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Medicine Group Research Article Article ID: igmin358

Endoscopic Aspects of Lesions Secondary to Helicobacter pylori Infection in two Hospitals in Douala: A Cross-Sectional Study over a Three-year Period

Bernard Bertrand Bille Eyoum 1,6 * ,
Fiacre Servais Bagnaka Eloumou 2 ,
Christiane Sike Médi 3,6 ,
Jethro Roland Misse Ngangue Ekwala 1 ,
Claudia Laurence Ntonga 6 ,
Agnes Malongue 7 ,
Chimi Fotso 8 ,
Stephane Fotsing 8 ,
Clementine Kamdem 8 ,
Roger Gilbert Ateba 8 ,
Bertrand Claude Mokou 8 ,
Brigitte Laure Mabeku Kouitcheu 4 and
Jules-Roger Kuiate 5
Gastroenterology

Received 13 Aug 2026 Accepted 20 Aug 2026 Published online 21 Aug 2026

Abstract

Background: Helicobacter pylori infection is a major cause of gastroduodenal diseases and is strongly associated with gastric carcinogenesis. Endoscopy plays a key role in identifying mucosal lesions related to this infection. However, data on the endoscopic aspects of H. pylori–associated lesions remain scarce in Cameroon. This study aimed to describe the endoscopic features of lesions associated with Helicobacter pylori infection in two hospitals in Douala over a three-year period.

Methods: This analytical cross-sectional study included 842 patients who underwent upper gastrointestinal endoscopy with gastric biopsies. The diagnosis of H. pylori infection was established using histology (reference method), rapid urease testing, and bacterial culture. Histological lesions, including mononuclear and polymorphonuclear infiltration, glandular atrophy, and intestinal metaplasia, were assessed according to the updated Sydney classification and compared according to H. pylori infection status.

Results: The prevalence of H. pylori infection was 73.2% by histology, 67.7% by rapid urease test, and 42.9% by bacterial culture. The most common endoscopic lesions were superficial gastritis (28.4%) and erosive gastritis (22.3%), followed by duodenal ulcers (16.8%) and gastric ulcers (10%). The prevalence of H. pylori infection was particularly high in duodenal ulcers (91.9%), gastric ulcers (82.1%), and gastric cancer (100%). High positivity rates were also observed in superficial gastritis (70.7%), erosive gastritis (64.9%), and patients with normal endoscopic findings (63.6%). H. pylori infection was significantly associated (p < 0.01) with severe mononuclear and polymorphonuclear infiltration, glandular atrophy, and intestinal metaplasia.

Conclusion: This study confirms the high prevalence of H. pylori infection and its significant association with inflammatory, ulcerative, and precancerous gastric lesions. These findings support the major role of H. pylori in the pathophysiological cascade leading to gastric cancer and highlight the importance of early detection and eradication strategies.

Introduction

Helicobacter pylori infection is recognized as the main cause of chronic gastritis, peptic ulcer disease, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma [1–3]. Several diagnostic methods are currently available for detecting H. pylori infection in the gastric mucosa, including the ^13C-urea breath test, stool antigen detection, serology, polymerase chain reaction (PCR), rapid urease testing, bacteriological culture, and histological examination of gastric biopsies [4–7].

Among these diagnostic techniques, histopathological examination of gastric biopsies obtained during endoscopy remains an essential method because it allows the simultaneous detection of H. pylori and evaluation of gastric mucosal lesions [8–10]. With the development of endoscopic techniques, histopathological diagnosis based on endoscopic biopsies has become increasingly common and plays a central role in the assessment of both tumoral and non-tumoral gastric lesions.

However, histological evaluation of H. pylori infection also presents several limitations. In routine pathology practice, infection severity is often described using qualitative grading systems such as mild, moderate, or severe, or using semi-quantitative notations such as +, ++, and +++. These descriptions may not fully reflect the histopathological characteristics of the infection or provide precise information regarding its relationship with gastric carcinogenesis.

Previous studies have shown that H. pylori infection can induce structural changes in the gastric mucosa, including epithelial hyperproliferation and glandular atrophy [11,12]. Due to its strong association with gastric cancer, the bacterium has been classified as a group I carcinogen by the World Health Organization [13,14]. Consequently, increasing attention has been given to screening and eradication strategies aimed at preventing gastric cancer.

Several studies have investigated the relationship between H. pylori infection and histological lesions such as chronic gastritis, glandular atrophy, and intestinal metaplasia. These lesions represent key stages in the multistep process of gastric carcinogenesis described by the Correa cascade [15–19]. Furthermore, eradication of H. pylori has been shown to significantly reduce the risk of gastric cancer development [20–22].

Despite the high prevalence of Helicobacter pylori infection in developing countries, data on the endoscopic features of associated lesions remain limited in African settings. This cross-sectional study, conducted over three years in two hospitals in Douala, aimed to describe the endoscopic aspects of lesions associated with H. pylori infection and to assess their distribution among patients undergoing upper gastrointestinal endoscopy.

Methods

This was a cross-sectional study conducted among patients undergoing upper gastrointestinal endoscopy at Laquintinie Hospital and Douala General Hospital in Douala, Cameroon, over a three-year period from August 2014 to December 2016. The minimum required sample size was calculated using Lorentz’s formula:

N= Z²XP(1P) m²

where the confidence level was set at 95% (Z = 1.96), the expected prevalence was based on the global Helicobacter pylori prevalence of 50% [38, 39] (p = 0.50), and the precision margin was set at 5% (m = 0.05), yielding a theoretical minimum requirement of 384 patients. To enhance statistical power and compensate for potential missing data, recruitment was expanded across both hospital sites, resulting in a total of 842 eligible participants included in the study.

