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First, we wish to thank Dr Quach and his coauthors1 for their interest in our study. We are flattered by their statement that our numbers are ‘quite convincing’ and will attempt to mitigate their concerns.2
The authors are correct in that the eradication of Helicobacter pylori does not abolish all gastric cancer (GC) risk in patients with long-standing atrophic gastritis.3–5 This broad statement, however, requires some clarifications.
The operative link for gastritis assessment (OLGA) Group was and is aware of the limitations of the staging system. Gastritis staging should be viewed as a step forward in improving the consistency of the interdisciplinary communication of GC risk in individual patients.6
The results of our study (confirmed by more recent data7) can help provide a solid clinicobiological rationale for designing secondary prevention strategies for GC. Such strategies should be modulated by a wide spectrum of variables, such as bacterial biology, host-related factors, as well as local epidemiological and socioeconomic conditions.
All models of secondary prevention strategies include occasional failures: for example, ‘interval colorectal cancers’ do not significantly impair the overall effectiveness of the screening colonoscopy. Similarly, while OLGA staging cannot be expected to prevent all GCs in all epidemiological contexts, it may play a reliable role in cancer risk assessment. This is the realistic goal we strive to achieve when advocating the widespread use of this staging strategy.
After recognising the significantly increased GC risk associated with high-risk OLGA stages, the second part of Dr Quach and his coauthors’ letter focuses on the possible occurrence of GC in H. pylori-eradicated subjects. Cancer development in these patients is well documented in both the Eastern and Western literature. Evidence has been also provided on the histologically proven regression of mucosal atrophy and intestinalisation, while the clinicopathological relevance of spasmolytic polypeptide-expressing metaplasia (SPEM) has been less extensively explored.8
Gastric cancer development decades after H. pylori eradication needs to be more deeply investigated. In particular, other risk factors should be considered, including eradication failure, reinfection, consistency of gastritis staging (SPEM is often histologically underscored), coexisting syndromic cancer-prone diseases, gastric autoimmunity and other yet unknown environmental factors.
Finally, we wish to emphasise that we do not see a dichotomy between the ‘histology-based’ and the ‘endoscopy-based’ prediction of GC risk. These two strategies are complementary rather than antagonistic, and their choice in practice should be determined on the basis of operative local conditions. We cannot support excluding the microscopic information in high-risk patients to save the cost of histopathology. Innumerable potentially useful biopsy samples have been and continue to be discarded after using them for the urea-based assessment of H. pylori infection, which could be equally or better detected by histology while simultaneously providing useful information on the state of the gastric mucosa.9
We are in complete agreement with Dr Quach and his coauthors’ position that an ethical approach requires centring prevention strategies on our patients. While the availability of different technical methodologies and the conditions of local health-system networks are pivotal to the strategies chosen, we should always attempt to use the best available of different, yet complementary, diagnostic approaches (serology, endoscopy, pathology) framed in the epidemiological context of H. pylori prevalence and GC incidence.10
Footnotes
Contributors Submitted by MR as the corresponding author.
Competing interests None declared.
Provenance and peer review Not commissioned; internally peer reviewed.
Patient consent for publication Not required.