Non-steroidal anti-inflammatory drug-induced enteropathy as a major risk factor for small bowel bleeding: a retrospective study

Lim, Doo-Ho; Jung, Kyoungwon; Lee, Seung Bum; Park, In Kyu; Jeong, Hee; Park, Jae Ho; Kim, Byung Gyu; Jung, Seok Won; Jeong, In Du; Kim, Jae Hyun; Kim, Sung Eun; Moon, Won; Park, Moo In; Park, Seun Ja

doi:10.1186/s12876-020-01329-5

Cited by 8 publications

(5 citation statements)

References 46 publications

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“…In this situation, administration of S. boulardii CNCM I-745, in both preventive and curative protocols, resulted in a significant reduction in small bowel damage, as documented by a significant decrease in type 1-3 lesions, suggesting a protective effect on intestinal mucosa against NSAID-induced enteropathy. In addition, S. boulardii CNCM I-745 administration was effective in counteracting the decrease in blood haemoglobin (regarded as an indirect index of enteric bleeding [Bjarnason et al, 2018;Fornai et al, 2014Fornai et al, , 2016Fornai et al, , 2020Lim et al, 2020]) associated with NSAID treatment. Thus providing the first experimental demonstration that such therapeutic intervention could represent a valuable tool to reduce digestive bleeding associated with NSAID-induced intestinal injury.…”

Section: Discussionmentioning

confidence: 99%

Use of Saccharomyces boulardii CNCM I‐745 as therapeutic strategy for prevention of nonsteroidal anti‐inflammatory drug‐induced intestinal injury

D’Antongiovanni

Antonioli

Benvenuti

et al. 2023

British J Pharmacology

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Background and PurposeThe use of nonsteroidal anti‐inflammatory drugs (NSAIDs) can be associated with severe adverse digestive effects. The aim of this study was to examine the protective effects of the probiotic S. boulardii CNCM I‐745 in a rat model of diclofenac‐induced enteropathy.Experimental ApproachEnteropathy was induced in 40‐wk‐old male rats by intragastric diclofenac (4 mg/kg BID for 14 days). S. boulardii CNCM I‐745 (3 g/kg BID by oral gavage) was administered starting 14 days before (preventive protocol) or in concomitance (curative protocol) with diclofenac administration. Ileal damage, inflammation, barrier integrity, gut microbiota composition, and TLRs‐NF‐kB‐pathway were evaluated.Key ResultsDiclofenac elicited intestinal damage, along with increments of myeloperoxidase, malondialdehyde, tumor necrosis factor and interleukin‐1β, overexpression of TLR‐2/‐4, MyD88, and NF‐kB p65, increased faecal calprotectin and butyrate levels as well as a decrease in blood hemoglobin levels, occludin and butyrate transporter MCT1 expression. In addition, diclofenac provoked a shift of bacterial taxa in both faecal and ileal samples. Treatment with S. boulardii CNCM I‐745, in both preventive and curative protocol, counteracted the majority of these deleterious changes. Only preventive administration of the probiotic counteracted NSAID‐induced decreased expression of MCT1 and increase in faecal butyrate levels. No significant changes were observed for the occludin expression after probiotic treatment.Conclusion and ImplicationsTreatment with S. boulardii CNCM I‐745 prevents diclofenac‐induced enteropathy through anti‐inflammatory and antioxidant activities. Such effects are likely to be related to increased tissue butyrate bioavailability, through an improvement of butyrate uptake by the enteric mucosa.

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Section: Discussionmentioning

confidence: 99%

Use of Saccharomyces boulardii CNCM I‐745 as therapeutic strategy for prevention of nonsteroidal anti‐inflammatory drug‐induced intestinal injury

D’Antongiovanni

Antonioli

Benvenuti

et al. 2023

British J Pharmacology

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“…10–40% and 50% of chronic NSAID users develop upper or lower GI ulcers respectively ( Yamagata and Hiraishi, 2007 , Higuchi et al., 2009 ; Endo et al., 2015 ). NSAID-associated enteropathy has gained much attention due to the introduction of new diagnostic devices such as video capsule endoscopy and device-assisted enteroscopy ( Maiden, 2009 ; Scarpignato and Bjarnason, 2019 , Lim et al., 2020 ). Erosive lesions are observed throughout the small intestine when low dose aspirin users are subjected to capsule endoscopy in low dose aspirin users ( Iwamoto et al., 2014 ).…”

Section: Introductionmentioning

confidence: 99%

A novel drug-like water-soluble small molecule Focal Adhesion Kinase (FAK) activator promotes intestinal mucosal healing

Wang

Gallardo‐Macias

Vomhof-DeKrey

et al. 2023

Current Research in Pharmacology and Drug Discovery

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“…According to the Korean CE registry report, the primary reason for CE examinations was obscure GI bleeding (OGIB) (62.7% cases) [ 7 ] and drug-induced SB enteropathy, the incidences of which increase with age [ 8 ]. A recent hospital-based study also showed that drug-induced enteropathy was the most prevalent etiology of SB bleeding identified in CE [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

Association between eupatilin and reduction in small bowel bleeding in aspirin users and aspirin plus acid suppressant users

Lee

Nam

et al. 2023

Korean J Intern Med

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Background/Aims: Capsule endoscopy (CE) has shown that low-dose aspirin occasionally causes small bowel (SB) bleeding. We herein evaluated the protective effects of mucoprotective agents (MPAs) on SB bleeding in aspirin users using the nationwide database of claims data from the National Health Insurance Service (NHIS).Methods: As CE is an insured procedure, we constructed an aspirin-SB cohort using NHIS claims data, with a maximum follow- up period of 24 months. Patients with anemia, melena, or hematochezia that occurred within 4 weeks before and after performing CE were suspected to have SB bleeding. A Cox proportional hazards regression model was used to determine the risk factors for SB bleeding. Subgroup analyses were conducted among patients who used acid suppressants, such as proton pump inhibitors (PPIs) and histamine-2 receptor antagonists.Results: A total of 15,542 aspirin users were included. Anticoagulant use (hazard ratio [HR], 3.22), high Charlson comorbidity index score (≥ 2) (HR, 3.54), and PPI use (HR, 2.85) were significantly associated with SB bleeding, whereas eupatilin use (HR, 0.35) was a preventive factor. SB bleeding occurred more frequently in concurrent users of acid suppressants than in nonusers (1.3% vs. 0.5%). Subgroup analysis revealed that eupatilin significantly reduced the risk of SB bleeding in aspirin users with concurrent use of acid suppressants (HR, 0.23 vs. 2.55).Conclusions: Eupatilin was associated with a reduced risk of SB bleeding in both aspirin users and those with concomitant use of acid suppressants. Eupatilin use should be considered for aspirin users, especially for those concomitantly taking acid suppressants.

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Non-steroidal anti-inflammatory drug-induced enteropathy as a major risk factor for small bowel bleeding: a retrospective study

Cited by 8 publications

References 46 publications

Use of Saccharomyces boulardii CNCM I‐745 as therapeutic strategy for prevention of nonsteroidal anti‐inflammatory drug‐induced intestinal injury

Use of Saccharomyces boulardii CNCM I‐745 as therapeutic strategy for prevention of nonsteroidal anti‐inflammatory drug‐induced intestinal injury

A novel drug-like water-soluble small molecule Focal Adhesion Kinase (FAK) activator promotes intestinal mucosal healing

Association between eupatilin and reduction in small bowel bleeding in aspirin users and aspirin plus acid suppressant users

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