Pediatric patients who receive early anti-TNF therapy for their Crohn’s disease are less likely to develop penetrating but not stricturing complications, new research shows.
The North American observational study of about 900 children newly diagnosed with Crohn’s disease also combined microbiology and genetic information to stratify the risk of complications.
The research team found 9% of children developed complications within four years of diagnosis. Older age, African-American race, anti-Saccharomyces cerevisiae antibodies (ASCA) and CBir1 seropositivity were associated with disease complications.
Genes regulating extracellular matrix were induced in patients who developed strictures whereas genes regulating inflammation were induced in people developing penetrating disease.
Commenting on the study, paediatric gastroenterologist Professor Jane Andrews said : “This is the way of the future and will help avoid over-treating patients at low risk and under-treating other patients, especially with regards to aggressive treatment.”
“Being able to tell a person they do not have signs they are at high risk of developing complications is good news. It helps reassure patients and relieves their anxiety.”
However Professor Andrews, head of IBD Services at the Royal Adelaide Hospital and Clinical Professor at the University of Adelaide, told the limbic some of the tests used in the risk-prediction model were not yet available in clinical practice.
“The testing for ileal genes is only available in the research setting and very expensive. However if it turns out to be useful, it will come into clinical use, ” she said.
“We need to see some of this validated in another cohort and ideally in a randomised controlled trial for those with particular gene signatures.”
The study also implicated Veillonella species with penetrating disease and Ruminococcus with stricturing disease.
However Professor Andrews warned against targeting particular organisms as they were quite likely to be different depending on the environment and diet in different populations.
“It might not be the particular identity of the organism that matters but their particular function or metabolic products,” she said.
“Antibiotics also restrict the microbiome and increase the risk of C. difficile infection,” she added.