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Lina Darzehaf1
, Did Loubna2*
, Boucheikhchouk Mehdi2
and Amara Hichem3
1
Department of Biochemistry, Badji Mokthar Annaba University, Algeria
2
Biodiversity and Ecosystem Pollution Laboratory, Chadli Bendjedid El Tarf University, Algeria
3
Department of pathological anatomy, El Tarf Hospital, Algeria
Involvement of Helicobacter Pylori in the Genesis of Precancerous Stomach Lesions:
Epidemiological Aspects Based on an Algerian Study
*
Corresponding author:
Did Loubna,
Biodiversity and Ecosystem Pollution Laboratry,
Chadli Bendjedid El Tarf University, Algeria,
E-mail: db.loubna@yahoo.fr
Received: 11 Oct 2022
Accepted: 20 Oct 2022
Published: 25 Oct 2022
J Short Name: AJSCCR
Copyright:
©2022 Did Loubna. This is an open access article dis-
tributed under the terms of the Creative Commons Attri-
bution License, which permits unrestricted use, distribu-
tion, and build upon your work non-commercially
Citation:
Did Loubna, Involvement of Helicobacter Pylori in the
Genesis of Precancerous Stomach Lesions: Epidemio-
logical Aspects Based on an Algerian Study. Ame J Surg
Clin Case Rep. 2022; 5(13): 1-4
Keywords:
H. pylori; Prevalence; Chronic gastritis; Atrophy; Fundic
antrum; Histological activity
1. Abstract
Helicobacter Pylori is a bacterium involved in the genesis of pre-
cancerous lesions of the stomach. This infection is universally
prevalent but is higher in developing countries. A retrospective
study spread over 3 years (2018-2019-2020) was conducted at the
pathological anatomy laboratory of the Chadli Bendjedid Hospital
in El Tarf, northeast Algeria. All patients were submitted to a fib-
erscope, and the diagnosis was established by histological exami-
nation. The results show that of the 134 patients examined, 100%
were diagnosed with chronic gastritis. The prevalence of H. pylori
infection was 61.94%; 63.86% of women were affected, and the
most susceptible age group was 50-59 years; 36.14% of men were
affected, mainly in the age group 30-39 years. Locally, the fun-
dic antrum area appeared to be the most affected (81.93%) with
moderate chronic atrophic gastritis (78.57%) and silent activity
(94.28%), which favors the development of cancer cells.
2. Introduction
In 1982, J. Robin Warren and Barry J. Marshall identified a bac-
terium colonizing the gastric mucosa and named it Helicobacter
Pylori (H. pylori) [1]. Numerous studies have shown its etiopatho-
genic role in several gastric and duodenal diseases (gastritis, ulcer,
lymphoma, gastric cancer) [2]. Other associations between H. py-
lori infection and certain extra digestive diseases have been report-
ed [3]. It is estimated that about half of the world’s population is
infected with H. pylori, mainly in developing countries.
However, it affects 70-90% of the population in developing coun-
tries, making it a real public health problem [4]. In these countries,
about 80% of the subjects are infected in childhood and remain so
throughout their lives [5, 6 ]. In industrialized countries, the prev-
alence varies from 20 to 40%. The mode of transmission of H. py-
lori is still unclear. As H. pylori has been isolated from stool, saliva
and dental plaque, this suggests that transmission is possible via
the oral or fecal route [7]. Our work is based on an epidemiological
study to determine the prevalence of detected chronic gastritis and
the presence of H. pylori over the 3 years (2018- 2019- 2020) as
well as demographic variables and site of infection, with the type
of atrophy.
3. Patients and Method
A retrospective and descriptive study was conducted at the patho-
logical anatomy laboratory of the Chadli Bendjedid Hospital of El
Tarf. The study involved 134 patients with gastric pathologies and
was spread over 3 years (2018-2019-2020). Our work consisted of
a consultation of the department’s analysis register, made available
to us, and from which we proceeded to a census of gastritis cases
diagnosed in the laboratory from biopsies sent by the attending
physician. Demographic (age and sex) and clinical information
was also collected.
4. Studied Variables
Five types of variables were recorded for this study: variability
related to the prevalence of detected chronic gastritis and the pres-
ISSN 2689-8268 Volume 5
American Journal of Surgery and Clinical Case Reports
Clinical Paper Open Access
Volume 5 | Issue 13
ence of H. pylori over the study period, the demographic variable
(age and sex), a variable related to the site of infection, the type of
atrophy, and finally the histological activity.
