Fibrosis Associated Protein Inhibitor (FAPI) Radiotracer-based Imaging to Identify Fibrotic Intestinal Crohn's Disease

Crohn's Disease (CD) is a chronic inflammatory condition that can affect any part of the intestine and currently has no cure. It affects 6.8 million people worldwide with UK healthcare costs in excess of £1 billion per year. Recent data suggests that the despite significant progress in treatments over the last 2 decades to help control disease, up to half of patients still develop progressive bowel scarring that require surgery and up to 70% needing surgery within 10-20 years from diagnosis. Unfortunately this is not a cure and some still require repeat surgery. These features have a devastating impact on an individual including education, work and social life. All our current treatments focus on resolving inflammation but there are no treatments targeting fibrosis, its activity and its progression. A major hurdle in our progress towards anti-fibrotic treatments and advancing care in CD has been our inability to identify bowel scarring accurately using non-invasive tests; this being critical in developing new treatments that prevent permanent bowel damage. We are also unable to identify early stage scarring (fibrosis) and once established we are unable to differentiate between different stages of scarring severity. The investigators aim to investigate a novel method that can identify early scarring and track progressive bowel damage by tracking cells that cause fibrosis. In this study the investigators will use a 'dye', also known as fibrosis associated protein inhibitor (FAPI), that tracks scarring and its activity in the intestine. The presence and amount of FAPI within an area of scarring can be detected using our current imaging tests (positron emission tomography and Computer Tomography imaging: PET/CT). If successful, this study will be the first method for detecting scarring activity in CD and have the potential to revolutionise care for this condition and facilitate new drug development to halt the processing of scarring (fibrosis) and improve the outcomes for patients with CD.