Secondary Logo

Journal Logo

Panesophageal-Gastroesophageal Junction Adenocarcinoma in a Patient without Barrett's Mucosa

19

Ali, Sobia M.D.; Parameswaran, Ganapathi M.D.; Kothari, Tarun M.D.

American Journal of Gastroenterology: September 2005 - Volume 100 - Issue - p S29
Supplement Abstracts Submitted for the 70th Annual Scientific Meeting of the American College of Gastroenterology: ESOPHAGUS
Free

Internal Medicine, Unity Health System, Rochester, NY.

Purpose: We report the occurrence of Panesophageal-gastroesophageal adenocarcinoma in a patient without Barrett's mucosa. We believe this is the first reported case of this clinical entity. Although several case reports have been published about distal esophageal and gastroesophageal adenocarcinoma, none have reported pan-esophageal adenocarcinoma on the initial presentation, in absence of Barrett's mucosa. 56 year old male presented with complaints of dysphagia and odonophagia for two weeks, and a 25lb weight loss in the last two months. Past medical history included hypertension, but no history of GERD, or tobacco use. The patient underwent an upper GI series, showing numerous superficial ulcerations involving the entire esophagus. Subsequently an upper gastrointestinal endoscopy was performed, showing an ulcerated mass at the cardia of stomach and severe ulcerative esophagitis involving the entire esophagus. Biopsies were taken, from the thoracic esophagus till the gastric mass in 7 places, each at 3–4 cm intervals. Biopsy results showed poorly differentiated adenocarcinoma in all specimens. No evidence of Barrett's mucosa was found and a stain was negative for H. pylori. An abdominal CT scan showed extensive metastatic disease. The patient was referred to an oncologist for further workup.

Esophageal adenocarcinoma represents 50% of all esophageal carcinomas. Evolution of esophageal adenocarcinoma usually begins with GERD, leading to metaplastic Barrett's esophageal mucosa finally developing into adenocarcinoma. Adenocarcinoma, however may occur in the absence of Barrett's mucosa, as was the case with our patient. We believe the patient had spread of tumor originating in the gastric cardia, later spreading to the esophagus. Two mechanisms contributing to gastric cardia adenocarcinoma are thought to be H. pylori, and the resultant effects of GERD induced damage, both, not seen in our patient. Studies have shown upto 40% of patients diagnosed with esophageal adenocarcinoma may not have any reported symptoms of GERD. On reviewing case reports of esophageal adenocarcinoma and time of onset of symptoms, we found that these patients had involvement of only the distal esophagus at time of presentation. Interestingly, our patient in spite of this extensive involvement, remained asymptomatic until the very end. Our literature search revealed no prior reports of such extensive disease, with such a time compressed clinical course. The rapidity of spread of tumor in this case raises the question of surveillance endoscopy.

© The American College of Gastroenterology 2005. All Rights Reserved.