Prevention of NSAID-Associated Gastrointestinal Lesions: A Comparison Study Pantoprazole<i>versus</i>Omeprazole

Reguła, Jarosław; Butruk, E; Dekkers, C. P. M.; Boer, S. Y. De; Raps, Dieter; Szabó, László; Terjung, Andreas; Thomas, Kathy B.; Lühmann, R; Fischer, Renate

doi:10.1111/j.1572-0241.2006.00686.x

Cited by 64 publications

(45 citation statements)

References 28 publications

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“…Approximately 30 million patients consume NSAIDs on a daily basis (1). However, NSAIDs have limitations; they induces gastropathy, and ϳ107,000 patients are hospitalized every year due to NSAIDrelated gastrointestinal complications (3).…”

Section: Nsaidsmentioning

confidence: 99%

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Tryptamine-Gallic Acid Hybrid Prevents Non-steroidal Anti-inflammatory Drug-induced Gastropathy

Pal

Dey

Alam

et al. 2012

Journal of Biological Chemistry

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Background: Non-steroidal anti-inflammatory drugs (NSAIDs) induce gastropathy by promoting mitochondrial pathology, oxidative stress, and apoptosis in gastric mucosal cells. Results: We have synthesized SEGA (3a), a tryptamine-gallic acid hybrid, which prevents NSAID-induced gastropathy by preventing mitochondrial oxidative stress, dysfunction, and apoptosis. Conclusion: SEGA (3a) bears an immense therapeutic potential against NSAID-induced gastropathy. Significance: This novel molecule is a significant addition in the discovery of gastroprotective drugs.

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Section: Nsaidsmentioning

confidence: 99%

“…2 are the most popular drugs commonly used throughout the world for the treatment of pain, inflammation, rheumatic disorders, and osteoarthritis (1,2). Approximately 30 million patients consume NSAIDs on a daily basis (1).…”

Section: Nsaidsmentioning

confidence: 99%

Tryptamine-Gallic Acid Hybrid Prevents Non-steroidal Anti-inflammatory Drug-induced Gastropathy

Pal

Dey

Alam

et al. 2012

Journal of Biological Chemistry

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“…Non-steroidal anti-inflammatory drugs (NSAIDs), 2 commonly used for the treatment of arthritis and other musculoskeletal disorders are considered to be one of the most important causative factors for gastric damage (1)(2)(3). Although various mechanisms have been suggested for NSAID-induced gastric ulcer (4 -7), recent studies suggest that increased apoptotic cell death and simultaneous block of mucosal cell renewal play major roles in the development of mucosal lesion (8 -10).…”

mentioning

confidence: 99%

Lansoprazole Protects and Heals Gastric Mucosa from Non-steroidal Anti-inflammatory Drug (NSAID)-induced Gastropathy by Inhibiting Mitochondrial as Well as Fas-mediated Death Pathways with Concurrent Induction of Mucosal Cell Renewal

