Risk factors for small-bowel mucosal breaks in chronic low-dose aspirin users: data from a prospective multicenter capsule endoscopy registry

Endo, Hideki; Shimizu, Eiji; Taniguchi, Leo; Kessoku, Takaomi; Komiya, Yasuhiko; Ezuka, Akiko; Kawamura, Harunobu; Taguri, Masataka; Higurashi, Takuma; Ohkubo, Hidenori; Yamada, Eiji; Takahashi, Hirokazu; Inamori, Masahiko; Maeda, Shin; Sakaguchi, Takashi; Hata, Yasuo; Nagase, Hajime

doi:10.1016/j.gie.2014.03.024

Cited by 59 publications

(69 citation statements)

References 26 publications

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“…In this work, concomitant use of PPI was associated with a reduced risk of UGB but not LGB[3]. In fact, there was a significant increase in the risk of LGB with PPI use, which has also been detected by other authors[3-8]. Due to the intrinsic nature of observational studies, the finding was explained as probably due to a “confounding by indication” bias.…”

Section: Proton Pump Inhibitor Treatment and Risk Of Lower Gastrointesupporting

confidence: 56%

Protons pump inhibitor treatment and lower gastrointestinal bleeding: Balancing risks and benefits

Lué

Lanas

2016

WJG

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Proton pump inhibitors (PPIs) represent a milestone in the treatment of acid-related diseases, and are the mainstay in preventing upper gastrointestinal bleeding in high-risk patients treated with nonsteroidal anti-inflammatory drugs (NSAIDs) or low-dose aspirin. However, this beneficial effect does not extend to the lower gastrointestinal tract. PPIs do not prevent NSAID or aspirin-associated lower gastrointestinal bleeding (LGB). PPIs may increase both small bowel injury related to NSAIDs and low-dose aspirin treatment and the risk of LGB. Recent studies suggested that altering intestinal microbiota by PPIs may be involved in the pathogenesis of NSAID-enteropathy. An increase in LGB hospitalization rates may occur more frequently in older patients with more comorbidities and are associated with high hospital resource utilization, longer hospitalization, and increased mortality. Preventive strategies for NSAID and aspirin-associated gastrointestinal bleeding should be directed toward preventing both upper and lower gastrointestinal damage. Future research should be directed toward identifying patients at low-risk for gastrointestinal events associated with the use of NSAIDs or aspirin to avoid inappropriate PPI prescribing. Alternatively, the efficacy of new pharmacologic strategies should be evaluated in high-risk groups, with the aim of reducing the risk of both upper and lower gastrointestinal bleeding in these patients.

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Section: Proton Pump Inhibitor Treatment and Risk Of Lower Gastrointesupporting

confidence: 56%

Protons pump inhibitor treatment and lower gastrointestinal bleeding: Balancing risks and benefits

Lué

Lanas

2016

WJG

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“…The Lewis score is widely used to assessed the small intestinal mucosal injuries, such as Crohn’s disease and inflammatory changes in aspirin users [18]. Based on the algorithm of the score, the small intestine was divided into three tertiles, according to the small intestinal transit time.…”

Section: Methodsmentioning

confidence: 99%

Type 2 Diabetes Mellitus Is Associated with More Serious Small Intestinal Mucosal Injuries

et al. 2016

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BackgroundClinical and experimental research has revealed that diabetes mellitus (DM) is characterized by intestinal hypomotility, gut microbial dysbiosis, increased gut permeability, microcirculation disorders, circulatory changes, and dysfunction of intestinal stem cells, which may be linked to inflammation of intestinal mucosa. However, the relationship between type 2 DM (T2DM) and macroscopic small intestinal mucosal injuries is still unclear. Therefore, we retrospectively studied capsule endoscopy data to determine the relationship between T2DM and small intestinal mucosal injuries.Materials and MethodsWe compared the records of 38 T2DM patients with those of 152 non-DM patients for small intestinal mucosal injuries. Different types of mucosal injuries and Lewis scores were compared between T2DM and non-DM patients. The relationships between patients with or without different types of diabetic complications and the Lewis score was assessed. Moreover, the relationships between insulin resistance and Lewis score, between HbA1c and Lewis score, were also both assessed.ResultsThe prevalence of a villous edema in subjects with T2DM was significantly higher than in those without DM (P < 0.001), but incidence of ulcers was not different (P = 1.000). With T2DM, the Lewis score was also significantly higher (P = 0.002). In addition, subjects with diabetic nephropathy showed significantly higher Lewis scores than patients without diabetic nephropathy (P = 0.033). In Pearson’s correlation tests, the homeostasis model assessment of insulin resistance (HOMA-IR) value was correlated positively with the Lewis score (γ = 0.175, P = 0.015), but no statistical correlation was found between HbA1c level and Lewis score (γ = 0.039, P = 0.697).ConclusionsSubjects with T2DM, especially those with diabetic nephropathy, have higher Lewis scores and more serious small intestinal mucosal lesions.

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“…Endo et al [23] showed that PPIs were the risk factors for LDA-induced small intestinal damage. In addition, a meta-analysis performed by Lo and Chan [24] indicated that the use of PPIs was statistically associated with SIBO.…”

Section: Significance Of Dysbiosis In Nsaid-induced Small Intestinal mentioning

confidence: 99%

Microbiota Plays a Key Role in Non-Steroidal Anti-Inflammatory Drug-Induced Small Intestinal Damage

Otani¹,

Tanigawa²,

Watanabe³

et al. 2017

Digestion

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Background: Non-steroidal anti-inflammatory drugs (NSAIDs) damage the small intestine by causing multiple erosions and ulcers. However, to date, no established therapies and prophylactic agents are available to treat such damages. We reviewed the role of intestinal microbiota in NSAID-induced intestinal damage and identified potential therapeutic candidates. Summary: The composition of the intestinal microbiota is an important factor in the pathophysiology of NSAID-induced small intestinal damage. Once mucosal barrier function is disrupted due to NSAID-induced prostaglandin deficiency and mitochondrial malfunction, lipopolysaccharide from luminal gram-negative bacteria and high mobility group box 1 from the injured epithelial cells activate toll-like receptor 4-signaling pathway and nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 inflammasome; this leads to the release of proinflammatory cytokines such as tumor necrosis factor-α and interleukin-1β. Proton pump inhibitors (PPIs) are often used for the prevention of NSAID-induced injuries to the upper gastrointestinal tract. However, several studies indicate that PPIs may induce dysbiosis, which may exacerbate the NSAID-induced small intestinal damage. Our recent research suggests that probiotics and rebamipide could be used to prevent NSAID-induced small intestinal damage by regulating the intestinal microbiota. Key Messages: Intestinal microbiota plays a key role in NSAID-induced small intestinal damage, and modulating the composition of the intestinal microbiota could be a new therapeutic strategy for treating this damage.

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Risk factors for small-bowel mucosal breaks in chronic low-dose aspirin users: data from a prospective multicenter capsule endoscopy registry

Cited by 59 publications

References 26 publications

Protons pump inhibitor treatment and lower gastrointestinal bleeding: Balancing risks and benefits

Protons pump inhibitor treatment and lower gastrointestinal bleeding: Balancing risks and benefits

Type 2 Diabetes Mellitus Is Associated with More Serious Small Intestinal Mucosal Injuries

Microbiota Plays a Key Role in Non-Steroidal Anti-Inflammatory Drug-Induced Small Intestinal Damage

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