RT Journal Article
SR Electronic
T1 ADTU-04 Faecal calprotectin in PSC-IBD: a novel marker of cholangitis
JF Gut
JO Gut
FD BMJ Publishing Group Ltd and British Society of Gastroenterology
SP A61
OP A61
DO 10.1136/gutjnl-2018-BSGAbstracts.120
VO 67
IS Suppl 1
A1 Polychronis Pavlidis
A1 Yasser El-Sherif
A1 Ben Warner
A1 Shraddha Gulati
A1 Konstantinos Sarras
A1 Ellie Alberts
A1 Joe Segal
A1 Tamir Rashid
A1 Phil Harrison
A1 John Devlin
A1 Michael Heneghan
A1 Alberto Fueyo
A1 Gwion Emlyn
A1 Hadil Abu Arqoub
A1 Patrick Dubois
A1 Deepak Joshi
A1 Nick Powell
A1 Bu’ Hayee
YR 2018
UL http://gut.bmj.com/content/67/Suppl_1/A61.1.abstract
AB Introduction Primary sclerosing cholangitis (PSC) is a chronic inflammatory condition of the bile ducts leading to fibrosis and end stage liver disease. A lack of robust non-invasive biomarkers has been hindering disease monitoring and development of optimal therapies. We have previously noted that the high levels of faecal calprotectin (fcal) seen in PSC-IBD patients belie the mild or quiescent intestinal inflammation. An unsupervised proteomics study identified biliary calprotectin as a potential biomarker. Here, we test the hypothesis that fcal is a marker of biliary injury in PSC.Methods We analysed paired endoscopic activity data (UCEIS) and fcal results of patients with PSC-IBD (n=20) or UC (n=20) who underwent colitis surveillance in the context of a colitis surveillance pilot study. Relevant clinical data was recorded prospectively. Recruiting consecutive patients attending for ERCP (n=6) allowed for the concomitant testing of biliary and faecal calprotectin.Results As expected, fcal strongly correlated with severity of mucosal injury (UCEIS) in UC [r=0.82, 95% CI(0.58, 0.92), p<0.0001]. However, the correlation was weaker in PSC-IBD [r=0.59, 95% CI(0.19, 0.82), p=0.006]. Moreover, in patients with PSC-IBD and quiescent colitis (UCEIS: 0–1) fcal concentration was significantly higher in comparison to UC patients with comparable endoscopic activity [279 ug/g (10, 1560) vs. 30 (10, 161), p=0.015)]. A trend towards abnormal liver biochemistry was seen in those PSC-IBD with higher fcal [ALP: 250IU/L (113, 561) vs. 83 (59, 170), p=0.06, GGT: 351 U/L (117, 1014) vs. 51 (29, 153) p=0.02, AST: 53 U/L (26, 85) vs. 37 (22, 43), p=ns]. UC patients with quiescent colitis and fcal >150 had a higher risk of colitis relapse in 12 months [HR=7.6, 95% CI(1.8, 33.6)] in comparison to those with fcal <150. However, in patients with PSC-IBD and quiescent colitis a fcal >150 was associated instead with a higher risk of cholangitis associated complications (need for antibiotics or stent insertion), HR=6.5, 95% CI(1.3, 33.9). Strikingly, biliary calprotectin concentration showed a strong correlation with fcal concentration (r=0.90, p=0.04). Interestingly, immunostaining of biliary brushings for calprotectin demonstrated positive staining in cholangiocytes as well as neutrophils and macrophages.Conclusion In patients with PSC-IBD and quiescent colitis the identification of a raised fcal is likely to herald complications of inflammation in the bile ducts rather than the colon. In this setting, fcal may be a valuable prognostic biomarker of cholangitis. Additionally, our data suggest that in PSC, the source of raised fcal may also be the damaged biliary epithelium.