Annals of African Medicine

REVIEW ARTICLE
Year
: 2021  |  Volume : 20  |  Issue : 1  |  Page : 1--8

Helicobacter pylori and association between its positivity and anatomotopographic settlement in the stomach with the host age range


Tuncer Ozturk1, Demet Sengul2, Ilker Sengul1,  
1 Department of General Surgery, Giresun University Faculty of Medicine, TR28100 Giresun, Turkey
2 Department of Pathology, Giresun University Faculty of Medicine, TR28100 Giresun, Turkey

Correspondence Address:
Dr. Demet Sengul
The Founder Chief, Department of Pathology, The United Education Laboratories, Giresun University Faculty of Medicine, Gazipasa Compound, Gazi Avenue, TR28100 Giresun
Turkey

Abstract

Helicobacter pylori (H. pylori) is a Gram-negative, helically shaped flagellated bacterium. Major diseases associated with H. pylori infection include peptic ulcer, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. The incidence of H. pylori in the anatomotopographic regions of the stomach, such as antrum, corpus, fundus, and incisura angularis, has been investigated. Do the rates of H. pylori in the settlements change over time according to the age ranges of the hosts? Does this change affect the diseases caused by or related to H. pylori? It is estimated that the outcomes, which have been obtained, may provide a new perspective in terms of understanding the etiopathogenesis of H. pylori-induced diseases. A comprehensive literature search of PubMed/MEDLINE databases had been conducted using a combination of terms, “Helicobacter pylori,” “Sydney System,” “stomach,” “pyloric antrum,” “gastric corpus,” “stomach cancer,” and “Helicobacter pylori and age.” There are very few articles examining the relationship between the topographic locations of H. pylori and host age range in the English language literature. Therefore, it is also purposed to emphasize the outcomes of our current research about the mentioned topic. In our opinion, similar studies should reveal the settlement and age range in the different geographic locations and societies as in our study. We believe that these findings will contribute to the efforts for understanding overtly of H. pylori-induced disease of the stomach.



How to cite this article:
Ozturk T, Sengul D, Sengul I. Helicobacter pylori and association between its positivity and anatomotopographic settlement in the stomach with the host age range.Ann Afr Med 2021;20:1-8


How to cite this URL:
Ozturk T, Sengul D, Sengul I. Helicobacter pylori and association between its positivity and anatomotopographic settlement in the stomach with the host age range. Ann Afr Med [serial online] 2021 [cited 2021 Apr 13 ];20:1-8
Available from: https://www.annalsafrmed.org/text.asp?2021/20/1/1/311175


Full Text



 Background



Description

H. pylori, belonging to Genus Helicobacter, Family Helicobacteraceae, Order Campylobacterales, Class Epsilonproteobacteria, Phylum Proteobacteria, Domain Bacteria, is a Gram-negative, helically shaped flagellated bacterium associated with many gastric diseases.[1],[2] The Genus Helicobacter includes about 35 species, consisting of one of them, H. pylori.[3] The most common and important diseases of H. pylori infection are peptic ulcer (10%), gastric adenocarcinoma (1%–3%), and lymphoid tissue lymphoma associated with primary gastric mucosa (mucosa-associated lymphoid tissue [MALT]).[4] H. pylori is a microaerophilic bacterium living in the mucosal parts of the stomach.[5],[6],[7] Colonization with H. pylori is often associated with the progression of gastrointestinal disorders, i.e., gastritis, peptic ulcer disease, gastric cancer, and MALT lymphoma.[8] The variety and severity of the diseases depend on the condition of the host's immune system, the pathogenicity of H. pylori and the presence of environmental factors, such as diet, stress, hygiene standard or presence of infections.[5]

H. pylori, fecal–oral or oral–oral contagion, is located in various parts of the stomach.[9] H. pylori involvement is present in approximately 50% of people in the upper gastrointestinal tract.[10] H. pylori has different mechanisms to escape the acidic gastric environment in which pH is about 2.0. These mechanisms are production of urease, flagellar mobility, and chemotaxis required for invasion of the stomach epithelium.[11] Urease catalyzes the hydrolysis of urea to bicarbonate and ammonia. Urea is present in abundant amounts in the stomach; therefore, the pH approaches a neutral range.[12]

Geographic distribution

The prevalence of H. pylori infection is changing worldwide, roughly 10% in developed Western countries and 80% in developing countries such as India.[13],[14] Clinical findings are seen at approximately 20%. H. pylori tends to decrease in many regions of the world. Evidence from the studies in Europe supports the downward trend. In some countries in the Middle East, the prevalence of H. pylori remained relatively stable. In a meta-analysis published last year, H. pylori prevalence was reported as very low in Australia and the surrounding regions (24.4%). However, the highest rate was observed in Africa (79.1%). The annual recurrence rate of H. pylori infection was 4.3%. The prevalence of human development index and infection was related to the recurrence rate. Several studies have investigated the relationship between H. pylori infection and the population data, social conditions, drinking water source, and dietary factors. In several studies, the insects and yeasts have been emphasized in the transmission of H. pylori.[15] Although there is an attenuation in gastric cancer rates in the developed countries, the most common cancer in the world is one of the causes of death.[16],[17] There is an increase in global mortality rates of gastric cancer due to population growth and life expectancy.[17] Approximately 75% of total gastric cancer patients are presumed to be H. pylori-induced inflammation and injury.[18] H. pylori colonized people for tens of thousands of years.[19] During this time, they survived the aggressive environment of the stomach and survived the host immune system.[20] H. pylori invades the gastric epithelial surfaces by spreading to the mucus layer.[21] Recently, it has been found that H. pylori has proliferated in the glands, has a recurrent gastrointestinal spread, and can provide niche to bacteria.[22],[23]

