Helicobacter pylori Infection, Clinical Features, and Nutritional Aspects: Comparison
Please note this is a comparison between Version 1 by Duygu AĞAGÜNDÜZ and Version 4 by Birsen Yılmaz.

Helicobacter pylori (H. pylori) is a 0.5–1 µm wide, 2–4 µm long, short helical, S-shaped Gram-negative microorganism. It is mostly found in the pyloric region of the stomach and causes chronic gastric infection. It is estimated that these bacteria infect more than half of the world’s population. The mode of transmission and infection of H. pylori is still not known exactly, but the faecal–oral and oral–oral routes via water or food consumption are thought to be a very common cause. In the last three decades, research interest has increased regarding the pathogenicity, microbial activity, genetic predisposition, and clinical treatments to understand the severity of gastric atrophy and gastric cancer caused by H. pylori. Studies have suggested a relationship between H. pylori infection and malabsorption of essential micronutrients, and noted that H. pylori infection may affect the prevalence of malnutrition in some risk groups. On the other hand, dietary factors may play a considerably important role in H. pylori infection, and it has been reported that an adequate and balanced diet, especially high fruit and vegetable consumption and low processed salty food consumption, has a protective effect against the outcomes of H. pylori infection. 

  • H. pylori
  • nutrition
  • infection
  • diet
  • clinical treatment

1. H. pylori Infection Epidemiology

There are many abstudies outn the prevalence of H. pylori, and its risk factors and pathways [1][2][3][9,17,18]. It is claimed that half of the world’s population is infected with H. pylori, but it is clear that more evidence-based research is still needed. The incidence of this infection is higher in low socioeconomic status groups and developing countries [4][19]. Vilaichone et al. found that the prevalence of H. pylori varies not only from country to country but also in different regions of the same country [5][20]. Its prevalence is significantly difficult to determine, as no health system compiles registry-based results of the prevalence of H. pylori in developing countries [6][21].
According to the regional prevalence estimates, there are approximately 4.4 billion H. pylori-infected people worldwide [7][22]. The countries with the highest H. pylori burden compared with the general population were found to be Nigeria, Portugal, Estonia, Kazakhstan, and Pakistan, and the lowest burden was in Switzerland [6][21]. In the study of Mezmale et al. (2020), a high prevalence of H. pylori infection was determined in Russia, Jordan, Iran, China, Canada, and Latin American countries [8][23].
Studies conducted in Turkey show that the rate of H. pylori infection is high. For example, in a study by Uyanıkoğlu et al. in 2010, 918 of 1298 patients who had antrum biopsy were positive for H. pylori. The prevalence of H. pylori infection is similar in males and females, and the incidence of H. pylori infection is 73.2% between the ages of 14 and 30, 71.5% between the ages of 31 and 45, 68.6% between the ages of 46 and 60, and 70.4% between the ages of 61 and 88 [9][24].  In a study conducted by Özen et al. in 2011, 161 of 473 children studying in four different primary and secondary schools in Istanbul were found to be H. pylori-positive [10][25]. Similarly, Özaydın et al. screened 4622 people for H. pylori infection in 55 cities using the C-urea breath test in 2013, and 3852 people (2075 females and 1777 males) were found to be positive for H. pylori [11][26]. In the review by Hooi et al., it was reported that three studin es were conducted in Turkey up to 2015, the total number of participants was 6036, and the prevalence was 77.2% [6][21]. In a study conducted by Soylu et al. in 2019, the number of H. pylori-positive patients was found to be 46 (21 females and 25 males) in biopsy samples taken from 88 patients (53 females and 35 males) aged 18–77 years with dyspeptic complaints. Compared with the total number of participants, male patients were found to be more H. pylori-positive [12][27]. A Istudy conducted in Nepal, it was reported that 18.2% of 6- to 59-month-old children, 14% of boys and 16% of girls aged 10–19 years, and 40% of non-pregnant women aged 20–49 years were infected with H. pylori [13][28].

2. H. pylori Transmission

Although the mode of transmission of H. pylori is not known exactly, it is thought that it can be transmitted directly from one person to another or indirectly from the environment to people [14][29]. Person-to-person transmission is thought to be the primary mode of transmission, especially in developed countries. Food- and waterborne transmission are more likely in developing countries and H. pylori spreads more rapidly in areas with poor hygienic conditions [15][16][30,31].
TIn a study evaluating the prevalence of H. pylori infection in the rural community, Goodman et al. reported that people who are consumers of raw vegetables are more likely to be infected. Moreover, swimming in streams and rivers and using streams as drinking water may increase infection because of contamination by irrigation water or unpurified water [17][32]. Although some studies suggested that the transmission of H. pylori is from environmental contamination to food products, there is insufficient evidence to confirm this information [15][18][30,33]. It is accepted that interpersonal transmission routes are more frequent than environmental exposures. However, special attention should be paid to the sources of contamination (unhygienic water) that may lead to contamination through food [14][29].
Person-to-person transmission is thought to occur through the oral–oral, faecal–oral, gastric–oral, or sexual routes [14][29]. The literature indicates that H. pylori is present in the dental plaque and saliva of infected individuals [19][20][21][34,35,36], which shows that H. pylori infection spreads at a much higher rate than expected and, especially, transmission between family members is very frequent [22][37].

