ISSN: 2147-2092
Helicobacter Pylori: Background, Diagnostic Methods and Nutritional Aspects
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Literature Review with Cases
VOLUME: 36 ISSUE: 3
P: 358 - 366
July 2025

Helicobacter Pylori: Background, Diagnostic Methods and Nutritional Aspects

Gazi Med J 2025;36(3):358-366
Vanessa Urie Kasum 1
Firdaus Hayati 1
Syed Sharizman Syed Abdul Rahim 2
Nik Amin Sahid Nik Lah 1
Serene En Hui Tung 3
1. Department of Surgery, Faculty of Medicine and Health Sciences, Universiti Malaysia Sabah, Sabah, Malaysia
2. Department of Public Health Medicine, Faculty of Medicine and Health Sciences, Universiti Malaysia Sabah, Sabah, Malaysia
3. Division of Nutrition and Dietetics, School of Health Sciences, International Medical University, Kuala Lumpur, Malaysia
No information available.
No information available
Received Date: 14.04.2024
Accepted Date: 21.05.2025
Online Date: 11.07.2025
Publish Date: 11.07.2025
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ABSTRACT

Helicobacter pylori (H. pylori) bacteria have infected one-half of the world’s population. The subset of H. pylori colonization with persistent inflammation is associated with an increased risk of developing gastritis, peptic ulcer disease, gastric cancer, and iron-deficiency anaemia. There are extra-gastric diseases that potentially can weaken the immune system and thus expose the host cells to bacterial infection. Accurate diagnosis of H. pylori infection is crucial for proper eradication treatment. There are several invasive and non-invasive methods available for H. pylori detection, and each of the methods has its advantages and disadvantages. In addition, nutritional status plays an important role in the progression of the H. pylori infection, which is further discussed in this review. We believe that there will be continuous improvements in the diagnostic methods and pharmaceutical treatments in the management of H. pylori infection. The emphasis on nutritional intake in the individual diet should also be implemented in the primary healthcare setting to reduce the incidence of H. pylori infection.

Keywords:
Diagnosis, diet, eradication treatment, gastritis

INTRODUCTION

Approximately one-half of the world’s population is infected with Helicobacter pylori (H. pylori) (1). It has been estimated that
H. pylori bacteria infect 90% of patients with duodenal ulcers and 80% of patients with gastric ulcers. H. pylori bacterium is a spiral gram-negative bacterium in a group called Epsilon proteobacteria class that can colonize the human stomach, especially the upper gastrointestinal tract site (2). The milestone discovery of H. pylori by Australian doctors, Barry J. Marshall and Robin Warren, has altered the diagnosis and treatment of stomach-related diseases (3). Although the curved bacteria had been reported, it was not until 1982 that Warren and Marshall identified the bacteria as the cause of chronic gastritis.

Initially, Marshall failed to develop an animal model for the experiments, so he decided to do a self-experiment by drinking a culture of the bacteria obtained from his patient (4). He developed nausea, vomiting, and achlorhydria 3 days after drinking the culture, and on day 8, the repeated endoscopy and biopsy results showed gastritis and positive H. pylori infection. He recovered with antibiotic and bismuth treatment, which eventually fulfilled Koch’s third and fourth postulates for the role of H. pylori and gastritis. Koch’s postulates were established to assess the microorganism that causes a disease (5). The bacteria were initially recognized as Campylobacter pylori, which was then renamed to H. pylori, as it has a helical physical structure and is mostly found in the pyloric region of the stomach (6).

H. pylori bacteria enter the body through oral and travel to the digestive system for colonization (7). It starts with a small subset of colonization and develops more serious outcomes over time, and massive colonization of H. pylori results in peptic ulcer, duodenal ulcer, or gastric cancer (8). The routes of transmission of H. pylori remain unclear. The most common routes of transmission are person-to-person, faecal-to-oral and environmental exposures (9). In developing countries, plausible environmental factors include untreated water, poor sanitation, and crowded living places that contribute to the spread of H. pylori bacteria (10).

