Helicobacter Pylori Infection Correlates with Risk of Abdominal Aortic Aneurysm
The H. pylori bacterium is famously associated with stomach ulcers; a researcher gave himself stomach ulcers by drinking a mix containing H. pylori to prove the point, in one of the more widely publicized self-experiments of recent history. Here, researchers review the evidence for H. pylori infection to correlate with the risk of suffering an aneurysm of the abdominal aorta. An aneurysm is a weakened blood vessel wall that forms a bulge at risk of rupture. In a major vessel such a rupture is frequently fatal. Inflammatory signaling is thought to be involved in the formation of an aneurysm, so one can consider that the persistent presence of a pathogen such as H. pylori may contribute via their effects on the inflammatory environment. There may be other mechanisms involved, however.
Abdominal aortic aneurysm (AAA) is a condition of considerable clinical importance, characterized by the dilation and weakening of the abdominal aorta. While several risk factors have been identified, recent studies have suggested a potential link between Helicobacter pylori infection (HPI) and the development of AAA. Abdominal aortic aneurysms pose a significant public health challenge, particularly among the elderly population. The prevalence of AAA increases with age, affecting a total of 35.12 million individuals, and its rupture can lead to catastrophic outcomes, including massive internal hemorrhage and mortality. Identifying modifiable risk factors is crucial for prevention and early intervention. Traditionally associated with gastric ulcers and gastritis, H. pylori is a bacterium that colonizes the gastric mucosa. However, recent investigations have explored its potential involvement in other systemic conditions, including cardiovascular diseases. It is hypothesized that chronic inflammation induced by H. pylori infection may contribute to the pathogenesis of AAA.
This study aims to quantify the association between Helicobacter pylori (H. pylori) infection and AAA development through a systematic review and meta-analysis, emphasizing numerical results for clarity. Following PRISMA guidelines, PubMed, SCOPUS, Medline, and Embase searches were conducted. Data extraction and quality assessment were performed using standardized tool. Among the 8 selected studies, H. pylori infection exhibited a statistically significant overall risk ratio of 1.54 for AAA development. Subgroup and sensitivity analyses were conducted to address high heterogeneity, revealing consistent results. These findings underscore the importance of further research to elucidate underlying mechanisms and inform preventive strategies and interventions aimed at mitigating the risk of AAA in individuals with H. pylori infection.