Helicobacter Pylori Infection IgG Biomarker

Optimal Takeaways

Helicobacter pylori is a pathogenic bacterium that commonly infects the gastric mucosa and contributes to gastritis, gastric and duodenal ulcers, gastric carcinoma, and ulcerative esophagitis. 

It has also been associated with metabolic syndrome, diabetes, and increased risk of cardiovascular disease as well. Detection of IgG antibodies in the blood indicate exposure and likely infection and is the most common antibody tested.

Standard Range: 0.00 - 0.89 Index

The ODX Range: 0.00 - 0.79 Index      

Low levels of anti- H. pylori IgG antibodies suggest absence of infection.

High levels (positive) anti-H. pylori IgG antibodies indicate infection with H. pylori, a pathogen that causes gastrointestinal inflammation (Zojaji 2013), more advanced gastritis (acute and chronic), gastric ulcer, duodenal ulcer,  gastric carcinoma, and ulcerative esophagitis (Pagana 2021). Infection is also associated with metabolic syndrome, increased triglycerides, fasting glucose, HOMA-IR, and blood pressure (Upala 2016).

Overview

Helicobacter pylori (H. pylori) is a type of bacteria that dwells in the mucosal lining of the stomach. Its presence is a risk factor for chronic gastritis, gastric and duodenal ulcers, ulcerative esophagitis, and gastric carcinoma. Measurement of IgG anti-H. pylori antibody in the blood is a relatively non-invasive way to screen for and detect active exposure. The antibody will increase two months after exposure/infection and can stay elevated for more than a year, even after treatment (Pagana 2021).

In one study of 170 dyspeptic patients, 62% were diagnosed with H. pylori infection. Those diagnosed had a serum IgG antibody level greater than 70 U/mL, while those negative for H. pylori had a level below 30 U/mL. Levels between 30 and 70 U/mL warrant additional assessment. At least 90% of those infected with H. pylori will have detectable IgG antibodies and the vast majority will have active gastritis (Chen 2002).

Infection with H. pylori is considered the most common infection globally. Its effects expand beyond the gastrointestinal tract and can contribute to inflammation and cardiovascular disease. In one case-control study, H. pylori (especially more virulent strains) and elevated CRP were significantly more prevalent in post-MI patients than in controls (Khodaii 2011). H. pylori may be an independent risk factor for coronary heart disease as well. In one cross-sectional study of 105 subjects, H. pylori was found in 48% of those with CHD versus 37% in those without CHD. The relationship between H. pylori and CHD was significant even after adjusting for diabetes, dyslipidemia, hypertension, and IL-6 and CRP levels (Rogha 2012).

A meta-analysis of 6 trials found that Infection with H. pylori was significantly associated with the incidence of metabolic syndrome and its characteristic elevations in triglycerides, fasting glucose, HOMA-IR, blood pressure, and BMI (Upala 2016). Individuals with diabetes may be at increased risk for H. pylori infection (Devrajani 2010). One clinical trial investigating H. pylori in diabetics found that hemoglobin A1C decreased significantly following treatment and eradication of infection (Zojaji 2013). Eradication of H. pylori significantly improved hemoglobin A1C levels even in diabetics with asymptomatic infection (Cheng 2019).

Conventional eradication of H. pylori has become complicated due to the development of antibiotic resistance. Alternative and adjuvant therapies are being explored including the use of probiotic microbes, phage technology, and plant-based compounds that can inhibit bacterial enzymes, support the host’s immune system, and modulate inflammation (Vale 2014).

Interestingly, a meta-analysis of observational studies suggests that O blood type may increase the odds of becoming infected with H. pylori by 16% compared to B or AB blood types (Chakrani 2018).

References

Chakrani, Zakaria et al. “Association Between ABO Blood Groups and Helicobacter pylori Infection: A Meta-Analysis.” Scientific reports vol. 8,1 17604. 4 Dec. 2018, doi:10.1038/s41598-018-36006-x

Chen, Tseng-Shing et al. “Immunoglobulin G antibody against Helicobacter pylori: clinical implications of levels found in serum.” Clinical and diagnostic laboratory immunology vol. 9,5 (2002): 1044-8. doi:10.1128/cdli.9.5.1044-1048.2002

Cheng, Kai-Pi et al. “Helicobacter pylori eradication improves glycemic control in type 2 diabetes patients with asymptomatic active Helicobacter pylori infection.” Journal of diabetes investigation vol. 10,4 (2019): 1092-1101. doi:10.1111/jdi.12991

Devrajani, Bikha Ram et al. “Type 2 diabetes mellitus: A risk factor for Helicobacter pylori infection: A hospital based case-control study.” International journal of diabetes in developing countries vol. 30,1 (2010): 22-6. doi:10.4103/0973-3930.60008

Khodaii, Zohreh et al. “Association of Helicobacter pylori infection with acute myocardial infarction.” Coronary artery disease vol. 22,1 (2011): 6-11. doi:10.1097/MCA.0b013e3283402360

Pagana, Kathleen Deska, et al. Mosby's Diagnostic and Laboratory Test Reference. 15th ed., Mosby, 2021.

Rogha, Mehran et al. “Is helicobacter pylori infection a risk factor for coronary heart disease?.” ARYA atherosclerosis vol. 8,1 (2012): 5-8.

Upala, Sikarin et al. “Association between Helicobacter pylori infection and metabolic syndrome: a systematic review and meta-analysis.” Journal of digestive diseases vol. 17,7 (2016): 433-40. doi:10.1111/1751-2980.12367

Vale, Filipa F, and Mónica Oleastro. “Overview of the phytomedicine approaches against Helicobacter pylori.” World journal of gastroenterology vol. 20,19 (2014): 5594-609. doi:10.3748/wjg.v20.i19.5594

Zojaji, Homayon et al. “The effect of the treatment of Helicobacter pylori infection on the glycemic control in type 2 diabetes mellitus.” Gastroenterology and hepatology from bed to bench vol. 6,1 (2013): 36-40.