Tapering the prednisone dosage while monitoring the patient's response is the most appropriate method to distinguish between weakness caused by a flare of inflammatory myopathy and glucocorticoid-induced toxic myopathy. The latter diagnosis is more likely in this patient with a normal serum creatine kinase level. In contrast, a flare of inflammatory myopathy, which can present the same way clinically, is associated with a marked increase in the serum creatine kinase level and evidence of irritable myopathy on electromyography (such as abnormal spontaneous necrosis or active muscle membrane damage from inflammation). If weakness improves after prednisone tapering, the patient should be given a glucocorticoid-free holiday or, if needed, switched to another agent. In contrast, if weakness worsens with tapering, an inflammatory flare should be suspected, and increasing the glucocorticoid dosage or adding another immunosuppressive therapy should be considered.

Intravenous immunoglobulin (IVIG) is a second-line therapy for severe inflammatory myopathies that are refractory to treatment with a glucocorticoid and at least one other immunosuppressive agent. Because glucocorticoid-induced myopathy is suspected in this patient, IVIG treatment is not warranted.

Increasing the prednisone dosage without evidence of active inflammation would be inappropriate and could worsen the patient's weakness, which is likely associated with glucocorticoid therapy.

A repeat muscle biopsy might show type 2 muscle fiber atrophy due to glucocorticoid myopathy, but these changes also are seen in disuse atrophy and other conditions and thus are nonspecific. Biopsy is also likely to show inflammatory changes but is unlikely to provide a definitive differentiation between a flare of inflammatory myopathy and glucocorticoid-induced myopathy.