A 38-year-old female presented with complaints of epigastric pain for 3 months along with abdominal fullness, nausea, vomiting and weight loss for the last 2 months. Initially, she was not able to tolerate solids, but, with the passage of time, she became intolerant to liquids also. She had a past history of pulmonary tuberculosis diagnosed on the basis of the symptoms and the sputum acid fast bacilli (AFB) smear positivity. There was no past surgical or blood transfusional history.
The patient underwent an upper gastrointestinal endoscopy that revealed narrowed pyloric opening with severe erythema and edema beyond which the GIF 150 scope could not be negotiated. Multiple biopsies were taken from the lesion that showed moderate active inflammation and mild Helicobacter pylori infection.
She was prescribed first-line therapy for H. pylori eradication, but the symptoms of abdominal fullness did not resolve. A computed tomography of the abdomen was performed that showed eccentric soft tissue thickening identified along the distal aspect of the stomach as well as along the pyloric canal, which was causing luminal narrowing and dilation of the proximal stomach. Adjacent fat stranding and few enhancing adjacent lymph nodes were noticed.
Because of the persistent symptoms, she underwent a second upper gastrointestinal endoscopy that showed similar findings of the mass in the pylorus with no reduction in size as compared with the previous examination. This time, the narrowed segment of the pylorus was dilated with a 12 mm CRE balloon. Subsequently, the pyloric opening was crossed successfully showing edematous bulb and normal distal duodenal folds. A repeat biopsy of the lesion showed no H. pylori organisms.
Because of the persistent symptoms, she underwent open laparotomy that showed bulky pylorus extending up to the first part of the duodenum. No extramural evidence of mass was noticed. A distal gastrectomy with controlled duodenal fistula and gastrojejunostomy was performed. The histopathology of the resected mass lesion showed irregular proliferation of a few mucinous cystically dialted glands lined by bland epithelial cells with abundant cytoplasm and basally located nuclei, intermixed with hypertrophied smooth muscle fibers reaching up to the deep muscle layer in the wall [Figure 1a-d]. Features were consistent with GPC. No dysplasia was seen. No H. pylori were detected. Foci of goblet cell metaplasia were noted. She made an uneventful recovery and, on follow-up, her symptoms improved markedly.