Gastric Antral Vascular Ectasia (GAVE)

Overview

Gastric antral vascular ectasia (GAVE, “watermelon stomach”) is a rare but important cause of non-variceal upper gastrointestinal bleeding, often presenting with chronic iron-deficiency anaemia or recurrent overt bleeding in older adults, particularly women [1–4]. It is frequently associated with systemic conditions such as liver cirrhosis (~30% of cases) and autoimmune/connective-tissue disease (especially systemic sclerosis). Although GAVE is often seen in patients with portal hypertension, it is pathophysiologically distinct from portal hypertensive gastropathy. Untreated, GAVE can lead to transfusion-dependent anaemia, hemodynamically significant upper GI haemorrhage, and procedure-related morbidity.^[1–4,7]

Anatomy and Physiology

• Gastric regions
  • Antrum is the distal stomach between incisura and pylorus; functions as a pump and grinder.
  • Contains thick circular muscle and prominent longitudinal folds, creating high mechanical stress during peristalsis.
    
• Vascular supply & drainage
  • Arterial supply from right and left gastric and gastroepiploic arteries; submucosal arterioles give rise to dense mucosal capillary plexus.
  • Venous drainage via submucosal veins → left and right gastric veins → portal venous system; pressure changes in portal system influence antral venous congestion.
    
• Mucosal defence & blood-flow regulation
  • Gastric mucosal blood flow is regulated by prostaglandins, nitric oxide, and neurohumoral factors in response to acid, food, and mechanical stimuli.
  • Adequate microcirculation is essential for epithelial repair; chronic congestion or shearing can remodel capillaries and venules.
    
• Antral motility
  • Strong phasic contractions mix chyme and drive it through pylorus; repetitive shearing forces act along longitudinal folds where vessels run.
  • Neurohormonal modulators (gastrin, VIP, prostaglandins) affect both motility and mucosal blood flow.

Aetiology and Risk Factors

Aetiology (multifactorial, incompletely understood)

• Chronic mechanical stress from strong antral peristalsis → repeated mucosal prolapse and trauma along longitudinal folds, promoting vascular ectasia and fibromuscular hyperplasia.
• Abnormal antral motility and gastric emptying, including “antral pump” dysfunction, possibly mediated by neurohormonal factors.
• Microvascular injury and remodeling driven by mucosal ischemia–reperfusion, venous congestion, and altered mucosal repair.
• Autoimmune-mediated microangiopathy in systemic sclerosis and other autoimmune diseases (e.g. anti–RNA polymerase III–positive SSc).[5]
• Contribution of portal hypertension in a subset of patients (especially cirrhotics), but GAVE can occur without portal hypertension and often persists despite portal-pressure reduction.[1,9,11]
• Possible hormonal influences (e.g. hypergastrinaemia, prostaglandins, vasoactive peptides) altering mucosal blood flow and angiogenesis.[1,3,6]
  

Risk factors

• Older age (typically >60–70 years).
• Female sex (female:male ~2:1).
• Liver cirrhosis and portal hypertension of any aetiology (~30% of GAVE patients).
• Autoimmune/connective-tissue disease: systemic sclerosis, primary biliary cholangitis, SLE, Sjögren’s, Raynaud’s phenomenon.
• Chronic kidney disease (especially dialysis-dependent).
• Cardiovascular disease and chronic heart failure.
• Metabolic disorders: type 2 diabetes mellitus, NAFLD/NASH-related cirrhosis.
• Bone-marrow transplantation, chronic immunosuppression.

Pathophysiology 

• Predisposing milieu
  • Systemic factors (cirrhosis, autoimmune disease, CKD, metabolic and vascular disease) alter hemodynamics, microvasculature, and repair capacity.
  • Antral hypermotility and mucosal prolapse increase mechanical shear at the distal antrum.
    
• Microvascular injury & congestion
  • Repetitive mucosal trauma and venous congestion cause focal capillary and venule dilation in lamina propria.
  • Increased mucosal blood flow and stasis favour microthrombi formation.
    
• Structural remodeling
  • Lamina propria develops:
    • Marked capillary/venule ectasia with fibrin thrombi.
    • Fibrohyalinosis and spindle-cell (smooth-muscle/fibroblast) proliferation → fibromuscular hyperplasia.
  • These changes produce elevated, friable longitudinal ridges or diffuse nodular/“honeycomb” mucosa.
    
• Clinical bleeding
  • Fragile ectatic vessels rupture with minor trauma or acid exposure → chronic occult bleeding (most common) or episodic overt haematemesis/melena.
  • Recurrent microbleeds cause iron-deficiency anaemia; severe lesions or superimposed coagulopathy can lead to acute massive haemorrhage.

Clinical Manifestations

• Chronic iron-deficiency anaemia (most common presentation)
• Overt upper GI bleeding: melena, haematemesis, “coffee-ground” vomiting (less frequent)
• Recurrent need for blood transfusions or IV iron despite PPI therapy.
• Non-specific upper GI symptoms: dyspepsia, early satiety, epigastric discomfort
• Symptoms/signs from associated conditions
  • features of cirrhosis (ascites, jaundice, encephalopathy)
  • systemic sclerosis (sclerodactyly, telangiectasia, Raynaud’s).

Diagnosis

Investigations

• FBC: microcytic hypochromic anaemia, sometimes normocytic in mixed disease.
• Iron studies: low ferritin, low transferrin saturation (iron-deficiency pattern).
• Coagulation profile, liver and renal function, autoimmune serology (context dependent).

