The effect of single‐dose naproxen on eicosanoid formation in human gastroduodenal mucosa

Treiber, Gerhard; Wex, Thomas; Link, Alexander; Laufer, Stefan; Malfertheiner, P.

doi:10.1111/j.1365-2036.2006.02725.x

Cited by 5 publications

(4 citation statements)

References 55 publications

(72 reference statements)

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“…This study has also shown that SLE patients who had received pulse methylprednisolone therapy and developed gastric mucosal damage had a significantly higher rate of NSAID/ aspirin use, lower gastric TXB2 and lower gastric PGE2 than those without gastric mucosa damage. This study also showed that patients who took NSAIDs/aspirin had significantly lower serum TXB2, lower serum PGE2, lower gastric TXB2, and lower gastric PGE2, which is consistent with other studies [18,22].Taken together, these observations suggest that lower gastric TXB2 and lower gastric PGE2 in these SLE patients with gastric mucosal injury may be due to NSAID/ aspirin effects rather than the methylprednisolone effect. This suggestion was supported by logistic regression analysis showing that NSAID/aspirin usage was the only risk factor for gastric mucosal injury in those SLE patients who had received pulse therapy.…”

Section: Discussionsupporting

confidence: 91%

“…These findings support that pulse methylprednisolone therapy does not inhibit COX-1 function of serum and gastric mucosa and does not cause gastric mucosal injury, although it decreases serum COX-2 activity, which is consistent with previous findings that inhibition of both COX-1 and COX-2 function is required for rat gastric mucosa injury [10]. Although the intra-and interassay variability of ELISA for PGE2 and TXB2 is reportedly high [18,22], Wilcoxon signed rank test was used in this inquiry to compare individual eicosonoids in the same patients before and after pulse therapy. In addition, all the eicosonoids were prepared and measured simultaneously to decrease intraand interassay variability.…”

Section: Discussionsupporting

confidence: 91%

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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: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 91%

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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“…One example of a drug that has this activity in horses is carprofen, which when given at the clinically recommended dosage of 0.7 mg/kg IV is a weak inhibitor of COX, but has some inhibitory action of 5‐LOX . There has been some concern that COX‐inhibiting NSAIDs may shunt arachidonic acid toward the LOX enzyme system, thereby enhancing inflammation, but this has not been consistently shown to be the case . Nonetheless, dual inhibitors of both COX and LOX remain a possibility for the future.…”

Section: Renal Effectsmentioning

confidence: 99%

The use of nonsteroidal anti‐inflammatory drugs in critically ill horses

Cook

Blikslager

2014

J Vet Emergen Crit Care

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“…Nachdem beide Cyclooxygenasen, COX-1 und COX-2, durch NSAR gehemmt werden, kommt es zu einer vermehrten Bildung von Leukotrienen über die 5-Lipooxygenase (5-LOX). Auch Leukotriene schädigen durch eine toxische Wirkung sowohl Gefäße in der Schleimhaut als auch die Schleimhautbarriere selbst [10,11].…”

Section: Nichtsteroidale Antirheumatika Und Acetylsalicylsäureunclassified

Ulkuskrankheit

Malfertheiner

Bellutti²

2006

Internist

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Treatment of peptic ulcer disease has undergone a radical change due to the discovery of its main cause, the Helicobacter pylori infection. The management of the chronic infection is now the primary aim. Treatment of peptic ulcer essentially consists of eradicating H. pylori. A current problem is the resistance developed by H. pylori to the antibiotics used in eradication regimen. Ulcers that are induced by nonsteroidal antirheumatic (NSAR) agents and acetylsalicylic acid are gaining in importance. Optimized inhibition of acid secretion with proton pump inhibitors has made it possible to both prevent and cure ulcers in the stomach and duodenum caused by NSAR agents.

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The effect of single‐dose naproxen on eicosanoid formation in human gastroduodenal mucosa

Abstract: SUMMARY BackgroundIn animal studies, aspirin and non-aspirin non-steroidal anti-inflammatory drugs contribute to gastroduodenal damage via cyclo-oxygenase inhibition and consecutive leucotriene formation (COX-LOX eicosanoid shunt).

Cited by 5 publications

References 55 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

The use of nonsteroidal anti‐inflammatory drugs in critically ill horses

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