Abstract
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.
Published Version
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