S3797 Silent Swarms: Incidental Discovery of Eosinophilic Colitis in an Asymptomatic Adult

Introduction: Eosinophilic colitis (EC), the rarest form of eosinophilic gastrointestinal disorders (EGIDs), is defined by eosinophilic infiltration of the colon without secondary causes such as infections, drugs, or systemic diseases. Presentations range from abdominal pain and diarrhea to incidental findings in asymptomatic patients. Diagnosis remains challenging due to lack of standardized criteria and overlap with other GI diseases. Case Description/Methods: A 69-year-old man with diabetes, hypothyroidism, hypertension, and treated hepatitis C underwent screening colonoscopy. He reported no gastrointestinal symptoms. Labs revealed mild eosinophilia. He denied recent medication changes, allergic history, or travel outside Puerto Rico months earlier. Random colon biopsies showed >100 eosinophils per high-power field, cryptitis, crypt abscesses, and no granulomas. WBC was 6.6, with an eosinophil count of 0.4 × 10³/μL (6.1%). Liver enzymes and stool parasite studies were unremarkable. With no identifiable secondary cause, a diagnosis of idiopathic EC was made. As he remained asymptomatic, corticosteroid therapy was deferred, and he was advised close follow-up. Discussion: Eosinophilic gastrointestinal disorders are categorized by anatomical location: esophagus, stomach, small bowel, colon, and by histologic layer involved: mucosal, muscular, or serosal. EC has the lowest prevalence (∼3/100,000). Mucosal disease causes malabsorption and diarrhea; muscular forms may lead to obstruction; serosal involvement can result in eosinophilic ascites. Our patient had mucosal EC without symptoms, an underrecognized subset. Histologic criteria (>65 eos/HPF) are widely used despite regional variability, with >100 eos/HPF being highly suggestive. Diagnosis requires exclusion of inflammatory bowel disease, parasitic infections, drug-induced colitis, and systemic eosinophilic syndromes. Endoscopic findings are nonspecific; thus, multisite biopsies are critical for diagnosis. Therapy is individualized due to limited data. Dietary elimination and corticosteroids (e.g., budesonide or prednisone) are commonly used. Emerging biologics like benralizumab and dupilumab show promise in targeting eosinophilic inflammation, though data remain limited. About 33% of patients experience acute flares, while 66% exhibit chronic persistence. Long-term surveillance is not standardized; however, close clinical monitoring is essential, especially in asymptomatic cases like ours, to detect disease progression and guide management.

Authors

Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001142648.53829.79
Primary Topic
Eosinophilic Esophagitis
Type
article
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article

S3797 Silent Swarms: Incidental Discovery of Eosinophilic Colitis in an Asymptomatic Adult

M Housam Nanah, Muhammad Naim Abdullah, Abdullah Hafeez, Omar Alkasabrah et al.
The American Journal of Gastroenterology
Eosinophilic Esophagitis
article

S3797 Silent Swarms: Incidental Discovery of Eosinophilic Colitis in an Asymptomatic Adult

M Housam Nanah, Muhammad Naim Abdullah, Abdullah Hafeez, Omar Alkasabrah, Sadia Rekhum, Faiza Jajja
article en

Abstract

Introduction: Eosinophilic colitis (EC), the rarest form of eosinophilic gastrointestinal disorders (EGIDs), is defined by eosinophilic infiltration of the colon without secondary causes such as infections, drugs, or systemic diseases. Presentations range from abdominal pain and diarrhea to incidental findings in asymptomatic patients. Diagnosis remains challenging due to lack of standardized criteria and overlap with other GI diseases. Case Description/Methods: A 69-year-old man with diabetes, hypothyroidism, hypertension, and treated hepatitis C underwent screening colonoscopy. He reported no gastrointestinal symptoms. Labs revealed mild eosinophilia. He denied recent medication changes, allergic history, or travel outside Puerto Rico months earlier. Random colon biopsies showed >100 eosinophils per high-power field, cryptitis, crypt abscesses, and no granulomas. WBC was 6.6, with an eosinophil count of 0.4 × 10³/μL (6.1%). Liver enzymes and stool parasite studies were unremarkable. With no identifiable secondary cause, a diagnosis of idiopathic EC was made. As he remained asymptomatic, corticosteroid therapy was deferred, and he was advised close follow-up. Discussion: Eosinophilic gastrointestinal disorders are categorized by anatomical location: esophagus, stomach, small bowel, colon, and by histologic layer involved: mucosal, muscular, or serosal. EC has the lowest prevalence (∼3/100,000). Mucosal disease causes malabsorption and diarrhea; muscular forms may lead to obstruction; serosal involvement can result in eosinophilic ascites. Our patient had mucosal EC without symptoms, an underrecognized subset. Histologic criteria (>65 eos/HPF) are widely used despite regional variability, with >100 eos/HPF being highly suggestive. Diagnosis requires exclusion of inflammatory bowel disease, parasitic infections, drug-induced colitis, and systemic eosinophilic syndromes. Endoscopic findings are nonspecific; thus, multisite biopsies are critical for diagnosis. Therapy is individualized due to limited data. Dietary elimination and corticosteroids (e.g., budesonide or prednisone) are commonly used. Emerging biologics like benralizumab and dupilumab show promise in targeting eosinophilic inflammation, though data remain limited. About 33% of patients experience acute flares, while 66% exhibit chronic persistence. Long-term surveillance is not standardized; however, close clinical monitoring is essential, especially in asymptomatic cases like ours, to detect disease progression and guide management.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 52%
Eosinophilic Esophagitis
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