S6106 Terminal Ileal Stricture Due To NSAID Enteropathy Mimicking Crohn’s Disease: A Diagnostic Dilemma

Introduction: nonsteroidal anti-inflammatory drug-induced enteropathy is a lesser-known cause of terminal ileitis and strictures and can closely mimic Crohn’s disease in clinical presentation, imaging, and endoscopic findings. Differentiating between the 2 is essential to avoid unnecessary immunosuppression or surgical intervention. Case Description/Methods: A 65-year-old man presented with epigastric pain, hematochezia, and unintentional weight loss. Contrast-enhanced computed tomography abdomen revealed a markedly abnormal 16 cm segment of thickened terminal ileum with adjacent mesenteric fat stranding, prominent lymph nodes, and regional vascular engorgement. These findings were strongly suggestive of active Crohn’s disease and led to a high index of suspicion for inflammatory bowel disease. Differential diagnoses included small bowel lymphoma or infectious ileitis; the elongated segment length made nonsteroidal anti-inflammatory drug enteropathy less likely based on typical imaging patterns. Colonoscopy showed ulceration and a moderate stricture in the terminal ileum. Initial biopsies revealed only focal acute inflammation without chronic architectural distortion or granulomas. Fecal calprotectin levels were elevated (rising from 418 to 1080), reinforcing concern for active intestinal inflammation. However, repeat endoscopic biopsies again lacked features of chronic inflammatory bowel disease. Following complete cessation of nonsteroidal anti-inflammatory drugs, the patient experienced significant clinical improvement, including 30-lb weight gain and resolution of gastrointestinal symptoms. Histologic re-review by a tertiary center supported nonsteroidal anti-inflammatory drug-induced ileitis as the sole diagnosis. Discussion: This case underscores the diagnostic challenge posed by nonsteroidal anti-inflammatory drug enteropathy when imaging mimics Crohn’s disease. The computed tomography scan findings—long-segment terminal ileal thickening, mesenteric fat stranding, reactive lymphadenopathy, and vascular engorgement—are classic for active Crohn’s and atypical for nonsteroidal anti-inflammatory drug injury, which is usually limited and less hyperemic. Elevated calprotectin further complicated the picture. Ultimately, the absence of histologic chronicity, full clinical remission after nonsteroidal anti-inflammatory drug withdrawal, and specialist review helped establish the correct diagnosis. This case highlights the need for cautious interpretation of radiologic and biochemical data, and emphasizes the importance of longitudinal clinical correlation in patients with ileal disease.

Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001152884.57789.3a
Primary Topic
Inflammatory mediators and NSAID effects
Type
article
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article

S6106 Terminal Ileal Stricture Due To NSAID Enteropathy Mimicking Crohn’s Disease: A Diagnostic Dilemma

The American Journal of Gastroenterology
Inflammatory mediators and NSAID effects
article

S6106 Terminal Ileal Stricture Due To NSAID Enteropathy Mimicking Crohn’s Disease: A Diagnostic Dilemma

article en

Abstract

Introduction: nonsteroidal anti-inflammatory drug-induced enteropathy is a lesser-known cause of terminal ileitis and strictures and can closely mimic Crohn’s disease in clinical presentation, imaging, and endoscopic findings. Differentiating between the 2 is essential to avoid unnecessary immunosuppression or surgical intervention. Case Description/Methods: A 65-year-old man presented with epigastric pain, hematochezia, and unintentional weight loss. Contrast-enhanced computed tomography abdomen revealed a markedly abnormal 16 cm segment of thickened terminal ileum with adjacent mesenteric fat stranding, prominent lymph nodes, and regional vascular engorgement. These findings were strongly suggestive of active Crohn’s disease and led to a high index of suspicion for inflammatory bowel disease. Differential diagnoses included small bowel lymphoma or infectious ileitis; the elongated segment length made nonsteroidal anti-inflammatory drug enteropathy less likely based on typical imaging patterns. Colonoscopy showed ulceration and a moderate stricture in the terminal ileum. Initial biopsies revealed only focal acute inflammation without chronic architectural distortion or granulomas. Fecal calprotectin levels were elevated (rising from 418 to 1080), reinforcing concern for active intestinal inflammation. However, repeat endoscopic biopsies again lacked features of chronic inflammatory bowel disease. Following complete cessation of nonsteroidal anti-inflammatory drugs, the patient experienced significant clinical improvement, including 30-lb weight gain and resolution of gastrointestinal symptoms. Histologic re-review by a tertiary center supported nonsteroidal anti-inflammatory drug-induced ileitis as the sole diagnosis. Discussion: This case underscores the diagnostic challenge posed by nonsteroidal anti-inflammatory drug enteropathy when imaging mimics Crohn’s disease. The computed tomography scan findings—long-segment terminal ileal thickening, mesenteric fat stranding, reactive lymphadenopathy, and vascular engorgement—are classic for active Crohn’s and atypical for nonsteroidal anti-inflammatory drug injury, which is usually limited and less hyperemic. Elevated calprotectin further complicated the picture. Ultimately, the absence of histologic chronicity, full clinical remission after nonsteroidal anti-inflammatory drug withdrawal, and specialist review helped establish the correct diagnosis. This case highlights the need for cautious interpretation of radiologic and biochemical data, and emphasizes the importance of longitudinal clinical correlation in patients with ileal disease.

The American Journal of GastroenterologyVol. 120(10S2)
Good health and well-being
Openalex Percentile: Top 32%
Inflammatory mediators and NSAID effects
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