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Table of Contents
Year : 2021  |  Volume : 13  |  Issue : 1  |  Page : 6-11

Helicobacter pylori-associated gastritis phenotypes in a South-Western Nigerian population

1 Department of Medicine, Benjamin Carson Snr. School of Medicine, Babcock University, Ilisan-Remo, Ogun State, Nigeria
2 Department of Pathology, College of Medicine, University of Ibadan, Ibadan, Oyo State, Nigeria
3 Department of Histopathology, Benjamin Carson Snr. School of Medicine, Babcock University, Ilisan-Remo, Ogun State, Nigeria
4 Department of Internal Medicine, Babcock University Teaching Hospital, Ilisan-Remo, Ogun State, Nigeria

Date of Submission22-Apr-2021
Date of Decision22-Apr-2021
Date of Acceptance25-Apr-2021
Date of Web Publication30-Jun-2021

Correspondence Address:
Dr. Abiodun Christopher Jemilohun
Department of Medicine, Benjamin Carson Snr. School of Medicine, Babcock University, Ilisan-Remo, Ogun State
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/njgh.njgh_21_20

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Background: The long-term outcomes of Helicobacter pylori infection ultimately depend on the distribution and extent of gastritis. Three main types of gastritis phenotypes which include pangastritis, antral-predominant gastritis, and corpus-predominant gastritis have been observed. Corpus predominant gastritis is more common in the parts of Asia with a high prevalence of gastric adenocarcinoma. This study was conducted to determine the prevalence of H. pylori-associated gastritis phenotypes in a South-western Nigerian population, a sub-Saharan African population.
Materials and Methods: The study was a cross-sectional prospective study which included 267 dyspeptic patients who had esophagogastroduodenoscopy at a tertiary health institution in South-west Nigeria. Five gastric biopsies were taken from each subject, and standard histologic examination was performed on the specimens. Both biopsy sampling and histologic examination followed the Updated Sydney System recommendations. The data generated were statistically analyzed. Continuous variables were presented as means ± standard deviation, whereas associations between the categorical variables were determined by the Pearson Chi-square test or Fisher's exact test. P ≤ 0.05 was considered statistically significant.
Results: The mean age was 46.1 (±15.4) years while the age range was 16–84 years. There were 160 (59.9%) female and 107 (40.1%) male participants. All participants had histological gastritis, whereas 79 (29.6%) were positive for H. pylori by histology. H. pylori infection was significantly associated with peptic ulcer disease. Among those who had H. pylori infection, 51 (64.6%) had pangastritis, 26 (32.9%) had antral-predominant gastritis, while 2 (2.5%) had corpus-predominant gastritis. The relationship between H. pylori infection and the gastritis phenotypes showed no statistical significance.
Conclusion: The prevalence of corpus predominant gastritis was low in our study population.

Keywords: Gastric cancer, gastritis phenotype, gastritis, Helicobacter pylori, precancerous lesions

How to cite this article:
Jemilohun AC, Ajani MA, Solaja TO, Uka AT. Helicobacter pylori-associated gastritis phenotypes in a South-Western Nigerian population. Niger J Gastroenterol Hepatol 2021;13:6-11

How to cite this URL:
Jemilohun AC, Ajani MA, Solaja TO, Uka AT. Helicobacter pylori-associated gastritis phenotypes in a South-Western Nigerian population. Niger J Gastroenterol Hepatol [serial online] 2021 [cited 2023 Mar 21];13:6-11. Available from: https://www.njghonweb.org/text.asp?2021/13/1/6/320303

  Introduction Top

Helicobacter pylori infection is often acquired in infancy but remains symptomless in most people until adulthood.[1] The organism penetrates the gastric mucosa and adheres to the gastric epithelial cells under the mucus layer where it causes damage to the cells.[2] The capacity of H. pylori to adapt to the hostile acidic gastric mucosa allows it to induce gastritis in all infected persons. The inflamed mucosa is very important for the long-term survival of the organism on the gastric mucosa as it supplies the nutrients that are required for the metabolism to the organism.[3] The underlying factor that facilitates H. pylori-induced gastroduodenal pathologies is gastritis.[4]

