ArticleBritish journal of clinical pharmacology2009
Gastric mucosal injury in systemic lupus erythematosus patients receiving pulse methylprednisolone therapy.
Article in British journal of clinical pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Review on recent advancements in understanding acetylsalicylic acid-induced gastrointestinal injury: mechanisms, medication, and dosage refinement.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- The 330 risk loci known for systemic lupus erythematosus (SLE): a review.Frontiers in lupus · 2024Article
- Helicobacter pylori infection and gastroduodenal lesions in patients with systemic lupus erythematosus.Clinical rheumatology · 2020Article
- The Contribution of Drugs andInternational journal of rheumatology · 2019Article
- A Rare Case of Systemic Lupus Erythematosus with Gastric Ulcer and Acute Pancreatitis: A Case Report and Literature Review.Gastroenterology research · 2018Article
- Drug use and upper gastrointestinal complications in children: a case-control study.Archives of disease in childhood · 2013Article
- The diminished expression of proangiogenic growth factors and their receptors in gastric ulcers of cirrhotic patients.PloS one · 2013Article
- Glucocorticoids are Gastroprotective under Physiologic Conditions.Therapeutic advances in chronic disease · 2011Article
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Authors and funding
9 authors.
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No grant is acknowledged in the PubMed record.
Abstract
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 B(2) and prostaglandin E(2) 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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