H Pylori Infection: The Ultimate Research-Backed Guide

Prevalence and Risk Factors 

The prevalence of Helicobacter pylori infection is approximately 50% worldwide, being as low as 30% in the United States and as high as 90% in developing countries.https://www.ncbi.nlm.nih.gov/books/NBK547758/ 

Asia, the prevalence of H. pylori is often higher than 50%. https://onlinelibrary.wiley.com/doi/epdf/10.1111/hel.12165 

most important risk factors for H. pylori infection. https://onlinelibrary.wiley.com/doi/epdf/10.1111/hel.12165

• Other infectious risk factors might include: 
• Living in a rural area https://onlinelibrary.wiley.com/doi/epdf/10.1111/hel.12165 
• Living in crowded homes https://onlinelibrary.wiley.com/doi/epdf/10.1111/hel.12165 
• Having contaminated sources of drinking water https://onlinelibrary.wiley.com/doi/epdf/10.1111/hel.12165
• Among the main lifestyle habits, smoking and alcohol consumption showed discordant results: although in most studies, there was no significant association with H. pylori infection. Some authors reported that regular smokers and drinkers were at higher risk. In contrast, in one study, regular alcohol drinking was a protective factor. https://onlinelibrary.wiley.com/doi/epdf/10.1111/hel.12165
  

Pathology and Infectious Consequences

• Infection results in an inflammatory disease state of the stomach source
• A team of researchers from Boston University, Harvard Medical School and Massachusetts Institute of Technology have shown that the bacterium that causes human stomach ulcers uses a clever biochemical strategy to alter the physical properties of its environment, allowing it to move and survive and further colonize its host.Contact with stomach acid keeps the mucin lining the epithelial cell layer in a spongy gel-like state. This consistency is impermeable to the bacterium Heliobacter pylori. However, the bacterium releases urease which neutralizes the stomach acid. This causes the mucin to liquefy, and the bacterium can swim right through it. Contributed by National Science Foundation, Zina Deretsky (PD-US GOV) https://www.ncbi.nlm.nih.gov/books/NBK547758/
• Infection  can lead to gastritis and resultant gastric atrophy of the HCL producing parietal cells. Can also contribute to the release of acid-inhibiting compounds (interleuin1beta). Source
• Gastritis as a result of H. pylori must be addressed by the primary care physician before late complications arise, such as atrophic gastritis (atrophic gastritis = inflammation based destruction of functional components of the stomach; can be permanent if prolonged) and pernicious anemia (B12 deficiency secondary to parietal cell destruction). https://www.ncbi.nlm.nih.gov/books/NBK547758/ 
• Of note, H. pylori infection is capable of causing both high and low levels of stomach acid.  http://pgnrc.sbmu.ac.ir/uploads/PUD.pdf 
• If the infection is localized to the antrum (grinding, lower compartment) of the stomach, it may cause excessive release of the acid-stimulating hormone gastrin OR inhibit the acid-regulating and reducing hormone somatostatin from being released to regulate gastrin secretion.source
• If there is a healthy amount of parietal cells that have not yet atrophied due to inflammation, this can result in high levels of stomach acidity as opposed to low levels of stomach acid. Source

Infectious Consequences

• Helicobacter pylori (H. pylori) is an important human pathogen involved in the pathogenesis of atrophic gastritis, gastroduodenal ulcer, gastric cancer, MALT lymphoma, idiopathic thrombocytopenic purpura, iron deficiency anemia and vitamin B12 deficiency https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4293486/ 
• Infection in infancy is thought to lead to pangastritis (low acid secretion status), whereas acuisition in later childhood may lead to a predominantly antral gastritis only (high acid load). https://www.researchgate.net/profile/Jagadish_Das2/publication/51382975_Epidemiology_and_Pathophysiology_of_Helicobacter_Pylori_Infection_in_Children/links/5543e37a0cf24107d396385a/Epidemiology-and-Pathophysiology-of-Helicobacter-Pylori-Infection-in-Children.pdf  
• Host genetic factors may determine why some individuals infected with H. pylori develop gastric cancer or ulcers while others do not. https://www.researchgate.net/profile/Jagadish_Das2/publication/51382975_Epidemiology_and_Pathophysiology_of_Helicobacter_Pylori_Infection_in_Children/links/5543e37a0cf24107d396385a/Epidemiology-and-Pathophysiology-of-Helicobacter-Pylori-Infection-in-Children.pdf

