Gastroenterologists' Assessment of EoE in Adults
A total of 162 adult EoE patients treated by six gastroenterologists (5 males, median age 46 years, range 39–65) specializing in EoE (each treated >50 EoE patients and performed >1,000 EGDs) were included into the study. The data on nine and four patients were excluded because of incomplete PRO or histopathology information (basal layer enlargement could not be evaluated because of suboptimal sample orientation), respectively. The data on 149 (N=107 males, 71.8%) patients were complete and used for further analyses. Patient characteristics are illustrated in Table 1. Of these, 79 patients (53.0%) had EoE symptom onset of >5 years before being recruited into the study. The predominant symptoms experienced by EoE patients were trouble swallowing and thoracic pain when swallowing. In the past 7 days, 88 patients (59.1%) reported trouble swallowing. The episodes of trouble swallowing were mostly of short duration, with only five patients reporting that episodes of trouble swallowing lasted >5 min. Twenty-eight patients (18.8%) experienced pain when swallowing. Rhinoconjunctivitis, asthma, and food allergies were reported by 89 patients (59.7%), 53 patients (35.6%), and 44 patients (29.5%), respectively. Gastroesophageal reflux disease was diagnosed in 47 patients (31.5%). In the past 12 months, 87 patients had been treated for EoE with swallowed topical corticosteroids (N=63, 42.3%), hypoallergenic diets (N=18, 12.1%), and/or esophageal dilation (N=27, 18.1%), before their participation in this study.
The median PhysGA of EoE activity was 4 (interquartile range 2–6, range 0–10). The PatGA was lower with a median of 2 (interquartile range 1–4, range 0–10). A moderate positive correlation between PhysGA and PatGA (rho=0.442, P<0.001) was observed (Figure 1a). The Bland–Altman plot (Figure 1b) evaluates the agreement between PhysGA and PatGA. A mean difference of 1.77 between PhysGA and PatGA was observed. The upper and lower 95% limits of agreement were 6.77 and −3.23, respectively.
The frequency of EoE-associated endoscopic and histologic alterations in the proximal and distal esophagus, as well as in the esophagus "overall," are shown in Table 2. Stricture(s) were detected in esophagi of 52 patients (34.9%), whereas white exudates were detected in esophagi of 51 patients (34.2%). The distribution of median values of PhysGA over the different severity categories of EoE-associated endoscopic findings and esophageal peak eosinophil counts for esophagus "overall" is shown in Figure 2. An increasing severity of EoE-associated endoscopic findings and esophageal peak eosinophil counts was associated with an increase in the value of PhysGA (particularly for the most severe categories of these findings).
The contribution of endoscopic and histologic findings as well as symptoms, either alone or together, to PhysGA is shown in Table 3. The contribution of endoscopic findings alone to PhysGA is shown as model 1 (Table 3). In general, all endoscopic findings examined were associated with the PhysGA, and the association was stronger with increasing severity of a given finding. For example, the predicted PhysGA increased by 0.87 points if the endoscopists detected mild fixed rings as opposed to no rings at all, and by 1.66 and 3.57 points if the endoscopists detected moderate and severe fixed rings, respectively. The predicted PhysGA increased by another 1.30 points if strictures were present. The regression model with all five major EoE-associated endoscopic findings explained 53% (R=0.53) of variability in PhysGA. When data for proximal and distal parts of the esophagus were analyzed separately, similar results as for esophagus "overall" were obtained (results available from authors).
The contribution of histologic findings to PhysGA is shown as model 2 (Table 3). The predicted PhysGA increased by 1.44 points if the pathologists detected 21–100 eosinophils per HPF in a biopsy as opposed to 0–5 eosinophils per HPF, and by 1.87 points if the pathologists detected >100 eosinophils per HPF. The predicted PhysGA increased by another 1.14 points if eosinophilic microabscesses were detected. The regression model that took into account peak eosinophil counts, eosinophilic microabscesses, and basal layer enlargement explained 30% (R=0.30) of variability in PhysGA. When data for proximal and distal parts of the esophagus were analyzed separately, similar results as for esophagus "overall" were observed (results available from authors). In addition, a subgroup analysis of data on 86 patients, whose biopsies contained lamina propria that could be evaluated, was conducted. Addition of lamina propria fibrosis did not explain additional variability above and beyond that already explained by peak esophageal eosinophil counts and eosinophilic microabscesses (results available from authors).
The combination of endoscopic and histologic findings explained 62% of PhysGA variability (model 3 in Table 3).
Model 4 shows the contribution of EoE-associated symptoms and behavioral adaptations to living with dysphagia to the PhysGA (Table 3). The predicted PhysGA increased with increasing severity and frequency of patient-reported symptoms. Key symptoms and behavioral adaptations to dysphagia together explained 49% of the variability in PhysGA.
The combination of EoE-associated endoscopic and histologic findings and key patient-reported symptoms (items of the EEsAI PRO instrument) explained 75% of PhysGA. Thus, physicians base their judgment of EoE overall severity on EoE-associated endoscopic findings and symptoms and, to a lesser extent, on histologic findings.
