Abstract
Objectives: This study aimed to provide reliable information on the impact of low-dose glucocorticoids (GCs) on the bone mineral density (BMD) of patients with rheumatoid arthritis (RA). Methods: This retrospective study enrolled 933 patients with RA who continued the consumption of GCs (GC group) and 100 patients who had discontinued consumption for >1 year (no-GC group). The BMD values were measured at baseline and follow-up, and the annual rate of change in BMD between the groups was compared using dual-energy X-ray absorptiometry. We used multiple linear regression analysis to identify the factors associated with changes in BMD. Results: The demographic characteristics and use of medical treatments affecting bone metabolism were similar between the two groups. Furthermore, there were no significant differences in the annual rate of changes in BMD and incidence of newly developed osteoporosis and incidental fractures between the two groups. Multiple linear regression analysis revealed that the disease activity score for 28 joints with erythrocyte sedimentation rate was the only factor affecting the annual rate of changes in BMD, and it was inversely proportional to changes in BMD. Conclusion: The benefits of GC therapy in attenuating inflammation compensate for the risk of osteoporosis if adequate measures to prevent bone loss are implemented in patients with RA.
Highlights
IntroductionRheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic, symmetrical, and progressive inflammatory polyarthritis [1]
There was no significant difference between the two groups in terms of age, sex, menopausal status, body mass index (BMI), smoking habits, alcohol consumption, or disease duration
The baseline bone biochemistry results did not deviate from the normal range and were similar between the two groups
Summary
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic, symmetrical, and progressive inflammatory polyarthritis [1]. Under pathological conditions of RA, the balance between bone resorption and formation is disrupted by the expression of pro-inflammatory cytokines that promote osteoclast differentiation and suppress the osteogenic activity of the osteoblasts [2]. Uncontrolled inflammation is transformed into hyperplastic invasive tissue, which destroys the cartilage and bone, leading to local and generalized bone loss [3]. This mechanism causes osteoporosis, a major complication of RA, which is a risk factor for fractures, impairs functional ability, deteriorates the quality of life, and further contributes to increased mortality [4]
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