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Glucocorticoid effects on skeletal muscle: benefit and risk in patients with autoimmune inflammatory rheumatoid diseases

Glucocorticoids have broad-spectrum immunosuppressive and anti-inf lammatory properties that have therapeutic effects for a variety of rheumatologic conditions, such as rheumatoid arthritis, vasculitidies, idiopathic inf lammatory myopathies (IIMs) and other connective tissue diseases. It has been estimated that approximately 1% of the general adult population take oral glucocorticoids at any given time, and that in older adults this rate may be as high as 2.5% [1]. In prescribing glucocorticoids to patients, clinicians are cognizant of the myriad adverse effects associated with these medications, but more effective therapeutic alternatives devoid of substantial deleterious effects are lacking. Individual patient susceptibility to adverse effects depends on glucocorticoid dose, duration of therapy, glucocorticoid receptor saturation levels and glucocorticoid receptor gene polymorphisms [2]. Common adverse effects associated with dose-dependent and cumulative glucocorticoid use include osteoporosis, cataracts, lipodystrophy, weight gain, systemic arterial hypertension, metabolic syndrome and adrenal suppression [3,4]. Osteoporosis is a particularly serious complication of long-term glucocorticoid therapy that is associated with a high personal and economic burden. In the USA alone, care of incident osteoporotic fractures was estimated to total close to US$17 billion in 2005 [5]. A landmark study demonstrated patients taking at least 7.5 mg daily of prednisolone or equivalent had significantly increased risks of vertebral, hip and nonvertebral fractures compared with patients using oral glucocorticoids at lower doses (<2.5 mg daily), where the median duration of glucocorticoid therapy was 28 days overall [6]. Still, according to van Staa et al., older patients and patients with arthritis are more likely to be on prolonged oral corticosteroid treatment for over 2 years compared with younger patients or those with chronic obstructive pulmonary disease, respectively [1]. Therefore, the burden of glucocorticoid therapy is especially high in a typical outpatient rheumatology clinic, where the mean age of patients referred from general practice is approximately 45 years, 18% of patients are 60 or older, and approximately half of all referrals are diagnosed with inf lammatory rheumatic diseases that typically require glucocorticoid therapy [7]. Similar to bone, skeletal muscle homeostasis is disrupted by glucocorticoids. Glucocorticoids not only decrease muscle anabolism by inhibiting amino acid transport into muscle [8], but also increase muscle catabolism by altering three major pathways: the myostatin signaling pathway, Glucocorticoid effects on skeletal muscle: benefit and risk in patients with autoimmune inflammatory rheumatoid diseases