It has been established beyond doubt that H. pylori gastritis is closely related to upper gastrointestinal pathologies that present clinically as dyspepsia such as peptic ulcer disease (PUD) and gastric cancer.[5] The long-term sequelae of the infection ultimately depend on the distribution and extent of the gastritis.[4] Three main gastritis phenotypes that are associated with distinct sets of pathophysiologic abnormalities and outcomes have been identified. The most prevalent phenotype presents as mild pangastritis with slight disruption of gastric acid secretion, this is also called simple or benign gastritis phenotype.[4] This phenotype is seen in asymptomatic participants who often do not develop serious gastrointestinal diseases. The second phenotype presents as antral-predominant gastritis with considerable sparing of the acid-producing mucosa of the stomach corpus. This is also known as the duodenal ulcer phenotype.[4] About 15% of infected persons have this type of phenotype, especially in the Western world where PUD is common.[6] The third phenotype, which is the most serious, presents as corpus-predominant gastritis with multifocal gastric atrophy, and hypo-or achlorhydria, the so-called gastric cancer phenotype.[7] This phenotype occurs in approximately 1% of infected persons and is more common in parts of Asia with a high prevalence of gastric adenocarcinoma.

Despite that Nigeria has one of the highest prevalence of H. pylori infection,[8] there has been no correlation between the prevalence of H. pylori infection and that of the upper gastroduodenal diseases apart from gastritis in the Nigerian population, the so-called African enigma.[9] Although Africa has a high prevalence of gastritis, the prevalence of PUD and gastric cancer in the African population is low as compared to the Western population.[9] Several studies have reported the high prevalence of H. pylori-associated gastritis in Nigerians, but they did not describe the gastritis phenotypes.[10],[11],[12],[13],[14] Campbell et al. demonstrated that Gambian adults and children mount up mainly mild chronic antral inflammation to H. pylori infection with low occurrences of gastric atrophy and intestinal metaplasia.[15]

According to the World Health Organization, Nigeria belongs to the region of the world with a low prevalence of gastric cancer (<3.7/100,000), whereas countries in Eastern Asia such as Japan and China have the highest incidence of gastric cancer worldwide (>16.5/100,000).[16] Naylor et al. previously demonstrated that Japanese patients with dyspepsia tend to have a higher prevalence of gastritis with more severe inflammation, more corpus predominant atrophy, and intestinal metaplasia as compared to English dyspeptic patients.[17] In light of the foregoing, we hypothesized that Nigerian patients with H. pylori-associated gastritis would have less of the corpus predominant gastritis phenotype than has been documented in the regions of the world like Japan with a high incidence of gastric cancer. Thus, this study was conducted to determine the prevalence of H. pylori-associated gastritis phenotypes in a South-western Nigerian population, a sub-Saharan African population, in order to test our hypothesis.

  Materials and Methods Top

Study design and setting

The study was a prospective, cross-sectional study conducted at the Digestive Endoscopy Unit of Babcock University Teaching Hospital (BUTH), Ilisan-Remo, Ogun State. The samples were taken from January 2017 to March 2019. The hospital is a tertiary health-care facility that serves as a referral center to the primary and secondary health-care facilities in Ilisan-Remo and neighboring communities in Ogun and Lagos States, Nigeria.

Study population and subject selection

The study population consisted of male and female patients aged 16–84 years with dyspepsia referred to the Digestive Endoscopy Unit of BUTH for esophagogastroduodenoscopy (EGD). Pregnant women, patients with history of gastric resection, and patients with gastric cancer were excluded from the study.

We defined dyspepsia as a chronic or recurrent pain or discomfort that is located in the central upper abdomen which is ascribable to the upper gastrointestinal tract. The pain or discomfort is often associated with food intake and/or hunger. Discomfort refers to a subjective negative feeling such as early satiety, excessive belching, bloating, nausea, or abdominal fullness. The Rome IV iteration requires a duration of at least 6 months for the diagnosis,[18] but the American College of Gastroenterology recommends a minimum period of 4 weeks for clinical purposes.[19]

Consecutive dyspeptic patients presenting at the endoscopy unit who consented to participate in the study were recruited. The demographic information, endoscopic findings, and histology results of the participants were recorded in a pro forma.

