Published online Jan 7, 2017. doi: 10.3748/wjg.v23.i1.135
Peer-review started: July 22, 2016
First decision: October 20, 2016
Revised: November 2, 2016
Accepted: November 23, 2016
Article in press: November 28, 2016
Published online: January 7, 2017
Processing time: 168 Days and 20 Hours
To evaluate whether repeated serum measurements of trefoil factor-3 (TFF-3) can reliably reflect mucosal healing (MH) in Crohn’s disease (CD) patients treated with anti-tumor necrosis factor-α (anti-TNF-α) antibodies.
Serum TFF-3 was measured before and after anti-TNF-α induction therapy in 30 CD patients. The results were related to clinical, biochemical and endoscopic parameters. MH was defined as a ≥ 50% decrease in Simple Endoscopic Score for Crohn’s disease (SES-CD).
SES-CD correlated significantly with CD clinical activity and several standard biochemical parameters (albumin, leukocyte and platelet counts, C-reactive protein, erythrocyte sedimentation rate, fibrinogen). In contrast, SES-CD did not correlate with TFF-3 (P = 0.54). Moreover, TFF-3 levels did not change significantly after therapy irrespectively of whether the patients achieved MH or not. Likewise, TFF-3 did not correlate with changes in fecal calprotectin, which has been proposed as another biochemical marker of mucosal damage in CD.
Serum TFF-3 is not a convenient and reliable surrogate marker of MH during therapy with TNF-α antagonists in CD.
Core tip: Mucosal healing (MH) is viewed as the holy grail of the efficacy of anti-tumor necrosis factor-α (anti-TNF-α) therapy for Crohn’s disease (CD), however performance of repeated colonoscopies is questionable for economical and safety reasons. We aimed to assess, whether serum trefoil factor-3 (TFF-3), a parameter engaged in maintaining mucosal integrity, could be useful in the assessment of MH. We found no correlation between TFF-3 and CD endoscopic activity and fecal calprotectin. Changes in TFF-3 did not reflect the degree to which MH was achieved. Thus, TFF-3 does not seem to be a reliable surrogate marker for MH in CD patients undergoing anti-TNF-α therapy.