Angelo Zullo1, Angela Rago2, Stefano Felici3, Stefano Licci4, Lerenzo Ridola5, Tommaso Caravita di Toritto6. 1. Gastroenterology and Digestive Endoscopy, 'Nuovo Regina Margherita' Hospital, Rome, Italy. angelozullo66@yahoo.it. 2. Haematology Unit, 'Nuovo Regina Margherita' Hospital, Rome, Italy. angela.rago@gmail.com. 3. Haematology Unit, 'Nuovo Regina Margherita' Hospital, Rome, Italy. sfelici51@gmail.com. 4. Pathology Unit, 'San Filippo Neri' Hospital, Rome, Italy. stefano.licci@hotmail.com. 5. Gastroenterology Unit, Sapienza University of Rome, Polo Pontino, Latina, Italy. lorenzo.ridola@tiscali.it. 6. Haematology Unit, 'Nuovo Regina Margherita' Hospital, Rome, Italy. tcaravita@yahoo.it.
Abstract
BACKGROUND AND AIMS: Patients with primary gastric lymphoma are at an increased risk of developing gastric cancer. Data on gastric precancerous lesions development in these patients are scanty. We assessed gastric precancerous lesions in a cohort of patients with primary lymphoma. METHODS: Data of patients with primary gastric lymphoma [mucosa-associated lymphoid tissue (MALT)- lymphoma or diffuse large B-cell lymphoma (DLBCL)] were analysed. Multiple (>10) biopsies were performed on gastric mucosa at each endoscopic control, beyond macroscopic lesions. Presence and distribution of intestinal metaplasia (IM) at baseline, the onset at follow-up, and progression through the stomach or transformation in the incomplete IM type were assessed. The onset of neoplastic lesions was recorded. RESULTS: Data of 50 patients (mean age of 63.6 ± 10.7 years; M/F: 25/25), including 40 with MALT-lymphoma and 10 with DLBCL, with median follow-up of 30.5 months (range: 9-108) and a median of 6 endoscopic controls (range: 3-14) were evaluated. At entry, IM was present in 12 (24%), and it developed in other 22 (57.9%) patients at a median follow-up of 6 (range: 3-40) months. Overall, progression of IM was observed in 7 (21.2%) cases, including extension in the stomach (n=5) or transformation into the incomplete type (n=2). Low-grade dysplasia was detected in 4, and indefinite dysplasia in other 7 patients. In one patient, low-grade dysplasia had progressed to high-grade and gastric adenocarcinoma of the fundus. CONCLUSIONS: Our data found a frequent onset and rapid progression of precancerous lesions on gastric mucosa of lymphoma patients. This observation could explain the increased incidence of metachronous gastric cancer in these patients.
BACKGROUND AND AIMS: Patients with primary gastric lymphoma are at an increased risk of developing gastric cancer. Data on gastric precancerous lesions development in these patients are scanty. We assessed gastric precancerous lesions in a cohort of patients with primary lymphoma. METHODS: Data of patients with primary gastric lymphoma [mucosa-associated lymphoid tissue (MALT)- lymphoma or diffuse large B-cell lymphoma (DLBCL)] were analysed. Multiple (>10) biopsies were performed on gastric mucosa at each endoscopic control, beyond macroscopic lesions. Presence and distribution of intestinal metaplasia (IM) at baseline, the onset at follow-up, and progression through the stomach or transformation in the incomplete IM type were assessed. The onset of neoplastic lesions was recorded. RESULTS: Data of 50 patients (mean age of 63.6 ± 10.7 years; M/F: 25/25), including 40 with MALT-lymphoma and 10 with DLBCL, with median follow-up of 30.5 months (range: 9-108) and a median of 6 endoscopic controls (range: 3-14) were evaluated. At entry, IM was present in 12 (24%), and it developed in other 22 (57.9%) patients at a median follow-up of 6 (range: 3-40) months. Overall, progression of IM was observed in 7 (21.2%) cases, including extension in the stomach (n=5) or transformation into the incomplete type (n=2). Low-grade dysplasia was detected in 4, and indefinite dysplasia in other 7 patients. In one patient, low-grade dysplasia had progressed to high-grade and gastric adenocarcinoma of the fundus. CONCLUSIONS: Our data found a frequent onset and rapid progression of precancerous lesions on gastric mucosa of lymphomapatients. This observation could explain the increased incidence of metachronous gastric cancer in these patients.