In 2015, around 4.4 billion people were infected with H. pylori worldwide and 950,000 new cases diagnosed with gastric cancer.[24] In some parts of the world, it is quite common, for instance, the East Asian countries, Japan, China, and Korea. The incidence of gastric cancer in these countries is about ten times that of the United States. The incidence of gastric cancer is almost two times higher in males than in females and observed 66% in rural and 47% in urban areas.[25] The successful colony of H. pylori in the stomach requires an age-related gastric physiology and special characteristics related to the host. H. pylori settles in childhood and continues for life.[26]

Diseases associated with Helicobacter pylori

H. pylori infection is associated with some of the most common disorders of the upper gastrointestinal tract.[27] Approximately 80% of the H. pylori infections do not give clinical signs. Permanent H. pylori colonization is the main risk factor for gastric and duodenal ulcer, lymphoid tissue lymphoma associated with gastric mucosa (MALT), and stomach adenocarcinoma.[28] Different treatment modalities had been described for H. pylori.[29],[30] The third leading cause of cancer deaths in the world is stomach adenocarcinoma and has been accepted as a cause of many disorders. H. pylori is the main cause of chronic active gastritis. Duodenal and gastric ulcer, low-grade B-cell lymphoma, and MALT lymphoma are other important clinical diseases.[27],[31],[32]

H. pylori, a gram-negative, flagellated, microaerophilic bacterium that selectively colonizes the gastric mucosa layer, is a Class I carcinogenic bacterium, colonizing the stomach in childhood.[33],[34] Approximately 10% of individuals with gastric epithelial colonization develop clinical disease and 90% remain subclinical. If left untreated, the infection may persist throughout life.[35] Up to now, about 20 different diseases associated with H. pylori have been identified; duodenal ulcer, gastric ulcer, adenocarcinoma of the distal stomach, MALT lymphoma, diabetes mellitus, cardiovascular disease, and autoimmune diseases.[36] Treatment failure of H. pylori infection is associated with bacterial resistance and poor patient compliance.[33],[36],[37]

Gastric cancer is the fifth most common cancer in the world and the third leading cause of cancer death.[24] Low stomach cancer rates in North America and Africa are high in Asia, Eastern Europe, and Central and South America. The incidence of gastric cancer varies widely according to geography regions.[38] Gastric cancer can occur in all parts of the stomach between the cardiac and the antrum. H. pylori colonization is known to increase the risk of cancer in other parts of the stomach, except for the cardiac region.[39] The relationship between H. pylori colonization and gastric cardia cancer varies according to geographical regions. In Western countries, there is a neutral or even negative relationship between gastric cardia cancer and H. pylori colonization, while high proportions reported for Eastern populations, namely China, Korea and Japan.[40]

H. pylori infection is associated with the development of different gastrointestinal diseases such as gastric ulcer, gastric cancer, mucosal lymphoid tissue (MALT) lymphoma, and biliary cancer and extragastric diseases such as ischemic heart diseases, type 2 diabetes mellitus, anemia, inverse metabolic features in obese people, and insulin resistance.[41],[42],[43],[44],[45],[46] H. pylori-related diseases occur only in a small percentage of infected people. This suggests that it has been colonized in the stomach without any clear signs of disease and that H. pylori plays a beneficial role in human health.[47],[48],[49],[50],[51],[52] Recent studies have shown that the decrease in the incidence of H. pylori is parallel to the increase in the incidence of allergy and autoimmune disease.[53] The absence of H. pylori is also associated with the incidence of multiple sclerosis and celiac disease.[54],[55],[56]

H. pylori has also been associated with diseases of various nongastrointestinal organs, including coronary heart disease, rosacea and idiopathic urticaria, autoimmune thyroid disease, dermatological diseases such as thrombocytopenic purpura and iron-deficiency anemia.[57]

Importance of gastric location for Helicobacter pylori

The virulence, anatomical location, environmental factors, and host genetics of H. pylori are important in transforming H. pylori infection into gastric cancer.[55] In Western countries, cardia cancer frequently involves a mixture of gastric cardia and esophageal adenocarcinomas due to the prevalance of Barrett's esophagus and adenocarcinoma of the esophagus.[56],[58] Taihang Mountains (China) are associated with a modest increase in the risk of both cardiac and noncardiac gastric adenocarcinoma in some high-risk regions worldwide for esophageal cancer.[59] This is not the case for gastric cardia adenocarcinoma. Taihang Mountains (China) are associated with a modest increase in the risk of both cardiac and noncardiac gastric adenocarcinoma in some high-risk regions worldwide for esophageal cancer.[59] Biopsy sampling is important for gastritis classification. However, the degree of inflammation and atrophy of different regions of the stomach with chronic gastritis has been discussed in just a few studies. Isajevs et al. analyzed the inflammatory, atrophic, and metaplastic changes in the big curvature and small curvature of the antrum and corpus mucosa. They examined the upper gastrointestinal endoscopy of a total of 420 patients, and the biopsy specimens were evaluated according to the updated Sydney classification. Histopathology revealed mononuclear and granulocyte inflammatory cells, which are more prominent in the curvature than the small curvature in the greater curvature. The degree of atrophy and intestinal metaplasia was more pronounced than the small curvature of the large curvature. The frequency of distribution of H. pylori did not differ in both the corpus and the curvature of the antrum. However, the degree of colonization of H. pylori is higher than the larger curvature in the small curvature. In addition, corpus atrophy was significantly higher than antrum atrophy. Severe atrophic, metaplastic, and inflammatory changes were more common in the small curvature than in the large curvature.[60]

