Background Avascular necrosis (AVN) of the hip is still one of the most serious complications associated with high-dose glucocorticoids (HDGC) treatment [1]; however, it has yet to be sufficiently appreciated among patients with collagen vascular diseases (CVD) other than lupus [2].

Objectives To clarify the frequency of AVN in each age and disease group of CVD, and risk factors for its development.

Methods Patients with CVD hospitalized in 2002-2009 were subjected to analysis.

Results Twenty-nine of the total 892 patients who had been hospitalized developed AVN of the hip afterwards. Since 28 (96.6%) of them had been treated with HDGC, i.e., prednisolone ≥30 mg/day for longer than 2 weeks or pulsed methylprednisolone (p-MPSL), only those with selected diseases who had received treatment with HDGC (n=268) were chosen and subjected to analysis. AVN occurred most frequently in miscellaneous small-vessel vasculitides (SV, n=2, 28.6%), followed by adult-onset Still disease (AOSD, n=3, 15.8%), systemic lupus erythematosus (SLE, n=16, 13.1%), microscopic polyangiitis (MPA, n=3, 7.3%), inflammatory muscle diseases (IMD, n=3), and Behcet disease (n=1, 6.3%).Although not significant, more than one HDGC treatment (odds ratio (OR): 2.04 (0.9289-4.4906), p=0.07), younger age (mean±standard deviation (SD): 43.3±18.1 years versus 49.6±19.5 years, p=0.1), p-MPSL (OR 1.74 (0.8-3.81), p=0.16) raised the risk of developing AVN. As for age, the risk of AVN was highest in those who received the first HDGC treatment in the teens (15.8%) and lowest (0%) in those who did in the eighties. The time to the development of AVN from the first treatment was significantly longer (6.91±3.55 years) in those who received more than one HDGC treatment than in those who received only one (3.80±2.67 years, p=0.02). It was observed that the patients with SLE (68.8%) and MPA (66.7%) tended to develop AVN late after several treatments, whereas all of the patients with AOSD and SV developed it earlier after only one treatment.

Conclusions Not only patients with lupus but also those with AOSD, IMD, and certain diseases of vasculitis syndromes who had been on treatment with HDGC were at risk for developing AVN of the hip. The way it developed was highly variable, mainly dependent on the underlying disease.

1. Migliaresi S, Picillo U, Ambrosone L, et al. Avascular osteonecrosis in patients with SLE: relation to corticosteroid therapy and anticardiolipin antibodies. Lupus 1994;3:37-41.

2. Weinstein RS. Glucocorticoid-induced osteonecrosis. Endocrine 2011 (in press)

Disclosure of Interest None Declared