by the ED+EGD and ED-only groups (61% vs 52% vs 34%; p=0.009) (Table 2). When compared to the ED-only and ED+EGD groups, the symptoms-only group was less likely to have narrowing (18% vs 35% and 27%; p=0.04) or undergo dilation (35% vs 56% and 43%; p=0.04) at time of follow-up endoscopy to assess tCS treatment response. Other endoscopic findings were similar between groups, though the symptoms-only group had numerically lower EREFS and ESS scores.
Table 2:
Treatment response to tCS by EFI type (symptoms only, ED only, ED + EGD)
| EFI symptoms only (n = 219) |
EFI with ER visit only (n = 35) |
EFI with ER visit and EGD (n = 104) |
p | |
|---|---|---|---|---|
| Type of steroid used (n, %) | 0.78 | |||
| Fluticasone | 72 (33) | 10 (29) | 28 (27) | |
| Budesonide | 147 (67) | 25 (71) | 76 (73) | |
| Mean steroid dose (mcg ± SD) | 1793 ± 637 | 1939 ± 1056 | 1772 ± 647 | |
| Post-treatment peak eosinophil count (mean eos/hpf ± SD) | 21.7 ± 30.8 | 46.7 ± 60.0 | 31.9 ± 47.6 | 0.001 |
| p value vs baseline | < 0.001 | 0.02 | < 0.001 | |
| Histologic response (n, %) | ||||
| <15 eos/hpf | 133 (61) | 12 (34) | 54 (52) | 0.009 |
| ≤6 eos/hpf | 113 (52) | 11 (31) | 49 (47) | 0.08 |
| <1 eos/hpf | 63 (29) | 4 (11) | 26 (25) | 0.09 |
| Global symptom response (n, %)* | 60 (79) | 10 (67) | 24 (75) | 0.58 |
| Post-treatment endoscopic findings (n, %) | ||||
| Normal | 46 (21) | 2 (6) | 8 (7) | 0.002 |
| Exudates | 57 (27) | 9 (26) | 24 (24) | 0.86 |
| Rings | 111 (51) | 21 (62) | 59 (58) | 0.37 |
| Edema | 55 (26) | 15 (44) | 32 (32) | 0.07 |
| Furrows | 97 (45) | 19 (56) | 53 (53) | 0.29 |
| Stricture | 78 (36) | 17 (50) | 47 (47) | 0.10 |
| Narrowing | 40 (18) | 12 (35) | 27 (27) | 0.04 |
| Crepe-paper mucosa | 0 (0) | 1 (3) | 3 (3) | 0.04 |
| Dilation | 75 (35) | 19 (56) | 43 (43) | 0.04 |
| Candida | 22 (10) | 2 (6) | 5 (5) | 0.25 |
| Endoscopic response (n, %) | 156 (72) | 24 (69) | 71 (69) | 0.86 |
| Post-treatment endoscopic severity (mean scores ± SD) | ||||
| EREFS** | 2.4 ± 2.0 | 2.8 ± 2.2 | 2.6 ± 1.8 | 0.51 |
| p value vs baseline | < 0.001 | 0.001 | < 0.001 | |
| ESS | 1.9 ± 1.5 | 2.4 ± 1.5 | 2.1 ± 1.3 | 0.08 |
| p value vs baseline | < 0.001 | 0.002 | < 0.001 |
available for n=76, 15, and 32
available for n=115, 143, and 38
Treatment response to dietary therapy by EFI type
In the overall EFI cohort, 192 (24%) patients had available data on dietary therapy for EoE and endoscopic follow-up to assess for treatment efficacy (Table 3). There were no differences observed between EFI groups and type of dietary therapy utilized. Empiric dietary therapy was the most common type of dietary therapy used across all EFI groups. All EFI groups largely had similar histologic and endoscopic responses to diet therapy (Table 3). The symptoms-only group was less likely to have edema on endoscopy compared to the ED-only and ED+EGD groups (23% vs 45% and 41%; p=0.03).