In a Russian study, conducted in Ryazan, the prevalence of H. pylori infection among the urban population was studied. 64.5% of the population studied were diagnosed as H. pylori infection. A total of 655 patients (638 adults and 17 children) were diagnosed with H. pylori infection. The prevalence of H. pylori infection was most commonly observed in 41–80 age group (66.9%). In addition, gender differences in the prevalence of H. pylori infection were detected in patients over 40 years of age. H. pylori infection in 41–80 years of age was 65.3% in men and 76.3% in women.[61]

Matsuhisa et al. reported that gastric ulcer was a common disease in Japan, whereas in Nepal, duodenal ulcers were common. Japanese patients infected with H. pylori have severe atrophic and metaplastic gastritis compared to Nepalese patients. The results may be related to the incidence of gastric cancer in Japanese. In older Japanese patients, dominant gastritis of the corpus was detected and antrum-dominant gastritis was found in all Nepalese patients. Matsuhisa et al. compared H. pylori-positive Asian adult populations with corpus-dominant gastritis, which is considered as one of the risk factors for gastric cancer.[62] The incidence and mortality of gastric cancer is high among Japanese and Chinese populations.

In Thailand, the incidence of gastric cancer is quite low, while in Vietnam, it is low. H. pylori-positive Chinese (Beijing), Thai, and Vietnamese patients were compared with Japanese patients with endoscopic diagnosis to compare antrum gastritis with corpus gastritis. The antrum gastritis rates of the Japanese were significantly higher than the other groups. The corpus-type gastritis was characteristic in the elderly Japanese and Chinese (Fuzhou).

However, Chinese (Beijing), Thai, and Vietnamese people (except those over 70 years of age) had antrum-type gastritis in all age groups. There is a similarity between the degree of H. pylori colonization and the neutrophil activity score. These results are parallel to the incidence of gastric cancer in Thailand and Vietnam populations. The incidence and mortality of gastric cancer is high among Japanese and Chinese people.[63]

We, Sengul and Sengul,[64] conducted a study to determine the H. pylori frequency and also to evaluate the connection of the location and age groups with the degree of H. pylori colonization, based on updated Sydney System for the histopathology results of endoscopic gastric mucosal samples of 373 cases, between February 2009 and February 2013. H. pylori was detected as at least one positive, 206 (55.2%), and negative, 167 (44.8%). H. pylori was positive for 73 of 147 (49.7%) in the corpus and 114 of 197 (57.9%) in the antrum. No difference was revealed, comparing the general stomach (P = 0.292), antrum (P = 0.896) and corpus (P = 0.184), age groups and also new subgroup (over and under 50, in the antrum), and the H. pylori colonization. We determined in our previous research that the H. pylori positivity was mostly present in the antrum and at the 45–64 age group, while no difference was detected between the location, six structured age groups, and subgroups with over and under 50 years, together with the degree of H. pylori colonization.[64]

Treatment modalities for Helicobacter pylori infections

Multiple antibiotic regimens have been evaluated in order to eradicate H. pylori.[65],[66],[67],[68] However, a number of regimens have consistently achieved the acceptable high eradication rates to date. There are also limited data on H. pylori antibiotic resistance rates to guide therapy. The selected treatment regimen must regard to local antibiotic resistance patterns (if known, with their possible allergenic effects), cost, side effects, and ease of administration for the medical agents. A resistance threshold of ≥15% is frequently utilized as an indicator in order to select an alternative empiric antibiotic regimen for H. pylori eradication purposes. In patients with risk factors for macrolide resistance, bismuth quadruple therapy is recommended to use, while clarithromycin-based triple therapy with a proton-pump inhibitor (PPI), amoxicillin, and clarithromycin for the ones without risk factors for that.[69],[70],[71] Alternative potential first-line treatment regimens consist of clarithromycin-based hybrid or sequential therapy.[72] Nevertheless, the clarithromycin-based hybrid therapy has not been universally endorsed; for instance, some North American guidelines recommendations run counter to utilization of the sequential therapy as a first-line regimen by adducing proofs of the deprivation of data from North American trials.[71] Recommendation for the duration of administration for clarithromycin-based triple therapy and bismuth quadruple treatment regimens is 14 days.[69],[70],[71] Bismuth quadruple therapy includes bismuth subsalicylate, metronidazole, tetracycline, and a PPI given for 14 days, while clarithromycin triple therapy comprises clarithromycin, amoxicillin, and a PPI, with the recommendation for a duration of 14 days.[71],[72],[73] Concomitant therapy involves clarithromycin, amoxicillin, nitroimidazole (tinidazole or metronidazole), and a PPI administered together with the duration of 10–14 days.[71],[72],[73] Gisbert et al.[74] reported that nonbismuth quadruple (concomitant) therapy was an effective, safe, and well-tolerated alternative to the triple therapy, while it was less complex than the sequential one. Therefore, they propounded that this regimen was being well suited for utilizing in settings, particularly where the efficacy of triple therapy would unacceptably low. Hybrid therapy subsumes amoxicillin and a PPI for 7 days, followed by the administration of amoxicillin, clarithromycin, nitroimidazole, and a PPI for 7 days.[75] Besides, the 10-day-sequential therapy regimen comprises amoxicillin and a PPI for 5 days, followed by clarithromycin and nitroimidazole (e.g., metronidazole) plus a PPI for 5 days.[76] In addition, levofloxacin resistance attenuates the eradication success rate of levofloxacin consisting of regimens by 20%–40%. However, levofloxacin triple therapy was revealed as might possess a role in the treatment of H. pylori species as a salvage regimen based on the results from international trials.[72] In order to confirm eradication, urea breath test, fecal antigen test, or upper endoscopy, 4 weeks or more after fulfilling medical antibiotic therapy, should be performed in all patients treated for H. pylori.[70]

