Pancolitis due to Tuberculosis Masquerading as Inflammatory Bowel Disease in a 43‐Year‐Old Woman: Diagnostic Challenges in a Resource‐Limited Setting—A Case Study and Literature Review From Ethiopia
Alemayehu Abebe Guji, Gashahun Mekonnen Dissassa, Melese Abere Gizaw, Daniel Rebuma Bekele, Merid Lemma Kebede, Kedir Negesso TukeniBackground
Gastrointestinal tuberculosis (GI TB) predominantly affects the ileocecal region, making primary colonic involvement exceptionally rare. In TB‐endemic, resource‐limited settings, differentiating colonic TB from inflammatory bowel disease (IBD)—particularly Crohn’s disease (CD)—presents a formidable diagnostic dilemma owing to overlapping clinical, radiological, and ileocolonoscopic features, often leading to diagnostic delays, misdiagnosis, and subsequent complications.
Initial Clinical Presentation, Treatment, and Diagnostic Re‐Evaluation
In May 2026, a 43‐year‐old Ethiopian woman presented to Jimma University Medical Center with a 10‐month history of progressive colicky abdominal pain, chronic watery diarrhea, postprandial nonbilious vomiting, and significant weight loss. Prior empirical regimens of antihelminthic agents and broad‐spectrum antibiotics administered at peripheral health facilities yielded no clinical improvement. Initial laboratory workup revealed microcytic hypochromic anemia (hemoglobin: 8.5 g/dL), a significantly elevated erythrocyte sedimentation rate (ESR) (92 mm/h), hypoalbuminemia (2.8 g/dL), and a normal carcinoembryonic antigen (CEA) level (4 ng/mL). Ileocolonoscopy demonstrated superficial ulceration involving the ascending colon and hepatic flexure in a continuous form with numerous inflammatory polyps, and a small deep ulceration at the terminal ileum. Initial histopathology demonstrated chronic active inflammation without evidence of malignancy or granuloma formation. With a presumed diagnosis of CD, treatment was initiated with prednisolone and azathioprine, which might have contributed to the suspected deterioration of the clinical condition, warranting re‐evaluation with contrast‐enhanced CT scan of the abdomen and pelvis, which demonstrated diffuse, long‐segment circumferential wall thickening involving the terminal ileum, the entire colon, and the rectum, alongside pericolic fat stranding, a mesenteric phlegmon, and multiple necrotic mesenteric lymph nodes, with the largest measuring 2 × 3 cm with peripheral rim enhancement. Fine‐needle aspiration cytology (FNAC) of the necrotic lymph nodes revealed epithelioid granulomas and characteristic caseous necrosis. With the above evidence, terminal ileitis and pancolitis due to TB were considered, immunosuppressive medications were discontinued, and standard antituberculosis therapy (2RHZE/4RH) was promptly initiated. The patient started to experience clinical improvement, achieving full resolution of her constitutional and abdominal symptoms and gaining weight at 1 month of follow‐up.
Conclusion
Diagnosing GI TB—especially in atypical sites such as the colon—presents a critical challenge in resource‐limited, TB‐endemic settings, where differentiating it from IBDs, especially CD, is vital to prevent severe complications from inappropriate therapy. To avoid misdiagnosing GI TB as IBD (which risks disseminated infection from immunosuppression) or IBD as TB (which worsens bowel stricture, fistulae, and perforation), clinicians must perform mandatory pretreatment TB screening using radiologic, immunologic, molecular, and culture modalities before initiating immunosuppressive agents. Furthermore, diagnostic accuracy requires obtaining deep submucosal biopsies during ileocolonoscopy to detect characteristic granulomatous lesions if present. Finally, when an empirical anti‐TB trial is necessary, it must be strictly time‐limited and followed by objective re‐evaluation at 8 weeks—including repeat endoscopy and biopsy—rather than relying solely on clinical symptomatic improvement.