Study population

Patients older than 15 years who underwent endoscopy for gastroduodenal disorders in the selected healthcare facilities were included. Consecutive sampling was used after obtaining informed consent.

The following patients were excluded:

  • Patients younger than 15 years
  • Patients receiving proton pump inhibitors
  • Gastritis associated with other conditions (reflux, suspected autoimmune origin, granulomatous gastritis)
  • Poor-quality or non-representative biopsies

Data collection

Data collected included demographic characteristics (age and sex), endoscopic findings and lesion location, and histopathological findings.

For each participant, nine gastric biopsy specimens were collected, including three from the antrum, three from the gastric body, and three from the angulus. The biopsy specimens were collected for histopathological examination and microbiological investigation according to the diagnostic procedures available and the quality of the specimens obtained.

Histopathological examination

Histopathological examination was performed using the modified Sydney classification. The evaluated parameters included chronic inflammatory infiltration, inflammatory activity, glandular atrophy, and intestinal metaplasia. Each parameter was graded as absent, mild, moderate, or severe.

H. pylori was identified on histological sections using modified Giemsa staining based on the presence of characteristic basophilic curved or spiral-shaped bacteria. The bacterial density was also assessed.

Microbiological diagnosis of H. pylori

The detection of H. pylori was performed using a rapid urease test and bacterial culture, in addition to histological examination.

The rapid urease test was performed using HelicotecUT® Plus and was interpreted at 5 minutes, 30 minutes, and 1 hour according to the manufacturer's instructions.

For bacterial culture, gastric biopsy specimens were inoculated onto appropriate selective culture media, including Mueller–Hinton agar supplemented with horse blood and Columbia agar with antibiotic supplementation, and incubated under microaerophilic conditions for seven days.

Bacterial identification was based on colony morphology, Gram staining, and biochemical tests, including oxidase, catalase, and urease reactions.

When a specific diagnostic test could not be performed because of insufficient specimen quality or inadequate specimen conditions, the corresponding test result was considered unavailable and was not used in the analysis of that diagnostic method. Participants with an unavailable result for one diagnostic procedure remained eligible for analyses based on the other available diagnostic information.

Definition of H. pylori infection

Histological examination was considered the reference method for the primary classification of H. pylori infection. The diagnostic results obtained by rapid urease testing and bacterial culture were analyzed according to the availability and quality of the corresponding specimens.

Ethical considerations

The study was conducted in accordance with the Declaration of Helsinki and received approval from the National Ethics Committee of Cameroon (Authorization No. 2014/03/425/L/CNE SRH/SP). Written informed consent was obtained from all participants.

Statistical analysis

Statistical analyses were performed using SPSS version 20®. Qualitative variables were described by their frequencies. Associations between variables were tested using the Chi-square test, with a significance level set at p < 0.05.

Results

Prevalence of Helicobacter pylori infection in the study population

The study revealed a high prevalence of Helicobacter pylori infection in the study population. Histological examination, considered the reference method, showed a high positivity rate (73.2%), indicating that nearly three-quarters of the patients were infected. The rapid urease test also showed a high positivity rate (67.7%), with good agreement with histology, confirming its satisfactory diagnostic performance.

In contrast, culture showed a lower positivity rate (42.9%) and a considerable proportion of tests not performed, probably due to technical constraints and limited sensitivity. Thus, histology remains the most reliable diagnostic method, followed by the rapid urease test, whereas culture appears to be less effective in this context (Table 1).

: Prevalence of Helicobacter pylori infection according to diagnostic method
  Diagnostic Methods
Number of patients (n) Percentage (%)
  Culture Negative 317 37.6
Not performed 164 19.5
Positive 361 42.9
Histology
(Gold standard)
Negative 226 26.8
Positive 616 73.2
Rapid urease test Negative 272 32.3
Positive 570 67.7

Endoscopic findings of participants

Analysis of the endoscopic data showed that gastroduodenal disorders were predominantly inflammatory lesions, particularly superficial gastritis (28.4%), followed by erosive gastritis (22.3%). Gastroduodenal ulcers were also frequent, with progressive duodenal ulcers accounting for 16.8% and progressive gastric ulcers for 10% of cases. Other conditions, including normal endoscopy, chronic gastritis, and non-progressive bulbar ulcers, were less common, while gastric tumors remained rare (1.7%). The distribution by sex was generally balanced, with a slight female predominance for erosive gastritis and a male predominance for duodenal ulcers and chronic gastritis (Table 2).

Table 2: Distribution of patients according to gastroduodenal disorders.
Endoscopic finding Women n (%) Men n (%) Total n (%)
Progressive duodenal ulcer 70 (14.8) 66 (17.8) 136 (16.8)
Progressive gastric ulcer 47 (10.0) 37 (10.0) 84 (10.0)
Non-progressive bulbar ulcer 18 (3.8) 22 (5.9) 40 (4.8)
Superficial gastritis 132 (28.0) 107 (28.9) 239 (28.4)
Erosive gastritis 122 (25.8) 66 (17.8) 188 (22.3)
Chronic gastritis 18 (3.8) 29 (7.8) 47 (5.6)
Gastric tumor 8 (1.7) 6 (1.6) 14 (1.7)
Normal endoscopy 56 (11.1) 32 (8.6) 88 (10.5)
Others* 1 (0.2) 5 (1.4) 6 (0.7)
Others include gastric polyps, hiatal hernia, ulcer scars, cardia incontinence, etc.