5. Statistical Method
The study of demographic data (age and sex) of the 134 patients,
as well as the clinical data, were collected and recorded, then pro-
cessed by Excel 2013 software and described by their numbers and
percentages.
6. Results
6.1. General characteristics of the sample studied
We studied the prevalence of detected chronic gastritis and the
presence of H. pylori over the study period. The study population
consisted of 134 biopsies from patients with gastric pathologies
sent for anatomopathological examination. Of these, 100% were
diagnosed as chronic gastritis. H. pylori was detected in 61.94% of
patients with chronic gastritis (Table 1).
6.2. Age and gender of patients
The 83 patients reported the presence of H. pylori with a mean age
of 51 years, of which 53 women and 30 men, the rate of (63.86%)
and (36.14%) were recorded, respectively. At the age of 30-39
years, men are affected by a rate of 26.66%, and a rate of 33.33%
is recorded at the age of 50-59 years in women, constituting the
largest rate of consultants. Table 2 shows the distribution of pa-
tients by age and gender.
Table 1: Prevalence of H. pylori.
134
Positive patients Negative patients
83 51
61.94% 38.05%
Table 2: Description of the study sample by gender and age.
Type Number %
Women 53 63.86%
Men 30 36.14%
Age group Number %
Woman Men Woman Men
-20 4 1 7.54% 3.33%
20-29 11 4 20.37% 13.33%
30-39 4 8 7.54% 26.66%
40-49 7 6 12.96% 20%
50-59 18 7 33.33% 23.33%
60-69 7 3 12.96% 10%
70-79 1 0 1.85% 0%
80-89 1 1 1.85% 3.33%
6.3. Variability according to the location of the lesion
Among the three areas of the stomach, the fundic antrum appears
to be the ideal location for H. pylori colonization, with a rate of
(81.93%), and (9.64%) for the pyloric antrum and (8.43%) for the
fundus (Figure 1).
Figure 1: Prevalence of gastritis due to H. pylori infection by the lesion
site.
6.4. Variability according to the presence and type of atrophy
The 83 patients with chronic gastritis with the presence of H. py-
lori (15.66%), superficial chronic gastritis, and (84.33%), moder-
ate type atrophic cases (78.57%) with silent activity (not active)
for a rate of (94.28%) presented as well as mild (4.29%) and severe
atrophic (17.14%) and chronic atrophic gastritis with histologic
activity (5.72%) (Figure 2 and Table 3).
Figure 2: Overall prevalence of histological activity in H. pylori-infected
chronic atrophic gastritis.
Table 3: The rate of different pathological types in the H. pylori-infected
population.
Superficial chronic gastritis Chronic atrophic gastritis
15.66% 84.33%
Slight Moderate Severe
17.14% 78.57% 4.29%
Volume 5 | Issue 13
ajsccr.org 2
7. Discussion
Epidemiological studies on H. pylori infection in chronic gastritis
are scarce in Algeria. This infection is widespread but is higher in
developing countries (78% inAlgeria, 71% in Morocco and 69% in
Ivory Coast) [8]. It is frequently linked to the poor socio-economic
status of families, determined mainly by the size of the dwelling
and its sanitary level, the risk of infection increases when several
people are in close contact, as in a large family [4]. However, these
conditions are improved in industrialized countries.
Our study population included 134 patients. The H. pylori preva-
lence was estimated to be (61.94%). Another study on H. pylori in-
fection in Morocco reported a rate of (69%). [9]. This frequency is
within the limits of the values reported by several African studies,
which vary from (56.4%) to (91.3%) and remains higher than in
European data, where this frequency does not exceed (45%) [10-
11]. In our epidemiological survey, a prevalence of the female sex
in chronic gastritis and H. pylori infection was reported with rates
of (60.44%) and (63.86%) respectively. Compared to the male sex,
(39.55%) chronic gastritis and (36.14%) H. pylori infection were
recorded. However, other studies noted the predominance of men
[12]. Essedik et al. (2013) did not find a significant difference in
prevalence between men [13].
