Gastric adenomas are epithelial premalignant neoplasms which may appear similar on endoscopic examination; however, histologically, they are classified into four distinct subtypes according to the World Health Organization (WHO) Classification of Tumors of the Digestive System: intestinal adenoma, foveolar-type adenoma, oxyntic gland adenoma, and pyloric gland adenoma. Each subtype has characteristic histologic features that are essential for accurate diagnosis, although distinction can be challenging due to overlapping morphologic patterns. Moreover, these entities differ in their potential for malignant transformation and in their associations with hereditary or syndromic conditions. The objective of this review is to provide a practical guide for the histopathologic diagnosis of gastric adenomas, summarize the evidence regarding their risk of associated malignancy or malignant transformation, and review current recommendations for clinical follow-up and management. Given that various lesions may present endoscopically as gastric polyps, this manuscript also reviews both epithelial and non-epithelial mimickers of gastric adenomas.

Gastric antral vascular ectasia (GAVE) is a rare vascular lesion of the stomach with an overall prevalence of approximately 0.09%, accounting for up to 4% of severe acute gastrointestinal bleeding and 4–6% of non-variceal bleeding in cirrhotic patients. GAVE predominantly affects older adults, with the majority of patients diagnosed at age 60 years or older, and is strongly associated with liver cirrhosis, autoimmune conditions such as systemic sclerosis, and, as increasingly recognized, metabolic syndrome. Three interrelated pathogenic mechanisms have been proposed: mechanical injury from gastric dysmotility, hormonal and vasoactive mediator dysregulation involving hypergastrinemia and prostaglandin E2, and microvascular injury with compensatory neoangiogenesis. Clinically, GAVE most commonly presents as chronic iron deficiency anemia from occult blood loss rather than overt hemorrhage. Endoscopic phenotypes include the classic linear striped “watermelon stomach,” a diffuse punctate or “honeycomb” pattern more commonly seen in cirrhotic patients, and a nodular variant. Distinguishing GAVE from portal hypertensive gastropathy is critical, as their management strategies differ substantially. The histologic triad of vascular ectasia, fibromuscular hyperplasia, and intravascular fibrin thrombi is central to pathologic diagnosis. Intravascular fibrin thrombi, when present, are highly specific for GAVE; CD61 immunohistochemistry serves as a highly useful adjunct in equivocal cases, though its sensitivity is limited by the focal nature of thrombosis and biopsy sampling. Endoscopic therapy remains first-line, with argon plasma coagulation as the most extensively studied modality and radiofrequency ablation demonstrating promising efficacy with potentially lower recurrence rates in preliminary comparative studies. Pharmacologic therapies lack robust evidence, and antrectomy is reserved for refractory cases. This review synthesizes the current understanding of GAVE across its epidemiology, pathogenesis, clinical and endoscopic features, histopathology, differential diagnosis, and management.