Observational Study
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 7, 2024; 30(29): 3479-3487
Published online Aug 7, 2024. doi: 10.3748/wjg.v30.i29.3479
Prevalence of Helicobacter pylori infection among patients with esophageal carcinoma
Miriam López-Gómez, Maria Morales, Rebeca Fuerte, Marta Muñoz, Pedro-David Delgado-López, Jorge Francisco Gómez-Cerezo, Enrique Casado
Miriam López-Gómez, Department of Medical Oncology, Precision Oncology Laboratory, Infanta Sofía University Hospital, San Sebastián de los Reyes 28231, Madrid, Spain
Maria Morales, Department of Medical Oncology, Infanta Sofía University Hospital, San Sebastián de los Reyes 28702, Spain
Rebeca Fuerte, Department of Internal Medicine, Infanta Sofía University Hospital, San Sebastián de los Reyes 28703, Madrid, Spain
Marta Muñoz, Department of Pathology, Infanta Sofía University Hospital, San Sebastián de los Reyes 28702, Spain
Pedro-David Delgado-López, Department of Neurosurgery, Burgos University Hospital, Burgos 09006, Spain
Jorge Francisco Gómez-Cerezo, Department of Internal Medicine, Infanta Sofía University Hospital and Henares University Hospital Foundation for Biomedical Research and Innovation, San Sebastian de los Reyes 28702, Madrid, Spain
Enrique Casado, Department of Medical Oncology, Infanta Sofia University Hospital and Henares University Hospital Foundation for Biomedical Research and Innovation, San Sebastian de los Reyes 28702, Madrid, Spain
Co-first authors: Miriam López-Gómez and Maria Morales.
Author contributions: López-Gómez M and Morales M wrote the manuscript; Morales M and Fuerte R curated the clinical data and performed the biostatistical analyses; Muñoz M selected the tumor tissue to be analyzed; Delgado-López PD drafted/edited the manuscript and reviewed the English version; Gómez-Cerezo JF and Casado E helped with clinical and scientific input and study design; López-Gómez M developed the study concept, interpreted the data and drafted/edited the manuscript; All authors edited the manuscript.
Institutional review board statement: Infanta Sofía University Hospital Institutional Review Board approval was obtained on June 1, 2023.
Informed consent statement: All study participants, or their legal guardian, provided informed written consent prior to study enrollment.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: Participants gave informed consent for data sharing at miriam.lopez@telefonica.net.
STROBE statement: The authors have read the STROBE Statement-checklist of items, and the manuscript was prepared and revised according to the STROBE Statement-checklist of items.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Miriam López-Gómez, PhD, Doctor, Department of Medical Oncology, Precision Oncology Laboratory, Infanta Sofía University Hospital, C/Paseo Europa 34, San Sebastián de los Reyes 28231, Madrid, Spain. miriam.lopez@telefonica.net
Received: April 24, 2024
Revised: June 24, 2024
Accepted: July 11, 2024
Published online: August 7, 2024
Processing time: 95 Days and 15.3 Hours
Abstract
BACKGROUND

Helicobacter pylori (H. pylori) is a widespread microorganism related to gastric adenocarcinoma (AC). In contrast, it has been reported that an inverse association exists between H. pylori infection and esophageal carcinoma. The mechanisms underlying this supposedly protective effect remain controversial.

AIM

To determine the prevalence of H. pylori infection in esophageal carcinoma patients, we performed a retrospective observational study of esophageal tumors diagnosed in our hospital.

METHODS

We retrospectively reviewed the prevalence of H. pylori infection in a cohort of patients diagnosed with esophageal carcinoma. Concomitant or previous proton pump inhibitor (PPI) usage was also recorded.

RESULTS

A total of 89 patients with esophageal carcinoma (69 males, 77.5%), with a mean age of 66 years (range, 26-93 years) were included. AC was the most frequent pathological variant (n = 47, 52.8%), followed by squamous cell carcinoma (n = 37, 41.6%). Fourteen ACs (29.8%) originated in the gastroesophageal junction and 33 (70.2%) in the esophageal body. Overall, 54 patients (60.7%) presented at stages III and IV. Previous H. pylori infection occurred only in 4 patients (4.5%), 3 with AC (6.3% of all ACs) and 1 with squamous cell carcinoma (2.7% of all squamous cell tumors). All patients with previous H. pylori infection had stage III-IV. Only one patient had received prior H. pylori eradication therapy, whereas 86 (96.6%) had received previous or concomitant PPI treatment.

CONCLUSION

In our cohort of patients, and after histologic evaluation of paraffin-embedded primary tumors, we found a very low prevalence of previous H. pylori infection. We also reviewed the medical history of the patients, concluding that the majority had received or were on PPI treatment. The minimal prevalence of H. pylori infection found in this cohort of patients with esophageal carcinoma suggests a protective role.

Keywords: Helicobacter pylori; Eradication; Esophageal tumor; Dysbiosis; Proton pump inhibitors; Carcinogenesis; Microbiota; Incidence

Core Tip:Helicobacter pylori (H. pylori) is involved in gastric carcinogenesis and its eradication has become widely accepted. However, recent studies suggest that it might have a role in maintaining homeostasis in the gastroesophageal junction cells and may have a protective role in esophageal carcinogenesis. The absence of this microorganism might contribute to dysbiosis and alterations in the esophageal microenvironment which might finally be involved in the onset of esophageal tumor. We are very much concerned that the prevalence of esophageal cancer increases after the universalization of H. pylori eradication.