A randomised trial of differentiated prednisolone treatment in active rheumatoid arthritis. Clinical benefits and skeletal side effects

Abstract

Objectives-To study benefits and skeletal side eVects of carefully monitored prednisolone treatment in patients with active rheumatoid arthritis. Methods-One hundred and two patients with active rheumatoid arthritis were randomly allocated to treatment with disease modifying anti-inflammatory drug (DMARD) alone or DMARD and prednisolone in a one year follow up study. Prednisolone was given in a dose regimen adapted to the disease activity of the individual patient. The mean dose was 6 mg and the mean cumulated dose was 2160 mg. Patients were followed up with disease activity parameters, radiograph of the hands (Larsen score), and bone mineral density (BMD) of the lumbar spine, distal forearm and hand. At one year 26 patients had withdrawn from the investigation leaving 76 patients for evaluation. Results-The results showed that disease activity in the prednisolone treated group was reduced within two weeks. In the DMARD alone group disease activity was gradually reduced over months. At six months there was no diVerence between the groups as evaluated by an improvement score using a number of ACR criteria. Prednisolone in the present set up was not able to protect significantly against radiological disease progression, although there was a trend towards less progression in Larsen score in the prednisolone group, a matter that was further underlined in an intention to treat analysis. BMD data revealed a significant reduction in spinal BMD in the prednisolone group, whereas prednisolone seemed to have a protective eVect against bone loss in the hand and distal forearm. Conclusions-This study does not allow any firm conclusions for or against the treatment of rheumatoid arthritis with prednisolone. The data suggest that the beneficial eVects of prednisolone are not as clear cut in established rheumatoid arthritis as in early disease. Furthermore the data indicate that treatment in the chosen relatively low dose does not provide suYcient control of disease. On the other hand the spinal bone loss observed in the prednisolone group does invite considerations about using higher doses.(Ann Rheum Dis 1999;58:713-718)

Meta‐Analysis of Tumor Necrosis Factor Inhibitors and Glucocorticoids on Bone Density in Rheumatoid Arthritis and Ankylosing Spondylitis Trials

“…We identified 11 eligible studies in patients with RA: 5 studies involved use of TNFi (total of 345 patients exposed to TNFi and 302 controls) (4,(12)(13)(14)(15) (Table 1) and 7 studies involved use of glucocorticoids (total of 445 patients exposed to glucocorticoids and 347 controls) (12,(16)(17)(18)(19)(20)(21) (Table 2). One study investigated the use of both TNFi and glucocorticoids (12) and was therefore included in both meta-analyses.…”

Oral Low-Dose Glucocorticoids Should Be Included in Any Recommendation for the Use of Non-Biologic and Biologic Disease-Modifying Antirheumatic Drugs in the Treatment of Rheumatoid Arthritis

“…All published RCTs confirm the more rapid achievement of better results in patients treated with low-dose GC combination therapy in clinical, functional and structural endpoints. Lower benefit is seen in cases of long-standing disease, indicating that the principle of the ‘window of opportunity' pertains to GC medication: the earlier, the better [28,29]. The structural effects of GCs are more evident when administered in the early phase of the disease.…”

03.02 Evaluation of anti-inflammatory effects of steroids and arthritis-related biotherapies in an in vitro co-culture model with immune cells and synoviocytes

“…Side effects of chronic steroid therapy are dose-related. At a low-dose (<7.5 mg/ day), many studies suggest that steroid treatment is relatively safe in RA (19,20), and even a very low dose (<5 mg/ml), can be sufficient to maintain remission without severe adverse events (21) but a better clinical response (22)(23)(24)(25). To identify their effects at the cellular level, an in vitro model based on interactions between mesenchymal cells and PBMC was used to mimic the in vivo inflammatory state.…”