Symptoms and When to See a Doctor 

Most people with H. pylori infection will never have any signs or symptoms. It's not clear why this is, but some people may be born with more resistance to the harmful effects of H. pylori. When signs or symptoms do occur with H. pylori infection, they may include:

1. Abdominal pain that's worse when your stomach is empty
2. Nausea
3. Loss of appetite
4. Frequent burping
5. Bloating
6. Unintentional weight loss
7. https://www.mayoclinic.org/diseases-conditions/h-pylori/symptoms-causes/syc-20356171 

Make an appointment with your doctor if you notice any persistent signs and symptoms that worry you. Seek immediate medical help if you experience:

1. Severe or persistent abdominal pain
2. Difficulty swallowing
3. Bloody or black tarry stools
4. Bloody or black vomit or vomit that looks like coffee grounds
5. https://www.mayoclinic.org/diseases-conditions/h-pylori/symptoms-causes/syc-20356171

Testing for H. pylori

Tests and procedures used to determine whether you have an H. pylori infection include:

• Blood test. Analysis of a blood sample may reveal evidence of an active or previous H. pylori infection in your body. However, breath and stool tests are better at detecting active H. pylori infections than is a blood test.
• Breath test. During a breath test, you swallow a pill, liquid or pudding that contains tagged carbon molecules. If you have an H. pylori infection, carbon is released when the solution is broken down in your stomach.Your body absorbs the carbon and expels it when you exhale. You exhale into a bag, and your doctor uses a special device to detect the carbon molecules. Acid-suppressing drugs known as proton pump inhibitors (PPIs), bismuth subsalicylate (Pepto-Bismol) and antibiotics can interfere with the accuracy of this test. Your doctor will ask you to stop taking those medications for a week or two before you have the test. This test is available for adults and children.
• Stool test. A laboratory test called a stool antigen test looks for foreign proteins (antigens) associated with H. pylori infection in your stool. As with the breath test, PPIs and bismuth subsalicylate can affect the results of this test, so your doctor will ask you to stop taking them for two weeks before the test.
• Scope test. You'll be sedated for this test, known as an upper endoscopy exam. During the exam, your doctor threads a long flexible tube equipped with a tiny camera (endoscope) down your throat and esophagus and into your stomach and duodenum. This instrument allows your doctor to view any irregularities in your upper digestive tract and remove tissue samples (biopsy).  These samples are analyzed for H. pylori infection. This test isn't generally recommended solely to diagnose an H. pylori infection because it's more invasive than a breath or stool test, but it may be used to diagnose H. pylori ulcers or if it's needed to rule out other digestive conditions.

https://www.mayoclinic.org/diseases-conditions/h-pylori/diagnosis-treatment/drc-20356177 

• The use of antimicrobial drugs and proton pump inhibitors as well as the presence of intestinal metaplasia may result in false-negative results. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4293486/ 

H. pylori infections like other major chronic infectious diseases (i.e., syphilis and tuberculosis) are associated with a long latent period before presenting clinically. As such, many infections will be discovered during this latent period. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4293486/  

Treatment and Management of Longterm Effects 

• Fortunately, Helicobacter pylori eradication treatment appears  to reduce gastric cancer risk. https://www.ncbi.nlm.nih.gov/books/NBK76788/ 
• Eradication of H. pylori reduced the risk of developing gastric cancer in patients with peptic ulcer diseases; however, the risk is higher in the patients with severe atrophic gastritis than those with mild or moderate atrophic gastritis. These data suggested that ‘‘the earlier, the better’’ in H. pylori eradication prevents gastric cancer. https://link.springer.com/content/pdf/10.1007/s00535-017-1407-1.pdf 
• Treatment and eradication of H. pylori may involve a number of combinations of targeted antibiotics, proton pump inhibitor medications, H2RAs, and bismuth compounds such as Pepto Bismol. Therapy may last 14 days. Regional considerations regarding specific antibiotics and risks for antibiotic resistance should be taken into account by prescribing physicians to improve therapeutic outcomes. Two antibiotics are commonly prescribed at once due to risks for antibiotic resistance.

