For the purpose of shedding some light upon the possible mechanisms involved in gallstone formation in patients with Crohn’s disease, we have investigated gallbladder emptying by means of ultrasonography in two groups of subjects: controls (n = 40) and Crohn’s disease (n = 30). Diminished gallbladder emptying after a liquid fatty-meal stimulus was observed in patients with Crohn’s disease when compared with controls (p < 0.001). Also, the values for the residual gallbladder volume (RGV) and maximal decrease in gallbladder volume (MDGV), both in milliliters and percentage were, respectively, increased (RGV = 9.6 ml) and diminished (MDGV = 14.8 ml; MDGV = 60.9%) in patients with Crohn’s disease when compared with controls (RGV = 5.9 ml, p < 0.001; MDGV = 19.9 ml, p = 0.003; MDGV = 77.8%, p < 0.001). Hence, reduced gallbladder emptying with consequent stasis might be a contributory factor to the increased prevalence of gallstones in Crohn’s disease.

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No fixed strategy is recommended after surgical resections in CD. Thus, the need for a personalized approach for each patient is emphasized, in accordance with several conditions and variables.

Biosimilars are not generic drugs. These are more complex medications than small molecules, with identical chemical structures of monoclonal antibodies that lost their patency over time. Besides identical to the original product at the end, the process of achieving its final forms differs from the one used in the reference products. These differences in the formulation process can alter final outcomes such as safety and efficacy of the drugs. Recently, a biosimilar of Infliximab was approved in some countries, even to the management of inflammatory bowel diseases. However, this decision was based on studies performed in rheumatologic conditions such as rheumatoid arthritis and ankylosing spondylitis. Extrapolation of the indications from rheumatologic conditions was done for Crohn's disease and ulcerative colitis based on these studies. In this article, the authors explain possible different mechanisms in the pathogenesis between rheumatologic conditions and inflammatory bowel diseases, that can lead to different actions of the medications in different diseases. The authors also alert the gastroenterological community for the problem of extrapolation of indications, and explain in full details the reasons for being care with the use of biosimilars in inflammatory bowel diseases without specific data from trials performed in this scenario.

The pathogenesis of nonsteroidal anti-inflammatory drug (NSAID) enteropathy is a complex process involving the uncoupling of mitochondrial oxidative phosphorylation and inhibition of cyclooxygenase (COX). Rofecoxib, a selective inhibitor of COX-2, has shown less gastric damage, but the same beneficial effect is not clear in the case of the small bowel. Fifty-seven male Wistar rats (250-350 g) were divided into three groups (N = 19 each) to evaluate the effect of this NSAID on the rat intestine. The groups received 2.5 mg/kg rofecoxib, 7.5 mg/kg indomethacin or water with 5% DMSO (control) given as a single dose by gavage 24 h before the beginning of the experiment. A macroscopic score was used to quantify intestinal lesions and intestinal permeability was measured using [ 51 Cr]-ethylenediaminetetraacetic acid ([ 51 Cr]-EDTA). The extent of intestinal lesion, indicated by a macroscopic score, was significantly lower when rofecoxib was administered compared to indomethacin (rofecoxib = 0.0 vs indomethacin = 63.6 ± 25.9; P < 0.05) and did not differ from control. The intestinal permeability to [ 51 Cr]-EDTA was significantly increased after indomethacin (control = 1.82 ± 0.4 vs indomethacin = 9.12 ± 0.8%; P < 0.0001), but not after rofecoxib, whose effect did not differ significantly from control (control = 1.82 ± 0.4 vs rofecoxib = 2.17 ± 0.4%; ns), but was significantly different from indomethacin (indomethacin = 9.12 ± 0.8 vs rofecoxib = 2.17 ± 0.4%; P < 0.001). In conclusion, the present data show that rofecoxib is safer than indomethacin in rats because it does not induce macroscopic intestinal damage or increased intestinal permeability.