Rofecoxib, a COX-2 inhibitor, does not inhibit human gastric mucosal prostaglandin production

Wight, Nicholas J.; Gottesdiener, Keith; Garlick, Nigel; Atherton, Clare T.; Novak, Sofia; Gertz, Barry J.; Calder, Nicole; Côté, Josée; Wong, Peggy; Dallob, A.; Hawkey, Chris J.

doi:10.1053/gast.2001.22432

Cited by 58 publications

(35 citation statements)

References 23 publications

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“…Blood COX-2 activity was measured as lipopolysaccharide (LPS)-induced PGE2, and blood COX-1 activity was measured as serum TXB2 [20]. LPS-induced PGE2 in whole blood, a marker of monocyte COX-2 activity, and serumgenerated TXB2 in whole blood, a marker of platelet COX-1 activity, were measured as in a previous study [20].…”

Section: Procedures and Measurementmentioning

confidence: 99%

“…LPS-induced PGE2 in whole blood, a marker of monocyte COX-2 activity, and serumgenerated TXB2 in whole blood, a marker of platelet COX-1 activity, were measured as in a previous study [20]. PGE2 and TXB2 were measured in duplicate using PGE2 and TXB2 enzyme-linked immunosorbent assay (ELISA) kit, respectively (Quantikine; R&D Systems Inc., Minneapolis, MN, USA).…”

Section: Procedures and Measurementmentioning

confidence: 99%

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Gastric mucosal injury in systemic lupus erythematosus patients receiving pulse methylprednisolone therapy

Luo

Chang

Chen

et al. 2009

Brit J Clinical Pharma

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Keywordsgastric mucosal injury, Helicobacter pylori, nonsteroidal anti-inflammatory drugs, pulse methylprednisolone therapy, systemic lupus erythematosus ---------------------------------------------------------------------- WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT• Whether glucocorticoids induce gastric mucosal injury remains uncertain, and Helicobacter pylori infection in steroid users has not been well evaluated in the past.• Pulse methylprednisolone therapy with the very high dose of steroid that is 100 times larger than the physiological dose will be a special model to evaluate whether glucocorticoids induce gastric mucosal injury. WHAT THIS STUDY ADDS• Use of nonsteroidal anti-inflammatory drugs/aspirin, but not H. pylori infection, increases gastric mucosal injury in systemic lupus erythematosus patients receiving pulse methylprednisolone therapy.• Very high-dose steroids de novo seem not to induce gastric mucosal injury in these patients.• However, a larger, case-controlled study enrolling a heterogeneous population is needed to clarify the role of glucocorticoids in gastric mucosal injury. AIMSWhether glucocorticoids induce gastric mucosal injury remains uncertain. We investigated whether very high-dose steroids caused gastric mucosal injury in systemic lupus erythematous (SLE) patients and evaluated the possible risk factors for mucosal injury. METHODSIn this prospective paired study, 67 SLE patients who had received pulse methylprednisolone therapy were enrolled. Each patient underwent endoscopic examination and tissue and blood sampling before and after pulse steroid therapy. Mucosal injury was diagnosed if the follow-up injury scale was higher than the initial scale. Examined parameters included Helicobacter pylori infection, cyclooxygenase (COX)-1 and COX-2 activity, and current nonsteroidal anti-inflammatory drug (NSAID) usage including aspirin. RESULTSEleven (16.4%) of 67 cases who developed gastric mucosal injury after pulse therapy had significantly higher rates of peptic ulcer history, NSAID/aspirin use, lower gastric thromboxane B2 and prostaglandin E2 levels when compared with cases without gastric mucosal injury (P < 0.05).Infection by H. pylori was not a risk factor for gastric mucosal injury. Multivariate logistic regression analysis showed that NSAID/aspirin use was the only risk factor for gastric mucosal injury in these patients (odds ratio 26.99, 95% confidence interval 4.91, 148.57, P < 0.0001). Pulse steroid therapy alone did not induce gastric mucosal injury in fifty SLE patients without taking any NSAID/aspirin. CONCLUSIONSUse of NSAIDs/aspirin, but not H. pylori infection, increases gastric mucosal injury in SLE patients receiving pulse methylprednisolone therapy. Very high-dose steroids de novo seem not to induce gastric mucosal injury in these patients. A larger case-controlled study enrolling a heterogeneous population is needed to clarify the role of glucocorticoids in gastric mucosal injury.

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Section: Procedures and Measurementmentioning

confidence: 99%

Section: Procedures and Measurementmentioning

confidence: 99%

Gastric mucosal injury in systemic lupus erythematosus patients receiving pulse methylprednisolone therapy

Luo

Chang

Chen

et al. 2009

Brit J Clinical Pharma

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“…Therefore, multiple randomized controlled trials were designed and executed to test the benefits of sulindac, and these confirmed the efficacy of this drug in inducing regression of adenomas (3,4,18). However, long-term use of NSAIDs generates gastrointestinal side effects such as bleeding and ulceration (19,20), and this fostered interest in developing more selective and targeted approaches (5,21), including use of COX-2 inhibitors. An initial randomized controlled trial in patients with FAP demonstrated that treatment with either of two doses of celecoxib (100 mg twice daily or 400 mg twice daily) significantly reduced the number of polyps in the colorectum (22).…”

Section: Discussionmentioning

confidence: 99%

Molecular targets and chemoprevention drug development in hereditary colorectal cancer syndromes

Borràs¹,

You²,

Vilar³

2014

AACR Education book

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“…Im Gegensatz zur Niere wird im Magen nur COX-1 exprimiert [25]. Die Gabe von NSAID führt durch eine COX-1-Inhibition zu einem Abfall der gastralen Prostaglandin-E 2 -Produktion, während COX-2-Inhibitoren keine Veränderungen bewirken [154,156].Außerdem verändern NSAID die Zusammensetzung und die sezernierte Menge des Schleims [97].…”

Section: Inzidenz Und Pathophysiologie Postoperativer Ulzeraunclassified

Nichtopioidanalgetika zur perioperativen Schmerztherapie

2004

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Non-opioid analgesics play a central role in the management of postoperative pain. In this review, the pharmacology, the analgesic efficacy and the side-effects of non-opioid analgesics are summarized. First, the pharmacology of diclofenac, acetyl salicylic acid, dipyrone, acetaminophen and the COX-2 inhibitors is described. Second, the analgesic efficacy of non-opioid analgesics is analyzed for moderate pain (e.g. ambulatory surgery) and for moderate to severe pain (e.g. abdominal surgery-in combination with opioids). There is limited evidence for an additive analgesic effect of two non-opioid analgesics. Third, the major side-effects of non-opioid analgesics are discussed in relation to the pathophysiology, the frequency and the clinical relevance of these effects. In particular, side-effects on the gastrointestinal tract (ulcus formation), on coagulation (bleeding and thrombosis), on the renal (renal insufficiency), the pulmonary (bronchospasm) and the hematopoetic systems (agranulocytosis) are described. Recommendations for the clinical use of non-opioid analgesics for perioperative pain therapy are given.

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Rofecoxib, a COX-2 inhibitor, does not inhibit human gastric mucosal prostaglandin production

Cited by 58 publications

References 23 publications

Gastric mucosal injury in systemic lupus erythematosus patients receiving pulse methylprednisolone therapy

Gastric mucosal injury in systemic lupus erythematosus patients receiving pulse methylprednisolone therapy

Molecular targets and chemoprevention drug development in hereditary colorectal cancer syndromes

Nichtopioidanalgetika zur perioperativen Schmerztherapie

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