Case Presentation: A 61-year-old woman with MEN1 (with associated hyperparathyroidism, parathyroid adenoma and pituitary microadenoma) and prior gastric carcinoid resection presented with 4 weeks of progressive exertional dyspnea, painful bilateral leg edema, and fatigue. She had not seen a doctor in 6 years, smoked cigarettes daily, and had not received routine cancer screening. Review of systems was otherwise negative. Vitals: 98.2°F, BP 153/84, HR 89. Labs: Hgb 4.2 g/dL, ferritin 8 ng/mL, vitamin B12 158 pg/mL, creatinine 0.64 mg/dL, calcium 11.1 g/dL, PTH 274 pg/mL. High sensitivity troponin was 18ng/L (normal: ≤14) and NT-Pro-BNP 1297 pg/mL (normal : ≤125 for age). Physical exam revealed a 3/6 systolic murmur, bibasilar rales, and 2+ bilateral edema. Venous duplex was negative for deep vein thrombosis. CT angiography was negative for pulmonary embolism but showed cardiomegaly with a small pericardial effusion. Transthoracic echocardiography showed LVEF 68% without valvular disease. She received 4 units of packed red blood cells with 20 mg IV furosemide after each unit, plus IV iron dextran (1 g) and IM vitamin B12 (1,000 µg). Esophagogastroduodenoscopy revealed innumerable fundic polyps; biopsies showed well-differentiated neuroendocrine tumors infiltrating the submucosa. Colonoscopy showed diverticulosis, internal hemorrhoids, and a 5-mm sessile serrated polyp. Hemoglobin improved to 7.5 g/dL with resolution of symptoms. She was discharged on pantoprazole 40 mg twice daily and oral iron, with endocrinology follow-up.
Discussion: MEN1 classically involves parathyroid, pituitary, and pancreatic/duodenal neuroendocrine tumors; gastric involvement is less common. MEN1-associated hypergastrinemia (often from gastrinoma/Zollinger–Ellison syndrome) drives enterochromaffin-like cell hyperplasia and multifocal fundic/body type II gastric NETs. These mucosal/submucosal lesions can ooze chronically, producing iron-deficiency anemia and, when severe, high-output physiology. In this patient, profound iron deficiency with low B12 explained dyspnea and edema, while daily NSAIDs likely compounded bleeding risk. The differential for profound microcytic anemia in this context includes NSAID gastropathy, bleeding angiodysplasias, malignancy, and small-bowel sources, but innumerable fundic NETs in a patient with MEN1 provide a unifying explanation for occult blood loss. Initial management centers on stabilization and repletion (packed red cells, iron, B12) plus acid suppression. Long-term strategies include endoscopic resection of dominant lesions, consideration of somatostatin analogs for symptomatic or progressive disease, and tumor-directed therapies; in diffuse or refractory cases, antrectomy may be considered. MEN1 surveillance should be re-established with biochemical testing (gastrin, chromogranin A), periodic EGD, and appropriate imaging in coordination with endocrinology and a neuroendocrine specialist.
Conclusions: In MEN1, diffuse fundic gastric NETs can cause chronic occult gastrointestinal bleeding and life-threatening iron-deficiency anemia. Early endoscopic evaluation is essential when MEN1 patients present with anemia—especially in the presence of additional bleeding risks such as NSAIDs. Prompt resuscitation, deficiency repletion, acid suppression, and coordinated endocrine/gastroenterology follow-up can reverse symptoms and address the underlying neoplasia while restoring guideline-based MEN1 surveillance.