In addition, H. pylori is found in our series if compared by age
groups. At the age of 30-39 years, men are affected by a rate of
26.66%. A rate of 33.33% is recorded at the age of 50-59 years in
women, constituting the highest rate among the consultants. Our
results are close to those obtained in developed countries, where
the highest prevalence (66%) is recorded at the age of 60 years
[12]. The site of H. pylori proliferation is the fundic antrum par ex-
cellence. Indeed, the antrum is colonized by H. pylori in (81.93%)
of our population. These results are in agreement with those of
the study conducted in the Gharb Chrarda-Beni Hssen region in
Morocco, which attributed (70.9%) of lesions to this site [14].
However, these values are still higher than those that Binan et al.
(2006) reported. Seoane et al. (2005) attributed 40% and 48.1%
of lesions to H. pylori at the antral site [15-16]. It should be noted
that the high presence of H. pylori in the fundic antrum is since
gastric biopsies are mainly performed at this level, which does not
prevent the bacteria from colonizing the entire mucosa, including
the pyloric region, hence its name.
On the other hand, H. pylori is the cause of several gastric pathol-
ogies. It is the cause of 80% of chronic atrophic gastritis [1]. These
results are in agreement with those found in our study. Indeed, H.
pylori is most frequently correlated with chronic atrophic gastritis,
with a prevalence of (84.38%). Our results are also in agreement
with those recorded in Morocco, where 91.8% of chronic atrophic
gastritis is correlated with H. pylori [13]. In the study population,
78.57% of atrophies are of the moderate type with silent (non-ac-
tive) activity for a rate of (94.28%).
The high rate of H. pylori infection reported in our survey and
its pathogenicity are related to the presence of numerous proteins
and cytotoxins (Cag A, Vag A). They generate cytotoxic power on
the cell (inhibition of phagosome-lysosome fusion or alteration of
the capacity to present antigens) [17]. This causes histopatholog-
ical changes in the cell, leading to atrophy. The predominance of
the moderate type of atrophy proves that the pathological process
evolves beyond the stage of mild atrophy and may lead to severe
atrophy with detrimental consequences for the gastric cell and the
organism as a whole. Silent (non-active) atrophies are the most
dangerous, as the disease potentially progresses silently to more
severe stages.
8. Conclusion
The results of our study are similar to those of other epidemiolog-
ical studies conducted in Morocco or several developing countries
for the prevalence of Helicobacter Pylori infection. A female prev-
alence of H. pylori was reported at 63.86% and 36.14% in males.
The results show that at the age of 30-39 years, men are affected
by a rate of 26.66%, and a rate of 33.33% is recorded at the age of
50-59 years in women, constituting the largest rate of consultants.
The fundic antrum seems to be the ideal place for H. pylori col-
onization with a rate of (81.93%), as well as atrophic (84.33%),
moderate (78.57%), and silent (non-active) cases with a rate of
(94.28%). Since the discovery in 1982 by Marshall and Warren of
the H. pylori bacterium in the pyloric antrum, numerous studies
have shown its etiopathogenic role in several gastric and duodenal
diseases (gastritis, ulcer, lymphoma, gastric cancer).
In our epidemiological survey, H. pylori was detected in 61.94%
of the study population (134 patients). The most infected age
group during these 3 years was between 21 and 59. Presence was
reported in women more than in men, with 63.86% and 36.14%,
respectively. H. pylori was most commonly correlated with chron-
ic atrophic gastritis with a prevalence of 84.38%, and 78.57% of
the atrophies were moderate, with low-grade dysplasia in 27% of
cases.
References
1. Marshall BJ, Warren JR. Unidentified curved bacilli in the stom-
ach of patients with gastritis and peptic ulceration. Lancet. 1984;
323(8390): 1311-5.
2. Mignon M. 2005 Nobel Prize in Medicine: Barry J. Marshall and
J. Robin Warren. Helicobacter pylori crowned. Medicine Sciences.
2005; 21(11): 993-994.
3. Longo-Mbenza B, Nsenga JN, Mokondjimobe E, Gombet T, Assori
IN, Ibara JR, et al. Helicobacter pylori infection identified as a car-
diovascular risk factor in Central Africans. Vasc Health Risk Manag.
2012; 6:455-61.
4. Malaty HM. Epidemiology of Helicobacter pylori infection. Best
Practice Research Clinical Gastroenterology. 2007; 21(2): 205-14.
Volume 5 | Issue 13
ajsccr.org 3
5. Brown LM. Helicobacter pylori: epidemiology and routes of trans-
mission. Epidemiol Rev. 2000; 22(2): 283-97.