Esophagogastroduodenoscopy and sampling

EGD was performed on all the subjects with either of two PKS series Karl Storz white-light forward-viewing video esophagogastroduodenoscopes by an endoscopist in line with global best practices. In compliance with the Updated Sydney System recommendations, five mucosal biopsies were taken from each patient's stomach: one each from the lesser (A1) and the greater curvature (A2) of the antrum, 2–3 cm from the pylorus; one from the lesser curvature of the body, about 4 cm proximal to the incisura angularis (B1); one from the center of the greater curvature of the body, approximately 8 cm from the cardia (B2); and one from the angularis incisura (IA).[20] The endoscopic features of each patient were recorded.


The five gastric biopsies were fixed in three separate 10% formaldehyde specimen bottles and labelled appropriately: Two from the antrum into one bottle, two from the body into one bottle, and one from the incisura angularis into one bottle. The samples were then taken to the histopathology laboratory for processing. Paraffin sections were stained with routine Hematoxylin and Eosin and Giemsa technique and examined microscopically. Tissue sections were graded in line with the Updated Sydney System of Classification and grading of gastritis for the following features: H. pylori density, neutrophilic activity, lymphocytic infiltration, and glandular atrophy. The severity of the inflammatory changes and grading were performed with a Visual Analog Scale as follows: l – mild; 2 – moderate; and 3 – severe. The presence of metaplasia was confirmed with a combination of periodic acid Schiff/Alcian blue stains.

Types of inflammation

  1. Chronic active gastritis (CAG) – lamina propria infiltration by neutrophil polymorphs, lymphocytes, and plasma cells
  2. Chronic nonspecific gastritis (CNG) – lamina propria infiltration by lymphocytes and plasma cells without neutrophilic infiltration.

Gastritis phenotypes

  1. Pangastritis had the same inflammation scores in the antrum and the body
  2. Antral predominant gastritis had higher inflammation score in the antrum than the corpus
  3. Corpus predominant gastritis had higher inflammation score in the corpus than the antrum.

Statistical analysis

We analyzed the data with the IBM Statistical Package for the Social Sciences (SPSS) for Windows, Version 21.0. Armonk, New York, United States of America. Continuous variables were presented as means ± standard deviation. Categorical variables were presented as frequencies and percentages. We compared the differences between the categorical variables by means of Pearson Chi-square test or Fisher exact test as occasion demanded. Statistical significance level for P ≤ 0.05.

Ethical consideration

We obtained ethical clearance from the Institutional Ethics Review Board. Both verbal and written informed consents were obtained from participants or the guardian in those who were <18 years. Information obtained from participants was kept confidential.

  Results Top

The demographic characteristics of the participants are depicted in [Table 1]. A total of 267 patients participated in the study. The mean age was 46.1 (±15.4) years while the age range was 16–84 years. There were 160 (59.9%) female and 107 (40.1%) male participants. Participants who were in their 40s had the highest representation totaling 63 (23.2%) while those who were <20 had the lowest representation (3.0%).
Table 1: Demographic characteristics and endoscopic findings among participants by age, gender,  Helicobacter pylori Scientific Name Search on (n=267)

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A total of 247 (92.5%) had endoscopic gastritis, 32 (12.0%) had gastric ulcer, 19 (7.1%) had duodenal ulcer while 7 (2.6%) had a combination of gastric and duodenal ulcers. More male participants (34.6%) had PUD than the female participants (14.6%) with a statistical significance (P < 0.001) [Table 1]. We found 74 (93.7%) participants with H. pylori infection had endoscopic gastritis while the remaining 4 (6.3%) participants did not have. Furthermore, 24 (32.4%) of participants with H. pylori infection had PUD with statistical significance (P = 0.039).

