Since 1994, the International Agency for Research on Cancer (IARC) classified H. pylori infection as a type 1 carcinogen with a level of imputation for gastric cancer comparable to that of tobacco for lung cancer and Hepatitis C virus for hepatocellular carcinoma. Since then, many epidemiological studies have confirmed the impact of H. pylori in gastric carcinogenesis.
Gastric atrophy and intestinal metaplasia represent the most important premalignant lesions in gastric carcinogenesis. The severity of gastric mucosal inflammation depends on the bacterium Helicobacter pylori (HP)‚ on the host and on environmental factors. The aim of our study is to determine the prevalence and factors associated with gastric atrophy and intestinal metaplasia in patients infected with Helicobacter pylori in a Moroccan population.
2. Patients and Methods
2.1. Study Description
This is a prospective randomized study over a period of 4 years (May 2009-January 2015) in the service of Hepatology and Gastroenterology in hospital university Hassan II of Fez in collaboration with microbiology and molecular laboratory and epidemiology service of Faculty of Medicine and Pharmacy Fes. The study comparing the efficacy and safety of sequential treatment with standard triple therapy. From this study we retrospectively studied gastric atrophy and intestinal metaplasia in patients infected with HP. Patients consent was obtained.
2.2. Inclusion Criteria
o Patients aged over 15 years;
o Presence of ulcer dyspepsia;
o Presence of a peptic ulcer;
o Presence of gastritis;
o Presence of esophagitis.
An upper endoscopy was performed in all patients, with five biopsies: two in the antrum, one at the angulus and two in the fundus.
HP detection was done by histology and/or polymerase chain reaction (PCR).
3.1. Studied Population
During the study period, 1190 patients were included of which 70% had HP infection (N = 833). The average age was 48.21 years [16 - 99 years], sex ratio M/F was 1.11. Sixty percent of patients were older than 45 years. Chronic smoking was found in 12% of cases (Table 1).
An upper endoscopy was performed in all patients, it was normal in 5.4% of patients (N = 45)‚ was found a gastritis in 63.6% (N = 530)‚ was found a peptic ulcer disease in 31% (N = 258) (Table 1).
3.2. Prevalence and Topography of Gastric Atrophy in Patients with HP Positive
Gastric atrophy was observed in 84% (N = 699) of patients infected with HP it was mild in 62%‚ moderate in 35% and severe in 3%. Gastric atrophy was localized in 70% in the antrum and in 30% in the fundus and in 24% in both.
3.3. Prevalence and Topography of Intestinal Metaplasia in Patients with HP Positive
Intestinal metaplasia was observed in 13.5% of patients (N = 112)‚ it was located in 10% of cases and diffuse in 90%.
3.4. Factors Associated with Atrophy and Metaplasia in Gastritis HP
As described in Table 2 the main factors associated with atrophy and metaplasia in gastritis HP follow:
Table 1. Patients’ characteristics.
Table 2. Factors associated with atrophy and metaplasia in gastritis HP.
*The p value defines the correlation between the gastric atrophy and each of the listed factors as well as the correlation between those latter ones and the intestinal metaplasia.
Gastric atrophy was observed in 82% of patients under 45 years and 91% of patients over 45 years of age (p = 0.8).
Intestinal metaplasia was noted in 12% of patients under 45 years and 17% of patients over 45 years (p = 0.9).
Age was not associated to the atrophy and métaplasia.
3.4.2. Density of HP
Intense density of HP was noted in 70% of patients with atrophy (p = 0.005) and in 80% of patients with metaplasia (p = 0.037).
3.4.3. Activity of Gastritis
Severe gastritis activity was noted in 87.3% of patients who have atrophy (p = 0.0001) and in 80% of patients who have metaplasia (p = 0.01).
3.4.4. CagA Status
In our study the CagA + status was not associated with either atrophy or intestinal metaplasia.
Fifty two percent of patients who present atrophy had CagA + status and 48% had CAG A− (p = 1.2).
Fifty five percent of patients who present metaplasia had CagA + status and 44.5% had Cag A− (p = 0.9).
3.4.5. Relationship between Atrophy and Metaplasia
Occurrence métaplasie is more detected in patients with severe atrophy 83.5% of patients presenting metaplasia had severe atrophy (p = 0.001).
It’s been 30 years since Correa proposed the cascade of histological events leading to the occurrence of gastric cancer  -  .
Gastric cancer is the terminal stage of a process vary from chronic gastritis‚ gastric atrophy and intestinal metaplasia  -  .
4.1. Gatric Atrophy Evaluation
Gastric atrophy is defined by a rarefaction of gastric glands. It can vary from mild atro- phy with reduction less than a third of the volume of the glands to severe atrophy with two-thirds reduction in the volume of glands   . The volume of the glands depends to the volume of the lamina propria wich can be enlarged particularly in concomitant inflammation by infiltration by lymphoplasmacytic element.
That is why in chronic active gastritis, the determination of gland volume is difficult and there is an overestimation of atrophy  .
In our study the prevalence of atrophy is 84%, which is a high prevalence, may be overestimated because of the presence of active gastritis.
4.2. Topography of Gastric Atrophy
The significance of gastric atrophy depends on its topography.
In HP infection the gastric atrophy has varying topographies it can be localized in the antrum and in this context it not considered pre-neoplastic lesion, if atrophy affects both the gastric antrum and the body in this case the atrophy causes hypochlorhydria and hypergastrinemia and constitutes a precancerous lesion  .
In a large cohort study of 1436 Japanese patients followed for 7 years the existence of a pan gastric atrophy or predominant in the gastric body was important risk factor for gastric cancer as opposed to the isolated antral gastritis  .
4.3. Intestinal Metaplasia
Intestinal metaplasia is characterized by replacement of the gastric mucosa by intestinal mucosa chronologically this lesion occurs later than gastric atrophy   .
Several epidemiological studies in China and Japan showed strong predictive value for cancer occurrence in patients with intestinal metaplasia, similar results were found in a population of western patients followed for 10 years, in this study 8.4% of patients with intestinal metaplasia developed cancer in 10 years  .
4.4. Interest of the Eradication of HP in Precancerous Lesions
Looking for and systematic eradication of HP in gastric cancer prevention does not yet the subject of consensus  .
Several studies have reported a regression of atrophy and metaplasia after eradication of HP  -  ‚ (Table 3).
4.5. Predictors Factors of Atrophy and Metaplasia
Several studies have examined the predictors factors of atrophy and metaplasia.
Age, smoking, history of smoking, alcohol and rurality are risk factors of gastric atrophy and intestinal metaplasia reported in some studies    .
Others studies reported the male gender as a risk factor for gastric atrophy and intestinal metaplasia  -  .
In our study the activity of gastritis and the density of the HP were factors associated
Table 3. Effect of Helicobacter pylori eradication in atrophic gastritis and intestinal metaplasia in studies with ≥2.5 a year follow-up  .
with atrophy. The density of HP and severe atrophy were factors associated with metaplasia.
In our study, the prevalence of atrophic gastritis and intestinal metaplasia in patients infected with Helicobacter pylori is 84% and 13.5% respectively, which is a high prevalence may be overestimated by inflammation.
The activity of gastritis and the density of the HP were factors associated with atrophy. The density of HP and severe atrophy were factors associated with metaplasia.
Our study did not assess the evolution of atrophy and metaplasia after eradication of HP.