Early research explained that person-to-person transmission occurs through two modes, namely, vertical and horizontal transmissions (11). The researchers explained that vertical transmission is spread among the same family members, while horizontal transmission involves contact from outside of the family or contaminated environments. The clustering of the H. pylori infection among family members is suggested to be due to genetic predisposition, close interpersonal contacts, and the same socioeconomic status (9). Dental plaque and saliva are typical means of transmission between family members (12).

The fact that H. pylori can survive in a pH environment as low as 1 and continue to create inflammation demonstrates its resilience (13). Figure 1 illustrates the anatomical structure of H. pylori bacteria and its function to induce inflammation in host cells. It can produce its cytoplasmic urease for enzymatic activity to convert urea to ammonia and carbon dioxide (14). The ammonia is responsible for neutralizing the acidic environment in the stomach to prevent the acid inhibition or damage of H. pylori bacteria. The presence of ammonia increases the pH in the gastric environment to protect the bacteria from gastric acid.

In contrast, H. pylori bacteria are unable to survive without urea at the extreme acidity (15). Due to urease activity, the gastric lining becomes less viscous, thus, allowing bacteria to adhere to the cells and colonize (16). H. pylori is a responsible agent that causes gastrointestinal diseases such as gastritis, peptic ulcer, duodenal ulcer, and stomach cancer (17). The severity of the disease depends on the immune system of the individual, the type of H. pylori strains, and environmental factors (18).

Diagnostic Test for H. pylori Infection

There are several methods to diagnose H. pylori infection. Each method has its advantages and disadvantages. An invasive test is biopsy-based that includes a rapid urease test (RUT), histological evaluation, and direct detection of H. pylori using polymerase chain reaction (PCR). On the other hand, there is also non-invasive treatment which includes serological tests, urea breath tests (UBT), and stool antigen tests (SAT). The comparison of the methods is provided in detail as shown in Table 1.

Rapid Urease Test

RUT can present the result in 1 hour, making it convenient for clinicians who need faster results (19). As mentioned, the principle of the RUT is based on the urease activity, which converts urea into ammonia and CO2 to neutralize the gastric environment for its survival, increasing gastric pH. Most of the H. pylori specimens will become red or pink color after 50 minutes of exposure to the medium, indicating the production of the ammonium ion and increased pH (20). Overall, the specificity of the UBT is more than 95%, but sensitivity is more than 85%.

The sensitivity of the test can be increased when more than 1 specimen is taken, preferably from the antrum and corpus of the gastric region (21). Additionally, RUT can be used in patients presenting with peptic ulcer bleeding. However, there are several limitations of RUT. First, RUT is influenced by bacterial urease concentration. Some cocci bacteria, such as Staphylococci and Streptococci, are involved in the production of urease activity, thus interfering with the detection of H. pylori bacteria (22). Secondly, RUT is influenced by antibiotics, pump-proton inhibitors (PPIs), bismuth, and achlorhydria, which can yield false-negative results (23). Hence, it is advisable to discontinue PPIs 2 weeks before, and antibiotics and bismuth 4 weeks before a UBT test (24). Finally, the RUT becomes less sensitive in the presence of formalin contamination in biopsy specimens.

Histological Evaluation

A histological test is the first method to detect H. pylori. It provides the assessment of the presence of H. pylori bacteria to the degree of inflammation caused by the infection (25). The use of the compound called Giemsa, hematoxylin, and eosin stains is sufficient to detect the H. pylori bacteria and the severity of the inflammation.  However, several factors influence the accuracy of the test, including the site and number of biopsies (23). An increase in the number of biopsies can decrease the result of false-negative because histological tests are unable to detect patchy H. pylori colonization. Another factor that can yield a false-negative result is the use of PPIs and antibiotics, as these medications can change the form of H. pylori to its cocci form, making it unable to detect H. pylori (26).

Polymerase Chain Reaction

PCR is used to detect bacteria and to characterize bacterial genes and antimicrobial resistance (22). It allows researchers to detect H. pylori DNA in biopsy samples, and the PCR reaction mixture is prepared according to the manufacturer (27). PCR samples are not only limited to the biopsy but PCR have also been improved by using stool and saliva specimens. Modification of PCR technology has increased the sensitivity to 80% and specificity up to 100% (21). PCR has several advantages. It can detect H. pylori bacteria in a short period; hence, it offers convenience in a large sample size. Since the PCR can be used in the detection of antibiotic resistance, it can guide clinicians in suggesting antibiotic therapy for the eradication of H. pylori bacteria (28).