Upper GI endoscopy (gold standard)

• Characteristic antral pattern of flat or slightly raised erythematous lesions:
  • Linear/striped (“watermelon stomach”) – red stripes radiating from pylorus along folds.
  • Diffuse/punctate (“honeycomb/diffuse GAVE”) – multiple red spots diffusely involving antrum, sometimes proximal extension.
  • Nodular GAVE – polypoid/nodular lesions overlapping with hyperplastic polyps.
• Lesions confined predominantly to antrum (may rarely extend proximally).
• Absence of typical PHG mosaic pattern in corpus/fundus.
  
• Histology – when diagnosis uncertain
  • Mucosal capillary and venule ectasia in lamina propria.
  • Fibrin thrombi within ectatic vessels.
  • Fibrohyalinosis and spindle-cell (smooth-muscle/fibroblast) proliferation.
  • Minimal inflammation.
    

Differential diagnosis

Condition	Typical site	Endoscopic pattern	Histology	Response to portal-pressure reduction (beta-blocker/TIPS)
GAVE	Antrum (± pylorus)	Linear “watermelon” stripes, diffuse “honeycomb”, or nodular lesions	Ectatic mucosal vessels with fibrin thrombi + fibromuscular hyperplasia (GAVE score >3)	Usually minimal
Portal hypertensive gastropathy (PHG)	Fundus & body	Mosaic “snakeskin” pattern with red/black spots	Non-specific congestion; no classic GAVE triad	Improves with reduced portal pressure
Gastric antral angiodysplasia (isolated)	Focal anywhere, including antrum	Isolated red spots or patches, not organised as stripes	Dilated vessels; lacks fibrohyalinosis pattern	Variable

Classification 

Endoscopic morphological classification

• Linear/striped GAVE (“watermelon type”) – longitudinal red stripes radiating from pylorus along antral folds; commonly described in non-cirrhotic and autoimmune patients.
• Diffuse/punctate GAVE (“honeycomb/ring pattern”) – innumerable small red spots or rings diffusely involving antrum, especially in cirrhosis and portal hypertension.
• Nodular GAVE – polypoid or nodular lesions with overlapping histologic features of gastric hyperplastic polyps; important because it may be mistaken for neoplasia.

Treatment

General principles

• Control acute bleeding
• Correct anaemia and iron deficiency
• Reduce recurrent bleeding and transfusion needs
• Treat underlying systemic disease.

Supportive / medical

• Resuscitation in acute bleeding: IV fluids, blood transfusions, correction of coagulopathy as per standard UGIB protocols.
• Iron replacement: oral or IV iron to correct deficiency; often needed long-term.
• Proton-pump inhibitors (PPIs): widely used to promote mucosal healing after ablation, although they do not treat GAVE per se.
• Blood transfusion
• Pharmacologic options with limited evidence (generally adjunctive/rescue)
  • Octreotide (especially in portal-hypertensive settings; benefit inconsistent).
  • Estrogen–progesterone therapy, tranexamic acid, or thalidomide described in case series; reserved for refractory cases due to adverse-effect profiles.

Endoscopic therapy – first-line definitive treatment

• Argon plasma coagulation 
• Endoscopic band ligation
• Radiofrequency ablation

Surgical / radiologic options

• Antrectomy or total gastrectomy
• Portal-pressure reduction (TIPS, surgical shunts, NSBBs)
  • Standard for PHG and varices, but inconsistent or minimal effect on GAVE; not primary therapy for GAVE, though may help coexisting PHG.

Management of underlying disease

• Optimise cirrhosis care (alcohol abstinence, viral suppression, metabolic control).
• Systemic sclerosis or other autoimmune diseases as per rheumatology guidance.

Complications & Prognosis

Complications

• Chronic transfusion-dependent iron-deficiency anaemia → iron overload, alloimmunisation, transfusion reactions.
• Acute massive upper GI bleeding → haemodynamic instability, ICU admission, increased mortality risk.
• Procedure-related: post-APC or RFA ulceration, pain, rare perforation or antral stenosis; post-EBL ulcer bleeding; anaesthesia/sedation risk.
• Surgical: anastomotic leak, infection, nutritional deficiencies, perioperative death
• Ongoing burden of frequent hospitalisations, endoscopies, and transfusions.

Prognosis

• Many patients have multiple comorbidities (liver disease, CKD, cardiovascular disease), but in-hospital mortality from GAVE-related bleeding is relatively low when managed appropriately
• Despite treatment, up to ~60% may remain at least intermittently transfusion-dependent, particularly those with advanced cirrhosis or diffuse disease.
• Long-term outcome largely driven by underlying conditions (e.g. severity of cirrhosis or systemic sclerosis) rather than GAVE alone.
• Favorable prognostic indicators: non-cirrhotic status, good response to endoscopic therapy with stabilised haemoglobin, fewer comorbidities.
• Poor prognostic indicators: decompensated cirrhosis, diffuse/ring-like GAVE requiring frequent transfusions, failure of multiple endoscopic modalities, need for surgery.

References 

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2. Cavallaro A, Tarantino I, Luca A, et al. Recurrent gastric antral vascular ectasia: a single center experience. Front Surg. 2024;11:1356409.
3. Kichloo A, El-Amir Z, Dahiya DS, et al. Gastric antral vascular ectasia: trends of hospitalizations and outcomes in the USA. Gastroenterology Res. 2021;14(4):244-52.
4. Patel U, Desai R, Desai J, et al. Predictors of blood transfusion and in-hospital outcomes in patients with gastric antral vascular ectasia: a nationwide population-based analysis. Ann Transl Med. 2019;7(3):46.
5. Parrado RH, Furst DE, Maranian P, Clements PJ. Gastric antral vascular ectasia in systemic sclerosis: a review. Int J Rheumatol. 2015;2015:762546.
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