Prevalence of Helicobacter pylori infection according to site and pathology

Analysis of Helicobacter pylori (Hp) prevalence according to biopsy site and endoscopic indications revealed a strong association between Hp infection and ulcerative lesions, particularly duodenal ulcers (Table 3).

Table 3: Prevalence of H. pylori according to biopsy site and endoscopic indications.
Endoscopic finding Site  
  Antrum (%) Body(%) Angulus(%) Total
HPP(%)
HPP HPN HPP HPN HPP HPN  
Duodenal ulcer 53(91.4) 5(8.6) 51(91.1) 5(8.9) 21(95.5) 1(4.5) 91.9
Gastric ulcer 39(84.8) 7(15.2) 18(78.3) 5(21.7) 12(80) 3(20) 82.1
Bulbar ulcer 15(93.8) 1(6.2) 9(52.9) 8(47.1) 4(57.1) 3(42.9) 70.0
Superficial gastritis 58(67.4) 28(32.6) 69(71.9) 27(28.1) 42(73.7) 15(26.3) 70.7
Erosive gastritis 44(68.8) 20(31.2) 42(57.5) 31(42.5) 36(70.6) 15(29.4) 64.9
Chronic gastritis 9(52.9) 8(47.1) 11(68.8) 5(31.2) 8(57.1) 6(42.9) 59.6
Gastric cancer 6(100)   3(100) - 5(100) - 100
Normal endoscopy 18(58.1) 13(41.9) 22(64.7) 12(35.3) 16(69.6) 7(30.4) 63.6
Others* 3(100) - 2(100) - - 1(100) 83.3
Otherss (gastric polyps, hiatal hernia, ulcer scars, cardia incontinence, etc.)
HPN (Helicobacter pylori negative); HPP (Helicobacter pylori positive)

According to endoscopic indications

H. pylori infection demonstrated a high prevalence across most gastroduodenal disorders evaluated. Positivity was particularly elevated in patients with duodenal ulcers (91.9%) and gastric ulcers (82.1%), consistent with its well-established association with peptic ulcer disease. High positivity rates were also observed in bulbar ulcers (70.0%), superficial gastritis (70.7%), and erosive gastritis (64.9%), whereas a more moderate prevalence was recorded in chronic gastritis (59.6%).

All diagnosed cases of gastric cancer were positive for H. pylori (100%). However, given the small size of this subgroup (n = 14), this finding should be interpreted cautiously and does not support generalized conclusions regarding absolute prevalence or causality. Notably, even among patients with normal endoscopic findings, H. pylori prevalence remained substantial (63.6%), indicating that bacterial colonization can occur in the absence of macroscopically visible mucosal lesions.

According to biopsy site

Hp positivity was most frequently detected in the antrum, consistent with the bacterium’s usual tropism. However, high prevalence in the body and angulus supports the use of multiple biopsy sites to optimize detection of infection.

Correlation between endoscopic and histological findings According to H. pylori infection status

Histological analysis revealed that inflammatory infiltration was present across all gastroduodenal disorders, with moderate to severe forms particularly common in gastritis and ulcers. Mononuclear infiltration (chronic inflammation) and polymorphonuclear infiltration (acute activity) were significantly more pronounced in Helicobacter pylori-positive (HPP) patients, especially in duodenal and gastric ulcers as well as gastric cancer (Table 4).

Table 4: Grades of mononuclear cell infiltration, polymorphonuclear cell infiltration, glandular atrophy, and intestinal metaplasia in the study patients
Endoscopic Lesion Mononuclear Cell Infiltration (Grade 0–3) n (%) Polymorphonuclear Cell Infiltration (Grade 0–3) n (%) Glandular Atrophy (Grade 0–3) n (%) Intestinal Metaplasia (Grade 0–3) n (%)
    0 1 2 3 0 1 2 3 0 1 2 3 0 1 2 3
Duodenal ulcer 136 45 51.7 1.4 2.4 7.5 30.8 30.9 30.8 36.4 3.8 19.4 26.3 9.1 7.7 25.0 18.4
Gastric ulcer 84 28.6 21.1 33.3 9.5 28.6 31.6 33.3 20.0 0 21.1 38.1 33.3 42.9 26.3 19.0 13.3
Bulbar ulcer 40 40 71.4 23.1 - 40 - 38.5 44.4 0 14.3 15.4 22.2 20 14.3 23.1 33.3
Superficial gastritis 239 37.5 39 17.9 21.0 12.5 29.3 23.1 35.5 18.8 25.8 23.2 14.6 31.3 17.1 16.1 17.7
Erosive gastritis 188 23.1 30.8 22 28.0 19.4 33.3 28.2 42.9 16.7 26.9 22 35.6 30.6 17.9 20.3 21.2
Chronic gastritis 47 20 25 18.2 8.7 40 25.1 54.5 56.5 - 13 18.2 21.7 40 12.5 9.1 37.5
Gastric cancer 14 - - - 70 30 30 - 60 50 - 30 70 - - - 60
Normal endoscopy 88 51.7 26.1 83.3 - 48.3 73.9 16.7 100 - - - - - - - -
Others* 6 100 - - - - 100 - 50 - - 50 - - - - 50
Others ( gastric polyps, hiatal hernia, ulcer scars, cardia incontinence etc.)

Glandular atrophy and intestinal metaplasia, considered precancerous lesions, were also more frequent in HPP patients, particularly in ulcers, advanced gastritis, and gastric cancer. These lesions were rare in patients with normal endoscopy. Gastric cancer showed a particularly strong association with infection, with all histological lesions observed in HPP patients in this series.