6. Bommelaer G, Stef A. Peptic ulcer disease: before and after Helico-
bacter pylori. Gastroenterol Clin Biol. 2009; 33(8-9): 626-634.
7. Everhart JE. Recent developments in the epidemiology of Helico-
bacter pylori. Gastroenterology Clinics of North America. 2000; 29
(3):78-559.
8. Faik M. Update on gastric infestation by Helicobacter pylori. Méde-
cine du Maghreb. 2000; 79: 17-19.
9. Hjoutei HA, et al. Helicobacter pylori infection in 755 patients with
digestive symptoms: Institut Pasteur du Maroc, 1998-2007 Eastern
MediterraneanHealth Journal La Revue de Santé de la Méditerranée
orient EMHJ. 2010; 16: 7.
10. Diomande MI, et al. Chronic gastritis and Helicobacter pylori infec-
tion in Côte d’Ivoire: a study of a series of 277 symptomatic patients.
Clinical and Biological Gastroenterology. 1991; 15(10): 711-716.
11. Sobalah GM, et al. Screening dyspepsia by serology to Helicobacter
pylori. Lancet. 1991; 338(13): 94-96
12. Ramanampamonjy RM, Randria MJD, Razafimahefa SH, Ratsiman-
disa R, Rajaonarivelo P. Seroprevalence of Helicobacter pylori infec-
tion in a Malagasy population sample. Bull Soc Pathol Exot. 2007;
100(1): 57-60.
13. Amel Essedik, et al. Epidemiological and clinical aspects of Helico-
bacter pylori infection through a Moroccan study Hegel. 2013; 3: 3.
14. Attaf N, et al. Epidemiological profile of Helicobacter pylori infec-
tion in the Gharb-Chrarda-Beni Hssen region. Biology & Health.
2004; 4(1): 25-3.
15. Binan Y, et al. Gastric cancer and Helicobacter pylori: results from an
endoscopy center in Abidjan. International Journal of Medical Sci-
ences. 2006; 8(1): 23-27.
16. Seoane A, et al. Helicobacter pylori and gastric cancer: relation-
ship to histologic subtype and tumor location. Gastroenterology and
Hepatology. 2005; 28 (2): 4-60.
17. Brent Polk 1, Richard M Peek Jr. Helicobacter pylori: gastric cancer
and beyond Nat Rev Cancer. June. 2010; 10(6): 403-14.
Volume 5 | Issue 13
ajsccr.org 4

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Involvement of Helicobacter Pylori in the Genesis of Precancerous Stomach Lesions: Epidemiological Aspects Based on an Algerian Study

  • 1. Lina Darzehaf1 , Did Loubna2* , Boucheikhchouk Mehdi2 and Amara Hichem3 1 Department of Biochemistry, Badji Mokthar Annaba University, Algeria 2 Biodiversity and Ecosystem Pollution Laboratory, Chadli Bendjedid El Tarf University, Algeria 3 Department of pathological anatomy, El Tarf Hospital, Algeria Involvement of Helicobacter Pylori in the Genesis of Precancerous Stomach Lesions: Epidemiological Aspects Based on an Algerian Study * Corresponding author: Did Loubna, Biodiversity and Ecosystem Pollution Laboratry, Chadli Bendjedid El Tarf University, Algeria, E-mail: db.loubna@yahoo.fr Received: 11 Oct 2022 Accepted: 20 Oct 2022 Published: 25 Oct 2022 J Short Name: AJSCCR Copyright: ©2022 Did Loubna. This is an open access article dis- tributed under the terms of the Creative Commons Attri- bution License, which permits unrestricted use, distribu- tion, and build upon your work non-commercially Citation: Did Loubna, Involvement of Helicobacter Pylori in the Genesis of Precancerous Stomach Lesions: Epidemio- logical Aspects Based on an Algerian Study. Ame J Surg Clin Case Rep. 2022; 5(13): 1-4 Keywords: H. pylori; Prevalence; Chronic gastritis; Atrophy; Fundic antrum; Histological activity 1. Abstract Helicobacter Pylori is a bacterium involved in the genesis of pre- cancerous lesions of the stomach. This infection is universally prevalent but is higher in developing countries. A retrospective study spread over 3 years (2018-2019-2020) was conducted at the pathological anatomy laboratory of the Chadli Bendjedid Hospital in El Tarf, northeast Algeria. All patients were submitted to a fib- erscope, and the diagnosis was established by histological exami- nation. The results show that of the 134 patients examined, 100% were diagnosed with chronic gastritis. The prevalence of H. pylori infection was 61.94%; 63.86% of women were affected, and the most susceptible age group was 50-59 years; 36.14% of men were affected, mainly in the age group 30-39 years. Locally, the fun- dic antrum area appeared to be the most affected (81.93%) with moderate chronic atrophic gastritis (78.57%) and silent activity (94.28%), which favors the development of cancer cells. 