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What is H. Pylori? Test & Treatment

Written by Joe Cohen, BS | Last updated:
Nattha Wannissorn
Medically reviewed by
Nattha Wannissorn, PhD | Written by Joe Cohen, BS | Last updated:
H. pylori in children

According to some estimates, more than half of the population is a host for Helicobacter pylori, which is most commonly acquired in childhood. Read on to find out when and how H. pylori infection is tested for and treated.

What is H. pylori?


Helicobacter pylori (H. pylori) is a gram-negative, spiral-shaped pathogenic bacterium that colonizes the stomach [1].

This bacterium is the second most commonly studied pathogen (after E. coli) [2]. Marshall and Warren were awarded the 2005 Nobel Prize in Medicine for linking the presence of H. pylori to inflammation of the stomach (gastritis) and peptic ulcer disease [3].

How Do You Get It?

Infection with H. pylori is most often acquired in early childhood and persists for life [4].

A specific immune response, skewed toward Th1, is triggered during the infection [5].

In spite of the immune response, H. pylori is frequently not cleared from the body completely because the bacterium is equipped with an array of mechanisms that allow it to evade or inhibit host responses [5].


This bacterium is one of the most prevalent human pathogens, infecting more than 50% of the human population [4]. H. pylori is present in approximately 70 – 80% of the population in developing countries and 13% – 50% of the population in developed countries [2].

In recent years, there has been a decrease in the prevalence of H. pylori infection in developed countries. In the United States, less than 6% of the children are infected by H. pylori. A similar trend is becoming apparent in other parts of the developed world [6].

Research indicates that H. pylori has been around at least since human migration out of Africa about 60,000 years ago [7].

H. pylori Test


The H. pylori bacterium can be detected in most biological fluids. This includes saliva, breath, blood, feces, and urine, in addition to the bacterium’s primary site of residence in the stomach lining [8].

Urease is an enzyme produced by H. pylori which can be used to detect its presence [8]. Common assessments include gastric biopsies for rapid urease detection (rapid urease test (RUT)), the 13C-urea breath test (13C-UBT) or fecal antigen determination (fecal antigen test (FAT)) [8].

Breath Test

The noninvasive 13C-UBT and FAT are of comparable diagnostic accuracy with biopsy-based tests and are the methods of choice in the test-and-treat setting and for controlling the effect of eradication treatments [8].

H. pylori is usually diagnosed with a breath test, though blood tests or other methods can be alternatively used.

How Effective Are Different Testing Methods?

Table: Different Methods of H. pylori Testing with Their Effectiveness (Sensitivity and Specificity) [9, 10]

Test Sensitivity Specificity
Urease (breath) test 67% 100%
Serology (blood) test for H. pylori antibodies 84% 60%
Stomach biopsy – histopathology (examining tissues under the microscope) 83% 100%
Stomach biopsy – H. pylori culture 64% 100%
Stool antigen test 86-97% (depending on antigen tested) 93-97%

Higher sensitivity (true positive rate) demonstrates that the test is better at detecting H. pylori in the true presence of H. pylori. Lower specificity (true negative rate) indicates that the test may show those without H. pylori as having H. pylori. This means that the stomach biopsy and blood test, for example, may not detect H. pylori in about 20% of people with H. pylori infections.

H. pylori serology test may detect antibodies against H. pylori either in individuals with active infections or even after infections have been eradicated. Therefore, the serology test is not a good test to follow up after H. pylori treatment [9].

H. pylori Treatment

Standard Eradication Treatment

Eradication of virulent H. pylori is necessary for people with the negative symptoms of infection, such as stomach ulcers. However, there are conflicting opinions whether asymptomatic H. pylori-positive children and adults should be treated, broadly because the antibiotic treatments themselves have strong side effects [11, 12].

The conventional treatment for H. pylori, called the standard triple therapy, consists of a short course of two antibiotics (typically clarithromycin and amoxicillin) along with proton pump inhibitors (stomach acid-reducing drugs, e.g. omeprazole or lansoprazole) [13, 14]. 14-day triple therapy was superior to the equivalent 7- or 10-day triple therapy [14].

Because H. pylori is adapted to an acidic environment, reducing stomach acid with a proton pump inhibitor inhibits H. pylori growth and is beneficial during the short-term standard triple therapy [15]. However, long-term treatment with PPI therapy can result in atrophy (wasting) of the stomach lining [15].

Standard treatment for H. pylori infection can alter healthy gut microbiota, leading to bloating, diarrhea, and nausea [13]. These side effects are estimated to affect over 50% of patients and are associated with decreased compliance and treatment failure [16]. Resistance to antibiotics or reinfection from remaining H. pylori bacteria can also cause the failure of the treatment to clear H. pylori.

The effectiveness of the standard triple therapy ranges between 60% and 80% [16].

Standard H. Pylori treatment involves triple therapy: two antibiotics and one proton pump inhibitor (PPI).

