H. pylori-Induced Higher C-Reactive Protein in Obese African Americans
Nuzhat R Siddiqui1, W Timothy Garvey, Mohammad A Khaled
1Department of Nutrition Sciences, University of Alabama at Birmingham Birmingham, AL 35294, USA.
Insights
Eradicating H. pylori infection significantly reduced systemic inflammation markers like CRP in African Americans. This suggests H. pylori contributes to chronic inflammation and related diseases in this population.
Area of Science:
- Medical Research
- Inflammation Biology
- Infectious Diseases
Background:
- African Americans exhibit higher susceptibility to chronic diseases like obesity, Type 2 Diabetes, and coronary heart disease (CHD).
- Systemic inflammation is a key factor in the development of these chronic conditions.
- Helicobacter pylori (H. pylori) infection, particularly cagA-positive strains, is more prevalent in African Americans, but its role in systemic inflammation is unclear.
Purpose of the Study:
- To investigate the impact of H. pylori (cagA) infection eradication on systemic inflammation in African Americans.
- To determine if H. pylori eradication affects markers of inflammation, specifically C-reactive protein (CRP).
- To explore the relationship between obesity (BMI) and the reduction in CRP levels post-H. pylori treatment.
Main Methods:
- A study involving 46 healthy African Americans over 40 years old with H. pylori (cagA) infection.
- Participants underwent treatment with a triple regimen to eradicate H. pylori.
- Assessment included baseline and post-treatment measurements of CRP, homocysteine (tHcy), folate, and vitamin B12, with H. pylori status confirmed by urea breath test (UBT).
Main Results:
- H. pylori eradication was successful in most participants (all but 3).
- A significant decrease in CRP levels was observed 2 months after H. pylori eradication (p=0.02).
- Obese individuals (BMI > 27) showed a more pronounced CRP reduction compared to leaner subjects, though CRP remained higher in the obese group post-eradication.
Conclusions:
- Chronic H. pylori infection is a significant contributor to systemic inflammation in African Americans.
- Eradication of H. pylori can reduce systemic inflammation, potentially mitigating risks for associated chronic diseases.
- Adiposity plays a residual role in maintaining elevated CRP levels even after H. pylori clearance.
Abstract:
African Americans are more susceptible to develop insulin resistance, obesity, Type 2 Diabetes, and coronary heart disease (CHD), and systemic inflammation is central to the pathophysiology of these chronic diseases. African Americans are also more likely to contract H. pylori (cagA) infections during their childhood. However, the contribution of H. pylori infection to the degree of overall systemic inflammation in these chronic diseases is not known. Therefore, we studied 46 apparently healthy African Americans, over 40 years of age who were, infected with H. pylori (cagA). These volunteers were assessed at baseline and after treatment with triple regimen drug therapy to eradicate H. pylori. All but 3 subjects were found to be free of this infection by urea breath test (UBT) after the treatment period. No hyperhomocysteinemia was found in these subjects and there were no significant changes in the level of homocysteine (tHcy), folate and B(12); however, CRP levels measured by high sensitivity assay showed a significant (p=0.02) decrease 2 months after the eradication. We further stratified CRP values according to the BMI < 27 and > 27. There was more profound reduction in CRP in the more obese group (i.e., BMI>27) from 54.26 ± 23.67 to 18.73 ± 17.39 mg/l (p=0.01), compared with the leaner subjects in whom CRP decreases from 8.88 ± 6.23 to 4.94 ± 6.21 mg/L (p=0.04), after eradication of the H. pylori (cagA) infection. The level of CRP, however, remained significantly higher in the obese subjects even after the eradication of this infection, indicative of a smaller residual influence of adiposity on CRP. Thus, a major component of systemic inflammation in African Americans may be attributable to chronic H. pylori infection.
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