Thanks for sharing a summary of the research, this is really interesting! I had some quick questions on the predictiveness of faecal calprotectin. Does that imply that it would make sense to take samples a lot more regularly and then proactively adjust medication? Or what other things could be done proactively if we know in advance that there is this elevated risk?
Yes it absolutely means that; and this is how we have been managing out IBD patients in Edinburgh for at least 10 years. We use the same assay so we can compare calprotectin values over time. We aim to follow the trend and adjust management accordingly. We are now working on modelling these trends mathematically in order to build a truly predictive model - this will enable personalised, proactive IBD care. Our other big paper on that was published last month - which is just the first step towards this. https://www.cghjournal.org/article/S1542-3565(25)01069-9/fulltext
Thanks for sharing a summary of the research, this is really interesting! I had some quick questions on the predictiveness of faecal calprotectin. Does that imply that it would make sense to take samples a lot more regularly and then proactively adjust medication? Or what other things could be done proactively if we know in advance that there is this elevated risk?
Yes it absolutely means that; and this is how we have been managing out IBD patients in Edinburgh for at least 10 years. We use the same assay so we can compare calprotectin values over time. We aim to follow the trend and adjust management accordingly. We are now working on modelling these trends mathematically in order to build a truly predictive model - this will enable personalised, proactive IBD care. Our other big paper on that was published last month - which is just the first step towards this. https://www.cghjournal.org/article/S1542-3565(25)01069-9/fulltext
Thank you very much for this fascinating work in such an important field.
As a patient advocate, I find the discrepancy between subjective experience and objective evidence of a flare particularly interesting.
While this is not fundamentally new, seeing it laid out so clearly is truly striking.
It would certainly also be interesting to understand how these differences arise.
Do subjective flares perhaps progress into objective flares at a later point in time?
Could subjective flares be driven by subclinical inflammation?
And where do these functional symptoms originate from?
Of course, none of us are interested in dismissing or invalidating patients’ lived experiences, so i am interestet in your perspective on this :)