Conflicts of Interest: Nothing to report.
Images in Hematology
Russell body gastritis†
Article first published online: 9 MAR 2010
Copyright © 2010 Wiley-Liss, Inc.
American Journal of Hematology
Volume 85, Issue 12, pages 951–952, December 2010
How to Cite
Habib, C., Gang, D. L., Ghaoui, R. and Pantanowitz, L. (2010), Russell body gastritis. Am. J. Hematol., 85: 951–952. doi: 10.1002/ajh.21702
- Issue published online: 23 NOV 2010
- Article first published online: 9 MAR 2010
- Manuscript Accepted: 1 MAR 2010
- Manuscript Received: 24 FEB 2010
Russell body gastritis, first described in 1998 , is a reactive gastric mucosal infiltration of plasma cells filled with cytoplasmic Russell bodies. Russell bodies are immunoglobulins present within dilated rough endoplasmic reticulum cisternae that have accumulated secondary to abnormal secretion . We present a case of Russell body gastritis occurring in a 75-year-old man with a history of alcohol use, renal failure, dyslipidemia, and prior rhabdomyolysis. He was noncompliant with reflux medications and reported intermittent coffee-ground emesis. Esophagogastroduodenoscopy with biopsy revealed esophagitis and nodular chronic active gastritis. The gastric antral mucosa exhibited regenerative changes and a dense chronic inflammatory infiltrate (Image 1) composed of numerous Russell body filled plasma cells, including Mott cells (Image 2). No lymphoepithelial lesions were identified. A CD138 immunostain (Image 3) confirmed that these were plasma cells and in situ hybridization studies for kappa and lambda light chains demonstrated their polyclonal distribution. Gastric biopsies were negative for Helicobacter pylori by immunohistochemistry.
To date, there have been 11 other published case reports of Russell body gastritis [1–10]. The average patient age is 57 years (range, 29–80 years), including seven males and five female patients. These patients presented primarily with gastric related symptoms including nausea, dyspepsia, and epigastric pain. Mucosal swelling and erythema appear to be relatively common endoscopic findings, and only a few cases exhibited erosion, ulceration, or a raised lesion endoscopically. The exact etiology of Russell body gastritis is unclear. However, nine (82%) of these reported cases were H.pylori positive, two individuals were positive for human immunodeficiency virus (HIV), and one also had Candida esophagitis. Another two patients had Epstein Barr virus (EBV)-associated gastric carcinoma. Except for one individual with a concomitant monoclonal gammopathy of undetermined significance (MGUS), none of these patients have manifested a plasma cell disorder.
Russell body gastritis is a diagnosis based on microscopic findings. The differential diagnosis on biopsy includes signet ring cell carcinoma, plasmacytoma, B-cell lymphoma with plasmacytic differentiation, and granular cell tumor. As highlighted in this, ancillary studies can be useful to demonstrate that these cells are polytypic plasma cells. Associated gastric carcinoma and infection (H.pylori, HIV, EBV, Candida) should also be excluded.