Non-gastrointestinal consequences of Helicobacter pylori infection
1Department of Public Health Sciences, St George's Hospital Medical School, London, UK.
Abstract:
Evidence relating H. pylori to non-gastrointestinal disease is sparse and inconclusive. Suggested mechanisms whereby infection might increase cardiovascular risk include release of acute-phase reactants including fibrinogen, reduction of HDL cholesterol, elevation of homocysteine levels and immunological cross-reactivity between bacterial and human heat shock proteins. Six published studies relating H. pylori seropositivity to various measures of ischaemic heart disease (IHD)-angiography, acute myocardial infarction, angina symptoms, or electro-cardiographic abnormalities-are all consistent with a modest (up to 2-fold) elevation in risk of IHD among infected subjects after adjustment for age, socioeconomic status and conventional cardiovascular risk factors. The pooled odds ratio from 1 longitudinal, 3 case-control and 2 cross-sectional studies is 1.4 (95% confidence interval 1.1-1.8). Further large-scale longitudinal studies are required to quantify the predictive value of seropositivity, to clarify the causal interpretation and to assess the underlying mechanisms for any link between H. pylori infection and ischaemic heart disease.
More Related Videos
10:44One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
Published on: June 18, 2016
08:24Profiling Luminal pH in Three-Dimensional Gastrointestinal Organoids Using Microelectrodes
Published on: July 5, 2024
Related Concept Videos
Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Peptic Ulcer
Gastritis II: Pathophysiology
Peptic Ulcer Disease II: Pathophysiology
Peptic Ulcer Disease III: Clinical Manifestations and Complications