However, PCR tests cannot be used for daily detection of H. pylori, like UBT and SAT, because of high prices and the requirement of high-tech equipment. Since the principle of PCR is based on genetics, it also might produce false-positive results because it can detect the DNA from dead bacteria (29). On the other hand, a PCR test also can result in a false-negative as the test is unable to detect H. pylori in coccoid form. H. pylori can mutate the genes by changing its shape to a coccoid form to survive under environmental conditions such as extreme pH, very low or high temperature, and oxygen tension (26). Last but not least, the specificity of the PCR is reduced with the presence of heavy metal, protein, and polysaccharides complexes (30).

Serological Test

A serological test is used for the detection of anti-H. pylori IgG antibody for the diagnosis of H. pylori infection. Individuals infected with H. pylori usually present with specific antibodies such as IgG, IgA, and IgM, which can be detected via serological tests (9). IgG predominantly responds to the presence of chronic H. pylori infection (22). Serological tests are widely used in epidemiological studies because they are easy, rapid, and affordable. It also offers sensitivity and specificity in the range of 80% to 90%, and it depends on the individual’s immune response, the duration of the exposure to the infection, nutritional status, and other antigen-related bacteria (22).

This rapid method also has high sensitivity in patients presenting with atrophy and is not influenced by antibiotics and PPIs; therefore, patients can continue taking the medications before the test (31). Serological tests have several disadvantages that limit their usefulness. This test cannot differentiate the past and present of the H. pylori infection; hence, it cannot be used to monitor the effectiveness of the eradication treatment (19). In fact, the serology result remains positive 3 years, after the treatment. The accuracy of the test is also lower in the low prevalence area which might produce false-positive result, thus further test by doing another diagnostic test such as histology, RUT and SAT to confirm the H. pylori infection  (32).

Urea Breath Test

UBT, which is characterized by its high sensitivity and specificity, is widely available (9). However, the specificity of the UBT decreases among infants younger than 2 years old, as it requires active cooperation and often yields false-positive results (33). The first UBT test was reported 7 decades ago by American biochemist when they did experimental study by injecting C urea intravenously into anaesthetized cats that were not secreting gastric juice. They found out that the amount of C- CO2 decreased in the breath and concluded that the colonization of Helicobacter felis bacteria was the culprit in the cat (34). The urease activity was abated after being treated with a mixture of penicillin, Terramycin, and sulphaguanidine in the cats.

Bacteria other than H. pylori are not present in the stomach except in patients with achlorhydria (35). As mentioned, H. pylori bacterium is involved in the mechanism that breaks down urea into ammonia and CO2 (14). CO2 enters the bloodstream and is subsequently exhaled in the lungs. Therefore, the CO2 with the labelled C is measurable in the diagnosis of the H. pylori infection. Before conducting the UBT, a tablet containing urea is swallowed, and the amount of the trapped labelled-CO2 is measurable in the exhalation. UBT offers a sensitivity of more than 95% and a specificity of more than 93%, with an affordable price (36). Besides, it can detect H. pylori bacteria in asymptomatic individuals, making it the gold standard for the diagnosis of H. pylori infection, especially among the elderly, children, and pregnant women, due to less radiation exposure (37). Although UBT has high sensitivity, there is a lack of data on antibiotic resistance that is important for eradication treatment (38). There is a chance of UBT yielding false-positive results that are induced by bacteria other than H. pylori, such as Helicobacter heilmannii, which is responsible for the process of urease activity (39). Patients who are on PPIs are also required to stop 2 weeks prior to UBT test because it can influence the results (31).