3. H. pylori Diagnosis

Each of the diagnostic tests used to detect the presence of H. pylori has advantages, disadvantages, and limitations, and the necessity of endoscopy is taken into account when classifying the methods. Histological evaluations using gastric biopsy specimens include rapid urease testing, culture, and polymerase chain reaction (PCR) [23][38]. Where invasive methods are time-consuming and not cost-effective, non-invasive diagnostic methods are used. Non-invasive tests include serological evaluation, stool antigen analyses, and the commonly used urea breath tests [24][39]. On the other hand, there is also non-Helicobacter pylori helicobacter (NHPH), which does not have a spiral morphology in the stomach [25][40]. Neither is the gold standard due to poor sensitivity or specificity. Combinations of more than one test give more reliable results [26][41].

4. H. pylori Pathogenesis

H. pylori is easily killed in hydrochloric acid solutions with a pH below 4.0. It is quite paradoxical for a microorganism whose primary site is the stomach. H. pylori continues to live in the lower part of the stomach by penetrating the mucus layer of the stomach through the contribution of its spiral shape and flagella [27][42]. To neutralise the acidic pH-related bactericidal activity against H. pylori, which can colonise the gastric epithelial surface, H. pylori hydrolyses urea to ammonia and carbon dioxide with the urease enzyme it produces [28][6]. In addition to its toxic effects on gastric mucosal epithelial cells, the ammonia formed increases the mucosal pH [29][43]. By damaging the protective mucus layer, which is rich in phospholipid and lipase, with the bacterial protease enzyme, it also delays the diffusion ability of H ions and increases its damaging effect [30][44].
It is known that H. pylori secretes a vacuole-forming cytotoxin (VacA) that adheres to the surface epithelium with adhesin proteins and causes vacuolization. The vacuole-forming cytotoxin induces host cell death through pore formation and apoptosis in mitochondrial membranes [31][45]. In addition to VacA, cytotoxin-associated antigen (CagA), known as an oncoprotein, is delivered into gastric epithelial cells and disrupts vesicular trafficking and autophagy pathways. IVarious st has beenudies have shown that cytotoxin-associated antigens affect the cell shape of bacterial proteins, disrupt cell assembly activity, increase cell motility, and are responsible for gastric ulcers and cancers [32][33][34][46,47,48].
Lipopolysaccharide (LPS), found in the outer membrane of H. pylori, is an effective immunomodulator in the human body and causes chronic inflammation by triggering the immune system. LPSs of H. pylori can mimic Lewis blood group antigens and, during infection, LPS can produce pathogenic anti-Lewis antibodies [35][49]. Lewis blood group antigens in the glycoprotein structure found on gastric epithelial surfaces mediate the binding of BabA, known as an adhesin, which binds to blood group antigens on the outer membrane of H. pylori, to surface mucosal cells and the gastric pit, and causes tissue destruction [36][50].

5. Conclusions

H. pylori is estimated to infect half of the world’s population and causes permanent infections as well as many health issues such as gastritis and MALT lymphoma, as well as peptic ulcer and gastric cancer. In H. pylori infection, there are some treatment limitations due to its ability to create resistance to antibiotic treatments in treatment strategies. Therefore, it has become necessary to seek alternatives to fight against H. pylori infection. Especially in the last few years, research has clearly shown the pathogenicity, microbial activity, and genetic predisposition to help understand the severity of gastric atrophy and gastric cancer caused by H. pylori. This situation is expected to affect the treatment process positively. Combination treatments, including with phytochemicals and probiotics found in natural products, seem to have beneficial effects in the eradication of H. pylori.
Due to the effects of hormones such as ghrelin and leptin, which control both growth and appetite, and the formation of malabsorption of various nutrients such as vitamin C, iron, cobalamin, and vitamin E in H. pylori-infected individuals, detailed nutritional information should be provided during and after treatment. It is important to provide optimal nutrition through the determination of strategies and the application of a suitable diet for the person by authorised dietitians. Besides, there have been some promising effects for probiotics added to treatment strategies; however, detailed research is needed. Most importantly, a diet rich in fruits and vegetables and reduced in salt and processed meat products has good prophylactic potential, especially against cancer in the eradication of H. pylori.
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