The patient underwent a gastric tangential resection, restricted to the portion of corpus of gastric wall involved by tumor and sparing almost all of the stomach (Figure ?(Figure3).3). patients with severe hypochlorhydria-related hypergastrinemia in order to earlier detect neuroendocrine polyps. contamination was unfavorable. An upper gastrointestinal endoscopy was performed. A two-cm single sessile protruding-type polyp was found in the greater curvature of the patients belly. Microscopic examination showed clumps of small round-oval shaped cells with areas arranged in a trabecular or Diclofenac diethylamine solid pattern in the gastric Diclofenac diethylamine mucosa (Physique ?(Figure1).1). There were no area of necrosis and the KI-67 index was 3%. Immunohistochemical staining showed that this cancer cells Diclofenac diethylamine were positive for neuron-specific enolase, cytokeratin and synaptophysin. The findings were those of a well-differentiated neuroendocrine carcinoma (carcinoid tumor). Mild chronic atrophic gastritis and Rabbit polyclonal to IL29 intestinal metaplasia were present in the surrounding, non-neoplastic tissue in the corpus of her belly. Thiazine staining for was unfavorable. Total body computed tomography showed no evidence of lymph node or hepatic metastases and confirmed a hypervascular 1.71.3 cm polyp in the belly (Determine ?(Figure2).2). The patient underwent a gastric tangential resection, restricted to the portion of corpus of gastric wall involved by tumor and sparing almost all of the belly (Physique ?(Figure3).3). Microscopic examination confirmed a well-differentiated, low-grade, neuroendocrine tumor of the belly infiltrating the submucosal layer with microvascular invasion. The margin of the resection was free of disease. Postoperative staging was pT1 according to the Union for International Malignancy Controls TNM Classification of Malignant Tumours (7th edition). The patients postoperative course was uneventful and she remained in a good clinical condition. Six months later, her serum gastrin was 2011 pg/mL. A total body computed tomography scan and an upper gastrointestinal endoscopy excluded recurrence of the disease. A gastric antral biopsy showed moderate chronic atrophic gastritis and intestinal metaplasia. Staining for was unfavorable. Immunohistochemical staining for cytokeratin and synaptophysin showed moderate hyperplasia of neuroendocrine gastric cells. No tumor recurrence was revealed. Open in a separate window Physique 1 Hematoxylin and eosin staining (100) of gastric biopsy showed trabecular structures of small round-oval cells (A); immunohistochemical staining (100) showed that this cytoplasm is usually positive for synaptophysin, which confirms the diagnosis of neuroendocrine carcinoma (B). Open in a separate window Physique 2 Stomach computed tomography scan showed a gastric polyp with arterial enhancement and an apical area of necrosis. Open in a separate window Physique 3 A gross photograph of the gastrectomy specimen showed a polyp (two cm in diameter) with an apical area of necrosis and the resected mucosal ring. Discussion A severe ( 1000 pg/mL) elevation of fasting serum gastrin concentration is usually suggestive for ZollingerCEllison syndrome; on top of this, the use of acid suppressant medication (both proton pump inhibitors or H2-receptor antagonists), the presence of contamination and autoimmune achlorhydric atrophic gastritis without or with pernicious anemia may lead to mild-to-moderate hypergastrinemia [4,5]. In our case, the absence of symptoms of classical gastrinoma and the persistence of extremely elevated gastrin after radical tumor excision rule out the diagnosis of ZollingerCEllison syndrome. The gastric biopsy performed six months after tumor resection showed chronic atrophic gastritis and intestinal metaplasia, with moderate hyperplasia of antral G cells; this data, together with vitamin Diclofenac diethylamine B12 deficiency anemia, suggest a hypochlorhydria-related hypergastrinemia. Although gastric parietal cell and intrinsic factor antibodies were both negative, cases of autoantibody-negative type A gastritis have been described . More than 100 cases of gastric carcinoids in patients with pernicious anemia are explained in the literature. Because the hormone gastrin regulates several important cellular processes in the gastric epithelium including proliferation, apoptosis, migration, invasion, tissue remodeling and angiogenesis , we hypothesize that this unusual and extremely elevated levels of gastrin facilitated the occurrence of gastric neuroendocrine tumor in this.