Clinical records of gastric anisakiasis cases diagnosed between April 2003 and May 2017 at St. Luke’s International Hospital (Tokyo, Japan), a tertiary referral center, were retrospectively reviewed. A total of 134 patients (54% men; mean age, 41.8 years) were diagnosed with symptomatic gastric anisakiasis, with subsequent endoscopic removal of the larvae during this period. We reviewed the presence of atrophic gastric mucosa using the modified Kimura-Takemoto classification [3]. Interestingly, 83.6% (112/134) of the patients had no atrophy, 10.4% (14/134) had limited atrophy (antral and antral-predominant atrophy: C-1, C-2), and only 5.9% had extensive atrophy (corpus-predominant and pan-atrophy: C-3, O-1, O-2, O-3). The prevalence of a non-atrophic stomach seemed high, considering the overall prevalence of Helicobacter pylori infection in Japan is approximately 40% [4]; we therefore assumed that a significant number of patients had asymptomatic parasitic infection.

Although factors associated with the development of symptomatic gastric anisakiasis remain unknown, the correlation between clinical symptoms and gastric atrophy may be significant. A previous study analyzing 45 Anisakis specimens from 35 patients revealed that larvae penetrated normal mucosa more frequently than atrophic mucosa, and that patients had a significantly higher risk of developing clinical symptoms with infection in normal mucosa [5]. We speculate that the clinical manifestations of gastric anisakiasis may be inversely related to H. pylori infection, given that atrophic gastritis is mostly due to H. pylori infection. Despite the possibility of selection bias in this report, further investigation is warranted to help clarify the mechanisms involved in the immune response to Anisakis larvae. With a decrease in prevalence of H. pylori infection among the younger population in East Asia, gastric anisakiasis may become more common.