LAUSR

A man in his 60s underwent esophagogastroduodenoscopy (EGD) because he found to be positive for serum Helicobacter pylori antibodies at a health checkup. He had no clinical symptoms. His grandparents had a history of gastric cancer. EGD revealed active gastritis due to H. pylori infection (Fig. 1a). Because a culture test showed tolerance for clarithromycin, he started H. pylori eradication therapy with amoxicillin 600 mg, metronidazole 250 mg, and rabeprazole 10 mg every 12 h twice a day for 7 days. EGD 2 months after eradication therapy showed that his active gastritis had improved, while a huge ulcerative lesion had arisen at the greater curvature of the fornix (Fig. 1b). Successful H. pylori eradication was confirmed by a urea breath test and a culture test. Biopsies of the ulcerative lesion were performed, and the specimens were diagnosed as diffuse large B-cell lymphoma (DLBCL) positive for CD10, CD20, BCL-2, and c-myc, which is double-expressor lymphoma (Fig. 2). DLBCL is a common subtype of primary gastric lymphoma that can also arise from a low-grade lymphoma as well. Double-expressor lymphoma is reportedly frequent in transformed lymphoma and is associated with a poor prognosis. In contrast to low-grade gastric mucosa-associated lymphoid tissue lymphoma, which is primarily cured with H. pylori eradication, high-grade DLBCL transformed from mucosa-associated lymphoid tissue lymphoma is believed to be H. pylori-independent, and chemotherapy is the mainstay treatment. In the present case, whether DLBCL arose de novo in the stomach or transformed from low-grade lymphoma is unclear. Furthermore, active gastritis due to H. pylori infection may have hampered the diagnosis of the lymphoma lesion before H. pylori eradication therapy. We usually perform follow-up EGD about a year after H. pylori eradication therapy in order to survey metachronous early gastric cancer. However, early follow-up EGD after eradication therapy should be considered in cases where the endoscopic visibility is poor due to mucus of active gastritis induced by H. pylori infection.