Gastric Antral Vascular Ectasia As A Rare Complication Of Imatinib Therapy: Case Series

Abstract

Background: Gastric antral vascular ectasia (GAVE) is a rare but clinically significant cause of upper gastrointestinal bleeding, characterized endoscopically by longitudinally dilated vessels in the gastric antrum resembling a “watermelon stomach”. While GAVE is often associated with systemic conditions such as cirrhosis and autoimmune disease, drug-induced etiologies must be considered in hematologic patients, particularly those receiving tyrosine kinase inhibitors (TKIs) like imatinib mesylate (IM).

Case Ilustration: We report three hematologic patients who developed gastrointestinal bleeding after several months of IM therapy. Endoscopic evaluation revealed typical GAVE lesions. Clinical and endoscopic improvement was observed following IM discontinuation. Two patients were successfully transitioned to nilotinib without recurrence of bleeding, and follow-up endoscopy confirmed regression of GAVE lesions.

Discussion: The consistent temporal relationship between IM administration and GAVE onset supports a potential causal link. Although the molecular mechanisms remain unclear, local mucosal irritation and vascular changes induced by IM have been proposed. Management of GAVE includes hemodynamic stabilization, supportive therapy, and endoscopic intervention for active bleeding. However, in drug-related cases, discontinuation of the offending agent and switching to an alternative TKI proved effective and low-risk. Supportive measures alone are insufficient to prevent recurrence if the underlying trigger is not addressed.

Conclusion: This case series underscores the importance of considering drug-induced etiologies in hematologic patients presenting with upper GI bleeding. Thorough medication history, multidisciplinary evaluation, and appropriate therapeutic adjustments are essential. Discontinuation of imatinib and transition to alternative TKIs can prevent recurrence and promote regression of GAVE lesions. Further prospective studies are needed to clarify the molecular mechanisms underlying TKI-associated GAVE and to establish evidence-based clinical guidelines.