Gastric antral vascular ectasia

An 84-year-old male was admitted in September 2009 with exertional dyspnoea and chest pain. He had a history of hypertension, carotid artery stenosis and colonic polyps. 

Presentation

Clinical examination was unremarkable. CXR was normal. Electrocardiogram showed sinus rhythm. Troponin I was negative. Haemoglobin was 9.0g/dI with hypochromic, microcytic picture. Platelets and international normalisation ratio were normal. Iron was low (3.6), as was ferritin level (14.1). Renal and liver function tests were normal. 

CT scan of abdomen and pelvis did not show any significant abnormality. Oesophagogastroduodenoscopy (OGD) showed gastritis at cardia, pyloric erythema with distended intramucosal vessels, and no active bleeding. Colonoscopy showed diverticular disease in the sigmoid colon and a small polyp in the transverse colon. Histological examination of the antral gastric biopsy showed focal intestinal metaplasia. Biopsy from the cardia showed normal morphology. Histological examination of the colonic polyp showed tubular adenomatous polyp. 

Treatment

The patient was treated with iron infusion and proton pump inhibitors. Repeated upper GI endoscopy in November 2009 showed the characteristic appearance of severe gastric antral vascular ectasia (GAVE), an uncommon but significant cause of severe acute or chronic gastrointestinal blood loss. The syndrome was first described in 1953 by Rider et al regarding a gastrectomy specimen of an elderly woman as “an erosive type of gastritis with marked venocapillary ectasia”.

In 1984, Jabbari et al defined GAVE as “longitudinal antral folds converging on the pylorus, containing visible columns of tortuous red ectatic vessels”.² Histological appearances were described as hyperplasia of the mucosa with capillary ectasia and thrombosis, fibromuscular hyperplasia of the lamina propria and abnormal vessels in the submucosa.

Physical and internal symptoms

GAVE is sometimes called ‘watermelon stomach’ because the characteristic endoscopic appearance of longitudinal rows of flat, reddish stripes is suggestive of a watermelon. The red stripes represent ectatic and sacculated mucosa vessels.³ The common clinical presentations are:

• Iron deficiency anaemia (88%)
• Faecal occult blood (FOB) positive (42%)
• Melena (15%)
• Haematemesis (3%)
• And, rarely, haematochezia (1%).⁴

There is a single report of GAVE presenting with gastric outlet obstruction.⁵

Most patients with GAVE suffer from chronic medical conditions. Liver cirrhosis is found in 30% of GAVE patients.⁶ At endoscopy, GAVE requires careful discrimination from portal hypertensive gastropathy. An association with autoimmune diseases, particularly atrophic gastritis and achlorhydria, is recognised.⁷ Other associations include:

• Scleroderma
• Bone-marrow transplantation
• Chronic renal failure
• Ischaemic heart disease
• Hypertension
• Valvular heart disease
• Familial Mediterranean fever
• Acute myeloid leukaemia.

Common misdiagnosis

It is widely believed that GAVE is under-recognised and is often misinterpreted as antral gastritis.⁸ Four distinct endoscopic patterns have been described. Most patients have antral disease with classic raised ridges covered by ectatic vascular tissue radiating out from the pylorus. Other patterns include lesions arranged in radiating flat stripes, scattered multiple mucosal lesions, or a mixture of the above patterns.

The treatment options for GAVE include pharmacological, surgical and endoscopic therapies. Some of the pharmacological treatments that have been reported are corticosteroid, hormonal therapy, octreotide and tranexamic acid. However, these were mainly case reports or small case series.⁷

Endoscopic therapy is the mainstay of conservative treatment. Endoscopic coagulation with a heater probe, gold probe, argon plasma coagulator or laser therapy obliterates the vascular ectasia and decreases the degree of bleeding. 

Endoscopic band ligation has also been reported. Surgical resection provides the most definite therapy for GAVE, and antrectomy is by far the most used procedure. However, surgery has significant morbidity and mortality, as most patients are elderly with significant comorbid illnesses.

References

1. Rider JA, Klotz AP, Kirsner JB. Gastritis with veno-capillary ectasia as a source of massive gastric haemorrhage. Gastroenterol 1953; 24: 118-123
2. Jabbari M, Cherry R, Lough JO et al. Gastric antral vascular ectasia: the watermelon stomach. Gastroenterol 1984; 87: 1165–1170
3. Ito M, Uchida Y, Kamano H, Nishioka M. Clinical comparisons between two subsets of gastric antral vascular ectasia. Gastrointes Endosc 2001; 53(7): 764-770
4. Gretz JE, Achem SR. The watermelon stomach: Clinical presentation, diagnosis, and treatment. Am J Gastroenterol 1998; 93: 890-895
5. Tuveri M, Borsezio V, Gabbas A, Mura G. Gastric antral vascular ectasia. An unusual cause of gastric outlet obstruction. Surgery Today 2007; 37: 503-505
6. Ward EM, Raimondo M, Rosser BG et al. Prevalence and natural history of gastric antral vascular ectasia (GAVE) in patients undergoing orthoptic liver transplantation. J Clin Gastroenterol 2004; 38: 898-900
7. Calam J, Klotz AP, Kirsner JB. Gastritis with venocapillary ectasia as a source of massive gastric haemorrhage. Gastroenterology 1953; 24: 118-123
8. Gostout CJ, Viggiano TR, Ahlquist DA et al. The clinical and endoscopic spectrum of the watermelon stomach. J Clin Gastroenterol 1992; 15: 256-632