Abstract
BackgroundGlucocorticoids (GCs) are used in ~ 60% of patients with rheumatoid arthritis (RA). Although disease-modifying, they also have significant adverse effects. Understanding factors associated with GC use may help minimise exposure. The aims of the present study were to describe oral GC use in RA; determine any change in use over time; and determine factors associated with oral GC use, commencement or cessation.MethodsAdult patients with RA were identified in the Australian Rheumatology Association Database (ARAD), a national Australian registry that collects long-term outcome data from patients with inflammatory arthritis. Patients were categorised by their ARAD date of entry (DOE), with population-averaged logistic regression and transition state analysis used to determine any change in GC use over time. Fixed-effects panel regression was used to examine whether GC current use was associated with pain/arthritis activity/Health Assessment Questionnaire (HAQ) scores or medication use. Transition state analysis was used to assess whether these factors influenced the commencement or cessation of GCs.ResultsA total of 3699 patients with RA completed a baseline ARAD questionnaire (73% female, mean age 57 years). The probability of GC use decreased over time according to ARAD DOE: September 2001 to March 2005, 55% (95% CI 52–58%); March 2005 to September 2008, 47% (45–49%); September 2008 to March 2012, 42% (39–45%); and March 2012 to October 2015, 39% (34–43%) (p < 0.001). Conventional synthetic disease-modifying anti-rheumatic drugs (OR 10.13; 95% CI 8.22–12.47), non-steroidal anti-inflammatory drugs (1.18; 1.02–1.37) and opioids (2.14; 1.84–2.48) were associated with GC current use, as were lower pain scores (0.94; 0.90–0.98), higher arthritis activity scores (1.09; 1.05–1.14) and poorer HAQ scores (1.52; 1.30–1.79). Use of biologic disease-modifying anti-rheumatic drugs (bDMARDs) was not associated with GC current use (0.98; 0.83–1.15) or GC cessation (HR 0.87; 95% CI 0.75–1.01), but it was associated with GC commencement (0.54; 0.47–0.62).ConclusionsThe probability of oral GC use decreased over time, with reduced commencement and increased cessation of GCs. The modest effect of bDMARDs on GC cessation was not statistically significant.
Highlights
Glucocorticoids (GCs) are used in ~ 60% of patients with rheumatoid arthritis (RA)
In Australia, Biologic disease-modifying anti-rheumatic drug (bDMARD) can be prescribed for RA only by rheumatologists, and prescribing is restricted on the basis of the following criteria: (1) The patient has severe, active RA; (2) the patient has failed a 6-month intensive Conventional synthetic disease-modifying anti-rheumatic drug (csDMARD) trial with a minimum of two agents for a minimum of 3 months each; (3) the patient can demonstrate failure to achieve an adequate response to 6 months of intensive prior treatment by an elevated erythrocyte sedimentation rate > 25 mm/h and/or an elevated C-reactive protein level > 15 mg/L, and the patient has an active joint count of ≥ 20 active joints or ≥ 4 major active joints
Change in GC use over time, according to Australian Rheumatology Association Database (ARAD) date of entry To test the hypothesis that GC use may vary over time, the probability of GC use throughout follow-up was examined according to DOE categories
Summary
Glucocorticoids (GCs) are used in ~ 60% of patients with rheumatoid arthritis (RA). diseasemodifying, they have significant adverse effects. Glucocorticoids (GCs) are used in ~ 60% of patients with rheumatoid arthritis (RA) globally [1] They have been shown to have disease-modifying properties [2], they are associated with significant adverse effects [3, 4]. Patients with severe disease resistant to conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs) prior to the introduction of bDMARDs may have been more likely to receive GCs than those with resistant disease and early access to bDMARDs. Previous studies have shown that bDMARDs can have a GC-sparing effect in RA, with a significant GC dose reduction seen in those commenced on bDMARDs compared with those who are not [7,8,9,10,11]. GC cessation rather than reduction should be the goal of therapy
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