Related Experiment Videos
Gastric Glomus Tumor Mimicking a Neuroendocrine Tumor: A Case Report Highlighting Diagnostic Pitfalls
Susumu Ohwada1, Shinji Sakurai2, Yuhei Nakano1
1Center of Gastroenterology and Oncology, IMS Ota Chuo General Hospital, Ota, Gunma, Japan.
Introduction:
Gastric glomus tumors (GGTs) are rare mesenchymal neoplasms arising from the modified smooth muscle cells of the glomus body. Their subepithelial location and pronounced hypervascularity overlap considerably with gastrointestinal stromal tumors (GISTs) and neuroendocrine tumors (NETs) on imaging and in small biopsy specimens, making an accurate preoperative diagnosis challenging; as a result, such lesions are frequently diagnosed after surgical resection.
Case Presentation:
A 38-year-old asymptomatic woman was found to have a 25-mm well-circumscribed, hypervascular submucosal lesion with a small central depression and minute ulceration in the upper gastric body during a routine health-screening esophagogastroduodenoscopy (EGD). Endoscopic ultrasonography (EUS) demonstrated a heterogeneous hypoechoic mass arising from the third sonographic layer without evidence of muscularis propria invasion. Contrast-enhanced CT showed a hypervascular lesion with no regional lymphadenopathy or distant metastasis. Conventional forceps biopsies targeting the minute ulceration, evaluated with hematoxylin and eosin (H&E) staining alone, were interpreted as consistent with a NET, leading to a provisional diagnosis of a type III gastric NET. Because of the diagnostic uncertainty surrounding the NET diagnosis, and because the EUS and CT showed no evidence of deep or nodal spread, the patient underwent laparoscopic and endoscopic cooperative surgery (LECS) with a local full-thickness gastric resection rather than upfront gastrectomy with lymphadenectomy, and the defect was repaired through a protective mini-laparotomy. Definitive histopathology demonstrated uniform round-to-spindle cells arranged in a perivascular sheet pattern within a myxoid stroma. Immunohistochemistry (IHC) showed focal positivity for α-smooth muscle actin (α-SMA) and negativity for KIT (CD117), CD34, chromogranin A, synaptophysin, desmin, and the S-100 protein, confirming a GGT. All surgical margins were negative, and no recurrence has been observed over 5 years of follow-up.
Conclusions:
A GGT must be included in the differential diagnosis of hypervascular gastric subepithelial lesions (SELs), including those with a nested, NET-like architecture. H&E staining alone is insufficient for a definitive diagnosis; direct communication with the pathologist and comprehensive IHC profiling are indispensable. LECS is a favorable and effective organ-preserving strategy for localized gastric SELs when the diagnosis remains uncertain despite the preoperative evaluation.