Search in the Abstract Database

Search Abstracts 2016

* = Presenting author

P054 Soluble GPVI is raised in patients with inflammatory bowel disease and anaemia

S. J. Montague1, A. Chauhan*2, E. E. Gardiner3, R. K. Andrews3, 
S. P. Watson1, T. Iqbal4

1Institute of Biomedical Research, University of Birmingham, Centre for Cardiovascular Sciences, College of Medical and Dental Sciences, Birmingham, United Kingdom, 2Centre for Liver Research, and National Institute of Health Research Birmingham Liver Biomedical Research Unit, Institute of Biomedical Research, College of Medical and Dental Science, Birmingham, United Kingdom, 3Monash University, Australian Centre for Blood Diseases, Melbourne, Australia, 4Queen Elizabeth Hospital, Department of Gastroenterology, Birmingham, United Kingdom


Iron deficiency anaemia (IDA) is common in patients with inflammatory bowel disease (IBD). Although multifactorial, chronic intestinal bleeding particularly at sites of inflammation is one of the key mechanisms accounting for iron deficiency. Platelets have been recognised to have a critical role in maintaining vascular integrity during inflammation. Further, platelet activation and thrombocytosis have been described during periods of intestinal inflammation. The immunoglobulin GPVI is a platelet receptor for collagen and fibrin that plays a critical role in maintaining vascular integrity at sites of inflammation. GPVI is shed upon platelet activation and is a recognised marker of platelet activation. In the present study, we sought to investigate whether soluble GPVI (sGPVI) levels correlate with severity of IDA and IBD. Aim: To determine if sGPVI levels correlate with either disease activity or iron deficiency anaemia in patients with active inflammatory bowel disease.


Double spun plasma was isolated from citrated blood taken from patients with inflammatory bowel disease (n = 42). sGPVI was measured in the plasma using a sGPVI sandwich enzyme-linked immunosorbent assay (ELISA). sGPVI levels in the plasma of patients were compared with healthy controls and correlated with the levels of haemoglobin, C-reactive protein (CRP), and ferritin.


sGPVI levels were significantly raised above control levels in patients with active ulcerative colitis (UC; p < 0.01) but not Crohn’s disease (CD). In addition, sGPVI levels positively correlated with the degree of anaemia in UC and CD. sGPVI levels were significantly higher in patients with haemoglobin levels < 120g/L compared with patients with haemoglobin levels >120 g/L (p < 0.01). Further, patients with more active disease (as gauged by CRP) exhibited a negative correlation between serum ferritin and sGPVI (Spearman’s r-value = -0.5).


sGPVI levels were raised in patients with active UC. In addition, there was a negative correlation between the level of sGPVI and haemoglobin, and in patients with active disease, ferritin levels negatively correlated with sGPVI. This suggests that blood loss from inflamed luminal surfaces (and the resultant iron deficiency anaemia) correlates with platelet activation. sGPVI may represent a novel marker to predict development of IDA in patients with inflammatory bowel disease.