Results
Patient and Physician Characteristics
A total of 162 adult EoE patients treated by six gastroenterologists (5 males, median age 46 years, range 39–65) specializing in EoE (each treated >50 EoE patients and performed >1,000 EGDs) were included into the study. The data on nine and four patients were excluded because of incomplete PRO or histopathology information (basal layer enlargement could not be evaluated because of suboptimal sample orientation), respectively. The data on 149 (N=107 males, 71.8%) patients were complete and used for further analyses. Patient characteristics are illustrated in Table 1. Of these, 79 patients (53.0%) had EoE symptom onset of >5 years before being recruited into the study. The predominant symptoms experienced by EoE patients were trouble swallowing and thoracic pain when swallowing. In the past 7 days, 88 patients (59.1%) reported trouble swallowing. The episodes of trouble swallowing were mostly of short duration, with only five patients reporting that episodes of trouble swallowing lasted >5 min. Twenty-eight patients (18.8%) experienced pain when swallowing. Rhinoconjunctivitis, asthma, and food allergies were reported by 89 patients (59.7%), 53 patients (35.6%), and 44 patients (29.5%), respectively. Gastroesophageal reflux disease was diagnosed in 47 patients (31.5%). In the past 12 months, 87 patients had been treated for EoE with swallowed topical corticosteroids (N=63, 42.3%), hypoallergenic diets (N=18, 12.1%), and/or esophageal dilation (N=27, 18.1%), before their participation in this study.
The Relationship Between Physician Global Assessment of EoE Activity and Patient Global Assessment of EoE Symptom Severity
The median PhysGA of EoE activity was 4 (interquartile range 2–6, range 0–10). The PatGA was lower with a median of 2 (interquartile range 1–4, range 0–10). A moderate positive correlation between PhysGA and PatGA (rho=0.442, P<0.001) was observed (Figure 1a). The Bland–Altman plot (Figure 1b) evaluates the agreement between PhysGA and PatGA. A mean difference of 1.77 between PhysGA and PatGA was observed. The upper and lower 95% limits of agreement were 6.77 and −3.23, respectively.
The Relationship Between Physician Global Assessment of EoE Activity and EoE-associated Endoscopic and Histologic Findings
The frequency of EoE-associated endoscopic and histologic alterations in the proximal and distal esophagus, as well as in the esophagus "overall," are shown in Table 2. Stricture(s) were detected in esophagi of 52 patients (34.9%), whereas white exudates were detected in esophagi of 51 patients (34.2%). The distribution of median values of PhysGA over the different severity categories of EoE-associated endoscopic findings and esophageal peak eosinophil counts for esophagus "overall" is shown in Figure 2. An increasing severity of EoE-associated endoscopic findings and esophageal peak eosinophil counts was associated with an increase in the value of PhysGA (particularly for the most severe categories of these findings).
Contribution of Endoscopy, Histology, and Symptoms to the Physician Global Assessment of EoE Activity
The contribution of endoscopic and histologic findings as well as symptoms, either alone or together, to PhysGA is shown in Table 3. The contribution of endoscopic findings alone to PhysGA is shown as model 1 (Table 3). In general, all endoscopic findings examined were associated with the PhysGA, and the association was stronger with increasing severity of a given finding. For example, the predicted PhysGA increased by 0.87 points if the endoscopists detected mild fixed rings as opposed to no rings at all, and by 1.66 and 3.57 points if the endoscopists detected moderate and severe fixed rings, respectively. The predicted PhysGA increased by another 1.30 points if strictures were present. The regression model with all five major EoE-associated endoscopic findings explained 53% (R=0.53) of variability in PhysGA. When data for proximal and distal parts of the esophagus were analyzed separately, similar results as for esophagus "overall" were obtained (results available from authors).
The contribution of histologic findings to PhysGA is shown as model 2 (Table 3). The predicted PhysGA increased by 1.44 points if the pathologists detected 21–100 eosinophils per HPF in a biopsy as opposed to 0–5 eosinophils per HPF, and by 1.87 points if the pathologists detected >100 eosinophils per HPF. The predicted PhysGA increased by another 1.14 points if eosinophilic microabscesses were detected. The regression model that took into account peak eosinophil counts, eosinophilic microabscesses, and basal layer enlargement explained 30% (R=0.30) of variability in PhysGA. When data for proximal and distal parts of the esophagus were analyzed separately, similar results as for esophagus "overall" were observed (results available from authors). In addition, a subgroup analysis of data on 86 patients, whose biopsies contained lamina propria that could be evaluated, was conducted. Addition of lamina propria fibrosis did not explain additional variability above and beyond that already explained by peak esophageal eosinophil counts and eosinophilic microabscesses (results available from authors).
The combination of endoscopic and histologic findings explained 62% of PhysGA variability (model 3 in Table 3).
Model 4 shows the contribution of EoE-associated symptoms and behavioral adaptations to living with dysphagia to the PhysGA (Table 3). The predicted PhysGA increased with increasing severity and frequency of patient-reported symptoms. Key symptoms and behavioral adaptations to dysphagia together explained 49% of the variability in PhysGA.
The combination of EoE-associated endoscopic and histologic findings and key patient-reported symptoms (items of the EEsAI PRO instrument) explained 75% of PhysGA. Thus, physicians base their judgment of EoE overall severity on EoE-associated endoscopic findings and symptoms and, to a lesser extent, on histologic findings.
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