Do non-steroidal anti-inflammatory drugs increase colonic permeability?

Jenkins, A. P.; Trew, D R; Crump, Barbara; Nukajam, W S; Foley, J. A.; Menzies, I. S.; Creamer, B.

doi:10.1136/gut.32.1.66

Cited by 76 publications

(47 citation statements)

References 19 publications

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“…Impaired barrier function intensifies antigen access, which in turn leads to an exaggerated immune stimulation that initiates or perpetuates inflammation (2). Increased intestinal permeability has been described in inflammatory bowel disease (3)(4)(5)(6)(7)(8)(9)(10)(11), atopic eczema (12), celiac disease and dermatitis herpetiformis (13), cystic fibrosis (14,15), alcohol consumption (16), use of nonsteroidal antiinflammatory drugs (17)(18)(19)(20), and acute infectious diarrhea (12,21). On the other hand, decreased intestinal permeability has been demonstrated in Blastocystis hominis infection (22).…”

Section: Introductionmentioning

confidence: 99%

Intestinal permeability in strongyloidiasis

Werneck-Silva

Sipahi

Damião

et al. 2001

Braz J Med Biol Res

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The objective of the present study was to assess intestinal permeability in patients with infection caused by Strongyloides stercoralis. Twentysix patients (16 women and 10 men), mean age 45.9, with a diagnosis of strongyloidiasis were evaluated. For comparison, 25 healthy volunteers (18 women and 7 men), mean age 44.9, without digestive disorders or intestinal parasites served as normal controls. Intestinal permeability was measured on the basis of urinary radioactivity levels during the 24 h following oral administration of chromium-labeled ethylenediaminetetraacetic acid ( 51 Cr-EDTA) expressed as percentage of the ingested dose. The urinary excretion of 51 Cr-EDTA was significantly reduced in patients with strongyloidiasis compared to controls (1.60 ± 0.74 and 3.10 ± 1.40, respectively, P = 0.0001). Intestinal permeability is diminished in strongyloidiasis. Abnormalities in mucus secretion and intestinal motility and loss of macromolecules could explain the impaired intestinal permeability.

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Section: Introductionmentioning

confidence: 99%

Intestinal permeability in strongyloidiasis

Werneck-Silva

Sipahi

Damião

et al. 2001

Braz J Med Biol Res

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“…This effect is believed to be caused by an increased mucosal permeability (16). Paradoxically, it has been speculated that this is due to the inhibition of the cyclooxygenase-dependent oxidation of arachidonic acid resulting in the depletion of endogenous prostaglandins (13).…”

Section: Introductionmentioning

confidence: 99%

Ibuprofen inhibits cystic fibrosis transmembrane conductance regulator-mediated Cl- secretion.

