Abstract
IntroductionGlucocorticoid (GC)-induced osteoporosis is a frequent complication in patients with rheumatoid arthritis. However, little information exists about the consequences of GC use in patients with early arthritis. Here we describe the variables underlying the use of GC in early arthritis, as well as its effect on bone-mineral density.MethodsData from 116 patients in our early arthritis register were analyzed (90 women; median age, 52.5 years, interquartile range (IQR, 38.5-66); 6-month median disease duration at entry (IQR, 4-9)). In this register, the clinical and treatment information was recorded systematically, including the cumulative GC dose. Lumbar spine, hip, and forearm bone-mineral density (BMD) measurements were performed at entry and after a 2-year follow-up. A multivariate analysis was performed to establish the variables associated with the use of GCs, as well as those associated with variations in BMD.ResultsOf the patients with early arthritis studied, 67% received GCs during the 2-year follow-up. GCs were more frequently prescribed to elderly patients, those with higher basal disease activity and disability, and patients with positive rheumatoid factor. When adjusted for these variables, GCs were less frequently prescribed to female patients. The use of GCs was associated with an increase of BMD in the ultradistal region of the forearm, although it induced a significant loss of BMD in the medial region of the forearm. No relevant effect of GC was noted on the BMD measured at other locations.ConclusionsThe frequent use of GCs as a "bridge therapy" in patients with early arthritis does not seem to be associated with relevant loss of bone mass. Moreover, cumulative GC administration might be associated with an increase of juxtaarticular BMD.
Highlights
Glucocorticoid (GC)-induced osteoporosis is a frequent complication in patients with rheumatoid arthritis
To assess whether oral and intraarticular/ soft tissue injection had equivalent effects on bone-mineral density (BMD), we developed a model with two independent variables, one for the cumulative GC dose prescribed orally and another for the cumulative GC dose administered as soft-tissue and joint injections
The prescription of GCs increased by 45.4% during the first 6 months, and it gradually decreased to only 17.3% by the end of the follow-up period (Figure 1a)
Summary
Glucocorticoid (GC)-induced osteoporosis is a frequent complication in patients with rheumatoid arthritis. We describe the variables underlying the use of GC in early arthritis, as well as its effect on bone-mineral density. Rheumatoid arthritis (RA) is a systemic and chronic inflammatory disease that has been associated with disability, the existence of comorbidities, and decreased life expectancy [1,2]. One of the most striking side effects of this drug is GC-induced osteoporosis (GIOP), a complication in patients with RA that can be prevented [11,12,13]. Establishing the real contribution of GCs to OP in RA is challenging because bone mineral loss is of multifactorial origin in these patients, and it may be influenced by inflammatory cytokines, inactivity, GCs, disease-modifying antirheumatic drugs (DMARDs), as well as the classic risk factors for OP
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