Published: May 2009


Corticosteroids and avascular necrosis

Prescriber Update 30(2): 14
May 2009

CARM has received a number of reports of avascular necrosis (AVN) in association with corticosteroid use. The reports describe the involvement of major joints such as hips, knees and ankles, often with bilateral involvement.

International reports have also included other joints, including the shoulder and wrists. AVN usually causes significant chronic pain and reduced mobility, with some patients requiring joint replacements.

The pathogenesis of AVN is not yet fully understood, but may involve steroid induced osteoblast apoptosis.

The CARM reports involve patients who were prescribed corticosteroids for asthma, immunosuppression in transplant recipients, polymyalgia rheumatica, rheumatoid arthritis, eczema, and cerebral oedema. International reports of AVN have included an association with the use of pulse steroid therapy in multiple sclerosis.

AVN usually occurs with high doses of corticosteroids over a period of a few weeks to several years. Other known risk factors for AVN\ include: alcoholism, infections, hyperbaric events, storage disorders, marrow infiltrating diseases, coagulation defects, sickle cell anaemia and some autoimmune diseases.

As some patients who develop AVN remain asymptomatic, the severity of symptoms cannot be taken as a guide to the severity or stage of AVN.

As the clinical outcome is dependent on the stage at which diagnosis of AVN is made, prescribers should be alert to symptoms of joint pain in patients using corticosteroids and are advised to investigate these symptoms early. In the presence of a confirmed diagnosis of AVN, stopping or interrupting corticosteroid treatment should be considered. Prescribers should also consider investigating for further conditions associated with AVN such as, myeloproliferative diseases, coagulation disorders, and autoimmune conditions.

  1. Assouline-Dayan Y. Chang C. Greenspan A. Schoenfeld Y. Gershwin ME. (2002), Pathogenesis and natural history of osteonecrosis. Seminars in Arthritis and Rheumatism, 32(2): 94 – 124.


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