Abstract
Background
Glucocorticoids are frequently employed in systemic lupus erythematosus (SLE) patients and play a critical role in the induction therapy of lupus nephritis (LN), despite their many side effects, including steroid-induced diabetes (SID). Information regarding SID in SLE patients is quite scant.
Purpose
The aim of this study was to determine risk factors associated with the development of SID in patients with LN.
Research Design
A nested case-control study was conducted.
Study sample
We included patients with biopsy-proven LN, who received induction treatment with steroids.
Data Collection and/or Analysis
Out of the total of 358 patients, 35 (9.7%) developed SID.
Results
Patients with SID had more metabolic risk factors, including the metabolic score for insulin resistance (METS-IR); more factors related with lupus activity, with higher SLEDAI and SLICC-DI scores; and lower cumulative pre-induction steroid dose. A higher percentage of patients who developed SID received steroid pulses and a lower percentage received antimalarials. After logistic regression, the variables significantly associated with the development of SID were the SLEDAI index (OR 1.25 [95% CI 1.04–1.50], p 0.01), SLICC-DI (OR 4.93 [95% CI 2.14–11.3], p < 0.001), METS-IR (OR 1.17 [95% CI 1.04–1.32], p 0.009), delta METS-IR at 6 months (OR 1.20 [95% CI 1.03–1.39], p 0.01), and the use of antimalarials (OR 0.14, [95% CI 0.02–0.85], p 0.03). After propensity score matching, METS-IR remained a significant predictor of SID. Patients with METS-IR >36.8 were at higher risk (OR: 2.83, 95% CI: 1.09–7.36, p = 0.034).
Conclusions
In conclusion, SDI development in patients receiving induction therapy for LN is associated with both classic metabolic risk factors and SLE-specific factors, and antimalarial use could be associated with a protective effect. Rheumatologists should be aware of this potential complication, in order to implement appropriate management strategies.
Get full access to this article
View all access options for this article.
