Gastric Antral Vascular Ectasia: An Ongoing Case

Lan S. Wang, MD; David M. Feldman, MD; David L. Carr-Locke, MD


January 11, 2011


Gastric antral vascular ectasia (GAVE) is a relatively rare cause of gastrointestinal (GI) bleeding that mainly affects women aged 70 years and older. Despite the obscurity of its true incidence, a large case series has found that GAVE accounts for 4% of upper GI bleeding.[1] Comorbid conditions include autoimmune disease (eg, systemic sclerosis), liver cirrhosis, renal failure, and heart disease.

GAVE was first described in 1953 by Rider and colleagues[2] as "an erosive type of atrophic gastritis with marked veno-capillary ectasia." Three decades later, in 1984, Jabbari and colleagues[3] coined the term "watermelon stomach" to describe the classic endoscopic appearance. Soon thereafter, the distinctive histologic characteristics of mucosal vascular ectasia (due to increases in both the size and number of capillaries), intravascular fibrin microthrombi, and fibromuscular hyperplasia (due to spindle cell proliferation) were defined.[4]

The etiology of GAVE remains incompletely described. Theories include: (1) mechanical stress due to increased gastric peristalsis; (2) spindle cell proliferation due to hypergastrinemia, which is frequently observed in GAVE patients, leading to a rise in venous hydrostatic pressure; and (3) local proliferation of neuroendocrine cells, producing high levels of vasoactive substances (eg, vasoactive intestinal polypeptide and serotonin) that lead to vascular dilation.

The most common clinical presentation of GAVE is chronic occult bleeding that leads to symptomatic iron deficiency anemia, although acute massive bleeding has also been documented. Frequently, the patient is unresponsive to iron repletion therapy alone and becomes transfusion dependent.

Endoscopic appearance is usually sufficient to establish this diagnosis. In cases of uncertainty, biopsy can be helpful. Westerhoff and colleagues[5] described immunohistochemical staining for vascular markers CD31 and CD34 as well as the platelet marker CD61 to help highlight the increased mucosal microvessel density and microthrombi. In patients with cirrhosis, portal hypertension, and bleeding antral lesions with an unusual appearance, this technique can help to distinguish GAVE from portal hypertensive gastropathy. This distinction is crucial because successful treatment of portal hypertension is curative in portal hypertensive gastropathy but useless in GAVE.

Treatment of GAVE with medications such as beta blockers, corticosteroids, progesterone and estrogen, octreotide, tranexamic acid, thalidomide, and cyproheptadine has been reported in small series with mixed results.

Although surgery (ie, antrectomy) is frequently curative, it remains the treatment of last resort due to high rates of morbidity and mortality. The risk is partially attributed to the advanced age and severe comorbidities seen in GAVE patients. However, risk may decrease with newer techniques such as laparoscopic surgery. Although endoscopic treatments such as heater probe coagulation and neodymium:yttrium-aluminum-garnet laser therapy have been successfully used in the past, they have been largely replaced by argon plasma coagulation (APC). Compared with older modalities, APC can treat larger areas at a time, has more symmetrical spread of treatment, and boasts lower rates of complication. Within the past 2 years, novel endoscopic treatment options such as band ligation, mucosal resection, and cryotherapy have shown great promise.

The following case describes a 66-year-old man with a fairly typical presentation of GAVE.