Case Presentation

MG is a 56-year-old female with no significant past medical history who presented to TJUH in October 2007 with a two year history of abdominal pain and weight loss. At presentation, she described her pain as non-radiating, 7 out of 10, gnawing, burning and located in the epigastrum and left upper quadrant. The pain initially occurred approximately 15 minutes postprandially and lasted 30 minutes. Over the two year period, the pain progressed to lasting for hours following meals. Dietary modifications and food consistency did not help the pain. The patient began avoiding oral intake, and her weight declined from 120 to 80 pounds. She denied nausea, vomiting, diarrhea, constipation, hematochezia, melena and change in stool frequency. Over the two years prior to admission the patient had an extensive workup with multiple gastroenterologists. Her initial workup included a colonoscopy, EGD, abdominal ultrasound and computerized tomography (CT) of the abdomen and pelvis. These were all reportedly normal and the patient was diagnosed with irritable bowel syndrome and treated symptomatically with a PPI. Due to lack of improvement, a second gastroenterologist repeated the EGD/colonoscopy and diagnosed her with peptic ulcer disease secondary to multiple gastric ulcers. She was treated with a PPI and carafate. A capsule study showed gastric and jejunal ulcers with cobblestone appearance of the small bowel which led to the diagnosis of Crohn’s disease. She was treated briefly with Pentasa. The patient sought care as an outpatient at TJUH Division of Gastroenterology. Mesenteric ischemia was initially high on the differential. An MRA of the abdomen revealed patent mesenteric vessels. Other workup included gastric emptying scan, push enteroscopy, endoscopic ultrasound (EUS), full-thickness biopsy in the operating room, fasting gastrin level, and an NSAID level. These studies were mostly inconclusive. Other studies including an octreotide scan, gastrin levels, and chromogranin A levels were either normal or inconclusive. Furthermore, it was discovered that the gastric pH was 4.4, arguing against a gastrin producing tumor as seen in Zollinger-Ellison Syndrome.