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

Authors


Associate Professor Hsiao-Yi Lin, MD, Division of Allergy, Immunology, and Rheumatology, Department of Medicine, Taipei Veterans General Hospital, 201 Shih-Pai Road, Section 2, Taipei 11217, Taiwan.
Tel: + 886 2 2875 7521
Fax: + 886 2 2871 7195
E-mail: hylin@vghtpe.gov.tw

Abstract

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.

AIMS

Whether 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.

METHODS

In 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.

RESULTS

Eleven (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.

CONCLUSIONS

Use 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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