A Case of Combined Gastric Carcinoid Tumor and Adenocarcinoma in Chronic Atrophic Gastritis

Abstract

Purpose: Gastric carcinoids (GCs) are infrequent and account for ˜8.7% of all gastrointestinal (GI) carcinoids. Although patients with chronic atrophic gastritis are at increased risk for the development of GC tumors and adenocarcinoma, the coexistence of both tumors in the stomach is a very rare finding. Case: 54 y/o asymptomatic female with history of hypothyroidism and hypertension presented with anemia. There was no history of smoking, alcohol or drug use. Upper endoscopy showed a 3 x 4 cm mass in the gastric body. A 4 mm nodule in the body adjacent but separate from the mass and a 3 mm nodule in the fundus were also found. Atrophic gastritis was seen (Picture 1). Pathology reported the gastric mass as a moderately differentiated adenocarcinoma. Gastric nodules were reported as well-differentiated neuroendocrine tumors (carcinoid tumors). Immunohistochemical stains of chromogranin, synaptophysin and low molecular cytokeratin were positive, supporting the diagnosis (Picture 2). H. pylori was not seen. Lab data: Hb=11.3, Hct=35.4, MCV=69.4, PTH=68.3, Urine HIAA-5= 9, Gastrin=2113. Chest, abdomen and pelvic CT showed no lymphadenopathy or metastasis. Both gastric adenocarcinoma and carcinoid tumors were limited to the submucosa with no lymph node involvement on surgical specimens. Discussion: GCs are often asymptomatic and usually diagnosed during endoscopy performed for different reasons. They mainly arise from gastric enterochromaffin-like (ECL) cells. Chronic stimulation by hypergastrinemia may cause ECL cells hyperplasia and their transformation to carcinoid tumors. GCs are classified into 3 types. Type 1 (70-85%) is linked to type A gastritis. Type 2 (5-10%) is associated with Zollinger-Ellison Syndrome, mostly in the context of MEN-1. Type 3 (15-25%) is not related to hypergastrinemia and has more aggressive course. Histochemistry (chromogranin A and synaptophysin) is used to identify malignant transformation of ECL cells. Endoscopic ultrasound, CT and MRI are useful for staging. The risk of gastric adenocarcinoma in patients with athrophic gastririts is 3-18 times higher than an age-matched population. The coexistence of these two independent tumors located in the same anatomic area (collision tumor) is very rare. GCs <1 cm can be treated endoscopically. Surgical resection should be considered with more advanced carcinoid disease or in association with adenocarcinoma. Conclusion: Chronic atrophic gastritis is related to increased risk for the development of GCs and adenocarcinoma. The coexistence of both tumors in the stomach is a very rare finding. Chronic stimulation by hypergastrinemia may have a trophic effect on both gastric neuroendocrine and epithelial cells.