Glucocorticoids currently still play a clear role in the treatment of patients with early RA, in part because these agents have a rapid onset of action. Patients begin to feel relief of symptoms within a few hours of treatment initiation, thus allowing glucocorticoids to act as a bridging therapy that fills the gap until other medications begin to kick in, which may take several weeks. Thus, short-term therapy (ie, typically a duration of 1-3 months) with low-dose glucocorticoids can play an appropriate role in the management of early RA. However, with long-term glucocorticoid use, even with lower doses, there are concerns about numerous adverse effects (eg, Cushingoid phenotype).

There are certain groups of patients with comorbidities that raise particular concerns. For example, even only 2 weeks of glucocorticoid treatment in patients with diabetes or hypertension can have an untoward effect on the comorbid condition. These are not strict contraindications, however, and they can usually be managed by adjusting medication dosages (eg, increasing insulin dosage based on blood glucose levels). That said, some of the newer agents and some agents under development also appear to have a relatively fast onset of action (ie, approximately 1 week) and, in the future, it is possible that emerging agents could start to fill this role, obviating the need for bridging therapy.

Low-dose glucocorticoids are generally safe as long as they are used at or below an equivalent of 10 mg per day of prednisone, which is akin to normal physiologic production. At this dose, they do not produce a dramatic improvement in the RA-associated immune pathology, so patients may still have some disease activity. There are other agents, however, that can control disease activity, so we no longer have to rely on glucocorticoids to do that. I would often say that, if you have a patient with RA on more than 10 mg of prednisone per day, or for longer than 3 months, you are doing something wrong. Now, some patients do feel good on glucocorticoids and they may experience a burst of energy, perhaps with some euphoria, so we are cautious about the number of tablets we prescribe for at-home use. In our practice, we have a mandate that patients must contact us before they experiment with the dose on their own.

In the literature, there has been some concern that glucocorticoid use can delay the receipt of appropriate biologic therapy. I think that this concern may be more relevant in parts of the world where glucocorticoids are used more extensively to control disease activity; the clinician might assume that the patient is doing well, and it is not until glucocorticoid-related adverse events occur that the physician is prompted to move on to a biologic or small molecule agent.