 Discussion



H. pylori is a spiral-shaped, Gram-negative special bacterium that selectively holds the gastric mucosa, living in a microaerophilic environment which usually leads to a pronounced disease condition and persistent inflammation.[63] However, in some cases, chronic active gastritis, peptic ulcer, lymphoid tissue lymphoma due to mucosa, and even gastric adenocarcinoma may develop. The evidence of oral–oral transmission is reported, though human–human passage has not been fully established.[64],[65],[66],[67],[68]

H. pylori prevalence varies concerning the ethnicity and the geographic regions. Lee et al. reported that the positivity of H. pylori was recognized as 48.3%, 67.4%, and 77.9% in the American, Korean, and Japan cases, respectively, and the antrum was the most common location.[77] In the studies, conducted in different regions in Turkey, H. pylori positivity was detected as 52.8%, 62.7%, 71%, 78.4%, 87%, 89.8%, 25.2%, 64%, 58.4%, and 70.1% in Thrace region, Istanbul, Erzurum, Erzincan, Van, Sanliurfa, Kırsehir, Konya, Kayseri, and Sivas.[78],[79],[80],[81],[82],[83],[84],[85],[86],[87],[88] In December 2018, we reported the H. pylori positivity as 55.2% in Giresun.[62] Our positivity is just between the positivity of American and Korean-Japan groups with the frequent location of the antrum (57.9%), concerning the corpus (49.7%).[62]

H. pylori has been found to colonize the most common gastric antrum as a result of various studies conducted in different parts of the world. It colonizes some parts of the stomach.[81] H. pylori localization is being more intense in the antrum.[89],[90] We reported that H. pylori positivity was 49.7% in the corpus, while 57.9% in the antrum. There was no significant association between H. pylori localization and H. pylori colonization degree. H. pylori localization in the antrum did not reveal a significant age.[62]

The EUROGAST study group examines the prevalence of H. pylori infection in Europe, North Africa, North America, and Japan covering 17 different geographically defined populations in two age groups, 25–34 and 55–64.[83] The EUROGAST study detected the higher infection prevalence in the older group (61.4%) than the younger one (34.9%).[83] Sengul and Sengul.[64] studied six age groups at the end of 2018 and reported the frequency of H. pylori, regarding the age groups as 15–34 age group (57.1%), 35–44 age group (49.1%), 45–64 age group (64.5%), 65–74 age group (53.7%), 75–84 age group (59.4%), and above 85 years (3.33%).[62] There was no significant relationship between H. pylori colonization and age groups (P > 0.05). Reported the highest positivity in the 3rd group, 45–65 age group, 64.5%, which revealed so similarity with the positivity of EUROGAST study group, 61.4% for their 55-64 age group.[64],[83]

The prevalence of H. pylori, ethnic group, and geographical varies according to regions.[84] A Chile study reported 29% H. pylori positivity using the fast urease test and endoscopic biopsy samples. The infection prevalence of the age group of 40–49 years was 38.1%, the highest rate. They also reported the attenuation of the prevalence of H. pylori to 28.9% from 44.9% during the period of 11 years.[85]

H. pylori-related diseases are increasing in proximal stomach parts with increasing age. The pathogenesis and mechanism of H. pylori-related diseases in the proximal stomach has not been explained. Stomach environment changes with age. H. pylori colonization appears to be affected by this change.

In a Chinese study, 180 cases with the symptoms of dyspepsia were divided into the young, middle-aged, and old groups and the endoscopic gastric biopsies had been obtained from five locations in each case as the large curvature (middle corpus, mid-antrum), small curvature (middle corpus, mid-antrum), and incisura angularis. The results of this study revealed that the H. pylori infection rate had increased with age in the corpus location. In addition, H. pylori density had increased in the corpus in the elderly patients while the antrum and incisura angularis had not increased. A significant positive relationship between H. pylori infection, mucosal inflammation, and pyloric metaplasia severity with increasing age in the corpus was reported. H. pylori involvement had shifted from the distal to proximal with increased age. In this case, the spread of the pyloric glands increases from distal to proximal. In the same way, the rate of pyloric metaplasia increased with the risk of aggravated H. pylori infection with associated inflammation in the elderly.[86] In a US study, the age-related changes in the gastric mucosa and their association with H. pylori had been examined. They collected data from a large national pathology database of 895.323 cases who underwent esophagogastroduodenoscopy between January 2008 and December 2013. Various gastric histopathologies were expressed as a percentage according to prevalence, sex, and age. Throughout life, gastric mucosa became abnormal in 50% of participants. Gastric mucosa abnormalities were also found to be high in patients with high H. pylori infection. The chronic active gastritis was detected in 22% of the biopsies associated with H. pylori. The reactive gastropathy was observed in 18% of biopsies. It is increasing with age. Most of the pathological conditions detected in histological analysis are caused by H. pylori infection.[87]

On December 2018, we reported our 4-year single-center experience with 373 cases, of which 344 had the endoscopic gastric biopsies, obtained from the antrum and corpus locations. H. pylori positivity had revealed 57.9% in the antrum and 49.7% in the corpus.[73] The rest of 29 cases had the results from the locations of fundus, corpus and antrum, and fundus and corpus and antrum. No significant association between the anatomic localization and H. pylori positivity could be exhibited. An alternate taxonomy in terms of the subgroups, under and over 50 years old, had been performed, and no statistical difference had been detected as the antrum localization, the most common location for H. pylori positivity, was selected as the anatomic pilot region.[62]

H. pylori infection is estimated to affect approximately 50% of the world population.[88] In another estimate, the average prevalence of H. pylori infection in the world was given as 58%.[89] In our study, the overall H. pylori positivity was 55.2%.[62] Because of the irregular distribution of H. pylori in the gastric mucosa, biopsies from various regions of the stomach may increase the diagnostic yield for detection of H. pylori.[90] H. pylori infection is a major health problem in China and its prevalence ranges from 41.5% to 72.3% according to population and geographic region.[91] According to geographical regions, age, and socioeconomic status, it ranges between 39.9% and 84.2%.[92]