[Table 2] shows the distribution of the gastric premalignant conditions among the participants. A total of 68 (25.5%) had mucosal atrophy, of which 53 (19.9%) were mild while 15 (5.6%) were moderate in severity. Five participants (1.9%) each had mucosal metaplasia and dysplasia which were all mild in severity. No participant had the severe forms of any of the three premalignant conditions. Invariably, 68% of the premalignant conditions were mild mucosal atrophy.{Table 2ss}

The distribution of the gastritis phenotypes among participants in relation to age, gender, H. pylori infection, inflammation type, and precancerous lesions is presented in [Table 3]. All the participants had gastritis, 79 (29.6%) were positive for H. pylori infection by histology while 74 (27.7%) had at least one of the premalignant conditions. Among those who had H. pylori infection, 51 (64.6%) had pangastritis, 26 (32.9%) had antral-predominant gastritis, while 2 (2.5%) had corpus-predominant gastritis. The relationship between H. pylori infection and the gastritis phenotypes showed no statistical significance. Irrespective of H. pylori status, a total of 179 (67.0%) had pangastritis (simple gastritis phenotype), 78 (29.2%) had antral predominant gastritis (duodenal ulcer phenotype) while 10 (3.7%) had corpus predominant gastritis (gastric cancer phenotype). Of note is that the female participants and those in their 30s had the highest rates of corpus predominant gastritis, but none of the relationships showed statistical significance. Concerning inflammation types, 250 (93.6%) participants had CAG while 17 (6.4%) had CNG. No participant with corpus predominant gastritis had CNG.
Table 3: Gastritis phenotypes distribution among subjects in relation to age, gender, Helicobacter pylori and precancerous lesions (n=267)

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  Discussion Top

Our finding of 100% gastritis among the participants is similar to previous studies from Nigeria that yielded prevalence rates of gastritis that were well above 90% among dyspeptic patients.[10],[21],[22] The 29.6% prevalence of H. pylori infection observed in this study may be considered low bearing in mind that older studies in the Nigerian population generally showed prevalence rates that were >50% (53%–94.5%).[23],[24],[25],[26],[27],[28],[29],[30],[31],[32] However, recent findings by researchers of prevalence rates that are less the 40% suggest that the prevalence of H. pylori infection in Nigeria may be declining.[12],[33],[34] Two reasons may be responsible for this observation. First, the unregulated nature of antibiotic use in Nigeria.[35],[36] Anyone who feels he needs antibiotics could easily procure them over the counter without prescription from a pharmacy or a patent medicine store. Second, empirical prescription of H. pylori eradication therapies for dyspeptic patients by primary care physicians in Nigeria which has become widespread.

Our finding of a positive association between H. pylori infection and PUD is consistent with what is already known. The projected lifetime risk of developing PUD in a person with H. pylori infection is around 10%–20%, which is about 3–4 folds higher than in noninfected persons.[2] H. pylori infection could be diagnosed in 60%–100% of patients with gastric ulcer and in 90%–100% of patients with duodenal ulcer.[2]

The low prevalence of precancerous gastric lesions in spite of high prevalence of chronic gastritis among Nigerians with dyspepsia has been previously reported.[12],[13],[37] Our finding regarding gastric precancerous lesions in this study further corroborates the previous observations. More especially that the majority of the premalignant conditions detected were mild mucosal atrophy.

Just like we hypothesized, we found fewer subjects who had corpus predominant gastritis (2.5%) among the participants with H. pylori infection in our study as compared to what obtained in the Japanese population (18%).[17] Although we found less corpus predominant gastritis among our participants, the value is not too far from what obtained among a British population (7%).[17] This observation is worthy of note for three reasons: the previously observed a high prevalence of H. pylori infection in the Nigerian population,[8] the high prevalence of CagA (96.4%) and VacA (92.8%) which are known bacterial virulence factors among H. pylori isolates from Nigeria and the high prevalence of chronic gastritis among the population.[34] These should ordinarily have led to higher prevalence rates of the more severe forms of gastritis, precancerous lesions, and gastric cancer in the Nigerian population but this is not to be. This study, again, brings to the fore the H. pylori African enigma which we believe deserves to be unraveled.

  Conclusion Top

The prevalence of corpus predominant gastritis was low in our study population. This correlates with the low rate of gastric cancer in the Nigerian population.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

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  [Table 1], [Table 2], [Table 3]


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