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Amyloidosis is commonly systemic, occasionally organ-limited, and rarely a solitary localized mass. The latter, commonly referred to as tumoral amyloidosis, is described as occurring in nearly every organ/tissue. Only a few reports of gastric amyloidosis exist today. We describe a 72 year-old black male from Barbados presenting with 3 d of diffuse abdominal pain. His medical history included Non-Hodgkin's Lymphoma diagnosed five years ago, status-post six rounds of cyclophosphamide, adriamycin, vincristine, prednisone chemotherapy, and currently was in remission. On computed tomography scan of the abdomen, thickening and calcification of the gastric wall was noted along with pneumatosis. On esophagogastroduodenoscopy, a large circumferential friable mass was seen from the gastroesophageal junction to the body. A large non-bleeding 3 cm polyp was also seen in post bulbar area of duodenum. Biopsies were stained with Congo red and gave green birefringence under polarized light, consistent with tumoral amyloidosis. Positron emission tomography scan revealed diffuse gastric mucosa uptake compatible with gastric malignancy without metastatic foci. Treatment for gastric amyloidomas has presently been one of observation or, at most, resection of the amyloid mass. It is not known if our patient required the same approach or if this warranted the re-institution of chemotherapy for Non-Hodgkin's Lymphoma. Until more reports of tumoral amyloidosis are made known, treatment as well as prognosis remain uncertain.

BACKGROUND: Gastro-oesophageal reflux disease complications may reflect imbalances between protective and injurious factors. Through its effects on cell growth, leptin may influence oesophageal mucosal homeostasis. AIMS: To determine whether leptin receptors are present in the oesophagus, and whether serum or gastric leptin levels are associated with oesophageal inflammation and metaplasia. METHODS: From patients referred for upper endoscopy, biopsies were obtained from the stomach and distal oesophagus, and serum samples were collected. Patients were classified as having normal, inflamed or Barrett's oesophagus. Quantitative immunohistochemistry was performed on representative sections, and leptin levels in plasma and gastric biopsy samples were determined by specific immunoassay. RESULTS: Of 269 individuals enrolled, 105 were Helicobacter pylori-negative. Of the 88 patients with complete oesophageal biopsies, 44 were normal, 24 were inflamed and 20 were Barrett's oesophagus. Receptors for leptin were highly expressed on oesophageal epithelial cells, with similar density and staining pattern in all three conditions, and plasma and antral leptin levels did not differ significantly. Patients with Barrett's had significantly (p = 0.01) higher fundic leptin levels (median 202 (interquartile range 123-333) pg/mg) compared with normal (126 (78-221) pg/mg) or inflamed (114 (76-195) pg/mg) oesophagus. In multivariate analysis, for every twofold increase in fundic leptin, the odds of having Barrett's was 3.4 times (95% CI 1.5 to 7.6) higher compared with having a normal oesophagus. CONCLUSIONS: Leptin receptor expression on oesophageal epithelial cells provides a pathway for leptin-mediated signal transduction. Variation in gastric leptin production could contribute to differential oesophageal healing and metaplasia progression