Mucosal and faecal neutrophil gelatinase-associated lipocalin as potential biomarkers for collagenous colitis
Autor: | Elin Synnøve Røyset, Arne K. Sandvik, Celia Escudero-Hernández, Silje Thorsvik, Atle van Beelen Granlund, Ingunn Bakke, Andreas Münch, Torunn Bruland, Gunnar Andreas Walaas, Ann Elisabet Østvik |
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Rok vydání: | 2021 |
Předmět: |
Adult
Male Original Article—Alimentary Tract Budesonide China medicine.medical_specialty Colitis Collagenous Enzyme-Linked Immunosorbent Assay Microscopic colitis Gastroenterology and Hepatology Inflammatory bowel disease Gastroenterology Feces Lipocalin-2 Internal medicine Gastroenterologi medicine Humans Calprotectin Chronic diarrhoea Irritable bowel syndrome Collagenous colitis business.industry Middle Aged medicine.disease Faecal calprotectin Biomarker (medicine) Immunohistochemistry Female business Biomarkers medicine.drug |
Zdroj: | Journal of gastroenterology Journal of Gastroenterology |
ISSN: | 1435-5922 0944-1174 |
DOI: | 10.1007/s00535-021-01814-y |
Popis: | Background Collagenous colitis (CC) is an inflammatory bowel disease where chronic diarrhoea is the main symptom. Diagnostic markers distinguishing between CC and other causes of chronic diarrhoea remain elusive. This study explores neutrophil gelatinase-associated lipocalin (NGAL) and its mRNA lipocalin2 (LCN2) as histological and faecal disease markers in CC. Methods NGAL/LCN2 were studied in colonic biopsies from CC patients before and during budesonide treatment using RNA sequencing (n = 9/group), in situ hybridization (ISH) (n = 13–22/group) and immunohistochemistry (IHC) (n = 14–25/group). Faecal samples from CC (n = 3–28/group), irritable bowel syndrome diarrhoea (IBS-D) (n = 14) and healthy controls (HC) (n = 15) were assayed for NGAL and calprotectin. Results NGAL/LCN2 protein and mRNA expression were upregulated in active CC vs HC, and vs paired samples of treated CC in clinical remission. IHC and ISH localized increased NGAL/LCN2 mainly to epithelium of active CC, compared to almost absence in HC and treated CC. In contrast, calprotectin was solely expressed in immune cells. Despite great individual differences, faecal NGAL was significantly increased in active CC compared to HC, IBS-D and treated CC and had high test sensitivity. Faecal calprotectin levels were variably increased in active CC, but the values remained below usual clinical cut-offs. Conclusion NGAL/LCN2 is upregulated in the epithelium of active CC and reduced during budesonide-induced clinical remission to the level of HC and IBD-S. This was reflected in NGAL faecal concentrations. We propose NGAL as an IHC marker for disease activity in CC and a potential faecal biomarker discriminating CC from HC and IBS-D. |
Databáze: | OpenAIRE |
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