2. Introduction In 1982, J. Robin Warren and Barry J. Marshall identified a bac- terium colonizing the gastric mucosa and named it Helicobacter Pylori (H. pylori) [1]. Numerous studies have shown its etiopatho- genic role in several gastric and duodenal diseases (gastritis, ulcer, lymphoma, gastric cancer) [2]. Other associations between H. py- lori infection and certain extra digestive diseases have been report- ed [3]. It is estimated that about half of the world’s population is infected with H. pylori, mainly in developing countries. However, it affects 70-90% of the population in developing coun- tries, making it a real public health problem [4]. In these countries, about 80% of the subjects are infected in childhood and remain so throughout their lives [5, 6 ]. In industrialized countries, the prev- alence varies from 20 to 40%. The mode of transmission of H. py- lori is still unclear. As H. pylori has been isolated from stool, saliva and dental plaque, this suggests that transmission is possible via the oral or fecal route [7]. Our work is based on an epidemiological study to determine the prevalence of detected chronic gastritis and the presence of H. pylori over the 3 years (2018- 2019- 2020) as well as demographic variables and site of infection, with the type of atrophy. 3. Patients and Method A retrospective and descriptive study was conducted at the patho- logical anatomy laboratory of the Chadli Bendjedid Hospital of El Tarf. The study involved 134 patients with gastric pathologies and was spread over 3 years (2018-2019-2020). Our work consisted of a consultation of the department’s analysis register, made available to us, and from which we proceeded to a census of gastritis cases diagnosed in the laboratory from biopsies sent by the attending physician. Demographic (age and sex) and clinical information was also collected. 4. Studied Variables Five types of variables were recorded for this study: variability related to the prevalence of detected chronic gastritis and the pres- ISSN 2689-8268 Volume 5 American Journal of Surgery and Clinical Case Reports Clinical Paper Open Access Volume 5 | Issue 13
  • 2. ence of H. pylori over the study period, the demographic variable (age and sex), a variable related to the site of infection, the type of atrophy, and finally the histological activity. 5. Statistical Method The study of demographic data (age and sex) of the 134 patients, as well as the clinical data, were collected and recorded, then pro- cessed by Excel 2013 software and described by their numbers and percentages. 6. Results 6.1. General characteristics of the sample studied We studied the prevalence of detected chronic gastritis and the presence of H. pylori over the study period. The study population consisted of 134 biopsies from patients with gastric pathologies sent for anatomopathological examination. Of these, 100% were diagnosed as chronic gastritis. H. pylori was detected in 61.94% of patients with chronic gastritis (Table 1). 6.2. Age and gender of patients The 83 patients reported the presence of H. pylori with a mean age of 51 years, of which 53 women and 30 men, the rate of (63.86%) and (36.14%) were recorded, respectively. At the age of 30-39 years, men are affected by a rate of 26.66%, and a rate of 33.33% is recorded at the age of 50-59 years in women, constituting the largest rate of consultants. Table 2 shows the distribution of pa- tients by age and gender. Table 1: Prevalence of H. pylori. 134 Positive patients Negative patients 83 51 61.94% 38.05% Table 2: Description of the study sample by gender and age. Type Number % Women 53 63.86% Men 30 36.14% Age group Number % Woman Men Woman Men -20 4 1 7.54% 3.33% 20-29 11 4 20.37% 13.33% 30-39 4 8 7.54% 26.66% 40-49 7 6 12.96% 20% 50-59 18 7 33.33% 23.33% 60-69 7 3 12.96% 10% 70-79 1 0 1.85% 0% 80-89 1 1 1.85% 3.33% 6.3. Variability according to the location of the lesion Among the three areas of the stomach, the fundic antrum appears to be the ideal location for H. pylori colonization, with a rate of (81.93%), and (9.64%) for the pyloric antrum and (8.43%) for the fundus (Figure 1). Figure 1: Prevalence of gastritis due to H. pylori infection by the lesion site. 6.4. Variability according to the presence and type of atrophy The 83 patients with chronic gastritis with