Glucocorticoids, Inflammation and Bone.

The current review on glucocorticoids (GCs), inflammation and bone is focused on three aspects: (1) the mutual effects between GCs, inflammation and bone in inflammatory rheumatic diseases, (2) current views on fracture risk assessment in patients using GCs and (3) non-pharmacological and pharmacological treatment to prevent fractures in GC-using patients with inflammatory rheumatic diseases. The use of GCs results in increased risk for fractures due to both direct and indirect negative effects of GCs on bone mass, and on bone and muscle strength. However, also the underlying inflammatory rheumatic disease is associated with the increased bone loss and fracture risk due to the chronic inflammation itself, and due to disability/immobility caused by active disease or joint destruction.

Management of osteoporosis in rheumatoid arthritis patients.

Introduction: In rheumatoid arthritis (RA) patients, the risk of both vertebral and non-vertebral fractures is roughly doubled, which is for an important part caused by inflammation-mediated amplification of bone loss and by immobilization. New treatments have become available in the last two decades to treat both RA and osteoporosis.

Areas Covered: Epidemiology and assessment of osteoporosis and fracture risk (including the influence of RA disease activity and bone-influencing medications such as glucocorticoids), the importance of vertebral fracture assessment in addition to bone density measurement in patients with RA, the use of disease-modifying antirheumatic drugs and their effects on generalized bone loss, and current and possible future anti-osteoporotic pharmacotherapeutic options are discussed with special focus on RA.

Metabolic effects of high-dose prednisolone treatment in early rheumatoid arthritis: balance between diabetogenic effects and inflammation reduction.

Objective: To investigate the dose-related effects of glucocorticoid treatment on glucose tolerance, beta cell function, and insulin sensitivity in patients with early active rheumatoid arthritis (RA).

Methods: A randomized, controlled, single-blind trial was conducted in 41 patients with early active RA. At the beginning of the trial patients had not been treated for their RA, and were randomized to begin treatment with prednisolone at 60 mg/day or 30 mg/day.

Changes in macrophage inhibitory factor correlate with changes in bone mineral density in glucocorticoid-treated patients with rheumatoid arthritis.

Objectives: To investigate whether changes in bone density and turnover are associated with changes in inflammatory mediators in RA patients treated with glucocorticoids (GCs) upon vitamin D treatment in comparison with alendronate treatment.

Methods: RA patients (n = 40) on long-term oral GC treatment received either alfacalcidol or alendronate. At baseline and after 18 months, we measured cytokines capable of antagonizing GCs [macrophage migration inhibitory factor (MIF), IL-13 and IL-7], cytokines causing T-cell differentiation (IL-6, IL-7, IL-12, IL-10 and IL-23) and cytokines produced by effector T cells (IFN-γ, IL-4, IL-17, IL-22).

Current view of glucocorticoid co-therapy with DMARDs in rheumatoid arthritis.

Glucocorticoids are widely used anti-inflammatory and immunosuppressive drugs for rheumatoid arthritis (RA). The disease-modifying potential of low to medium doses of glucocorticoids has been reconfirmed in the past decade, and co-administration of DMARDs and glucocorticoids has become standard in many treatment protocols, especially those for early disease stages but also for long-standing RA. The glucocorticoid regimens used range from continuous low doses to intermittent high doses.

High incidence rate of vertebral fractures during chronic prednisone treatment, in spite of bisphosphonate or alfacalcidol use. Extension of the alendronate or alfacalcidol in glucocorticoid-induced osteoporosis-trial.

Objectives: In the 18 month "alendronate or alfacalcidol in glucocorticoid-induced osteoporosis"-trial (STOP-trial) patients with rheumatic diseases who started glucocorticoids were randomised to anti-osteoporosis therapy with either daily alendronate (10 mg) or alfacalcidol (1 microg). In the present observational open follow-up study of the STOP-trial, we report the long-term effects of risk factors on the incidence and pattern of vertebral fractures, assessed using the Genant method.

Results: Of the 201 included patients in the STOP-trial, 163 completed the trial and of those 116 underwent a follow-up radiography of the spine.

Low-dose glucocorticoid therapy in rheumatoid arthritis: an obligatory therapy.

Glucocorticoids (GCs) are used extensively in patients with rheumatoid arthritis (RA). Recent data on the efficacy of these drugs in alleviating symptoms of inflammation, but also in retarding erosive damage, are presented. In addition, a critical review of the rather limited literature on adverse effects of chronic use of low dose GCs is given.

Are glucocorticoids DMARDs?

Disease modifying antirheumatic drugs (DMARDs) are drugs used in rheumatoid arthritis (RA) to control the disease and to limit joint damage and improve long-term outcome. The last decade evidence has accumulated that suggests that low dosages of glucocorticoids are indeed able to control the disease and limit the destruction. This role is especially present in early disease and in combination with other drugs.