Published online Aug 8, 2020. doi: 10.4292/wjgpt.v11.i3.40
Peer-review started: January 14, 2020
First decision: April 8, 2020
Revised: May 11, 2020
Accepted: July 18, 2020
Article in press: July 18, 2020
Published online: August 8, 2020
Processing time: 203 Days and 19.1 Hours
Neovascularisation is a common feature of gastrointestinal (GI) vascular disorders with differing aetiologies and presentations; including small bowel angiodysplasia (SBA), gastral antral vascular ectasia and portal hypertensive gastropathy. These lesions are all common causes of recurrent or chronic intestinal bleeding especially in adults above 60 years. GI vascular malformations and bleeding in SBA have been associated with varying disturbances in angiogenesis, however, the precise mechanisms underlying these conditions remain unclear. Our hypothesis is that response to a variety of upstream triggers including portal hypertension, hypoxia and inflammation, which may be regulated at a local level by common angiogenic regulators including Angiopoietin 1 (Ang-1), Ang-2 and vascular endothelial growth factor (VEGF) may be responsible for these conditions.
At present, the precise mechanisms underlying these conditions remain unclear and assessment of angiogenic factors across several GI vascular disorders associated with recurrent bleeding and anaemia has not been reported. In addition, there is currently no specific treatment for these vascular conditions, the development of which is limited by a deficient knowledge of the underlying pathophysiology.
The overarching aim of our work is to identify angiogenic factors associated with the condition which may be useful both as diagnostic and prognostic markers and as future treatment targets.
Using enzyme-linked immunosorbent assay, concentrations of Ang-1, Ang-2 and VEGF were measured from 2 serum tubes of blood using standard phlebotomy techniques. Categorical data was compared with a Chi2 Test. Serum levels of angiogenic factors were expressed as a mean and compared between groups using the Student t-test. Results were controlled for patient demographics including age, gender and haemoglobin level. A P value of < 0.05 was considered significant.
We observed a common reduction in Ang-1 levels and elevation in Ang-2 levels across several GI vascular disorders compared to controls. Differences in Ang-1/Ang-2 ratios among vascular disorders compared to controls suggest disease-specific modulation. This warrants further investigation as potential biomarkers and therapeutic targets.
Our novel pilot study shows the common alteration in Ang-1 and Ang-2 levels across a variety of GI disorders. This suggests that the modulation of these angiogenic factors may play a vital role in these GI vascular conditions. This shows the value of these factors as potential biomarkers and therapeutic targets.
Targeting these angiogenic factors could potentially serve as diagnostic or prognostic biomarkers and therapeutic targets in a clinical setting.