Published online Mar 28, 2013. doi: 10.3748/wjg.v19.i12.2000
Revised: January 5, 2013
Accepted: January 18, 2013
Published online: March 28, 2013
Processing time: 112 Days and 18.5 Hours
Helicobacter pylori (H. pylori) is a pathogen and the most frequent cause of gastric ulcers. There is also a close correlation between the prevalence of H. pylori infection and the incidence of gastric cancer. We present the case of a 38-year-old woman referred by her primary care physician for screening positron emission tomography-computed tomography (PET-CT), which showed a nodular strong accumulation point with standardized uptake value 5.6 in the gastric fundus. Gastroscopy was then performed, and a single arched ulcer, 12 mm in size, was found in the gastric fundus. Histopathological examination of the lesion revealed chronic mucosal inflammation with acute inflammation and H. pylori infection. There was an obvious mitotic phase with widespread lymphoma. Formal anti-H. pylori treatment was carried out. One month later, a gastroscopy showed a single arched ulcer, measuring 10 mm in size in the gastric fundus. Histopathological examination revealed chronic mucosal inflammation with acute inflammation and a very small amount of H. pylori infection. The mitotic phase was 4/10 high power field, with some heterotypes and an obvious nucleolus. Follow-up gastroscopy 2 mo later showed the gastric ulcer in stage S2. The mucosal swelling had markedly improved. The patient remained asymptomatic, and a follow-up PET-CT was performed 6 mo later. The nodular strong accumulation point had disappeared. Follow-up gastroscopy showed no evidence of malignant cancer. H. pylori-associated severe inflammation can lead to neoplastic changes in histiocytes. This underscores the importance of eradicating H. pylori, especially in those with mucosal lesions, and ensuring proper follow-up to prevent or even reverse early gastric cancer.