Gastric Antral Vascular Ectasia Pathogenesis and the Link to the Metabolic Syndrome
Purpose of Review
Gastric antral vascular ectasia (GAVE) is a well-described source of chronic blood loss. We aim to review the previously hypothesized etiologies of GAVE and focus on recent proposed mechanisms, including metabolic syndrome. We will support these theories with newly discovered clinical associations and possible therapeutic implications.
Historically, GAVE has been associated with connective tissue disease and liver disease. Based on these associations and its histologic appearance, GAVE has presumed to be caused by mechanical- and hormonally mediated injury. Recent findings have been notable for a clinical association with aspects of the metabolic syndrome. Therefore, the pathogenic etiology may be akin to aspects of the metabolic syndrome via microvascular injury and neoangiogenesis.
The potential etiologies of GAVE include hypergastrinemia, mechanical injury, and microvascular injury with neovascular proliferation particularly in the metabolic syndrome. Further research is needed to evaluate these proposed mechanisms and potential targets for treatment.
KeywordsGAVE Gastric antral vascular ectasia Metabolic syndrome Pathophysiology Motility Gastrin
Compliance with Ethical Standards
Conflict of Interest
The authors declare that they have no conflict of interest.
Human and Animal Rights and Informed Consent
This article does not contain any studies with human or animal subjects performed by any of the authors.
Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major Importance
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