A 42-year-old woman without a history of vomiting in infancy presented to the emergency department with postprandial abdominal distension and repeated vomiting but no abdominal pain. Laboratory examination showed normal results, including a normal serum Helicobacter pylori antibody level, except for mild anemia. Abdominal computed tomography (CT) showed gastric dilatation and wall thickening of the distal stomach (Fig. , asterisk, arrow). Endoscopy and contrast gastrography revealed gastric outlet obstruction due to stenosis of the antral and pyloric region (Fig. ), and a deep ulcer in the stenotic antrum (Fig. ). She was admitted to our hospital and treated with nasogastric tube drainage, fasting, and administration of a proton pump inhibitor. Three days later, her symptoms improved and she could start to take a liquid diet. Ten days after the initiation of treatment, she was asymptomatic and could eat a normal diet. Follow-up endoscopy performed on hospital day 12 showed a healing ulcer in the prepyloric region (Fig. ) and a distinct opening to the duodenum at the edge of the healing ulcer that was different from the original pylorus. Endoscopic ultrasonography (EUS) revealed circumferential thickening of the muscularis propria layer of the pylorus with a maximum thickness of over 10 mm (Fig. , arrowheads). Pathological examination of multiple biopsy specimens taken from the ulcer and surrounding mucosa showed no evidence of malignancy. Since the patient was asymptomatic, she was discharged from the hospital on hospital day 21. Additional follow-up endoscopic examinations revealed a clear double pylorus (Fig. , arrows). The endoscope could easily pass through both channels to the duodenum. Based on her clinical course and findings of clinical images, she was diagnosed as having gastric outlet obstruction due to AHPS that was improved by spontaneous double channel pylorus formation. Six months after onset, CT showed residual wall thickening of the distal stomach without gastric dilatation (Fig. , arrow) and EUS revealed residual circumferential thickening of the muscularis propria layer of the pylorus, indicating that she still had AHPS although she did not have any abdominal symptoms.\nOur patient's clinical and imaging findings suggested that the double pylorus formed in our patient in the following manner. When we retrospectively reviewed the endoscopic images from the EGD examination that the patient had undergone 1 year prior to the current admission, antral narrowing was observed. She may have had asymptomatic AHPS at that time. When the patient came to the emergency room, endoscopy and contrast gastrography revealed gastric outlet obstruction due to stenosis and a deep ulcer in the stenotic antrum. During the hospital admission, the deep ulcer made a fistula with the duodenum that would eventually become a double pylorus. After double pylorus formation, the patient no longer had symptoms of AHPS and she was discharged from the hospital.
The patient was a 67-year-old man, who arrived at the emergency department and referred with chronic epigastric pain and dyspepsia over the last 6 months and felt weakness. He suffered from diabetes mellitus type 2 and high blood pressure and took medications for both diseases. Currently, he reported that he periodically took nonsteroidal anti-inflammatory drugs (NSAIDs) for arthralgia during the last year, without taking inhibitor of gastric acid and he denied having black or bloody stools. Physical examination revealed only mild upper abdominal tenderness and the blood tests showed microcytic anemia with hemoglobin 10.1 g/L and iron deficiency with ferritin 13 ng/mL and iron 27 µg/dL. He underwent an esophagogastroduodenoscopy and colonoscopy as an outpatient due to gastrointestinal symptoms and microcytic anemia. The colonoscopy was normal, while the esophagogastroduodenoscopy revealed a normal esophagus, gastritis with erosions, a double pylorus and a normal duodenum. Specifically, an accessory channel connected the lesser curvature of the prepyloric antrum to the duodenal bulb and the endoscope was able to easily pass via both of the pyloric channels ().\nFurthermore, the Helicobacter pylori quick test proved positive, while histological examinations of gastric antrum and corpus showed chronic active gastritis in both of them and H&E stain revealed a large amount of Helicobacter pylori bacteria. Finally, the patient was treated successfully with concomitant therapy for the eradication of Helicobacter pylori (metronidazole 500 mg, amoxicillin 1g, clarithromycin 500 mg and lansoprazole 30 mg, twice a day for 10 days). The eradication was verified via a stool antigen test for Helicobacter pylori, 1 month after treatment. In addition, he took iron supplements, continues to take proton pump inhibitor once a day and has limited the use of NSAIDs. The symptoms were eliminated after a few weeks from the inception of therapy and the hemoglobin was normal after 5 months. Two years later, a follow-up endoscopy revealed that the bridge between the two channels was disappeared and there was only single large opening (). The stomach, duodenum and esophagus were normal. In addition, biopsies were taken from the gastric antrum and body, which showed chronic inactive gastritis, while H&E stain proved to be negative for Helicobacter pylori.