Case-control study of corticosteroids and other drugs that either precipitate or protect from the development of scleroderma renal crisis
Article first published online: 14 MAY 2004
Copyright © 1998 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 41, Issue 9, pages 1613–1619, September 1998
How to Cite
Steen, V. D. and Medsger, T. A. (1998), Case-control study of corticosteroids and other drugs that either precipitate or protect from the development of scleroderma renal crisis. Arthritis & Rheumatism, 41: 1613–1619. doi: 10.1002/1529-0131(199809)41:9<1613::AID-ART11>3.0.CO;2-O
- Issue published online: 14 MAY 2004
- Article first published online: 14 MAY 2004
- Manuscript Accepted: 19 MAR 1998
- Manuscript Received: 4 AUG 1997
- Scleroderma Federation
- United Scleroderma Foundation
- Arthritis Foundation
- Western Pennsylvania Chapter (Shoemaker Fund), Pittsburgh
To determine whether the initiation of corticosteroids or other types of therapy affects the development of scleroderma renal crisis (SRC).
Using a case-control study, 110 patients with systemic sclerosis who developed SRC between 1981 and 1993 were closely matched with controls on sex, race, age, disease duration, skin score, levels of creatine phosphokinase, and presence of tendon friction rubs. Corticosteroid use was determined prior to the onset of SRC in cases or prior to the first visit in controls. Cases were compared with matched controls using McNemar's matched-pair analysis and conditional logistic regression analysis. The effects of other drugs, including D-penicillamine, nonsteroidal anti-inflammatory drugs (NSAIDs), calcium channel blockers, and angiotensin-converting enzyme (ACE) inhibitors, were also evaluated.
In the 6 months prior to SRC onset or to the first visit, high-dose corticosteroids (≥15 mg/day prednisone or equivalent) were administered significantly more frequently in SRC patients (36%) than in the controls (12%) (McNemar's odds ratio 4.37, 95% confidence interval 2.03-9.43, P < 0.0001). New use of low-dose steroids, continuous use of any steroid dose, NSAIDs, calcium channel blockers, and ACE inhibitors were not associated with an increased risk of SRC. Antecedent D-penicillamine therapy may have been protective against the development of SRC in controls.
This retrospective case-control study has shown a significant association between antecedent high-dose corticosteroid therapy and the development of SRC. These results should discourage the use of high-dose corticosteroids in patients with early diffuse scleroderma who are at increased risk of developing SRC.