Clinical trial: comparison of ibuprofen‐phosphatidylcholine and ibuprofen on the gastrointestinal safety and analgesic efficacy in osteoarthritic patients

Lanza, Frank L.; Marathi, Upendra; Anand, Bhupinderjit S.; Lichtenberger, Lenard M.

doi:10.1111/j.1365-2036.2008.03765.x

Cited by 60 publications

(45 citation statements)

References 27 publications

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“…Thus, covalently linking phosphatidylcholine to aspirin, ibuprofen and other NSAIDs results in compounds with equivalent antiinflammatory properties to the parent drug, but with markedly reduced gastric toxicity [181] . This has been demonstrated in endoscopic clinical trials for an aspirin derivative [181] , and also with an ibuprofen derivative [182] , though in the latter trial, statistical significance was only seen in an older subset of the patients studied. Recently, Lichtenberger et al [78] demonstrated that pre-associating aspirin with phosphatidylcholine greatly reduced the small intestinal damage produced by intraduodenal administration of this compound, as compared to aspirin alone.…”

Section: Novel Intestinal-sparing Nsaidsmentioning

confidence: 78%

Mechanisms, prevention and clinical implications of nonsteroidal anti-inflammatory drug-enteropathy

Wallace¹

2013

WJG

151

148

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This article reviews the latest developments in understanding the pathogenesis, detection and treatment of small intestinal damage and bleeding caused by nonsteroidal anti-inflammatory drugs (NSAIDs). With improvements in the detection of NSAID-induced damage in the small intestine, it is now clear that this injury and the associated bleeding occurs more frequently than that occurring in the stomach and duodenum, and can also be regarded as more dangerous. However, there are no proven-effective therapies for NSAIDenteropathy, and detection remains a challenge, particularly because of the poor correlation between tissue injury and symptoms. Moreover, recent studies suggest that commonly used drugs for protecting the upper gastrointestinal tract (i.e. , proton pump inhibitors) can significantly worsen NSAID-induced damage in the small intestine. The pathogenesis of NSAIDenteropathy is complex, but studies in animal models are shedding light on the key factors that contribute to ulceration and bleeding, and are providing clues to the development of effective therapies and prevention strategies. Novel NSAIDs that do not cause small in- FRONTIER

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Section: Novel Intestinal-sparing Nsaidsmentioning

confidence: 78%

Mechanisms, prevention and clinical implications of nonsteroidal anti-inflammatory drug-enteropathy

Wallace¹

2013

WJG

151

148

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“…There is robust evidence to support the notion that an impaired bile acid to phospholipid ratio contributes to the damage caused by ASA/NSAIDs [48][49][50][51]. Indeed, bile salts at high concentrations are detergent molecules that solubilize hydrophobic lipids (cholesterol) and phospholipids in micelles, allowing bile formation, cholesterol disposal, and intestinal lipid absorption.…”

Section: Fxr and Nsaid-induced Gastroenteropathymentioning

confidence: 83%

Bile acid activated receptors are targets for regulation of integrity of gastrointestinal mucosa

et al. 2015

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Bile acids are the end product of cholesterol metabolism. Synthesized in the liver, primary bile acids are secreted by hepatocytes and are transformed by intestinal microbiota into secondary bile acids. In addition to their role in cholesterol and lipid absorption, bile acids act as signaling molecules activating a family of nuclear and G-protein-coupled receptors collectively known as bile acid activated receptors (BARs). These receptors are expressed at high density in enterohepatic tissues, but their expression occurs throughout the body and their activation mediates regulatory functions of bile acids on lipids and glucose metabolism and immunity. In the gastrointestinal tract, BARs maintain intestinal integrity, and their deletion makes the intestine more susceptible to the damage caused by acetylsalicylic acid and nonsteroidal anti-inflammatory drugs (NSAIDs). Deficiency in farnesoid X receptor and G-protein-coupled bile acid receptor 1 genes alters the expression/activity of cystathione c-lyase and endothelial nitric oxide synthase, two genes involved in the synthesis of hydrogen sulfide and nitric oxide, i.e., two gaseous mediators that have been shown to be essential in maintaining the intestinal homeostasis. In addition, farnesoid X receptor regulates the expression of transporters required for secretion of phospholipid by hepatocytes. Because phospholids attenuate intestinal injury caused by acetylsalicylic acid and NSAIDs, BAR agonism could be exploited to protect the intestinal mucosa against injury caused by anti-inflammatory medications. This approach might be useful in the prevention of so-called NSAID enteropathy, a common clinical condition occurring in long-term users of NSAIDs, which is not effectively prevented either by cotreatment with proton pump inhibitors or by the use of coxibs.

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“…In a 4-day study, performed on healthy volunteers, the gastric injuring action of aspirin, assessed through endoscopic examination, was significantly reduced in subjects administered with soy phosphatidylcholine, although in both treatment groups prostaglandin levels in gastric biopsies were significantly reduced (Anand et al, 1999). Recently, Lanza et al (2008) evaluated the digestive safety of ibuprofen chemically combined with phosphatidylcholine in osteoarthritic patients, observing a better tolerability of this association in comparison with ibuprofen alone. CINODs have been developed exploiting the concept that NO, released locally in the gastric mucosa, would enhance the mucosal blood flow and reduce leukocyte adherence in the gastric microcirculation.…”

Section: Novel Therapeutic Options For Prevention and Treatment Of Gamentioning

confidence: 99%

Pathophysiology of Gastric Ulcer Development and Healing: Molecular Mechanisms and Novel Therapeutic Options

Fornai¹,

Antonioli²,

Colucci³

et al. 2011

Peptic Ulcer Disease

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Clinical trial: comparison of ibuprofen‐phosphatidylcholine and ibuprofen on the gastrointestinal safety and analgesic efficacy in osteoarthritic patients

Abstract: SUMMARY BackgroundChronic use of NSAIDs is associated with gastrointestinal (GI) toxicity that increases with age.

Cited by 60 publications

References 27 publications

Mechanisms, prevention and clinical implications of nonsteroidal anti-inflammatory drug-enteropathy

Mechanisms, prevention and clinical implications of nonsteroidal anti-inflammatory drug-enteropathy

Bile acid activated receptors are targets for regulation of integrity of gastrointestinal mucosa

Pathophysiology of Gastric Ulcer Development and Healing: Molecular Mechanisms and Novel Therapeutic Options

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