Clinical, medical and diagnostics
A study found distinct antibody profiles in blood samples collected up to 10 years before Crohn’s disease or ulcerative colitis was diagnosed but clinical testing will require further validation
Distinct antibody patterns were detectable in blood samples up to 10 years before some people received a diagnosis of inflammatory bowel disease (IBD), researchers reported at United European Gastroenterology Congress 2026, in Barcelona, Spain. The findings could help scientists understand early disease development but do not yet establish a screening test.
IBD includes Crohn’s disease and ulcerative colitis, conditions in which abnormal immune responses contribute to inflammation and damage in the digestive system. Researchers analysed 2,000 serum samples from 500 people: 200 who later developed Crohn’s disease, 200 who developed ulcerative colitis and 100 healthy controls. Samples came from diagnosis and approximately two, four and 10 years earlier.
The team examined antibody responses to about 357,000 microbial, viral, food-related and immune-associated antigens and identified 123,980 distinct antibodies. Antibody diversity was lower in people who later developed either condition than in controls. The researchers also found different patterns: Crohn’s disease was associated with increased responses to herpesviruses and flagellin, while responses to some encapsulated bacteria declined towards diagnosis. In ulcerative colitis, responses to herpesviruses and autoantigens rose, while reactivity to encapsulated pathogens fell.
Machine-learning models distinguished people who later developed Crohn’s disease or ulcerative colitis from controls up to 10 years before diagnosis, with area-under-the-curve values of 0.90 and 0.84, respectively. A separate model distinguished future complicated from non-complicated Crohn’s disease with a value of 0.85. These measures describe performance in the study dataset and require independent validation.
Lead author Dr. Arno Bourgonje said the patterns could help researchers investigate disease subtypes and identify people who might benefit from closer assessment. The authors said the next steps include testing the signatures in diverse, prospective populations, comparing them with existing markers and determining whether a reproducible, affordable assay could improve clinical outcomes.
The samples were collected at diagnosis and at intervals of approximately two, four and 10 years beforehand, allowing the team to compare how antibody profiles changed as diagnosis approached. Across the dataset, the analysis identified a very large number of distinct antibody responses, with lower overall diversity in people who later developed Crohn’s disease or ulcerative colitis than in healthy controls.
The antibody patterns also varied with the form and course of disease. In Crohn’s disease, stronger responses to herpesviruses and antibodies against bacterial flagellin were especially apparent in people who later had complicated or ileal disease. Responses to encapsulated bacteria declined towards diagnosis. In ulcerative colitis, herpesvirus and autoantigen responses rose while reactivity to encapsulated pathogens fell.
The authors described the work as proof of principle. A model’s ability to distinguish groups in this dataset does not show how it would perform in routine screening, where disease prevalence and patient characteristics differ. They called for independent, diverse cohorts, comparison with genetic and clinical markers, and evidence that a targeted test changes care or outcomes.
ILM 51.6 Sept 2026