Side effects of nonsteroidal anti-inflammatory drugs on the small and large intestine in humans

Bjarnason, Ingvar; Hayllar, Jeremy; Aj, MacPherson; As, Russell

doi:10.1016/0016-5085(93)90667-2

Cited by 947 publications

(595 citation statements)

References 169 publications

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“…It is well established that the administration of indomethacin in dosages comparable to that used in the present study increases small intestinal permeability about 2-3 fold (Bjarnason et al, 1986(Bjarnason et al, , 1989(Bjarnason et al, , 1993, which is in line with our results. Intestinal permeability after taking indomethacin for 7 days reverts back to normal within 1 week (Bjarnason et al, 1991).…”

Section: Discussionsupporting

confidence: 93%

“…This is regarded as the first step in the development of gastrointestinal injury (Somasundaram et al, 1995(Somasundaram et al, , 1997. This uncoupling causes efflux of hydrogen and calcium ions from mitochondria and promotes oxygen radical damage (Bjarnason et al, 1993;Carafoli, 1987). Owing to this oxidative stress, tight junctions are damaged and paracellular permeability increases.…”

Section: Discussionmentioning

confidence: 99%

“…However, if the intestinal permeability is increased, excessive penetration of luminal aggressive agents and antigens may attract local and circulating neutrophils which cause the release of reactive oxygen species (Bjarnason et al, 1993) and the initiation of gastrointestinal inflammation (Wallace, 1993;Soderholm & Perdue, 2001). This inflammation increases permeability to a greater extent, resulting in permeation of luminal aggressive agents through the mucosa and aggravation of local tissue inflammation which, in turn, leads to increased permeability (Ferry et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

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Recombinant human lactoferrin ingestion attenuates indomethacin-induced enteropathy in vivo in healthy volunteers

2003

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Objective: To determine whether recombinant human lactoferrin ingestion inhibits nonsteroidal antiinflammatory drugs (NSAID)-induced gastroenteropathy in vivo in healthy volunteers as a model for disorders associated with a rise in permeability of the stomach and the small intestine. Design: A randomized crossover dietary intervention. Subjects and interventions: In all, 15 healthy volunteers (age 2371.4 y) were tested. A sucrose and a lactulose/rhamnose (L/R) permeability test was performed to assess gastroduodenal and small intestine permeability as indicator of NSAID-induced gastroenteropathy. All subjects consumed standardized meals for 2 days. On the second day at time ¼ À24 h each subject ingested a drink containing 5 g recombinant human lactoferrin or placebo during breakfast. At t ¼ À9 h, subjects ingested the same drink with 75 mg of the NSAID indomethacin and after an overnight fast at t ¼ À1 h subjects consumed the drink and 50 mg indomethacin. After 1 h, at t ¼ 0, a permeability test was performed. Results: Small intestine permeability after indomethacin and placebo was significantly higher (L/R ratio ¼ 0.036; 0.014-0.092, Po0.05) compared to the permeability observed after ingestion of indomethacin and lactoferrin (0.028; 0.015-0.056), whereas gastroduodenal permeability did not differ between the two interventions (P ¼ 0.3). Conclusion: Oral recombinant human lactoferrin supplementation during a short-term indomethacin challenge reduced the NSAID-mediated increase in small intestinal permeability and hence may provide a nutritional tool in the treatment of hyperpermeability-associated disorders. Sponshorship: Grant and human recombinant lactoferrin donated from Agennix Inc., Houston, TX.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Recombinant human lactoferrin ingestion attenuates indomethacin-induced enteropathy in vivo in healthy volunteers

2003

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“…Permeability increases in pathologic conditions including IBD [4] , celiac disease [11,12] , and with the administration of NSAIDs [13,14] . When permeability is increased the gastrointestinal tract is exposed to bacterial and dietary antigens.…”

Section: Introductionmentioning

confidence: 99%

Gastrointestinal lesions associated with spondyloarthropathies

Orlando

Renna²,

Perricone³

et al. 2009

WJG

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Subclinical gut inflammation has been described in up to two-thirds of patients with spondyloarthropathies (S pA). Ar t hr i t is represents an extra-intestinal manifestation of several gastrointestinal diseases, including inflammatory bowel disease (IBD), Whipple's disease, Behcet's disease, celiac disease, intestinal bypass surgery, parasitic infections of the gut and pseudomembranous colitis. Moreover about twothirds of nonsteroidal anti-inflammatory drug users demonstrate intestinal inflammation. Arthritis may manifest as a peripheral or axial arthritis. The spondyloarthropathy family consists of the following entities: ankylosing spondylitis, undifferentiated s p o n d y l o a r t h r i t i s , r e a c t i ve a r t h r i t i s , p s o r i a t i c arthritis, spondyloarthritis associated with IBD, juvenile onset spondyloarthritis. This topic reviews the major gastrointestinal manifestations that can occur in patients with SpA and in nonsteroidal antiinflammatory drugs users.

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“…What is not in doubt is that conventional NSAIDs cause damage throughout the whole of the gastrointestinal tract (stomach and small bowel and occasionally the large bowel) (Bjarnason et al 1993). Basic research, almost all of which comes from rodents using NSAID doses far greater than in man (as per kg weight), shows that the damage is initiated by the biochemical actions of the drugs (Somasundaram et al 1995) which leads to cellular damage that progresses to micro-and macroscopic damage by the interaction between the luminal contents of the organs (acid in the stomach and bile and bacteria in the small bowel) and impaired mucosal defence, microvascular blood flow and oxygenation all playing an important role.…”

mentioning

confidence: 99%

Serious upper gastrointestinal complications of NSAIDs and COX-2 selective agents

Sisson

Bjarnason

2011

Inflammopharmacol

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Side effects of nonsteroidal anti-inflammatory drugs on the small and large intestine in humans

Cited by 947 publications

References 169 publications

Recombinant human lactoferrin ingestion attenuates indomethacin-induced enteropathy in vivo in healthy volunteers

Recombinant human lactoferrin ingestion attenuates indomethacin-induced enteropathy in vivo in healthy volunteers

Gastrointestinal lesions associated with spondyloarthropathies

Serious upper gastrointestinal complications of NSAIDs and COX-2 selective agents

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