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Two recent papers by Leal et al1 and by Yarur et al2 focalised their attention on the mechanisms of Tumour Necrosis Factor α (TNF) inhibition by anti-TNFα in patients suffering from IBDs. In particular, Yarur et al found that the ration anti-TNF/TNF in tissue was highest in uninflamed areas and lowest in severely inflamed areas, and claimed that TNFα overexpression in local tissue inflammation characterised serves as a sink for anti-TNF.1 Moreover, Leal et al found that anti-TNFα therapy significantly downregulates a subset of inflammatory genes even in patients who fail to achieve endoscopic remission, suggesting that these genes may not be dominant in driving inflammation in non-responders.2
We reported herein our experience in assessing TNFα mucosal expression and mucosal healing (MH) in UC under treatment with infliximab (IFX). We revised the MH and TNFα expression before and after IFX treatment in …
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