the presence of H. py- lori (15.66%), superficial chronic gastritis, and (84.33%), moder- ate type atrophic cases (78.57%) with silent activity (not active) for a rate of (94.28%) presented as well as mild (4.29%) and severe atrophic (17.14%) and chronic atrophic gastritis with histologic activity (5.72%) (Figure 2 and Table 3). Figure 2: Overall prevalence of histological activity in H. pylori-infected chronic atrophic gastritis. Table 3: The rate of different pathological types in the H. pylori-infected population. Superficial chronic gastritis Chronic atrophic gastritis 15.66% 84.33% Slight Moderate Severe 17.14% 78.57% 4.29% Volume 5 | Issue 13 ajsccr.org 2
  • 3. 7. Discussion Epidemiological studies on H. pylori infection in chronic gastritis are scarce in Algeria. This infection is widespread but is higher in developing countries (78% inAlgeria, 71% in Morocco and 69% in Ivory Coast) [8]. It is frequently linked to the poor socio-economic status of families, determined mainly by the size of the dwelling and its sanitary level, the risk of infection increases when several people are in close contact, as in a large family [4]. However, these conditions are improved in industrialized countries. Our study population included 134 patients. The H. pylori preva- lence was estimated to be (61.94%). Another study on H. pylori in- fection in Morocco reported a rate of (69%). [9]. This frequency is within the limits of the values reported by several African studies, which vary from (56.4%) to (91.3%) and remains higher than in European data, where this frequency does not exceed (45%) [10- 11]. In our epidemiological survey, a prevalence of the female sex in chronic gastritis and H. pylori infection was reported with rates of (60.44%) and (63.86%) respectively. Compared to the male sex, (39.55%) chronic gastritis and (36.14%) H. pylori infection were recorded. However, other studies noted the predominance of men [12]. Essedik et al. (2013) did not find a significant difference in prevalence between men [13]. In addition, H. pylori is found in our series if compared by age groups. At the age of 30-39 years, men are affected by a rate of 26.66%. A rate of 33.33% is recorded at the age of 50-59 years in women, constituting the highest rate among the consultants. Our results are close to those obtained in developed countries, where the highest prevalence (66%) is recorded at the age of 60 years [12]. The site of H. pylori proliferation is the fundic antrum par ex- cellence. Indeed, the antrum is colonized by H. pylori in (81.93%) of our population. These results are in agreement with those of the study conducted in the Gharb Chrarda-Beni Hssen region in Morocco, which attributed (70.9%) of lesions to this site [14]. However, these values are still higher than those that Binan et al. (2006) reported. Seoane et al. (2005) attributed 40% and 48.1% of lesions to H. pylori at the antral site [15-16]. It should be noted that the high presence of H. pylori in the fundic antrum is since gastric biopsies are mainly performed at this level, which does not prevent the bacteria from colonizing the entire mucosa, including the pyloric region, hence its name. On the other hand, H. pylori is the cause of several gastric pathol- ogies. It is the cause of 80% of chronic atrophic gastritis [1]. These results are in agreement with those found in our study. Indeed, H. pylori is most frequently correlated with chronic atrophic gastritis, with a prevalence of (84.38%). Our results are also in agreement with those recorded in Morocco, where 91.8% of chronic atrophic gastritis is correlated with H. pylori [13]. In the study population, 78.57% of atrophies are of the moderate type with silent (non-ac- tive) activity for a rate of (94.28%). The high rate of H. pylori infection reported in our survey and its pathogenicity are related to the presence of numerous proteins and cytotoxins (Cag A, Vag A). They generate cytotoxic power on the cell (inhibition of phagosome-lysosome fusion or alteration of the capacity to present antigens) [17]. This causes histopatholog- ical changes in the cell, leading to atrophy. The predominance of the moderate type of atrophy proves that the pathological process evolves beyond the stage of mild atrophy and may lead to severe atrophy with detrimental consequences for the gastric cell and the organism as a whole. Silent (non-active) atrophies are the most dangerous, as the disease potentially progresses silently to more severe stages. 