A 65-year-old female with history of chronic alcohol use was hospitalized for sudden onset of hematemesis. She also reported few days of nausea and vomiting associated with worsening ascites. She denied any significant past medical history except for a ruptured ovarian cyst at age of 30 years that required emergent surgery. Patient had a long history of alcohol use (two glasses of vodka daily) for over 10 years. Physical exam showed scleral icterus, there was mild abdominal distention with epigastric tenderness, no hepatosplenomegaly was noted. No signs of encephalopathy or asterixis were seen. Blood test showed hemoglobin 10.4 × 10 g/dL, white blood cell count of 7.7 × 103 cells/µL and platelet count of 190 × 103 cells/µL. Her prothrombin time and international normalized ratio (INR) were elevated at 1.4 and 14.3 s, respectively. Liver function test showed aspartate transaminase 140 U/L, alanine transaminase 29 U/L, alkaline phosphatase 332 U/L, total bilirubin 9.6 mg/dL (direct 7.4 mg/dL, indirect 2.2 mg/dL). Few hours after admission, she developed an episode of hematemesis with drop in hemoglobin to 7.7 g/dL. Emergent endoscopy showed a non-bleeding 2 cm prepyloric gastric antral ulcer (). Biopsy of the ulcer base was negative for malignancy or H. pylori.\nFollow-up endoscopy at an interval of 6 weeks showed a healing prepyloric antral ulcer with mild portal hypertensive gastropathy (). Patient had a repeat endoscopy at 4 months for persistent nausea and vomiting which again showed a healing antral ulcer. She continued to drink alcohol and was intermittently followed by her the primary care physician. She also reported daily NSAID use for abdominal pain and nausea. She had multiple emergency department (ED) visits for the same complaints and underwent repeat endoscopy which showed a duodenal ulcer (). She was managed with pantoprazole twice daily and was advised to avoid NSAIDs and alcohol. She also underwent extensive workup for recurrent nausea and vomiting which were all unremarkable. Systemic disorders including but not limited to neurological cause, adrenal, parathyroid and diabetes were also ruled out.\nShe again presented to the ED for worsening nausea and vomiting associated with upper abdominal pain. Endoscopy, now 7 years from the discovery of the initial lesion, showed a GDF. The prepyloric antral ulcer had fistulized into the duodenal bulb creating the appearance of a double pylorus (). Biopsy of the ulcer base was again negative for malignancy or H. pylori. H. pylori stool antigen and serum H. pylori antibody test were also negative. She was discharged on oral proton pump inhibitor and has been followed up with gastroenterology for management of Laennec’s cirrhosis. With more frequent outpatient follow up, alcohol abstinence and use of acid-suppression medication, she had gradual improvement in her symptoms in about 1 - 2 months.
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.