Dasatinib is a potent second-generation tyrosine kinase inhibitor widely used in chronic myeloid leukemia (CML) treatment, particularly in patients intolerant to imatinib. While generally well-tolerated, dasatinib can cause various adverse effects including pleural effusions, cytopenias, and gastrointestinal symptoms. However, progressive enterocolitis resembling inflammatory bowel disease (IBD) is rarely reported and poses diagnostic challenges due to clinical and endoscopic similarities to IBD.

A 71-year-old female with a 20-year history of achalasia was diagnosed with chronic myeloid leukemia in 2021 following evaluation for leukocytosis and typical hematological findings. Initial treatment with imatinib 400 mg daily was discontinued due to severe facial edema. Subsequently, dasatinib 100 mg daily was initiated as second-line therapy.

Concurrent with dasatinib initiation, the patient developed new gastrointestinal symptoms previously absent in her medical history, including abdominal pain, intermittent diarrhea, altered bowel habits, and occasional hematochezia. These symptoms progressively worsened over subsequent years despite achieving hematological remission.

Physical examination in 2021 revealed stable vital signs with mild diffuse abdominal tenderness without hepatosplenomegaly. Laboratory investigations confirmed BCR-ABL positivity establishing CML diagnosis, with leukocytosis (WBC >50,000/µL) and normal renal and hepatic function. Hematological remission was maintained throughout 2022-2025 follow-up period.

Colonoscopy performed in February 2022 revealed minimal terminal ileal hyperemia with edematous and granular colonic mucosa, raising suspicion for ulcerative colitis or Crohn's disease. Histopathological examination of biopsies showed chronic active colitis with cryptitis, terminal ileitis, and eosinophilic infiltration, but lacked granulomas or specific features diagnostic of IBD. Previous biopsies from November 2021 demonstrated similar chronic active colitis and cryptitis without diagnostic specificity.

Despite endoscopic findings suggestive of IBD, the absence of characteristic histopathological features and progressive symptom worsening during dasatinib therapy raised suspicion for drug-induced enterocolitis. In 2025, when gastrointestinal symptoms significantly intensified, dasatinib was discontinued.

Remarkably, within approximately two months of dasatinib discontinuation, all gastrointestinal symptoms completely resolved, providing strong evidence for drug-induced etiology rather than IBD.

This case demonstrates a rare but clinically significant adverse effect of dasatinib therapy. While gastrointestinal symptoms are recognized side effects of tyrosine kinase inhibitors, progressive enterocolitis mimicking IBD is uncommon and poses diagnostic challenges.

The temporal relationship between dasatinib initiation and symptom onset, progressive worsening during treatment, and complete resolution following discontinuation strongly supports drug-induced etiology. The endoscopic findings, while concerning for IBD, lacked supporting histopathological evidence, which is crucial for IBD diagnosis.

The mechanism underlying dasatinib-induced enterocolitis remains unclear but may involve disruption of intestinal epithelial barrier function or immune-mediated inflammatory responses. The eosinophilic infiltration observed in biopsies suggests possible allergic or hypersensitivity reaction.

Clinicians should maintain high suspicion for drug-induced enterocolitis in CML patients receiving dasatinib who develop new gastrointestinal symptoms, particularly when symptoms are progressive. Careful correlation between clinical presentation, endoscopic findings, and histopathological examination is essential to avoid misdiagnosis and inappropriate immunosuppressive therapy.

Dasatinib can cause progressive enterocolitis mimicking IBD in CML patients. Complete symptom resolution following drug discontinuation confirms the diagnosis and highlights the importance of considering drug-induced etiology before initiating immunosuppressive therapy for presumed IBD in patients receiving tyrosine kinase inhibitors.