Maity

Bindu

Choubey³

et al. 2008

Journal of Biological Chemistry

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We have investigated the mechanism of antiapoptotic and cell renewal effects of lansoprazole, a proton pump inhibitor, to protect and heal gastric mucosal injury in vivo induced by indomethacin, a non-steroidal anti-inflammatory drug (NSAID). Lansoprazole prevents indomethacin-induced gastric damage by blocking activation of mitochondrial and Fas pathways of apoptosis. Lansoprazole prevents indomethacin-induced up-regulation of proapoptotic Bax and Bak and down-regulation of antiapoptotic Bcl-2 and Bcl xL to maintain the normal proapoptotic/antiapoptotic ratio and thereby arrests indomethacin-induced mitochondrial translocation of Bax and collapse of mitochondrial membrane potential followed by cytochrome c release and caspase-9 activation. Lansoprazole also inhibits indomethacin-induced Fas-mediated mucosal cell death by down-regulating Fas or FasL expression and inhibiting caspase-8 activation. Lansoprazole favors mucosal cell renewal simultaneously by stimulating gene expression of prosurvival proliferating cell nuclear antigen, survivin, epidermal growth factor, and basic fibroblast growth factor. The up-regulation of Flt-1 further indicates that lansoprazole activates vascular epidermal growth factor-mediated controlled angiogenesis to repair gastric mucosa. Lansoprazole also stimulates the healing of already formed ulcers induced by indomethacin. Time course study of healing indicates that it switches off the mitochondrial death pathway completely but not the Fas pathway. However, lansoprazole heals mucosal lesions almost completely after overcoming the persisting Fas pathway, probably by favoring the prosurvival genes expression. This study thus provides the detailed mechanism of antiapoptotic and prosurvival effects of lansoprazole for offering gastroprotection against indomethacin-induced gastropathy.Non-steroidal anti-inflammatory drugs (NSAIDs), 2 commonly used for the treatment of arthritis and other musculoskeletal disorders are considered to be one of the most important causative factors for gastric damage (1-3). Although various mechanisms have been suggested for NSAID-induced gastric ulcer (4 -7), recent studies suggest that increased apoptotic cell death and simultaneous block of mucosal cell renewal play major roles in the development of mucosal lesion (8 -10). Healthy gastric mucosa is always under equilibrium between cell death and cell renewal (11, 12) and mucosal injury is developed when this balance is disturbed due to an increase in apoptosis and/or inhibition of cell proliferation (11,12). NSAIDs are shown to induce apoptosis in gastric mucosal cells through reactive oxygen species generation, cytochrome c release, activation of caspase-3, inhibition of survivin expression, and induction of Ca 2ϩ signaling (8,10,13,14). Caspase-3 activation is generally mediated through two main pathways, viz. the mitochondrial (internal) and death receptor (external) pathways (15, 16). In the mitochondrial pathway, up-regulation or activation of pro-apoptotic proteins and/or down-regulation or inactivat...

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“…The authors concluded that both doses of pantoprazole and omeprazole provide equivalent, effective, and well-tolerated primary prophylaxis against the endoscopic development of peptic ulcer disease in chronic NSAID users. 38 While most COX-2 inhibitors are no longer widely available due to safety concerns, these drugs provided an alternative strategy in primary and secondary prophylaxis of gastrointestinal complications related to chronic NSAIDs. Several large outcomes studies have demonstrated signifi cantly fewer clinically important upper gastrointestinal events in patients treated with selective COX-2 inhibitors compared to non-selective NSAIDs.…”

Section: Primary Prophylaxis Of Nsaid-induced Peptic Ulcer Diseasementioning

confidence: 99%

Treatment and chemoprevention of NSAID-associated gastrointestinal complications

Go¹

2008

TCRM

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Abstract:The use of non-steroidal anti-infl ammatory drugs has become ubiquitous worldwide and remains a common source of gastrointestinal morbidity. Antisecretory medications, particularly proton pump inhibitors, are effective in the treatment and prevention of NSAID-related gastrointestinal complications, including peptic ulcer disease and non-ulcer dyspepsia. A careful assessment of patients' risk factors for developing NSAID-related gastrointestinal complications should be undertaken prior to initiation of any NSAIDs. Patients who are considered at risk for developing gastrointestinal complications should receive concurrent antisecretory medical therapy to minimize the risk for GI complications.

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Prevention of NSAID-Associated Gastrointestinal Lesions: A Comparison Study PantoprazoleversusOmeprazole

Abstract: For patients taking NSAIDs continually, pantoprazole 20 mg o.d., pantoprazole 40 mg o.d., or omeprazole 20 mg o.d. provide equivalent, effective, and well-tolerated prophylaxis against GI lesions, including peptic ulcers.

Cited by 64 publications

References 28 publications

Tryptamine-Gallic Acid Hybrid Prevents Non-steroidal Anti-inflammatory Drug-induced Gastropathy

Tryptamine-Gallic Acid Hybrid Prevents Non-steroidal Anti-inflammatory Drug-induced Gastropathy

Lansoprazole Protects and Heals Gastric Mucosa from Non-steroidal Anti-inflammatory Drug (NSAID)-induced Gastropathy by Inhibiting Mitochondrial as Well as Fas-mediated Death Pathways with Concurrent Induction of Mucosal Cell Renewal

Treatment and chemoprevention of NSAID-associated gastrointestinal complications

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