H. pylori has been found to colonize the most common gastric antrum as a result of various studies conducted in different parts of the world. It colonizes some parts of the stomach.[89] Zhang et al. reported that H. pylori localization is being more intense in the antrum.[90] We reported the H. pylori positivity of 49.7% in the corpus, while 57.9% in the antrum. No significant association was recognized between H. pylori localization and H. pylori colonization degree. H. pylori localization in the antrum did not reveal a significant age.[64]

The EUROGAST study group examines the prevalence of H. pylori infection in Europe, North Africa, North America, and Japan covering 17 different geographically defined populations in two age groups, 25–34 and 55–64.[91] The EUROGAST study detected the higher infection prevalence in the older group (61.4%) than the younger one (34.9%).[91] Sengul and Sengul[64] studied six age groups at the end of 2018 and reported the frequency of H. pylori, regarding to the age groups as 15–34 age group (57.1%), 35–44 age group (49.1%), 45–64 age group (64.5%), 65–74 age group (53.7%), 75–84 age group (59.4%), and above 85 years (3.33%). There was no significant relationship between H. pylori colonization and age groups (P > 0.05). We reported the highest positivity in the 3rd group, 45–65 age group, (64.5%), which revealed so similarity with the positivity of 55–64 age group in EUROGAST study group, (61.4%).[64],[91]

The prevalence of H. pylori, ethnic group, and geographical varies according to regions.[92] A Chile study reported 29% H. pylori positivity using the fast urease test and endoscopic biopsy samples. The infection prevalence of the age group of 40–49 years was 38.1%, the highest rate. They also reported the attenuation of the prevalence of H. pylori to 28.9% from 44.9% during the period of 11 years. H. pylori-related diseases are increasing in proximal stomach parts with increasing age. The pathogenesis and mechanism of H. pylori-related diseases in the proximal stomach has not been explained. Stomach environment changes with age. H. pylori colonization appears to be affected by this change.[93]

 Conclusion



H. pylori leads to important diseases in the stomach and gastrointestinal tract. Although quite a few researches have been performed to date about H. pylori, few studies exist in the English language literature about whether its anatomotopographic gastric settlements in the stomach during the aging process alter its positivity [Figure 1]. We reported in our current previous study that the H. pylori positivity was being mostly in the antrum and at 45–64 age group, while no difference was observed between the location, six structured age groups, and subgroups with over and under 50 years, together with the degree of colonization for H. pylori.[64] We assert that the advanced multicentric studies should be performed on the topographic gastric localization and relevant age groups related to assessment evaluation of H. pylori which we suppose that it could be beneficial and essential for the progressive evaluation and follow-up of its leading diseases in the stomach.{Figure 1}

Financial support and sponsorship

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Conflicts of interest

There are no conflicts of interest.