Stool Antigen Test

SAT is a non-invasive method that was introduced after the UBT test. The test is designed to detect the antigen associated with H. pylori in the stool (40). There are 2 types of SAT; one is based on enzyme immunoassay (EIA) and the other is based on immunochromatography (ICA). Both tests yield high accuracy results, but in general, ICA provides less reliable results as compared to EIA (41). Early SAT used EIA based on polyclonal antibodies, which was then further improved by changing to monoclonal antibodies because they are more accurate with high sensitivity (42-43). The guidelines  created by the Japanese researchers suggested that SAT has a sensitivity of more than 96% and a specificity of more than 97% before the eradication (44).

SAT is a relatively inexpensive non-invasive method as it requires fewer high-technology equipment to detect H. pylori bacteria in the stool sample (45). it offers convenience as patients can take the stool sample at home. SAT does not require discontinuation of PPI as does UBT because some monoclonal antibodies are not affected by PPIs. The SAT has disadvantages. Since the principle of the SAT is dependent on the antigen reaction, hence, it is less accurate when the sample is obtained from watery or unformed stool because the consistency of  H. pylori specific antigen called serum pepsinogen I is diluted (46). SAT also has less accuracy in patients who underwent distal gastrectomy, with specificity decreased to 90.5%, altered bowel movements, and those on antibiotics and PPIs (21, 47).

H. pylori Infection-Related Disease Outcomes

H. pylori bacteria are known to cause inflammation in the stomach region. This inflammation can lead to the development of diseases such as chronic gastritis, peptic ulcer disease, gastric cancer, iron-deficiency anaemia and diabetes mellitus (T2DM).

Chronic Gastritis

The primary infection of the H. pylori bacteria resulting in chronic gastritis is accompanied by epigastric pain and is sometimes asymptomatic (48). Gastritis is defined as inflammation of the gastric lining and can manifest as acute or chronic (49). Acute gastritis is temporary inflammation followed by clinical manifestations such as nausea, vomiting, and indigestion. H. pylori bacteria favor the antrum region of the stomach to start the colonization before migrating to another region (50). It often develops with the involvement of hypochloridria and neutrophil inflammatory cell infiltration (51). Researchers suggest that neutrophils are the marker in the development of gastric cancer, which has been examined with fluorescence RNA in situ. Chronic gastritis is divided into 2 categories: atrophic and non-atrophic, with the primary causal factor being H. pylori infection (52-53). Non-atrophic gastritis could progress to atrophic gastritis if proper treatment is not received by patients.

Peptic Ulcer

An early study found that 15% of H. pylori-infected individuals developed peptic ulcer disease (54). Symptoms of the peptic ulcer include nausea, vomiting, weight loss, and stomach bleeding (55). A peptic ulcer is a   subset of the stomach and duodenum which extends into the submucosa (56). H. pylori bacteria cause inflammation, degeneration and injury to epithelial cells. Patients diagnosed with peptic ulcer disease are recommended to proceed with diagnostic tests for H. pylori bacteria because peptic ulcer can also be induced by non-steroidal anti-inflammatory drugs that are commonly used to relieve pain and reduce inflammation (57, 58).

Gastric Cancer

H. pylori infection is one of the strongest factors in the development of gastric cancer. H. pylori bacteria are persistent in producing inflammation in the stomach, which weakens the immune response if left untreated (59). Prolonged exposure to the inflammatory response predisposes gastric cells to become cancer (60). The inflammatory compounds attack healthy tissue and cause alteration in the DNA transcription hence resulting in DNA damage (61). This is the initial stage of gastric cancer. Further steps in the pathway are to promote cell proliferation and produce more reactive oxygen species that further damage the DNA and decrease the efficiency of DNA repair, resulting in cancer cell development (62).

Type 2 Diabetes Mellitus

A meta-analysis found that H. pylori bacteria increased the risk of T2DM by 27% (63). T2DM is characterized by insulin deficiency or insulin resistance (64). Insulin is a hormone that is secreted by the pancreas to maintain glucose homeostasis. In the cross-sectional study conducted in Cameroon, central region of Africa, about 73% of the subjects with H. pylori infection were diagnosed with T2DM (65). Infected patients with body mass index (BMI) of more than 25kg/m2 are more prone to develop T2DM compared to infected patients with normal BMI in the range of 18.5 to 24.9kg/m2. Symptoms vary and include dysphagia, early satiety, nausea and vomiting (66).