Overall, histological lesions—including chronic and active inflammation, atrophy, and metaplasia—were significantly more frequent in HPP patients (p < 0.01), confirming the central role of H. pylori in the initiation and progression of the gastric lesion cascade (inflammation → atrophy → metaplasia → cancer) and in gastric carcinogenesis.

These findings underscore the major role of H. pylori in the development, progression, and severity of gastroduodenal lesions, as well as its involvement in gastric cancer pathogenesis (Table 5).

Table 5: Rates of inflammation, activity, glandular atrophy, and intestinal metaplasia in patients according to Helicobacter pylori infection status
Endoscopic Lesion Infiltration of Mononuclear Cells Infiltration of Polymorphonuclear Cells Glandular Atrophy Intestinal Metaplasia
  HPP HPN HPP HPN HPP HPN HPP HPN
Duodenal ulcer 91.7a 8.3 91.5a 8.5 92.3a 7.7 92.6a 7.4
Gastric ulcer 80.0a 20.7 91.7a 8.3 77.3 22.7 77.8a 22.2
Bulbar ulcer 70.0a 30 50 50 88.9a 11.1 77.8a 22.2
Superficial gastritis 64.9a 35.1 75.0a 25 71.4a 28.6 69.6a 30.4
Erosive gastritis 69.2a 30.8 63.3a 36.7 58.7 41.3 68.3a 31.7
Chronic gastritis 57.1a 42.9 69.6a 30.4 40 60 57.1 42.9
Gastric cancer 100.0a 0 100.0a 0 100.0a 0 100.0a 0
Normal endoscopy 59.3 40.7 65.6 34.4 - - - -
Others* 100 0 100 0 100 0 50 50
aP<0.01 vs H pylori-negative group; HPP: Helicobacter pylori positive; HPN: Helicobacter pylori negatif

Discussion

Helicobacter pylori infection remains one of the most prevalent chronic bacterial infections worldwide, affecting more than half of the global population. In developing countries, particularly in Africa, the prevalence is considerably higher due to socioeconomic factors such as overcrowding, poor sanitation, and limited access to clean water [25]. The present study provides valuable data on the prevalence of H. pylori infection and its association with endoscopic and histopathological gastric lesions in a large cohort of patients undergoing upper gastrointestinal endoscopy in Cameroon.

Prevalence of Helicobacter pylori infection

The histological prevalence of H. pylori infection in this study was 73.2%. This finding is consistent with results reported in several African studies. In Cameroon, Ndjitoyap Ndam et al. reported a prevalence of 72.5% among dyspeptic patients [37], while Muteba et al. in Kinshasa found a prevalence of approximately 75% [36]. These figures are substantially higher than those reported in industrialized countries, where the prevalence generally ranges between 30% and 50% [29].

The high prevalence observed in low-resource settings is often explained by socioeconomic conditions, including crowded living environments, shared utensils, and limited hygiene facilities, which facilitate the transmission of the bacterium [25]. These findings highlight the persistent burden of H. pylori infection in developing countries and underline the importance of effective screening and eradication strategies.

In this study, the rapid urease test showed a positivity rate of 67.7%, which was slightly lower than that observed with histology but still demonstrated good diagnostic agreement. The rapid urease test is widely used due to its simplicity and rapid results. Previous studies have reported a sensitivity ranging from 85% to 95% and a specificity of approximately 95–100%, depending on the number and location of biopsies obtained during endoscopy [26]. The slightly lower sensitivity observed in the present study may be explained by variations in bacterial density or by the effect of previous proton pump inhibitor use, which can reduce bacterial load and urease activity.

Bacterial culture showed a lower positivity rate of 42.9%, which is consistent with the known limitations of this technique. Although culture remains the most specific method for diagnosing H. pylori infection, it requires strict transport and incubation conditions, including a microaerophilic environment and rapid processing of biopsy specimens. Any delay in sample processing or prior antibiotic exposure may reduce culture sensitivity [31]. Despite these limitations, culture remains valuable because it allows antimicrobial susceptibility testing, which is essential in the context of increasing antibiotic resistance [33].

Distribution according to endoscopic findings

The present study observed a strong cross-sectional association between H. pylori infection and gastroduodenal ulcer disease. Infection was detected in 91.9% of patients with duodenal ulcers and 82.1% of those with gastric ulcers. These findings are consistent with numerous international studies reporting that H. pylori is associated with approximately 70–90% of duodenal ulcers and 60–80% of gastric ulcers [26].

Similar results have been reported in African populations. For example, Ndjitoyap Ndam et al. found an infection rate of approximately 88% in patients with duodenal ulcers in Cameroon [37], while studies conducted in Cotonou reported rates exceeding 85% [30]. These findings reinforce the well-established involvement of H. pylori in ulcer formation through mechanisms involving mucosal inflammation, disruption of the gastric barrier, and alterations in gastric acid secretion.

In addition to ulcerative disease, high infection rates were also observed in patients with gastritis. Superficial gastritis and erosive gastritis showed infection rates of 70.7% and 64.9%, respectively. These findings reflect the close relationship between H. pylori colonization and gastric mucosal inflammation. Superficial gastritis often represents the initial stage of mucosal response to bacterial colonization.

