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.
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.