References

1Suerbaum S, Michetti P. Helicobacter pylori infection. N Engl J Med 2002;347:1175-86.
2Goodwin CS, Armstrong JA, Chilvers T, Peters M, Collins MD, Sly L, et al. Transfer of Campylobacter pylori and Campylobacter mustelae to Helicobacter gen. nov. as Helicobacter pylori comb. nov. and Helicobacter mustelae comb. nov., respectively. Int J Syst Bacteriol 1989;39:397-405.
3Vandamme P, Falsen E, Rossau R, Hoste B, Segers P, Tytgat R, et al. Revision of Campylobacter, Helicobacter, and Wolinella taxonomy: Emendation of generic descriptions and proposal of Arcobacter gen. nov. Int J Syst Bacteriol 1991;41:88-103.
4Peek RM Jr., Crabtree JE. Helicobacter pylori infection and gastric neoplasia. J Pathol 2006;2:233-48.
5Robinson K, Letley DP, Kaneko K. The human stomach in health and disease: Infection strategies by Helicobacter pylori. Curr Top Microbiol Immunol 2017;400:1-26.
6Malfertheiner P, Link A, Selgrad M. Helicobacter pylori: Perspectives and time trends. Nat Rev Gastroenterol Hepatol 2014;11:628-38.
7Venerito M, Vasapolli R, Malfertheiner P. Helicobacter pylori and gastric cancer: Timing and ımpact of preventive measures. Adv Exp Med Biol 2016;908:409-18.
8Dunne C, Dolan B, Clyne M. Factors that mediate colonization of the human stomach by Helicobacter pylori. World J Gastroenterol 2014;20:5610-24.
9Brown LM. Helicobacter pylori: Epidemiology and routes of transmission. Epidemiol Rev 2000;22:283-97.
10Smoak BL, Kelley PW, Taylor DN. Seroprevalence of Helicobacter pylori infections in a cohort of US Army recruits. Am J Epidemiol 1994;139:513-9.
11Keilberg D, Ottemann KM. How Helicobacter pylori senses, targets and interacts with the gastric epithelium. Environ Microbiol 2016;18:791-806.
12Celli JP, Turner BS, Afdhal NH, Keates S, Ghiran I, Kelly CP, et al. Helicobacter pylori moves through mucus by reducing mucin viscoelasticity. Proc Natl Acad Sci U S A 2009;106:14321-6.
13Choudhuri G, Mohindra S. Epidemiology of Helicobacter pylori in India. Indian J Gastroenterol 2000;19 Suppl 1:S3-5.
14Graham DY, Adam E, Reddy GT, Agarwal JP, Agarwal R, Evans DJ Jr., et al. Seroepidemiology of Helicobacter pylori infection in India. Comparison of developing and developed countries. Dig Dis Sci 1991;36:1084-8.
15Sjomina O, Pavlova J, Niv Y, Leja M. Epidemiology of Helicobacter pylori infection. Helicobacter 2018;23 Suppl 1:e12514.
16Ferro A, Peleteiro B, Malvezzi M, Bosetti C, Bertuccio P, Levi F, et al. Worldwide trends in gastric cancer mortality (1980-2011), with predictions to 2015, and incidence by subtype. Eur J Cancer 2014;50:1330-44.
17Bray F, Jemal A, Grey N, Ferlay J, Forman D. Global cancer transitions according to the Human Development Index (2008-2030): A population-based study. Lancet Oncol 2012;13:790-801.
18Amieva M, Peek RM Jr. Pathobiology of Helicobacter pylori-Induced gastric cancer. Gastroenterology 2016;150:64-78.
19Moodley Y, Linz B, Bond RP, Nieuwoudt M, Soodyall H, Schlebusch CM, et al. Age of the association between Helicobacter pylori and man. PLoS Pathog 2012;8:e1002693.
20Salama NR, Hartung ML, Müller A. Life in the human stomach: Persistence strategies of the bacterial pathogen Helicobacter pylori. Nat Rev Microbiol 2013;11:385-99.
21Schreiber S, Konradt M, Groll C, Scheid P, Hanauer G, Werling HO, et al. The spatial orientation of Helicobacter pylori in the gastric mucus. Proc Natl Acad Sci U S A 2004;101:5024-9.
22Keilberg D, Zavros Y, Shepherd B, Salama NR, Ottemann KM. Spatial and temporal shifts in bacterial biogeography and gland occupation during the development of a chronic ınfection. mBio 2016;7:e01705-16.
23Howitt MR, Lee JY, Lertsethtakarn P, Vogelmann R, Joubert LM, Ottemann KM, et al. ChePep controls Helicobacter pylori ınfection of the gastric glands and chemotaxis in the Epsilonproteobacteria. mBio 2011;2:e00098-11.
24Ferlay J, Soerjomataram I, Dikshit R, Eser S, Mathers C, Rebelo M, et al. Cancer incidence and mortality worldwide: Sources, methods and major patterns in GLOBOCAN 2012. Int J Cancer 2015;136:E359-86.
25Nagy P, Johansson S, Molloy-Bland M. Systematic review of time trends in the prevalence of Helicobacter pylori infection in China and the USA. Gut Pathog 2016;8:8.
26Huang JY, Sweeney EG, Sigal M, Zhang HC, Remington SJ, Cantrell MA, et al. Chemodetection and destruction of host urea allows Helicobacter pylori to locate the epithelium. Cell Host Microbe 2015;18:147-56.
27Kao CY, Sheu BS, Wu JJ. Helicobacter pylori infection: An overview of bacterial virulence factors and pathogenesis. Biomed J 2016;39:14-23.
28Hu Q, Zhang Y, Zhang X, Fu K. Gastric mucosa-associated lymphoid tissue lymphoma and Helicobacter pylori infection: A review of current diagnosis and management. Biomark Res 2016;4:15.
29Kim SY, Choi DJ, Chung JW. Antibiotic treatment for Helicobacter pylori: Is the end coming? World J Gastrointest Pharmacol Ther 2015;6:183-98.
30Parkin DM. The global health burden of infection-associated cancers in the year 2002. Int J Cancer 2006;118:3030-44.
31Choi IJ, Kook MC, Kim YI, Cho SJ, Lee JY, Kim CG, et al. Helicobacter pylori therapy for the prevention of metachronous gastric cancer. N Engl J Med 2018;378:1085-95.
32Leja M, Axon A, Brenner H. Epidemiology of Helicobacter pylori infection. Helicobacter 2016;21 Suppl 1:3-7.
33Yu X, Yang X, Yang T, Dong Q, Wang L, Feng L. Decreasing prevalence of Helicobacter pylori according to birth cohorts in urban China. Turk J Gastroenterol 2017;28:94-7.