Interestingly, H. pylori infection was also detected in 63.6% of patients with normal endoscopic findings. This observation indicates that bacterial colonization may occur even in the absence of macroscopically visible mucosal lesions. Similar results have been reported in previous studies conducted in Cameroon, which documented infection rates exceeding 60% in patients with macroscopically normal endoscopy [37]. These findings highlight the clinical utility of systematic gastric biopsy sampling during endoscopy, particularly in regions with a high prevalence of infection.

Histopathological correlations and cautious interpretation

Histopathological analysis demonstrated significant cross-sectional correlations between H. pylori status and both inflammatory and precancerous gastric lesions. Infected patients exhibited significantly higher levels of mononuclear and polymorphonuclear inflammatory infiltration, reflecting both chronic inflammation and active inflammatory activity.

Mononuclear cell infiltration is considered a hallmark of chronic H. pylori gastritis and reflects the host immune response to persistent bacterial colonization [24,25]. In this study, moderate to severe mononuclear infiltration was particularly common in patients with superficial gastritis, duodenal ulcers, and gastric ulcers.

Polymorphonuclear infiltration, which reflects active mucosal inflammation, was also frequently observed in erosive gastritis and ulcerative lesions. The presence of neutrophilic activity indicates ongoing mucosal damage associated with bacterial colonization [26].

Precancerous lesions such as glandular atrophy and intestinal metaplasia were significantly more frequent in H. pylori-positive patients. These observed associations align with the multistep model of gastric carcinogenesis described by Correa [27]. According to this framework, chronic gastritis, glandular atrophy, and intestinal metaplasia represent sequential histopathological changes associated with long-term infection. However, given the observational cross-sectional design of the present study, these findings represent single-point associations rather than direct evidence of temporal progression or causality.

All 14 patients diagnosed with gastric cancer in this series were positive for H. pylori infection (100%). While this finding is consistent with the established role of H. pylori as a group I carcinogen [13,14,28], it must be interpreted with caution. The gastric cancer subgroup represented a small fraction of the total study population (n = 14) 1.7%. Due to the low statistical power inherent to this small subgroup size, broad generalizations regarding absolute prevalence or causative necessity cannot be drawn. Further prospective, multi-center studies with larger subgroup cohorts are warranted to evaluate these carcinogenic dynamics in the Cameroonian population.

Clinical implications

The findings of this study emphasize the importance of early detection and eradication of H. pylori infection in high-prevalence settings. Screening and treatment strategies could significantly reduce the incidence of gastroduodenal ulcer disease and potentially prevent the progression of chronic gastritis to gastric cancer.

In addition, the high prevalence of infection observed even in patients with normal endoscopic findings supports the routine use of gastric biopsies during endoscopic examination in endemic regions.

Study limitations

This study has several limitations that should be considered when interpreting the results:

Study design: As a cross-sectional observational study, temporal relationships and direct causality between H. pylori infection, lesion progression, and carcinogenesis cannot be established.

Small subgroup sizes: Certain endoscopic diagnostic groups, particularly gastric cancer (n = 14) and chronic gastritis (n = 47), contained small sample sizes, limiting the statistical power and generalizability of subgroup-specific findings.

Missing diagnostic tests: Bacterial culture was not performed in 19.5% of cases (n = 164) due to technical and transport constraints. Although histology served as the primary reference standard, incomplete culture data may limit comprehensive microbiological evaluations.

Histological & image constraints: Limited or missing histological sections in a subset of samples may have led to an underestimation of patchy lesions such as glandular atrophy or intestinal metaplasia. Additionally, the lack of archived endoscopic image repositories prevented systematic iconographic re-evaluation.

Declarations

Author contributions

BBEB and LBKM contributed to the conceptualization of the manuscript, development of the measurement method, interpretation of results, and data analysis. BBEB was responsible for project coordination and overall management. BBEB carried out data collection. BBEB prepared the initial draft of the manuscript. BBEB and LBKM contributed to data collection, manuscript preparation, and coordination. All authors reviewed and approved the final version of the manuscript.

Ethical approval: The study was conducted in accordance with the Declaration of Helsinki and was approved by the National Ethics Committee of Cameroon.

Informed consent: Written informed consent was obtained from all participants.

Funding: The authors received no specific funding for this work.

Data availability: The data that support the findings of this study are available from the corresponding author upon reasonable request.

Competing interests: The authors declare no competing interests.

References

  1. Bomme M, Hansen JM, Wildner-Christensen M, Hallas J, Schaffalitzky de Muckadell OB. Effects of community screening for Helicobacter pylori: 13-year follow-up evaluation of a randomized controlled trial. Clin Gastroenterol Hepatol. 2017;15(11):1715–1723.e7. doi:10.1016/j.cgh.2017.06.006

  2. Mitsui Y, Miyoshi A, Okamoto K, et al. Different phenotypes of gastric fundic gland polyposis and cancer in patients with familial adenomatous polyposis depending on Helicobacter pylori Gastric Cancer. 2019;22(6):1294–1300. doi:10.1007/s10120-019-01005-y

  3. Zullo A, Hassan C, Cristofari F, et al. Effects of Helicobacter pylori eradication on early-stage gastric mucosa-associated lymphoid tissue lymphoma. Clin Gastroenterol Hepatol. 2010;8(2):105–110. doi:10.1016/j.cgh.2009.07.017

  4. Huh CW, Kim BW. Diagnosis of Helicobacter pylori Korean J Gastroenterol. 2018;72(5):229–236. doi:10.4166/kjg.2018.72.5.229

  5. Malfertheiner P, Megraud F, O’Morain CA, et al. Management of Helicobacter pylori infection: the Maastricht V/Florence consensus report. Gut. 2017;66(1):6–30. doi:10.1136/gutjnl-2016-312288