https://www.cag-acg.org/images/publications/Hp_Toronto_Consensus_2016.pdf ;

https://link.springer.com/content/pdf/10.1007/s00535-017-1407-1.pdf 

https://www.mayoclinic.org/diseases-conditions/h-pylori/diagnosis-treatment/drc-20356177   

• Pharmacologic doses of ascorbic acid have also shown some efficacy as an adjuvant therapy to traditional eradication therapy, and could possibly be helpful in hastening healing of H. pylori induced peptic ulcers: 
• Ascorbic acid plays a key role in healing and protection of the gastric mucosa from injurious insults. Vitamin C deficiency has repeatedly been linked with peptic ulcer disease and its complications. Its role in scavenging free radicals and reducing the inflammatory cascade, particularly in H. pylori induced gastritis, play a major preventive role in reducing the consequences of gastric inflammation including in reducing the deleterious effects of reactive oxygen species and NOC. These effects are reflected in population-based epidemiologic studies showing negative correlations between vitamin C intake and gastric cancer and endoscopic studies suggesting regression of precancerous lesion with ascorbic acid supplementation. Ascorbic acid supplementation has been associated with a decreased incidence of bleeding from peptic ulcer disease and with a reduction in NSAID-associated gastric mucosal damage. Pharmacologic doses of ascorbic acid also may improve the effectiveness of H. pylori eradication therapy. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3874117/ 
• The treatment group received 5 grams of vitamin C daily for four weeks and 8 patients achieved H. pylori eradication, measured by urease test of gastric biopsy, in the treatment group compared to no patients in the control group (P=0.006) (Table 4). Zojaji et al. randomized 312 patients to two groups; one group received amoxicillin, metronidazole, bismuth and omeprazole for two weeks and the other the same regimen plus 500 mg of ascorbic acid daily [81]. The addition of ascorbic acid resulted in an increase in eradication from 48.8% to 78% at 4 weeks (p<0.0001) (Table 4). Sezikli et al. randomized 160 patients to receive either lansoprazole, amoxicillin, clarithromycin, and bismuth subcitrate or this regimen plus 500 mg ascorbic acid b.i.d. and vitamin E (200 IU, b.i.d.) for 2 weeks [82]. H. pylori eradication increased from 60% to 93.5% with the addition of the vitamins (p<0.005) (Table 4). Chuang et al. randomized 171 patients into three therapies for 1 week. Group 1 received 20 mg omeprazole daily, 1 gram amoxicillin daily and 250 mg of clarithromycin twice daily, group 2 received the same regimen as group 1 plus 500 mg of vitamin C twice daily and group 3 received omeprazole, amoxicillin and 500 mg of clarithromycin twice daily without vitamin C supplementation [83]. The eradication rate increased from 68% in group 1 to 85% with the addition of ascorbic acid in group 2 (p=0.03). The difference in eradication rate was not significant between group 2 and group 3 suggesting that vitamin C supplementation might allow a reduction in the dose of clarithromycin required to eradicate H. pylori (Table 4). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3874117/ 

• Treatment may eradicate the infection and reverse inflammatory changes, but cannot reverse atrophy that has already occurred to functional components in the stomach. Source 
• While some gastric acid secretion may be restored with H. pylori eradication, restoration may never reach baseline or even normal levels of gastric acidity if damage is extensive. https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2036.2004.01948.x 
• If lasting damage exists, special attention may need to be paid to avoid deficiencies of B12, Iron, calcium, magnesium, etc. in the setting of prolonged acid-reducing medication use or parietal cell destruction and hypochlorhydria. 
• Betaine HCL supplementation may be useful in the case of hypochlorhydria or achlorhydria so long as no peptic ulcers are present, no acid-mediated disease processes are occurring, and no acid regulating medications are being taken. 
• Additional attention to food safety and risks of food-borne illness may be warranted in the setting of hypochlorhydria or achlorhydria given the loss of protective low stomach pH against ingested pathogens.
• Dietary strategies which lessen the risk of gastric cancers are likely a good idea: e.g. diet low in highly processed/preserved and salted foods and high in fresh fruits and vegetables (particularly those rich in vitamin C)  may be particularly important for gastric cancer prevention.