On closer reflection, I have a suspicion that there is nothing intrinsically wrong in using low-dose prednisone for OA patients. The problem is not in the patients or the medication, but in the lack of an OA disease-modifying drug. If a patient has active RA and I feel that low-dose prednisone is warranted until that patient’s methotrexate or other slow-acting medication has a chance to work, I am reasonably confident that I’ll be able to get the patient off prednisone eventually, or at least be able to lower the dose. In OA, the treatment strategy is intrinsically different because I have no such hope of ever getting the patient off prednisone, and I might possibly be condemning him or her to decades of prednisone. It’s not as if I can say, “Take this prednisone just until your glucosamine starts to work, and then we will taper off your prednisone.” That’s simply preposterous.
I suggest that the converse would also be true: If a true OA disease-modifying drug were to become available, I think many rheumatologists would feel less apprehensive about using low-dose prednisone as a bridge therapy. Until that disease-modifying drug arrives, low-dose prednisone for OA still looks like a last choice remedy from my perspective.
If I could only get that point across to this patient, my day would have been easier – but easy days in the clinic are an unreasonable expectation.
This column, “Inside Rheum,” regularly appears in Rheumatology News, an Elsevier publication. Dr. Greenbaum is a rheumatologist who practices in Greenwood, Ind.