  6. Sabbagh P, Mohammadnia-Afrouzi M, Javanian M, et al. Diagnostic methods for Helicobacter pylori infection: ideals, options, and limitations. Eur J Clin Microbiol Infect Dis. 2019;38(1):55–66. doi:10.1007/s10096-018-3414-4

  7. Lauwers GY, Fujita H, Nagata K, Shimizu M. Pathology of non-Helicobacter pylori gastritis: extending the histopathologic horizons. J Gastroenterol. 2010;45(2):131–145. doi:10.1007/s00535-009-0146-3

  8. Chatrangsun B, Vilaichone RK. Endoscopic diagnosis for Helicobacter pylori infection: white light imaging vs image-enhanced endoscopy. Asian Pac J Cancer Prev. 2021;22(9):3031–3038. doi:10.31557/APJCP.2021.22.9.3031

  9. Watanabe T, Nadatani Y, Suda W, et al. Long-term persistence of gastric dysbiosis after eradication of Helicobacter pylori in patients undergoing endoscopic submucosal dissection. Gastric Cancer. 2021;24(3):710–720. doi:10.1007/s10120-020-01141-w

  10. Tiwari A, Rai R, Dahal P, Regmi S. Prevalence of Helicobacter pylori in endoscopic gastric biopsies of chronic gastritis patients at a tertiary care centre. J Nepal Med Assoc. 2020;58(228):564–568. doi:10.31729/jnma.5210

  11. Wang Y, Shen L, Zhao G, et al. Histomorphological characteristics and pathological types of hyperproliferation of gastric surface epithelial cells. Gastroenterol Res Pract. 2021;2021:8828326. doi:10.1155/2021/8828326

  12. Wang YK, Zhou JL, Meng NL, Zhu CY, Wang SN, Chen XD. How does Helicobacter pylori infection cause gastric mucosal atrophy? Infect Drug Resist. 2022;15:3619–3629. doi:10.2147/IDR.S355981

  13. Suzuki H, Mori H. World trends for Helicobacter pylori eradication therapy and gastric cancer prevention strategy. J Gastroenterol. 2018;53(3):354–361. doi:10.1007/s00535-017-1407-1

  14. Khatoon J, Prasad KN, Rai RP, Ghoshal UC, Krishnani N. Association of heterogeneity of Helicobacter pylori cag pathogenicity island with peptic ulcer disease and gastric cancer. Br J Biomed Sci. 2017;74(3):121–126. doi:10.1080/09674845.2017.1278887

  15. Salar A. Gastric MALT lymphoma and Helicobacter pylori. Med Clin (Barc). 2019;152(2):65–71. doi:10.1016/j.medcli.2018.09.006

  16. Marques MS, Melo J, Cavadas B, et al. Afadin downregulation by Helicobacter pylori induces epithelial-to-mesenchymal transition in gastric cells. Front Microbiol. 2018;9:2712. doi:10.3389/fmicb.2018.02712

  17. Quach DT, Vilaichone RK, Vu KV, Yamaoka Y, Sugano K, Mahachai V. Helicobacter pylori infection and related gastrointestinal diseases in Southeast Asia: an expert opinion survey. Asian Pac J Cancer Prev. 2018;19(12):3565–3569. doi:10.31557/APJCP.2018.19.12.3565

  18. El-Zimaity HM, Graham DY. Evaluation of gastric biopsy site and number for identification of Helicobacter pylori: role of the Sydney system. Hum Pathol. 1999;30(1):72–77. doi:10.1016/S0046-8177(99)90303-9

  19. Udoh MO, Obaseki DE. Histopathological evaluation of Helicobacter pylori-associated gastric lesions in Benin City, Nigeria. East Afr Med J. 2012;89(12):408–413

  20. El-Serag HB, Kao JY, Kanwal F, et al. Houston consensus conference on testing for Helicobacter pylori infection in the United States. Clin Gastroenterol Hepatol. 2018;16(7):992–1002.e6. doi:10.1016/j.cgh.2018.03.013

  21. Horiuchi Y, Fujisaki J, Yamamoto N, et al. Biological behavior of Helicobacter pylori-negative early gastric cancer. Gastric Cancer. 2016;19(1):160–165. doi:10.1007/s10120-014-0452-1

  22. Take S, Mizuno M, Ishiki K, et al. Low incidence of esophageal adenocarcinoma after Helicobacter pylori eradication in Japan. Clin Gastroenterol Hepatol. 2018;16(12):1995–1996. doi:10.1016/j.cgh.2018.03.030

  23. Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis: the updated Sydney system. Am J Surg Pathol. 1996;20(10):1161–1181

  24. Malfertheiner P, Megraud F, Rokkas T, Gisbert JP, Liou JM, Schulz C, et al. Management of Helicobacter pylori infection: the Maastricht VI/Florence consensus report. 2022;71(9):1724–1762

  25. Eusebi LH, Zagari RM, Bazzoli F. Epidemiology of Helicobacter pylori Best Pract Res Clin Gastroenterol. 2020;44–45:101704

  26. Chey WD, Leontiadis GI, Howden CW, Moss SF. ACG clinical guideline: treatment of Helicobacter pylori Am J Gastroenterol. 2017;112(2):212–239

  27. Correa P. Human gastric carcinogenesis: a multistep and multifactorial process. Cancer Res. 1992;52(24):6735–6740

  28. International Agency for Research on Cancer. Helicobacter pylori. IARC Monogr Eval Carcinog Risks Hum. 2012;100B:363–382

