S6433 A Gastric Masquerade: Glomus Tumor Mimicking Gastric Neuroendocrine Neoplasm

Introduction: Gastric glomus tumors (GGT) are rare mesenchymal neoplasms, estimated to comprise <1% of resected gastric lesions. Typically benign, they most commonly arise in the gastric antrum and are composed of modified smooth muscle cells. Clinically, they often present as submucosal masses with nonspecific symptoms, making diagnosis challenging. GGTs are frequently mistaken for gastrointestinal stromal tumors or gastric neuroendocrine tumors (GNET), due to similar clinical and endoscopic features. We present a case of a GGT that was initially suspected to be a GNET, highlighting the diagnostic challenges associated with this rare entity. Case Description/Methods: A 65-year-old man with a history of hypertension, gastroesophageal reflux disease (GERD), and anemia presented after an incidentally found gastric antral nodule during a previous esophagogastroduodenoscopy (EGD). Endoscopic ultrasound (EUS) revealed an approximately 9 × 9 mm hypoechoic submucosal nodule in the gastric antrum. Fine needle aspiration (FNA) revealed small uniform cells arranged in organoid nests within the smooth muscle wall, (+) CD56, weak synaptophysin, (-) for chromogranin, DOG1, and CD117, suggesting a well-differentiated grade 1 neuroendocrine tumor. Six months later, the patient underwent endoscopic submucosal dissection (ESD) for management. Histopathological examination revealed a glomus tumor, characterized by well-circumscribed nodules within the muscularis propria, composed of uniform round cells with a perivascular growth pattern and associated hyalinization. Immunohistochemistry (IHC) showed diffuse positivity for smooth muscle actin (SMA) and focal positivity for synaptophysin, with (-) staining for cytokeratin AE1/3 and chromogranin. Discussion: This case highlights the diagnostic challenges of GGTs, which often mimic other submucosal lesions due to overlapping clinical, endoscopic, and immunohistochemistry features. Some GGTs strongly express synaptophysin, resembling GNETs. Unlike GNETs, GGTs lack keratin expression and are centered in the muscularis propria. In this patient, initial FNA biopsy suggested a GNET, however final diagnosis of GGT was achieved only after ESD and comprehensive histopathological evaluation. While EUS-guided FNA can aid diagnosis, its yield may be limited by small sample size, making ESD with full-thickness biopsy more reliable. Clinicians should consider GGTs in the differential diagnosis of submucosal tumors, particularly cases with focal synaptophysin reactivity.