Two studies up to now have shown an association between adenosine deaminase activity and disease activity in patients with Crohn’s disease and ulcerative colitis. We conducted a similar study in Crohn’s disease and in addition evaluated fecal calprotectin which is a known accurate disease activity marker for IBDs. But, we found no association between ADA activity and disease activity (evaluated by CDAI). Also no association was between ADA activity and FC, CRP, or ESR. But, ESR, CRP, and FC were all associated with disease activity.
What could be the reason for this difference between the study results?
ADA is reported in current literature as a non-specific marker of inflammation and it has been found elevated in the serum of patients with chronic inflammatory disorders enclosing ulcerative colitis and Crohn's disease. On my opinion its levels could correlate more with CRP or ESR than with FC. This last marker is affected by the site and the extension of the disease and indicate a local rather than a general condition. Therefore, I should like to suggest you a comparison with CRP and ESR more than with CDAI or FC. In the case of a negative realationship, I suggest you a revision of the method of assay by a comparison with that reported in other papers. In the case this last check is convincing, my suggestion is to describe your experience in the form of brief report or letter to the Editor. Indeed, I found only a paper treating this topic on Pub Med.
I am agreed with Prof.Enzo entirely in that it may become a novel investigation: to compare the ADA and FC levels in a certain group of patients with Crohn's disease.
Some attention may be paid as to the sources of ADA and FC to explain that discrepancy. What is your opinion, are they produced by the same or by the different cells?