Karolinska Institutet, Department of Medicine Solna, Stockholm, Sweden; Karolinska University Hospital, Centre for Digestive Health, Department of Gastroenterology, Dermatovenereology and Rheumatology, Stockholm, Sweden.
Uppsala University, Department of Medical Sciences, Gastroenterology and Hepatology, Uppsala, Sweden.
Linköping University, Department of Biomedical and Clinical Sciences, Linköping, Sweden.
University of Gothenburg, Sahlgrenska Academy, Department of Microbiology and Immunology, Institute of Biomedicine, Gothenburg, Sweden.
Vestfold Hospital Trust, Department of Gastroenterology, Tønsberg, Norway.
Vestfold Hospital Trust, Department of Gastroenterology, Tønsberg, Norway; University of Oslo, Institute of Clinical Medicine, Oslo, Norway.
Thermo Fisher Scientific, Uppsala, Sweden; Uppsala University, Department of Medical Sciences: Respiratory, Allergy and Sleep Research, Uppsala, Sweden.
Thermo Fisher Scientific, Uppsala, Sweden.
Thermo Fisher Scientific, Uppsala, Sweden; Uppsala University, Department of Medical Sciences, Gastroenterology and Hepatology, Uppsala, Sweden.
Uppsala University, Department of Immunology, Genetics and Pathology, Uppsala, Sweden.
Gastrointestinal Genetics Lab, CIC bioGUNE - BRTA, Derio, Spain; Ikerbasque, Basque Foundation for Science, Bilbao, Spain; Department of Medicine and Surgery, LUM University, Casamassima, Italy.
University of Oslo, Institute of Clinical Medicine, Oslo, Norway; Akershus University Hospital, Department of Gastroenterology, Lørenskog, Norway.
University of Oslo, Institute of Health and Society, Oslo, Norway.
University of Oslo, Institute of Health and Society, Oslo, Norway; Oslo University Hospital, Department of Gastroenterology, Oslo, Norway.
Akershus University Hospital, Department of Gastroenterology, Lørenskog, Norway; Lovisenberg Diaconal Hospital, Department of Gastroenterology, Oslo, Norway.
Oslo University Hospital, Department of Gastroenterology, Oslo, Norway; Lovisenberg Diaconal Hospital, Unger-Vetlesen Institute, Oslo, Norway.
University of Gothenburg, Sahlgrenska Academy, Department of Microbiology and Immunology, Institute of Biomedicine, Gothenburg, Sweden.
Linköping University, Department of Biomedical and Clinical Sciences, Linköping, Sweden.
Uppsala University, Department of Medical Sciences, Gastroenterology and Hepatology, Uppsala, Sweden.
University of Oslo, Institute of Clinical Medicine, Oslo, Norway; Oslo University Hospital, Department of Gastroenterology, Oslo, Norway.
BACKGROUND AND AIMS: The diagnostic and prognostic properties of anti-integrin αvβ6 IgG autoantibodies in ulcerative colitis (UC) are poorly understood. We aimed to assess the diagnostic performance of anti-integrin αvβ6 autoantibodies and examine their association with disease outcomes.
METHODS: Serum samples from a Swedish inception cohort of patients with suspected inflammatory bowel disease (IBD, n=473) were analysed using an in-house fluorescence enzyme immunoassay based on EliA™technology. Findings were validated in a Norwegian population-based inception cohort (n=570). Diagnostic performance was assessed by calculating the area under the curve (AUC) with 95% confidence intervals (CIs) and determining sensitivity and specificity. Reclassification was evaluated using the net reclassification index.
RESULTS: In the discovery cohort, patients with UC, IBD-unclassified, or colonic Crohn's disease exhibited higher median autoantibody levels compared to symptomatic and healthy controls. In the validation cohort, the autoantibody demonstrated 79% sensitivity and 94% specificity for UC vs symptomatic controls at a cut-off of 400 UA/l. Its diagnostic performance (AUC=0.92, 95%CI 0.89-0.95) was superior to hs-CRP (AUC=0.65, 95%CI 0.60-0.70, P<0.001) and faecal calprotectin (fcalpro) (AUC=0.88, 95%CI 0.84-0.92, P=0.09). Combining the autoantibody with fcalpro further improved diagnostic accuracy (AUC=0.97, 95%CI 0.95-0.98) and patient reclassification (P<0.001). Autoantibody positivity was associated with a severe phenotype of UC, characterised by increased inflammatory activity and higher IL-17A and granzyme B levels. Higher autoantibody levels were linked to an aggressive disease course, remaining stable in aggressive UC but decreasing in indolent disease (P=0.003).
CONCLUSIONS: Anti-integrin αvβ6 is a reliable diagnostic and prognostic marker for UC, with potential clinical implementation.
Oxford University Press, 2025. Vol. 19, nr 5, artikkel-id jjaf062