Table 3:
Treatment response to dietary elimination by EFI type (symptoms only, ED only, ED + EGD)
| EFI symptoms only (n = 137) |
EFI with ER visit only (n = 11) |
EFI with ER visit and EGD (n = 44) |
p | |
|---|---|---|---|---|
| Type of diet (n, %)† | ||||
| Targeted | 28 (20) | 2 (18) | 9 (20) | 0.98 |
| Empiric | 91 (66) | 6 (55) | 28 (64) | 0.71 |
| Elemental | 4 (3) | 0 (00) | 0 (0) | -- |
| Post-treatment peak eosinophil count (mean eos/hpf ± SD) | 40.6 ± 51.1 | 49.3 ± 66.1 | 50.6 ± 57.5 | 0.52 |
| p value vs baseline | < 0.001 | 0.30 | 0.01 | |
| Histologic response (n, %) | ||||
| <15 eos/hpf | 56 (41) | 4 (36) | 17 (39) | 0.93 |
| ≤6 eos/hpf | 47 (34) | 3 (27) | 13 (30) | 0.78 |
| <1 eos/hpf | 22 (16) | 0 (0) | 6 (14) | 0.34 |
| Global symptom response (n, %)* | 82 (64) | 6 (60) | 23 (59) | 0.83 |
| Post-treatment endoscopic findings (n, %) | ||||
| Normal | 28 (20) | 0 (0) | 4 (9) | 0.07 |
| Exudates | 54 (39) | 3 (27) | 18 (41) | 0.70 |
| Rings | 74 (54) | 7 (64) | 29 (66) | 0.35 |
| Edema | 31 (23) | 5 (45) | 18 (41) | 0.03 |
| Furrows | 72 (53) | 8 (73) | 28 (64) | 0.23 |
| Stricture | 52 (38) | 5 (45) | 21 (48) | 0.49 |
| Narrowing | 31 (23) | 4 (46) | 16 (36) | 0.15 |
| Crepe-paper mucosa | 2 (1) | 0 (0) | 0 (0) | 0.67 |
| Dilation | 54 (39) | 5 (45) | 18 (41) | 0.92 |
| Endoscopic response (n, %)* | 58 (66) | 8 (73) | 24 (69) | 0.88 |
| Post-treatment endoscopic severity (mean scores ± SD) | ||||
| EREFS** | 2.6 ± 2.1 | 3.5 ± 2.4 | 3.3 ± 3.3 | 0.17 |
| p value vs baseline | < 0.001 | 0.43 | 0.38 | |
| ESS | 2.1 ± 1.6 | 2.5 ± 1.6 | 2.6 ± 1.6 | 0.12 |
| p value vs baseline | < 0.001 | 0.21 | 0.51 |
diet type unknown for 14, 3, and 7
available for n=128, 10, and 39 for symptoms and 88, 11, and 35 for endoscopy
available for n=127, 10, and 38
Discussion
Despite EoE being a leading cause of EFI, little is known about the spectrum of food impaction severity in patients with EoE, and whether differences in disease characteristics and treatment response exist between EoE patients who experience different EFI types. In this study, we found that most EFI symptoms in EoE patients are self-resolving, but that the majority of EoE patients who present to the ED with EFI symptoms will ultimately undergo an EGD. While most baseline characteristics are similar between EFI types, those patients requiring at least an ED visit have more fibrostenotic disease and are less likely to have histologic response with tCS therapy.
The gaps in our understanding of EFI in EoE are at least partially related to how prior studies have defined EFI. Most studies on EFI have included all patients presenting with EFI regardless of etiology and almost exclusively focused on cases of EFI that required endoscopic intervention to clear the food bolus [2–7,11–15]. We focused on EFI among a cohort of EoE patients, broadened the definition to include those with transient EFI symptoms or symptoms that resolved prior to EGD, and categorized patients into specific EFI types. Using this approach, we found that almost two-thirds of EoE patients who experience impaction symptoms do not seek or reach emergency care before symptoms resolve, and that one in ten seek care but do not require EGD before passing their obstruction. Esophageal biopsies are already underperformed in patients with EFI who undergo endoscopy [34,35], therefore, patients who do not present for emergent medical care or do present but do not undergo EGD at that time are potentially at high risk of being lost to follow-up and not receiving biopsies in a timely manner. In a study of 950 EoE patients that assessed for reported history of impaction symptoms in addition to EFI with documented EGD, Leigh and colleagues reported that ~38% of patients with some history of impaction had required endoscopic removal, meaning that other 62% of patients with EFI symptoms had not undergone EGD [36], rates that our similar to what we report. In another study of 721 EoE patients with a higher proportion of EFI patients requiring endoscopy, about half of those with symptoms of food impaction did not have endoscopic intervention [19]. Taken together, these results indicate that the burden of EFI symptoms may be greater than previously appreciated because most prior studies did not capture patients who did not require EGD. Indeed, these findings may help explain recent epidemiologic data showing that there were more than 700,000 ED visits for esophageal symptoms in males younger than 40 without an EoE diagnosis [8]. Future studies may benefit from using the terminology from the current study to report more detailed results of patients with EFI.