The pathogenesis of H. pylori in relation to T2DM is interesting. Gastritis related to H. pylori alters the secretion of hormones called gastrin and somatostatin (67). Gastrin stimulates the production of insulin while somatostatin decreases the production of insulin. H. pylori acts to promote the production of somatostatin and reduce gastrin, causing a decrease in the production of insulin and increasing the susceptibility of insulin to oxidative stress and inflammatory mediators (68-69). Other evidence indicates that T2DM itself can increase the risk of H. pylori infection because T2DM can impair the immune system of host cells, thus, increasing the susceptibility of infection (70). Besides, gastric motility is often disrupted in patients with T2DM, thereby increasing the risk of H. pylori colonization and inducing inflammation (71).

Iron-deficiency Anemia

Chronic gastritis related to H. pylori infection is closely associated with impairment of iron absorption, resulting in iron deficiency, anemia, and vitamin B12 deficiency (72). This clinical manifestation resulted from hypochlorhydria in the stomach, which subsequently impairs the absorption of dietary iron, which is necessary to metabolize ferric into ferrous form. H. pylori uses iron for its colonization and increases the production of hepcidin (73). The hormone hepcidin is released by the liver for iron metabolism. A reduction in the intragastric pH affects iron absorption from the diet (74). This has been demonstrated in the study conducted among school-aged children with H. pylori infection, who presented with elevated hepcidin levels and iron deficiency, compared to non-infected children (75).

Treatment For H. pylori Infection

H. pylori infection is often treated with antibiotics for a minimum of 2 weeks (76). The treatment also usually will include medication such as PPIs and bismuth subsalicylate, to help in the healing process by coating the ulcer base and protecting the stomach from further acid exposure (26, 77).

H. pylori Infection and Nutrition

Nutrition plays an important role in maintaining ecology in the gastric environment (2). The health ecology in the gastric environment is highly influenced by the host’s diet. The contribution of the nutrients to H. pylori is explained in detail as follows:

Salt

High intake of salt is associated with an increase in the risk of H. pylori infection and development of pre-malignancy (78). The consumption of salt in high amounts can destroy the gastric mucosal barrier, resulting in inflammation and, thus, favor colonization by H. pylori bacteria (79). One of the potential pathways is that high salt intake alters the viscosity and integrity of gastric mucosa, thus, promoting the colonization of H. pylori colonization and persistent inflammation forming gastric proliferation  and mutation in DNA (80). This has been demonstrated well in an early animal study whereby a high salt diet modifies the structure of gastric mucosa via an inflammatory process in mice infected with H. pylori (81). The loss of parietal cells, which secrete gastric acid, creates an achlorhydria environment, exacerbates the colonization of H. pylori, and enhances the process of carcinogenesis (82). Another interesting animal experimental study was conducted where researchers introduced a diet with a high concentration of salt, 87.5% sodium chloride, to Mongolian gerbils (83). 87.5% of sodium chloride is the starting concentration, approximately equivalent to 3 to 20% of salt in salted fish, 25% of salt in pickles, and 19% of salt in soy sauce. This mixture was given to the gerbil with no variation over a prolonged period. Over 60%     of the gerbils were infected with cagA+ H. pylori strain within 4 months of interventions.

Zinc

Zinc plays a pivotal role in the maintenance of DNA integrity, synthesis, repair and cell division (84). It is also involved in the defense mechanism to protect DNA from oxidative stress. Deficiency of zinc can impede DNA damage through the production of oxidative stress mediators and impair its role as a DNA repair agent. Previous studies clearly demonstrated the relationship between zinc deficiency and the role of H. pylori infection in the human mechanism (85). This has been confirmed in the case-control study whereby the H. pylori-infected group, presented with gastritis, peptic ulcer, and gastric cancer, having a lower level of serum zinc compared to the healthy control group (86).