8. Conclusion The results of our study are similar to those of other epidemiolog- ical studies conducted in Morocco or several developing countries for the prevalence of Helicobacter Pylori infection. A female prev- alence of H. pylori was reported at 63.86% and 36.14% in males. The results show that at the age of 30-39 years, men are affected by a rate of 26.66%, and a rate of 33.33% is recorded at the age of 50-59 years in women, constituting the largest rate of consultants. The fundic antrum seems to be the ideal place for H. pylori col- onization with a rate of (81.93%), as well as atrophic (84.33%), moderate (78.57%), and silent (non-active) cases with a rate of (94.28%). Since the discovery in 1982 by Marshall and Warren of the H. pylori bacterium in the pyloric antrum, numerous studies have shown its etiopathogenic role in several gastric and duodenal diseases (gastritis, ulcer, lymphoma, gastric cancer). In our epidemiological survey, H. pylori was detected in 61.94% of the study population (134 patients). The most infected age group during these 3 years was between 21 and 59. Presence was reported in women more than in men, with 63.86% and 36.14%, respectively. H. pylori was most commonly correlated with chron- ic atrophic gastritis with a prevalence of 84.38%, and 78.57% of the atrophies were moderate, with low-grade dysplasia in 27% of cases. References 1. Marshall BJ, Warren JR. Unidentified curved bacilli in the stom- ach of patients with gastritis and peptic ulceration. Lancet. 1984; 323(8390): 1311-5. 2. Mignon M. 2005 Nobel Prize in Medicine: Barry J. Marshall and J. Robin Warren. Helicobacter pylori crowned. Medicine Sciences. 2005; 21(11): 993-994. 3. Longo-Mbenza B, Nsenga JN, Mokondjimobe E, Gombet T, Assori IN, Ibara JR, et al. Helicobacter pylori infection identified as a car- diovascular risk factor in Central Africans. Vasc Health Risk Manag. 2012; 6:455-61. 4. Malaty HM. Epidemiology of Helicobacter pylori infection. Best Practice Research Clinical Gastroenterology. 2007; 21(2): 205-14. Volume 5 | Issue 13 ajsccr.org 3
  • 4. 5. Brown LM. Helicobacter pylori: epidemiology and routes of trans- mission. Epidemiol Rev. 2000; 22(2): 283-97. 6. Bommelaer G, Stef A. Peptic ulcer disease: before and after Helico- bacter pylori. Gastroenterol Clin Biol. 2009; 33(8-9): 626-634. 7. Everhart JE. Recent developments in the epidemiology of Helico- bacter pylori. Gastroenterology Clinics of North America. 2000; 29 (3):78-559. 8. Faik M. Update on gastric infestation by Helicobacter pylori. Méde- cine du Maghreb. 2000; 79: 17-19. 9. Hjoutei HA, et al. Helicobacter pylori infection in 755 patients with digestive symptoms: Institut Pasteur du Maroc, 1998-2007 Eastern MediterraneanHealth Journal La Revue de Santé de la Méditerranée orient EMHJ. 2010; 16: 7. 10. Diomande MI, et al. Chronic gastritis and Helicobacter pylori infec- tion in Côte d’Ivoire: a study of a series of 277 symptomatic patients. Clinical and Biological Gastroenterology. 1991; 15(10): 711-716. 11. Sobalah GM, et al. Screening dyspepsia by serology to Helicobacter pylori. Lancet. 1991; 338(13): 94-96 12. Ramanampamonjy RM, Randria MJD, Razafimahefa SH, Ratsiman- disa R, Rajaonarivelo P. Seroprevalence of Helicobacter pylori infec- tion in a Malagasy population sample. Bull Soc Pathol Exot. 2007; 100(1): 57-60. 13. Amel Essedik, et al. Epidemiological and clinical aspects of Helico- bacter pylori infection through a Moroccan study Hegel. 2013; 3: 3. 14. Attaf N, et al. Epidemiological profile of Helicobacter pylori infec- tion in the Gharb-Chrarda-Beni Hssen region. Biology & Health. 2004; 4(1): 25-3. 15. Binan Y, et al. Gastric cancer and Helicobacter pylori: results from an endoscopy center in Abidjan. International Journal of Medical Sci- ences. 2006; 8(1): 23-27. 16. Seoane A, et al. Helicobacter pylori and gastric cancer: relation- ship to histologic subtype and tumor location. Gastroenterology and Hepatology. 2005; 28 (2): 4-60. 17. Brent Polk 1, Richard M Peek Jr. Helicobacter pylori: gastric cancer and beyond Nat Rev Cancer. June. 2010; 10(6): 403-14. Volume 5 | Issue 13 ajsccr.org 4