34Yücel O, Sayan A, Yildiz M. The factors associated with asymptomatic carriage of Helicobacter pylori in children and their mothers living in three socio-economic settings. Jpn J Infect Dis 2009;62:120-4.
35Testerman TL, Morris J. Beyond the stomach: An updated view of Helicobacter pylori pathogenesis, diagnosis, and treatment. World J Gastroenterol 2014;20:12781-808.
36Gunaletchumy SP, Seevasant I, Tan MH, Croft LJ, Mitchell HM, Goh KL, et al. Helicobacter pylori genetic diversity and gastro-duodenal diseases in Malaysia. Sci Rep 2014;4:7431.
37Tanih NF, Okeleye BI, Naidoo N, Clarke AM, Mkwetshana N, Green E, et al. Marked susceptibility of South African Helicobacter pylori strains to ciprofloxacin and amoxicillin: Clinical implications. S Afr Med J 2010;100:49-52.
38Carneiro F. Stomach cancer. In: Steward B, editor. World Cancer Report. Lyon, France: International Agency for Research on Cancer; 2014. p. 383-91.
39International Agency for Research on Cancer. Infection with Helicobacter pylori. IARC Monogr Eval Carcinog Risks Hum 1994;61:177-40.
40Cavaleiro-Pinto M, Peleteiro B, Lunet N, Barros H. Helicobacter pylori infection and gastric cardia cancer: Systematic review and meta-analysis. Cancer Causes Control 2011;22:375-87.
41Shmuely H, Wattad M, Solodky A, Yahav J, Samra Z, Zafrir N. Association of Helicobacter pylori with coronary artery disease and myocardial infarction assessed by myocardial perfusion imaging. Isr Med Assoc J 2014;16:341-6.
42Liu J, Wang F, Shi S. Helicobacter pylori ınfection ıncrease the risk of myocardial ınfarction: A meta-analysis of 26 studies ınvolving more than 20,000 participants. Helicobacter 2015;20:176-83.
43Li JZ, Li JY, Wu TF, Xu JH, Huang CZ, Cheng D, et al. Helicobacter pylori ınfection ıs associated with type 2 diabetes, not type 1 diabetes: An updated meta-analysis. Gastroenterol Res Pract 2017. pii: 5715403.
44Xu MY, Cao B, Yuan BS, Yin J, Liu L, Lu QB. Association of anaemia with Helicobacter pylori infection: A retrospective study. Sci Rep 2017;7:13434.
45Chen CX, Mao YS, Foster P, Zhu ZW, Du J, Guo CY. Possible association between Helicobacter pylori infection and nonalcoholic fatty liver disease. Appl Physiol Nutr Metab 2017;42:295-301.
46Upala S, Sanguankeo A, Saleem SA, Jaruvongvanich V. Effects of Helicobacter pylori eradication on insulin resistance and metabolic parameters: A systematic review and meta-analysis. Eur J Gastroenterol Hepatol 2017;29:153-9.
47Bach JF. The effect of infections on susceptibility to autoimmune and allergic diseases. N Engl J Med 2002;347:911-20.
48Chen Y, Blaser MJ. Inverse associations of Helicobacter pylori with asthma and allergy. Arch Intern Med 2007;167:821-7.
49Cohen D, Shoham O, Orr N, Muhsen K. An inverse and independent association between Helicobacter pylori infection and the incidence of shigellosis and other diarrheal diseases. Clin Infect Dis 2012;54:e35-42.
50Islami F, Kamangar F. Helicobacter pylori and esophageal cancer risk: A meta-analysis. Cancer Prev Res (Phila) 2008;1:329-38.
51Perry S, de Jong BC, Solnick JV, de la Luz Sanchez M, Yang S, Lin PL, et al. Infection with Helicobacter pylori is associated with protection against tuberculosis. PLoS One 2010;5:e8804.
52Sonnenberg A, Dellon ES, Turner KO, Genta RM. The influence of Helicobacter pylori on the ethnic distribution of esophageal eosinophilia. Helicobacter. 2016;00:e12370.
53Miftahussurur M, Nusi IA, Graham DY, Yamaoka Y. Helicobacter, hygiene, atopy, and asthma. Front Microbiol 2017;8:1034.
54Efthymiou G, Dardiotis E, Liaskos C, Marou E, Tsimourtou V, Scheper T, et al. Anti-hsp60 antibody responses based on Helicobacter pylori in patients with multiple sclerosis: (ir) Relevance to disease pathogenesis. J Neuroimmunol 2016;298:19-23.
55Lochhead P, El-Omar EM. Helicobacter pylori infection and gastric cancer. Best Pract Res Clin Gastroenterol 2007;21:281-97.
56Helicobacter and Cancer Collaborative Group. Gastric cancer and Helicobacter pylori: A combined analysis of 12 case control studies nested within prospective cohorts. Gut 2001;49:347-53.
57Kuo CH, Chen YH, Goh KL, Chang LL. Helicobacter pylori and systemic disease. Gastroenterol Res Pract 2014;2014:358494.
58Kamangar F, Dawsey SM, Blaser MJ, Perez-Perez GI, Pietinen P, Newschaffer CJ, et al. Opposing risks of gastric cardia and noncardia gastric adenocarcinomas associated with Helicobacter pylori seropositivity. J Natl Cancer Inst 2006;98:1445-52.
59Kamangar F, Qiao YL, Blaser MJ, Sun XD, Katki H, Fan JH, et al. Helicobacter pylori and oesophageal and gastric cancers in a prospective study in China. Br J Cancer 2007;96:172-6.
60Isajevs S, Liepniece-Karele I, Svirina D, Santare D, Kaidaks S, Sivins A, et al. Different pattern of ınflammatory and atrophic changes in the gastric mucosa of the greater and lesser curvature. J Gastrointestin Liver Dis 2015;24:429-34.
61Zhestkova TV, Butov MA, Papkov SV. The prevalence of Helicobacter pylori infection among urban population. Ter Arkh 2018;90:17-20.
62Matsuhisa T, Miki M, Yamada N, Sharma SK, Shrestha BM. Helicobacter pylori infection, glandular atrophy, intestinal metaplasia and topography of chronic active gastritis in the Nepalese and Japanese population: The age, gender and endoscopic diagnosis matched study. Kathmandu Univ Med J (KUMJ) 2007;5:295-301.
63Matsuhisa T, Matsukura N, Yamada N. Topography of chronic active gastritis in Helicobacter pylori-positive Asian populations: Age-, gender-, and endoscopic diagnosis-matched study. J Gastroenterol 2004;39:324-8.
