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Gastric antral vascular ectasia (GAVE): an update on clinical presentation, pathophysiology and treatment
Christian P Selinger1, Yeng S Ang
1Department of Gastroenterology, Royal Albert Edward Infirmary, Wigan, UK. christian.selinger@web.de
Gastric antral vascular ectasia (GAVE), though a rare disorder, causes up to 4% of non-variceal upper GI bleeding. This paper gives an overview of studies examining clinical presentation and pathophysiology, and reviews the current evidence for invasive and non-invasive treatments. GAVE is often associated with systemic illnesses, such as cirrhosis of the liver, autoimmune connective tissue disorders, bone marrow transplantation and chronic renal failure. The pathophysiological changes leading to GAVE have not been fully explained and remain controversial. Patient presentation varies from chronic iron-deficiency anaemia to heavy acute gastrointestinal bleeding. It is important to differentiate GAVE from portal hypertensive gastropathy as GAVE does not respond to measures reducing portal pressures. Endoscopic ablation (Nd:YAG-laser or argon plasma coagulation) is the first-line treatment of choice. As evidence for pharmacological therapy with oestrogen (and/or progesterone), tranexamic acid or thalidomide stems from case reports only, these should be used if endoscopic measures have failed to stop chronic blood loss. Surgical antrectomy should be reserved for unresponsive cases as it is associated with a high mortality. Ultimately, treatment of the underlying medical co-morbidities may lead to resolution of GAVE.
Gastric antral vascular ectasia (GAVE), though a rare disorder, causes up to 4% of non-variceal upper GI bleeding. This paper gives an overview of studies examining clinical presentation and pathophysiology, and reviews the current evidence for invasive and non-invasive treatments. GAVE is often associated with systemic illnesses, such as cirrhosis of the liver, autoimmune connective tissue disorders, bone marrow transplantation and chronic renal failure. The pathophysiological changes leading to GAVE have not been fully explained and remain controversial. Patient presentation varies from chronic iron-deficiency anaemia to heavy acute gastrointestinal bleeding. It is important to differentiate GAVE from portal hypertensive gastropathy as GAVE does not respond to measures reducing portal pressures. Endoscopic ablation (Nd:YAG-laser or argon plasma coagulation) is the first-line treatment of choice. As evidence for pharmacological therapy with oestrogen (and/or progesterone), tranexamic acid or thalidomide stems from case reports only, these should be used if endoscopic measures have failed to stop chronic blood loss. Surgical antrectomy should be reserved for unresponsive cases as it is associated with a high mortality. Ultimately, treatment of the underlying medical co-morbidities may lead to resolution of GAVE.
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