Factors that Affect the Effectiveness of H. pylori Treatments


Lack of observance to doctor’s prescriptions is the main cause of eradication failure [2, 17]. Treatment compliance lower than 80% decreases treatment success rates [14].

Cytochrome P450 2C19 (CYP2C19) Mutation

Another cause of eradication failure is a mutation in cytochrome P450 2C19 (CYP2C19). CYP2C19 is the principal enzyme involved in the metabolism of proton pump inhibitors (omeprazole or lansoprazole). When CYP2C19 works more effectively than usual, the drugs get degraded faster and have lower efficacy [18].

CYP2C19 SNPs affecting the effectiveness of proton pump inhibitors include rs4244285(A) and rs4986893(A) [19].

H. pylori Reservoir in the Mouth

Dental plaque can act as a reservoir of H. pylori, making proper oral hygiene maintenance essential to preventing reinfection [20].

Several studies suggest that untreated periodontal disease increases the risk of becoming reinfected after H. pylori eradication. Reducing the number of oral H. pylori using an antiseptic mouthwash and/or periodontal treatment is recommended to improve the eradication rate following antibiotic therapy [21].

For example, in one study, the treatment of an oral infection increased the success rate of H. pylori eradication from the stomach from 61% to 82% [22].

Antibiotic Resistance

Increased resistance to the antibiotic clarithromycin has accounted for a dramatic decline in the efficacy of standard triple therapies across the world [23]. Alternative antibiotic regimens have been shown to overcome clarithromycin resistance and are now preferred treatments achieving improved eradication rates (over 90%) [23].

Factors like patient compliance, antibiotic resistance, and CYP enzyme activity might all affect the effectiveness of H. Pylori treatment.

H. pylori Interferes with the Host’s Metabolism

Nutrient Availability

H. pylori infection impairs the absorption of iron and vitamin B12 [24].

Vitamin C concentration is 20% lower in H. pylori-infected subjects [24].

The concentration of β-carotene and vitamin E in the stomach is also decreased [24].

Some studies also reported a decrease in folate absorption in infected individuals [24].

Hormones that Regulate Appetite

Several studies show that infected subjects have lower levels of ghrelin and a higher concentration of leptin.

Since leptin decreases appetite, and ghrelin stimulates the release of growth hormone, H. pylori infection could result in decreased growth, especially in children who are already at risk for malnutrition [24, 25].

In some studies of infected children, the eradication of H. pylori increased ghrelin levels and resulted in growth increases in both weight and height [26].

The research on the links between H. pylori and leptin are ghrelin levels are conflicting in some cases, however. The majority of studies found lower levels of circulating ghrelin in H. pylori-positive subjects in Asia and Europe but not in the United States.

Conflicting results were also obtained when the effect of H. pylori eradication on ghrelin levels was evaluated [25, 27]. In a study of infected veterans, ghrelin levels were nearly six-fold higher than pre-eradication, but leptin levels also increased significantly seven months following eradication [27].

Gut Microbiota

H. pylori alters the stomach bacterial community, increasing bacteria in the Proteobacteria, Spirochete, and Acidobacteria species and decreasing bacteria in the Actinobacteria, Bacteroidetes and Firmicutes species [13, 26].

H. pylori infection also alters the ratio of fecal Bifidobacterium/E. coli in children, but this can be improved by ingesting probiotics in the form of yogurt [26].

Limited data suggest that H. Pylori might alter vitamin absorption, the gut microbiome, and appetite-related hormones. More research is needed to confirm these hypotheses.


H. Pylori is a bacterial infection that most people acquire in childhood. More than half of the world’s population is a host for H. Pylori, but there’s been a drop in prevalence in developed countries.

H. Pylori is usually diagnosed with a breath test, but there are certain cases in which your doctor may think that a blood test or another method would be more suitable.

Standard treatment involves triple therapy: two antibiotics and one proton pump inhibitor (PPI). The effectiveness of this treatment can be affected by factors like patient compliance, antibiotic resistance, and CYP enzyme activity.

Further Reading

About the Author

Joe Cohen, BS

Joe Cohen, BS

Joe Cohen flipped the script on conventional and alternative medicine…and it worked. Growing up, he suffered from inflammation, brain fog, fatigue, digestive problems, insomnia, anxiety, and other issues that were poorly understood in traditional healthcare. Frustrated by the lack of good information and tools, Joe decided to embark on a learning journey to decode his DNA and track his biomarkers in search of better health. Through this personalized approach, he discovered his genetic weaknesses and was able to optimize his health 10X better than he ever thought was possible. Based on his own health success, he went on to found SelfDecode, the world’s first direct-to-consumer DNA analyzer & precision health tool that utilizes AI-driven polygenic risk scoring to produce accurate insights and health recommendations. Today, SelfDecode has helped over 100,000 people understand how to get healthier using their DNA and labs.
Joe is a thriving entrepreneur, with a mission of empowering people to take advantage of the precision health revolution and uncover insights from their DNA and biomarkers so that we can all feel great all of the time.


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