Antral mucosal perfusion is not increased in GAVE

ABSTRACT

Objectives: Although a common cause of intestinal blood loss, the pathophysiology of gastric antral vascular ectasia (GAVE) is not well understood. We aimed to evaluate gastric antral and body mucosal flow in GAVE patients compared to a control population using laser Doppler flowmetry.

Methods: 27 patients with GAVE and 11 control patients without GAVE were evaluated using an endoscopic LDF probe. The probe was placed in the gastric antrum and body in order to calculate standardized mucosal flow rates recorded as perfusion units (PU).

Results: Despite its hyperemic appearance and propensity to bleed, antral blood flow was not increased in GAVE: 115.5 PU (IQR: [94.4, 135.9 PU]) in GAVE versus 123.7 PU (IQR: [109.7, 186.5 PU]) in controls. There was a significant gradient between the gastric body and antral blood flow in GAVE (p < 0.001) that was not evident in controls.

Conclusion: These results indicate that antral mucosal blood flow is not increased in GAVE despite its grossly hyperemic appearance. A mild but statistically significant gradient was noted between the gastric antrum and body in patients with GAVE compared to controls. The pathophysiological significance of this finding is uncertain.

KEYWORDS:

• GAVE
• watermelon stomach
• anemia
• PPI
• gastric mucosal perfusion

Acknowledgments

The authors would like to acknowledge the support and guidance of Drs. Patrick Northup and Abdullah M. S. Al-Osaimi, Mr. Kevin Mays and the UVA endoscopy staff and the late Mr. Jack Chambers who provided philanthropic support, which made the work possible.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Additional information

Funding

This work was supported by the Philanthropy of Jack Chambers’ contribution to the UVA Hepatology Research fund.