64Sengul D, Sengul I. Frequency of Helicobacter pylori and association of location, six age groups, and assessment of borderline of 50-year based-age, based on the anatomic pilot region with the degree of Helicobacter pylori colonization. Bakirkoy Med J 2018;14:381-8.
65Fischbach LA, van Zanten S, Dickason J. Meta-analysis: The efficacy, adverse events, and adherence related to first-line anti-Helicobacter pylori quadruple therapies. Aliment Pharmacol Ther 2004;20:1071-82.
66Crowe SE. Helicobacter pylori ınfection. N Engl J Med 2019;380:1158-65.
67Gisbert JP, Gonzalez L, Calvet X. Systematic review and meta-analysis: Proton pump inhibitor vs. ranitidine bismuth citrate plus two antibiotics in Helicobacter pylori eradication. Helicobacter 2005;10:157-71.
68Graham DY, Hammoud F, El-Zimaity HM, Kim JG, Osato MS, El-Serag HB. Meta-analysis: Proton pump inhibitor or H2-receptor antagonist for Helicobacter pylori eradication. Aliment Pharmacol Ther 2003;17:1229-36.
69Malfertheiner P, Megraud F, O'Morain CA, Atherton J, Axon AT, Bazzoli F, et al. Management of Helicobacter pylori infection--the Maastricht IV/Florence Consensus Report. Gut 2012;61:646-64.
70Chey WD, Wong BC; Practice Parameters Committee of the American College of Gastroenterology. American college of gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol 2007;102:1808-25.
71Fallone CA, Chiba N, van Zanten SV, Fischbach L, Gisbert JP, Hunt RH, et al. The toronto consensus for the treatment of Helicobacter pylori Infection in adults. Gastroenterology 2016;151:51-69.
72Chey WD, Leontiadis GI, Howden CW, Moss SF. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. Am J Gastroenterol 2017;112:212-39.
73McColl KE. Clinical practice. Helicobacter pylori infection. N Engl J Med 2010;362:1597-604.
74Gisbert JP, Calvet X. Update on non-bismuth quadruple (concomitant) therapy for eradication of Helicobacter pylori. Clin Exp Gastroenterol 2012;5:23-34.
75Wang B, Wang YH, Lv ZF, Xiong HF, Wang H, Yang Y, et al. Review: Efficacy and safety of hybrid therapy for Helicobacter pylori infection: A systematic review and meta-analysis. Helicobacter 2015;20:79-88.
76Moayyedi P, Malfertheiner P. Editorial: Sequential therapy for eradication of Helicobacter pylori: A new guiding light or a false dawn? Am J Gastroenterol 2009;104:3081-3.
77Lee I, Lee H, Kim M, Fukumoto M, Sawada S, Jakate S, et al. Ethnic difference of Helicobacter pylori gastritis: Korean and Japanese gastritis is characterized by male- and antrum-predominant acute foveolitis in comparison with American gastritis. World J Gastroenterol 2005;11:94-8.
78Ümit H, Ünsal G, Tezel AO, Soylu AR. Helikobakter pilori infeksiyonu ve Benign Gastroduodenal Hastalıklar, Trakya Bölgesi Verileri. Trakya Üniver Tıp Fakültesi Derg 2010;27:400-03.
79Salih BA, Abasiyanik MF, Bayyurt N, Sander E. H pylori infection and other risk factors associated with peptic ulcers in Turkish patients: A retrospective study. World J Gastroenterol 2007;13:3245-8.
80Uyanıkoğlu A, Coşkun M, Binici DN, Uçar Ş, Kibar Yİ, Tay A, et al. Endoskopi yapılan hastalarda Helicobacter pylori sıklığı. Dicle Med J 2012;39:197-00.
81Demirtaş L, Sayar İ, Akbas EM, Özçiçek A, Özçiçek F, Timuroğlu A, et al. Endoskopi yapılan hastalarda Helicobacter pylori sıklığı ve yerleşim yerinin yaş ve cinsiyete göre dağılımı. Dicle Tıp Derg 2014;41:3507-11.
82Esen R, Dulger AC, Begenik H, Demirtas L, Ebinc S, Aytemiz E, et al. Prevalence of Helicobacter pylori in patients with brucellosis. J Investig Med 2012;60:895-7.
83Özardalı HG, Bitiren M, Nazlıgül Y, Yılmaz N. Şanlıurfa yöresinde noneroziv gastritlerde Helicobacter pylori sıklığı. Genel Tıp Derg 1998;8:149-52.
84Demir T, Turan M, Tekin A. Kırşehir bölgesindeki dispeptik hastalarda Helicobacter pylori antijen prevalansı. Dicle Tıp Derg 2011;38:44-8.
85Özdemir M, Baykan M. Dispeptik hastalarda H. pylori infeksiyonu tanısında H. pylori gaita antijeninin tanı değerinin incelenmesi. Genel Tıp Derg 2005;15:65-70.
86Kalem F, Ozdemir M, Baysal B. Investigation of the presence of Helicobacter pylori by different methods in patients with dispeptic complaints. Mikrobiyol Bult 2010;44:29-34.
87Arslan D, Tahan F, Demir F, Taşkın İ. Erciyes Üniversitesi Tıp Fakültesi Çocuk Polikliniğine başvuran sağlıklı çocuklarda Helicobacter pylori enfeksiyonunun seroprevalansı ve bunu etkileyen faktörler. Erciyes Tıp Derg 2006;28:192-6.
88Alim A, Ataş AD, Güneş T, Ataş M, Yıldırım M, Öztekin A, et al. Sivas ili merkezinde semptomatik ve asemptomatik yetişkin bireylerde Helicobacter pylori seroprevalansı. CÜ Tıp Fak Derg 2004;26:75-80.
89Correa P, Piazuelo MB. Natural history of Helicobacter pylori infection. Dig Liver Dis 2008;40:490-6.
90Zhang C, Yamada N, Wu YL, Wen M, Matsuhisa T, Matsukura N. Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer. World J Gastroenterol 2005;11:791-6.
91Epidemiology of, and risk factors for, Helicobacter pylori infection among 3194 asymptomatic subjects in 17 populations. The EUROGAST Study Group. Gut 1993;34:1672-6.
92Goh KL, Chan WK, Shiota S, Yamaoka Y. Epidemiology of Helicobacter pylori infection and public health implications. Helicobacter 2011;16 Suppl 1:1-9.
93Da Costa D, Guidotti F, Cabello N, Trigo F, Contreras C, Vergara F, et al. Helicobacter pylori infection detected during upper gastrointestinal endoscopy. Rev Med Chil 2018;146:555-61.