Abstract

Aims: Approximately 50% of rheumatoid arthritis (RA) patients require treatment with glucocorticoids (GC) to control inflammation [1]. Although effective, GC cause numerous adverse effects. Glucocorticoid-induced leucine zipper (GILZ) is an anti-inflammatory protein, which is up-regulated by GC. Although GILZ mediates the anti-inflammatory effects of GC, it appears to have osteogenic effects on bone [2]. This has raised interest in GILZ as a potential therapeutic approach, which could replicate the anti-inflammatory effects of GC while minimising the adverse effects [1]. Prior to examining GILZ as a therapeutic avenue, a greater understanding of its role in RA is needed. Methods: Clinical data was obtained from RA patients and medical records. Three control cohorts were also recruited, including 23 healthy controls, 25 patients with fibromyalgia and 44 patients with depression. Blood was taken from each participant. Following isolation of peripheral blood mononuclear cells (PBMC) from whole blood, RNA was extracted. Reverse transcription polymerase chain reaction (RT PCR) and quantitative real time PCR (qPCR) were performed to quantify GILZ expression. Results: GILZ expression was increased in RA patients compared to healthy controls, patients with fibromyalgia and patients with depression. Prednisolone use was associated with increased GILZ expression, and there was a weak positive correlation between GILZ expression and prednisolone dose. There was a strong negative correlation between GILZ adjusted for prednisolone dose and disease activity in RA patients. Conclusions: Our results suggest that patients who are better able to induce GILZ in response to GC may experience more significant improvement in disease activity with relatively lower doses of steroids.

Authors and Affiliations