Esophageal Leiomyoma-Associated Angiodysplasia in a Dog: A Long-Term Management Strategy

Abstract

Background: Angiodysplasia [AGD] is an uncommonvascular malformation defined as abnormally dilated and tortuous vessels within mucosal and submucosal layers, representing a rare cause of gastrointestinal [GI] bleeding in veterinary medicine. While AGD typically occurs inthe lower GI tract, its occurrence in the esophagus has not been previously reported in dogs. This report presentsthe first canine case of esophageal AGD, which was found to be associated with an esophageal leiomyoma at the gastroesophageal junction [GEJ]. It describes the clinicopathologic findings, proposes a pathophysiologic mechanism linking mechanical venous obstruction to vascular ectasia, and presents a long-term, minimally invasive management strategy.

Case: A 6-year-old neutered male mongrel dog was presented with a 3-month history of lethargy and anemia. Hematologic evaluation revealed severe microcytic, hypochromic anemia with markedly decreased serum iron concentration and transferrin saturation, consistent with iron deficiency anemia. Endoscopy identified dilated and tortuous vessels at the GEJ, and computed tomography confirmed a well-defined extraluminal esophageal mass compressing the distal esophagus. Histopathologic and immunohistochemical examinations confirmed an esophageal leiomyoma. Chronic extraluminal venous compression by the leiomyoma was suspected to contribute to localized venous stasis and secondary mucosal vascular ectasia. The dog was treated with oral ethinyl estradiol and levonorgestrel, combined with surgical debulking because complete resection was not feasible due to the mass location. Anemia resolved within 10 days of initiating hormonal therapy and did not recurduring 93 weeks of continuous hormonal treatment. At 53 weeks after the initiation of hormonal therapy, an intraluminal recurrence of the leiomyoma was detected and endoscopically removed; however, no recurrence of AGD or anemia was observed. Hormonal therapy was continued without adverse effects throughout follow-up.

Discussion: This case proposes a novel pathophysiologic mechanism in which chronic venous outflow obstruction at the high-tension GEJ region [Laplace’s law] may induce mucosal vascular ectasia consistent with AGD. Although a direct causal link cannot be definitively proven, the close anatomical association and sustained improvement of vascular lesions following decompression suggest that AGD developed secondary to venous obstruction caused by the leiomyoma. The findings extend the anatomic spectrum and pathophysiologic understanding of AGD in dogs. This case also underscores the diagnostic importance of integrating endoscopic and imaging modalities to identify underrecognized vascular lesions in anemic patients. Clinically, combined estrogen-progestin therapy, complemented by surgical debulking, achieved durable 93-week remission without recurrence of AGD, offering a feasible, minimally invasive option when invasive endoscopic ablation or surgery poses high-risk. Estrogen-progestin therapy likely promotes vascular stabilization through endothelial modulation and anti-angiogenic effects, providing durable hemostatic control. The absence of treatment-related complications supports the safety and efficacy of this long-term multimodal approach. This report broadens current knowledge of AGD in veterinary medicine and highlights a practical management strategy for tumor-associated AGD in anatomically constrained regions.

Keywords: angiodysplasia, dog, leiomyoma, hormone therapy, iron deficiency anemia.