  29. Katelaris P, et al. Global epidemiology of peptic ulcer disease. World J Gastroenterol. 2020;26(29):4153–4163

  30. Bola S, et al. Profil endoscopique des affections gastroduodénales à Cotonou. Rev Afr Gastroenterol. 2019

  31. Mégraud F, Lehours P. Helicobacter pylori detection and antimicrobial susceptibility testing. Clin Microbiol Rev. 2007;20(2):280–322

  32. World Health Organization. Helicobacter pylori and gastric cancer classification. Geneva: WHO; 2017

  33. World Gastroenterology Organisation. Global guideline: Helicobacter pylori in developing countries. 2023

  34. Ka O, et al. Profil histologique et endoscopique de l’infection à Helicobacter pylori au Sénégal. Mali Med. 2018;33(3):32–38

  35. Plummer M, Franceschi S, Vignat J, Forman D, de Martel C. Global burden of gastric cancer attributable to Helicobacter pylori. Int J Cancer. 2015;136(2):487–490

  36. Muteba J, et al. Profil endoscopique des gastrites à Kinshasa. Ann Afr Med. 2020

  37. Ndjitoyap Ndam EC, et al. Helicobacter pylori infection and upper gastrointestinal endoscopic findings in Cameroon. Pan Afr Med J. 2014;17:115

  38. Suzuki R, Shiota S, Yamaoka Y. Molecular epidemiology, population genetics, and pathogenic role of Helicobacter pylori. Infect. Genet. Evol. 2012; 12: 203–213. doi : 1016/j.meegid.2011.12.002

  39. Mentis A, Lehours P, Mégraud F. Epidemiology and Diagnosis of Helicobacter pylori infection. Helicobacter, 2015; 20: 1–7. doi : 10.1111/hel.12250

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Eyoum BBB, Eloumou FSB, Médi CS, Ekwala JRMN, Ntonga CL, Malongue A, Fotso C, Fotsing S, Kamdem C, Ateba RG, Mokou BC, Kouitcheu BLM, Kuiate JR. Endoscopic Aspects of Lesions Secondary to Helicobacter pylori Infection in two Hospitals in Douala: A Cross-Sectional Study over a Three-year Period. IgMin Res. August 21, 2026; 4(8): 341-348. IgMin ID: igmin358; DOI:10.61927/igmin358; Available at: igmin.link/p358

13 Aug, 2026
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  1. Bomme M, Hansen JM, Wildner-Christensen M, Hallas J, Schaffalitzky de Muckadell OB. Effects of community screening for Helicobacter pylori: 13-year follow-up evaluation of a randomized controlled trial. Clin Gastroenterol Hepatol. 2017;15(11):1715–1723.e7. doi:10.1016/j.cgh.2017.06.006

  2. Mitsui Y, Miyoshi A, Okamoto K, et al. Different phenotypes of gastric fundic gland polyposis and cancer in patients with familial adenomatous polyposis depending on Helicobacter pylori Gastric Cancer. 2019;22(6):1294–1300. doi:10.1007/s10120-019-01005-y

  3. Zullo A, Hassan C, Cristofari F, et al. Effects of Helicobacter pylori eradication on early-stage gastric mucosa-associated lymphoid tissue lymphoma. Clin Gastroenterol Hepatol. 2010;8(2):105–110. doi:10.1016/j.cgh.2009.07.017

  4. Huh CW, Kim BW. Diagnosis of Helicobacter pylori Korean J Gastroenterol. 2018;72(5):229–236. doi:10.4166/kjg.2018.72.5.229

  5. Malfertheiner P, Megraud F, O’Morain CA, et al. Management of Helicobacter pylori infection: the Maastricht V/Florence consensus report. Gut. 2017;66(1):6–30. doi:10.1136/gutjnl-2016-312288

  6. Sabbagh P, Mohammadnia-Afrouzi M, Javanian M, et al. Diagnostic methods for Helicobacter pylori infection: ideals, options, and limitations. Eur J Clin Microbiol Infect Dis. 2019;38(1):55–66. doi:10.1007/s10096-018-3414-4

  7. Lauwers GY, Fujita H, Nagata K, Shimizu M. Pathology of non-Helicobacter pylori gastritis: extending the histopathologic horizons. J Gastroenterol. 2010;45(2):131–145. doi:10.1007/s00535-009-0146-3

  8. Chatrangsun B, Vilaichone RK. Endoscopic diagnosis for Helicobacter pylori infection: white light imaging vs image-enhanced endoscopy. Asian Pac J Cancer Prev. 2021;22(9):3031–3038. doi:10.31557/APJCP.2021.22.9.3031

  9. Watanabe T, Nadatani Y, Suda W, et al. Long-term persistence of gastric dysbiosis after eradication of Helicobacter pylori in patients undergoing endoscopic submucosal dissection. Gastric Cancer. 2021;24(3):710–720. doi:10.1007/s10120-020-01141-w

  10. Tiwari A, Rai R, Dahal P, Regmi S. Prevalence of Helicobacter pylori in endoscopic gastric biopsies of chronic gastritis patients at a tertiary care centre. J Nepal Med Assoc. 2020;58(228):564–568. doi:10.31729/jnma.5210

  11. Wang Y, Shen L, Zhao G, et al. Histomorphological characteristics and pathological types of hyperproliferation of gastric surface epithelial cells. Gastroenterol Res Pract. 2021;2021:8828326. doi:10.1155/2021/8828326

