P099 Neutrophil gelatinase-associated lipocalin (NGAL) as biomarker in collagenous colitis

G.A. Walaas1, I. Bakke1,2, A.V. Granlund1,3, C. Escuderos-Hernândez4, T. Bruland1,2, E.S. Røyset1,5, S. Thorsvik2,6, A. Münch4,7, A.E. Østvik1,2,6, A.K. Sandvik1,2,3,6

1Norwegian University of Science and Technology, Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Trondheim, Norway, 2St. Olav’s University Hospital, Clinic of Medicine, Trondheim, Norway, 3Norwegian University of Science and Technology, Centre of Molecular Inflammation Research, NTNU, Trondheim, Norway, 4Linköping University, Department of Biomedical and Clinical Sciences BVK, Linköping, Sweden, 5St. Olav’s University Hospital, Department of Pathology, Clinic of Laboratory Medicine, Trondheim, Norway, 6St. Olav’s University Hospital, Department of Gastroenterology, Clinic of Medicine-, Trondheim, Norway, 7Linköping University Hospital, Department of Gastroenterology and Hepatology, Linköping, Sweden


Neutrophil gelatinase‐associated lipocalin (NGAL) is upregulated in the intestinal epithelium in inflammatory bowel disease and is a biomarker with sensitivity and specificity comparable to calprotectin. Microscopic colitis (MC) is a common cause of chronic, watery diarrhoea and represents an inflammatory bowel disease with unknown aetiology and pathogenesis. Diagnosis depends on histological evaluation of colonic biopsies. There is a need for non-invasive diagnostic tools, and this study examines the potential of NGAL as a biomarker in collagenous colitis (CC) as one of the two main histological forms of MC.


Gene expression of colonic biopsies (n = 9/group) from active CC, budesonide treated CC in clinical remission and healthy controls (HC) was explored by RNA-sequencing analysis. An extended set of colonic biopsies (n = 17–29/group) was also examined by immunohistochemistry (IHC) and in situ hybridisation (ISH). Faecal samples from the same patient groups, in addition to samples from patients with irritable bowel disease diarrhoea (IBS-D), were assayed for NGAL and calprotectin (Calpro) by ELISA.


The NGAL gene, LCN2, was significantly upregulated in active CC vs. HC (log2 2.694, fold change 6.471) adjusted p-value 0.005) and in pairs of active CC vs. treated CC LCN2 was significantly downregulated (log2 0.345, fold change −1.536), adjusted p-value 0.04). Both immunohistochemical staining and in situ hybridisation identified increased NGAL expression localised to the mucosal epithelial cells in active CC, compared with an almost absent and scarce expression in HC and treated CC, respectively. There were great individual differences in faecal concentrations of NGAL particularly in the active CC group, but the NGAL concentrations were significantly increased compared with HC, IBS-D and treated CC.


NGAL is upregulated and located mainly to the colonic epithelium of active CC and reduced in clinical remission after budesonide treatment. This is also reflected in the faecal concentrations. We propose NGAL as a valuable biomarker in evaluating the inflammatory activity related to CC and a potential faecal biomarker discriminating CC from IBS-D.