Alfred Hospital, Commercial Road, Prahran, Victoria 3181, Australia
SIR, Osteonecrosis [alternatively known as avascular necrosis (AVN)] involving up to three joints has been reported infrequently as a complication of HIV infection. Potential risk factors cited in sporadic case reports include the presence of HIV infection itself, the associated incidence of acquired antiphospholipid syndrome and other autoimmune phenomena, the hyperlipidaemic effect of protease inhibitors, and the prior use of corticosteroid therapy [17]. We present a case of avascular necrosis at eight separate sites in a HIV-positive patient.
Our patient, a 42-yr-old Caucasian homosexual male, presented 2 yr after a positive diagnosis of HIV infection, with an 18-month history of joint pain affecting his ankles, knees and hips, made worse by weight-bearing and walking. No joint swelling or evidence of synovitis was seen on musculoskeletal examination and there was no other evidence of connective tissue disease. A whole-body 99mTc methylene-diphosphate bone scan performed to look for inflammatory arthritis showed changes consistent with avascular necrosis bilaterally in the femoral heads, the talar domes, both lateral femoral condyles of the knees, and both glenohumeral joints. MRI scanning of the lower limb joints confirmed AVN at the six corresponding lower-limb joints affected on the bone scan. Anticardiolipin antibodies, lupus inhibitor screen and cryoglobulins were negative.
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To our knowledge, such extensive AVN in the setting of HIV has not been reported in the literature before. Although the diagnosis is made infrequently, its true prevalence is likely to be higher due to underdiagnosis on the part of treating physicians. A recent casecontrol trial reported a mean delay in diagnosis from onset of symptoms of 125 days [8]. Furthermore, a high prevalence of asymptomatic AVN of the hip has been demonstrated with MRI scanning in a large group of patients with HIV [9]. Given the increased longevity of AIDS patients receiving highly active antiretroviral therapy, many of these patients could go on to develop symptomatic disease unless potential risk factors are recognized and minimized.
Corticosteroid therapy in the treatment of other diseases is associated with a high rate of developing the radiological features of AVN on MRI, which can reverse after discontinuation of therapy [10, 11]. Of the risk factors for AVN proposed in HIV infection, only prior use of corticosteroids has been shown to be an independent risk factor in a recent controlled trial [12]. The onset of joint pain 6 months after high-dose dexamethasone treatment would be consistent with steroid-induced AVN and is the most likely precipitant in our patient.
Our case highlights the need for increased awareness of AVN in HIV-positive patients with joint pain. Clinicians need to be aware of the risks associated with corticosteroid therapy in this subgroup of patients, minimize its use when possible and investigate joint pain specifically for AVN so that disease-limiting interventions can be undertaken early.
Notes
Correspondence to: 20 Donnybrook Court, Beech Hill Road, Donnybrook, Dublin 4, Republic of Ireland.
References
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