  12. Wang YK, Zhou JL, Meng NL, Zhu CY, Wang SN, Chen XD. How does Helicobacter pylori infection cause gastric mucosal atrophy? Infect Drug Resist. 2022;15:3619–3629. doi:10.2147/IDR.S355981

  13. Suzuki H, Mori H. World trends for Helicobacter pylori eradication therapy and gastric cancer prevention strategy. J Gastroenterol. 2018;53(3):354–361. doi:10.1007/s00535-017-1407-1

  14. Khatoon J, Prasad KN, Rai RP, Ghoshal UC, Krishnani N. Association of heterogeneity of Helicobacter pylori cag pathogenicity island with peptic ulcer disease and gastric cancer. Br J Biomed Sci. 2017;74(3):121–126. doi:10.1080/09674845.2017.1278887

  15. Salar A. Gastric MALT lymphoma and Helicobacter pylori. Med Clin (Barc). 2019;152(2):65–71. doi:10.1016/j.medcli.2018.09.006

  16. Marques MS, Melo J, Cavadas B, et al. Afadin downregulation by Helicobacter pylori induces epithelial-to-mesenchymal transition in gastric cells. Front Microbiol. 2018;9:2712. doi:10.3389/fmicb.2018.02712

  17. Quach DT, Vilaichone RK, Vu KV, Yamaoka Y, Sugano K, Mahachai V. Helicobacter pylori infection and related gastrointestinal diseases in Southeast Asia: an expert opinion survey. Asian Pac J Cancer Prev. 2018;19(12):3565–3569. doi:10.31557/APJCP.2018.19.12.3565

  18. El-Zimaity HM, Graham DY. Evaluation of gastric biopsy site and number for identification of Helicobacter pylori: role of the Sydney system. Hum Pathol. 1999;30(1):72–77. doi:10.1016/S0046-8177(99)90303-9

  19. Udoh MO, Obaseki DE. Histopathological evaluation of Helicobacter pylori-associated gastric lesions in Benin City, Nigeria. East Afr Med J. 2012;89(12):408–413

  20. El-Serag HB, Kao JY, Kanwal F, et al. Houston consensus conference on testing for Helicobacter pylori infection in the United States. Clin Gastroenterol Hepatol. 2018;16(7):992–1002.e6. doi:10.1016/j.cgh.2018.03.013

  21. Horiuchi Y, Fujisaki J, Yamamoto N, et al. Biological behavior of Helicobacter pylori-negative early gastric cancer. Gastric Cancer. 2016;19(1):160–165. doi:10.1007/s10120-014-0452-1

  22. Take S, Mizuno M, Ishiki K, et al. Low incidence of esophageal adenocarcinoma after Helicobacter pylori eradication in Japan. Clin Gastroenterol Hepatol. 2018;16(12):1995–1996. doi:10.1016/j.cgh.2018.03.030

  23. Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis: the updated Sydney system. Am J Surg Pathol. 1996;20(10):1161–1181

  24. Malfertheiner P, Megraud F, Rokkas T, Gisbert JP, Liou JM, Schulz C, et al. Management of Helicobacter pylori infection: the Maastricht VI/Florence consensus report. 2022;71(9):1724–1762

  25. Eusebi LH, Zagari RM, Bazzoli F. Epidemiology of Helicobacter pylori Best Pract Res Clin Gastroenterol. 2020;44–45:101704

  26. Chey WD, Leontiadis GI, Howden CW, Moss SF. ACG clinical guideline: treatment of Helicobacter pylori Am J Gastroenterol. 2017;112(2):212–239

  27. Correa P. Human gastric carcinogenesis: a multistep and multifactorial process. Cancer Res. 1992;52(24):6735–6740

  28. International Agency for Research on Cancer. Helicobacter pylori. IARC Monogr Eval Carcinog Risks Hum. 2012;100B:363–382

  29. Katelaris P, et al. Global epidemiology of peptic ulcer disease. World J Gastroenterol. 2020;26(29):4153–4163

  30. Bola S, et al. Profil endoscopique des affections gastroduodénales à Cotonou. Rev Afr Gastroenterol. 2019

  31. Mégraud F, Lehours P. Helicobacter pylori detection and antimicrobial susceptibility testing. Clin Microbiol Rev. 2007;20(2):280–322

  32. World Health Organization. Helicobacter pylori and gastric cancer classification. Geneva: WHO; 2017

  33. World Gastroenterology Organisation. Global guideline: Helicobacter pylori in developing countries. 2023

  34. Ka O, et al. Profil histologique et endoscopique de l’infection à Helicobacter pylori au Sénégal. Mali Med. 2018;33(3):32–38

  35. Plummer M, Franceschi S, Vignat J, Forman D, de Martel C. Global burden of gastric cancer attributable to Helicobacter pylori. Int J Cancer. 2015;136(2):487–490

  36. Muteba J, et al. Profil endoscopique des gastrites à Kinshasa. Ann Afr Med. 2020

  37. Ndjitoyap Ndam EC, et al. Helicobacter pylori infection and upper gastrointestinal endoscopic findings in Cameroon. Pan Afr Med J. 2014;17:115

  38. Suzuki R, Shiota S, Yamaoka Y. Molecular epidemiology, population genetics, and pathogenic role of Helicobacter pylori. Infect. Genet. Evol. 2012; 12: 203–213. doi : 1016/j.meegid.2011.12.002

  39. Mentis A, Lehours P, Mégraud F. Epidemiology and Diagnosis of Helicobacter pylori infection. Helicobacter, 2015; 20: 1–7. doi : 10.1111/hel.12250

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