Devor

Schultz²

1998

J. Clin. Invest.

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We evaluated the acute effects of ibuprofen and salicylic acid on cAMP-mediated Cl Ϫ secretion (I sc ) in both colonic and airway epithelia. In T84 cells, ibuprofen inhibited the forskolin-dependent I sc in a concentration-dependent manner, having an apparent K i of 142 M. Salicylic acid inhibited I sc with an apparent K i of 646 M. We determined whether ibuprofen would also inhibit the forskolin-stimulated I sc in primary cultures of mouse trachea epithelia (MTE) and human bronchial epithelia (HBE). Similar to our results in T84 cells, ibuprofen (500 M) inhibited the forskolin-induced I sc in MTEs and HBEs by 59 Ϯ 4% ( n ϭ 11) and 39 Ϯ 6% ( n ϭ 8), respectively. Nystatin was employed to selectively permeabilize the basolateral or apical membrane to determine the effect of ibuprofen on apical Cl Ϫ (I Cl ) and basolateral K ϩ (I K ) currents after stimulation by forskolin. After forskolin stimulation, ibuprofen (500 M) reduced both the I Cl and I K ; reducing I Cl and I K by 60 and 15%, respectively. To determine whether this inhibition of I Cl was due to the inhibition of CFTR, the effects of ibuprofen and salicylic acid on CFTR Cl Ϫ channels in excised, inside-out patches from L-cells were evaluated. Ibuprofen (300 M) reduced CFTR Cl Ϫ current by 60 Ϯ 16% and this was explained by a short-lived block ( ‫ف‬ 1.2 ms) which causes an apparent reduction in single channel amplitude from 1.07 Ϯ 0.04 pA to 0.59 Ϯ 0.04 pA ( n ϭ 3). Similarly, salicylic acid (3 mM) reduced CFTR Cl Ϫ current by 50 Ϯ 8% with an apparent reduction in single channel amplitude from 1.08 Ϯ 0.03 pA to 0.48 Ϯ 0.06 pA ( n ϭ 4). Based on these results, we conclude that the NSAIDs ibuprofen and salicylic acid inhibit cAMP-mediated Cl Ϫ secretion in human colonic and airway epithelia via a direct inhibition of CFTR Cl Ϫ channels as well as basolateral membrane K ϩ channels. This may reduce their efficacy in conjunction with other therapeutic strategies designed to increase CFTR expression and/or function in secretory epithelia. ( J. Clin. Invest.

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“…The GIEQ provides the opportunity to measure a large amount of environmental exposures all at once, allowing analysis of interactions between different environmental exposures, as different exposures seem to have similar biological modus of effect. Gut permeability for example, seems to be affected by the use of non-steroidal anti-inflammatory drugs (NSAIDs) as well as smoking cigarettes [32,33]. One can imagine that combining both exposures will yield a different effect than that of individual evaluation per each factor.…”

Section: Discussionmentioning

confidence: 99%

Development and validation of a web-based questionnaire to identify environmental risk factors for inflammatory bowel disease: the Groningen IBD Environmental Questionnaire (GIEQ)

et al. 2018

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Background In the complex etiology of inflammatory bowel disease (IBD), the exposome is a major contributor. Though many environmental exposures have been identified, quality of evidence varies greatly and overall evidence for the exposome is inconclusive. A universal, precise, and reproducible measurement tool is needed to study the exposome in IBD. Methods We built the web-based Groningen IBD Environmental Questionnaire (GIEQ), an extensive and structured questionnaire measuring potentially involved environmental exposures, consisting of 848 items, subdivided into 15 categories. For validation, 76 IBD patients completed the GIEQ twice (2-month interval). Cohen's kappa and correlation coefficients were used to compare both fills. Internal consistency was evaluated using Cronbach's alpha tests. Proportional bias was examined using Bland-Altman plots. Results In general, we obtained a mean kappa coefficient of 0.78 (standard deviation 0.17) for categorical questions and a mean intraclass correlation coefficient of 0.88 (0.15) for numeric questions. Cronbach's alpha ranged from 0.64 to 1.0 with a mean of 0.79 (0.14). Bland-Altman plots showed proportional bias only for current physical activity score. Conclusions The GIEQ is a reliable measurement tool to study the exposome in IBD, enabling consistent measurement of an extended number of environmental factors and their interactions. Use of the GIEQ across IBD cohorts will lead to more standardized, generalizable, and comparable results. Also, the GIEQ can be used for calculation of an exposome risk score, applicable for secondary prevention by identifying high-risk patients as well as to analyze interactions between the exposome and other aspects of IBD etiology.

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Do non-steroidal anti-inflammatory drugs increase colonic permeability?

Cited by 76 publications

References 19 publications

Intestinal permeability in strongyloidiasis

Intestinal permeability in strongyloidiasis

Ibuprofen inhibits cystic fibrosis transmembrane conductance regulator-mediated Cl- secretion.

Development and validation of a web-based questionnaire to identify environmental risk factors for inflammatory bowel disease: the Groningen IBD Environmental Questionnaire (GIEQ)

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