A faecal protein biomarker for risk of Crohn’s Disease progression
An association between the protein Faecal calprotectin and risk of progression of Crohn’s disease is investigated in a new publication led by Prof Charlie Lees. Sept 2020
Crohn’s disease (CD) and ulcerative colitis (UC) are chronic inflammatory bowel diseases (IBD) characterised by relapsing and remitting intestinal inflammation, currently estimated to affect 1 in every 125 people in the UK. While the cause of IBD is not fully understood, it is believed that, in those genetically predisposed, an abnormal immune response of the intestinal mucosa to the gut microbiota is involved. This occurs in response to a variety of poorly characterised environmental triggers including aspects of habitual diet
CD shows progressive development in the majority of those affected, with approximately 60-70% eventually developing strictures and/ or fistula with time. It is widely held that this progression is a result of chronic intestinal inflammation. This irreversible bowel damage drives the risk of major surgery to over 50% within a 5 to 10 year period from diagnosis. A significant proportion of these patients will require a permanent ostomy – where bowel contents are diverted to a stoma ‘bag’ on the abdominal wall. Due to the prevalence and progressive nature of the disease, understanding risk factors and identifying effecting treatment options are of great importance. Healing of the intestinal mucosa has been associated with improved outcomes in CD patients including lower risk of relapse, hospitalisation and surgery.
A recent publication in the journal Clinical Gastroenterology and Hepatology, led Prof Charlie Lees, has investigated the association between the level of a protein biomarker, faecal calprotectin, and CD. It has previously been shown that there is a correlation between the level of faecal calprotectin and evidence of inflammation as detected through endoscopic examination. Indeed, a treatment strategy for CD that incorporates faecal calprotectin level is more effective in induction of mucosal healing, than one based solely on symptoms alone.
In their current publication Dr Nik Plevris working in Prof Lees’ team, aimed to determine whether normalisation of faecal calprotectin within 12 months of CD diagnosis was associated with reduced disease progression. Performing a retrospective cohort study to identify all cases of CD in the Lothian area between 2005 and 2017, they showed that those who displayed a normalised level of the protein within 12 months had a significantly lower risk of disease progression.
The results of the study confirm that decreased faecal calprotectin levels correlating to resolution of inflammation in the intestinal mucosa, within 12 months of diagnosis, is a valid prognostic marker for reduced progression of Crohn’s disease.
We have been using faecal calprotectin in routine clinical practice for over 10 years in the Edinburgh IBD unit. We know it helps differentiate inflammatory bowel disease from irritable bowel syndrome. In the IBD clinic we adopt a treat to target approach based on faecal calprotectin. We have now shown that early tight control based on calprotectin is associated with markedly improved outcomes in Crohn’s disease – less disease progression and fewer hospitalisations and surgeries.
We are working hard to improve outcomes for the many people across the UK and increasingly worldwide living with IBD. Moving forwards, we are looking to use digital health tools coupled with machine learning and artificial intelligence to build predictive models to guide treatment. Meantime, these new data show very practically how IBD teams and patients can today best utilise faecal calprotectin as a target early in Crohn’s disease course to achieve better long-term outcomes.
Read the paper in journal Clinical Gastroenterology and Hepatology doi.org/10.1016/j.cgh.2020.08.022
Professor Charlie Lees' Research Group website