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  • Author: Andrada-Viorela Gheorghe x
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Andrada-Viorela Gheorghe, Mihai Rimbas, Octav Ginghina, Andrada Spanu and Theodor Alexandru Voiosu


Background. Gastric neuroendocrine tumors (GI-NETs) are rare lesions, usually discovered incidentally during endoscopy. Based on their pathology, there are 4 types of GI-NETs. Type I are multiple small polypoid lesions with central ulceration located in the gastric body or the fundus, associated with atrophic gastritis usually noninvasive and very rarely metastatic. We report on a rare case of a gastric NET arising from the muscularis propria layer of the pyloric ring.

Case report. We present the case of a 65-year old woman with a history of alcoholic cirrhosis, investigated for melena. Upper endoscopy revealed a 30 mm submucosal pedunculated polypoid lesion located on the pylorus protruding in the duodenum, with normal overlying mucosa, fundic gastric atrophy and multiple small polyps at this level, with no active bleeding. CT scan did not reveal any distant metastases. An ultrasound endoscopy was performed, and a round hypoechoic heterogeneous solitary mass, evolving from the pyloric muscle was described. Considering a 30-mm tumor evolving from the gastric muscle layer in the absence of local invasion and with no distant metastases we decided against an endoscopical resection and we referred the patient to surgery. A laparoscopic wedge resection was performed. The pathology report described a 30/25 mm welldifferentiated neuroendocrine tumor invasive in the muscularis mucosa (pT3).

Conclusions. Usually, type I neuroendocrine tumors are located in the body or the fundus of the stomach without submucosal invasion. The interesting feature in our case was that the tumor originated from the pylorus, making it an atypical presentation for a neuroendocrine tumor.

Open access

Theodor Alexandru Voiosu, Andrada Viorela Gheorghe, Dan Adrian Bobeica, Andrei Mihai Voiosu and Radu Bogdan Mateescu


Tracheoesophageal fistula (TEF) is frequently congenital and requires surgical correction. TEF can also occur secondary to malignant esophageal tumors or benign diseases and these cases are managed by endoscopic means, such as closing the defect with metallic stents. Although esophageal injury can occur secondary to nonsteroidal anti-inflammatory drugs (NSAIDs), TEF secondary to chronic NSAIDs use has not been described in the literature.

We report the case of a male patient with refractory migraine and chronic use of NSAIDs, with a history of esophageal stenosis presenting with acute-onset total dysphagia. Upper gastrointestinal endoscopy and CT-scan revealed TEF located at 25 cm from the incisors. An esophageal stent was placed endoscopically, and 6 weeks a second stent was placed in a stent-in-stent manner to allow removal of both stents. Endoscopic control after the removal of the stents showed the persistence of the fistula, so a third stent was placed as a rescue therapy.

Against medical advice, the patient continued to use OTC painkillers and NSAIDs in large doses. Three months later, he was readmitted with total dysphagia and recent-onset dysphonia. CT scan revealed a new fistula above the already placed stent. A second metallic stent was endoscopically placed through the old stent to close the newly developed fistula. The patient was discharged on the third day with no complications and he remains well at 6 months follow-up.

Due to small cases studies, recurrent TEF remains a therapeutic challenge. Endoscopic therapy is usually an effective solution, but complex cases might require multiple treatment sessions.