H. pylori bacteria require zinc for nutrition to support its growth and colonization; thus, it needs to compete with calprotectin (87). Calprotectin is a zinc-binding protein that can be found in neutrophils, and the presence of calprotectin in the stomach region is closely related to the inflammatory response (88). It is released into the gut to chelate with zinc in response to bacterial infection. In response to calprotectin, the H. pylori bacterium alters its structure to decrease cell surface hydrophobicity to enhance its fitness in the presence of calprotectin to response when there is availability of the zinc (89). In the state of zinc deficiency, this increases susceptibility to inflammatory response, gastric inflammation, and DNA damage in the host cells.

Vitamin C

Adequate intake of vitamin C acts as a defence mechanism against infection. It is believed that high intake of vitamin C from fruits and vegetable sources reduces the risk of H. pylori infection (90). The antioxidant role of vitamin C is to protect the gastric mucosa from the inflammation caused by H. pylori infection, and it also reduce the production of carcinogens to prevent the colonization of H. pylori bacteria (91). Vitamin C has been shown to play a crucial role in inhibiting the activity of neutrophils induced by H. pylori infection (92). It has been demonstrated well in the study that the level of vitamin C in gastric acid and serum is lower in H. pylori-infected patients with gastritis and peptic ulcers (93).

In addition, vitamin C has been used as part of treatment to eradicate H. pylori (94). Whether increased vitamin C levels during the eradication period from intake of natural fruits and vegetables, along with the addition of vitamin C supplementation, increase the effectiveness of therapy is still a controversial issue. Normal dietary intake of vitamin C, about 40mg per day from fruits and vegetables, allows vitamin C to play its role as an antioxidant and enzymatic cofactor (95). Thus, nutritional management and education emphasizing a high daily intake of fruits and vegetables are important, especially among H. pylori-infected populations.

Probiotics

Probiotic bacteria called Lactobacillus and Bifidobacterium can be found widely in probiotic yoghurt drinks. The supplementation of probiotics during the H. pylori eradication period has improved the rate of success (96). Supplementation of probiotics by consuming yoghurt drinks two times a day for 6 months demonstrates a decrease in H. pylori urease compared to the infected group that only supplemented with milk (97). A meta-analysis examined The effect of Lactobacillus bacteria and reported that it improves by approximately 10 percent over placebo before antibiotic drug therapy (98). It plays a role as an antioxidant and an anti-inflammatory agent that later explains its role in decreasing stabilizing the gastric barrier (99).

The mechanism of probiotics against the severity of H. pylori infection is still unclear. However, a few researchers have suggested that probiotics may help in producing mucin to strengthen the gastric barrier and compete with H. pylori bacteria for adhesion receptors, as well as stabilize the gut barrier to prevent bacterial colonization (100). Moreover, Lactobacillus displays similar characteristics to H. pylori as both can survive in low pH environments in the stomach and protect the gut from inflammation induced by H. pylori bacteria (101). The longer the duration of yoghurt consumption, the better the effect in decreasing the density of H. pylori colonization in the gut (100). Intake of yoghurt in the long term was found to be a safe and effective strategy to prevent an infection.

CONCLUSION

The development of the current methods to detect H. pylori bacteria allows more accurate diagnosis of H. pylori infection to combat the disease outcomes associated with it. An accurate diagnosis helps to guide clinicians in choosing the appropriate eradication treatment for infected H. pylori individuals. The selection of the method depends on the sample size, the location, the clinical manifestation of the infected individual, and the pros and cons of the methods. The selection of more than one method is advisable in certain circumstances to further confirm the H. pylori diagnosis. Importantly, the nutritional status of the individual should not be overlooked as it undoubtedly influences disease outcomes related to H. pylori infection. We believe that there would be continuous improvement in the diagnostic method and pharmaceutical treatment in the management of H. pylori infection. The emphasis on nutritional intake in the individual diet also should be implemented in the primary healthcare setting to reduce the incidence of H. pylori infection.

Authorship Contributions

Surgical and Medical Practices: F.H., N.A.S.N.L., Concept: S.S.S.A.R., Design: Data Collection or Processing:Analysis or Interpretation:Literature Search: F.H., S.E.H.T., Writing: V.U.K.
Conflict of Interest: No conflict of interest was declared by the authors.
Financial Disclosure: The authors declared that this study received no financial support.

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