By categorizing EFI presentations by severity, we were also able to compare sub-populations of EoE patients. Patients with EFI requiring an endoscopy were more likely to be male, have a higher BMI, and have endoscopic findings of rings and strictures. They were also less likely to experience heartburn or abdominal pain. Patients with heartburn or abdominal pain may have a more inflammatory rather than fibrostenotic predominant disease phenotype, which could lead to more transient sensations of food impaction due to esophageal inflammation and edema. The higher burden of fibrostenotic disease among those with more severe EFI was expected, as these features are likely the primary driver of EFI, and there is data showing that these patients are at increased risk of EFI [18,19,37].
The relationship between EFI severity and EoE treatment response has not been previously studied, but successful EoE treatment is crucial in preventing future EFI [37,38]. In those treated with tCS in our study, the chance of histologic response decreased as the severity of EFI presentation increased. Whereas over 60% of patients in the symptoms-only group had histologic response, only one-third of patients requiring endoscopy responded. Though less dramatic, there were also differences in endoscopic response, with those in the symptoms-only group being less likely to have narrowing or require dilation at follow-up. These findings align with recent evidence showing a lower likelihood of response to tCS with more severe baseline disease (graded by the Index of Severity for Eosinophilic Esophagitis (I-SEE), which incorporates history of food impaction) [23], as well as with data showing fibrostenotic disease may be more treatment refractory [39,40]. In contrast, the histologic and endoscopic response to dietary therapy was similar regardless of EFI severity. While tCS and dietary therapy treatment outcomes were not compared directly, we observed that endoscopic response was similar between groups, whereas those treated with tCS therapy were more likely than those treated with diet therapy to have histologic and symptom response. These results could inform how clinicians understand and communicate the likelihood of response based on initial severity of EFI presentation to patients.
There are several limitations to this study. Our findings represent data from a retrospective cohort of patients at a single institution. That said, all patients were newly diagnosed with EoE (rather than referred as complex prevalent cases) and are overall reflective of the general EoE population. EFI in other patients from the database, or different types of EFI in the included patients, may have occurred at institutions that do not share the same electronic medical record, and these data may not have been captured in our analysis. The smaller sample size for certain cohort subgroups, particularly the ED-only group who went on to receive dietary therapy, may limit what conclusions can be drawn about those subgroups. However, large treatment sample sizes for both tCS and dietary therapy were available for analysis for the other EFI groups. Due to the retrospective study design, EFI events were defined by clinician documentation rather than a standardized definition and the exact timing and number of EFI events prior to diagnosis could not obtained. There was not enough available information to include data on the following: accommodating or compensatory behaviors while eating, the proportions of patients in the ED+EGD group who were diagnosed at the time of EFI event or who required endoscopic removal of food bolus, esophageal stricture diameter, treatment response to PPI therapy, or the number of patients who were lost to follow-up after their initial diagnosis. This study also had strengths. To our knowledge, it is the first to stratify EoE patients by EFI severity. Further, we were able to leverage a large patient database to compare these specific groups of patients with high levels of granularity for both baseline characteristics and treatment outcomes.
In conclusion, categorizing patients by severity and type of EFI in EoE allows observations about how these patients differ in their disease presentation and treatment response. Since most EoE-related EFI symptoms are transient and self-resolving, further research could aim to identify predictors of those who ultimately require emergent care. EFI patients who require at least an ED visit have more fibrostenotic disease and are overall less responsive to tCS. Such findings can help inform prognosis and management approach, particularly as suboptimally managed patients can further progress to fibrostenosis and successful treatment is associated with decreased future EFI risk.
Financial support:
This study was supported by T32 DK007634 and NIH T35 DK007386.
Disclosures:
Dr. Dellon is a consultant for Abbott, Abbvie, Adare/Ellodi, Aimmune, Akesobio, Alfasigma, ALK, Allakos, Amgen, Apogee, Apollo, Aqilion, Arena/Pfizer, Aslan, AstraZeneca, Avir, Biorasi, Bryn, Calypso, Celgene/Receptos/BMS, Celldex, Eli Lilly, EsoCap, Eupraxia, Dr. Falk Pharma, Ferring, GSK, Gossamer Bio, Holoclara, Invea, Knightpoint, Landos, LucidDx, Morphic, Nexstone Immunology/Uniquity, Nutricia, Parexel/Calyx, Phathom, Regeneron, Revolo, Robarts/Alimentiv, Salix, Sanofi, Shire/Takeda, Target RWE, Third Harmonic Bio, Upstream Bio; receives research funding from Adare/Ellodi, Allakos, Arena/Pfizer, AstraZeneca, Celldex, Eupraxia, Ferring, GSK, Meritage, Miraca, Nutricia, Celgene/Receptos/BMS, Regeneron, Revolo, Shire/Takeda; and has received an educational grant from Allakos, Aqilion, Holoclara, Invea. Dr. Redd is a consultant for Sanofi. None of the other authors report any potential conflicts of interest with this study.
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