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Avascular necrosis in HIV
Puja Mehta1, Mark Nelson, Alexander Brand
1Department of Rheumatology, Chelsea and Westminster Hospital, London, UK.
Avascular necrosis (AVN) is an emerging complication of HIV infection. The incidence of AVN in HIV patients is greater than the general population. Although the incidence has increased in the HAART era, the aetiology remains unclear. We report our experience of AVN from our tertiary referral HIV centre and evaluate risk factors for its development. Review of MRI reports of HIV-positive patients between 2007 and 2010 identified 22 patients with AVN (19 men, 3 women). Case notes and electronic records were reviewed. Twenty-two patients developed AVN, among 6,487 HIV patients attending our centre (0.34% incidence; 95% CI, 0.2-0.48%). 68% of patients had multi-joint involvement. The median nadir CD4 count was 52 cells/μL. 73% of patients had more than two risk factors including HAART (91%), protease inhibitors (68%), hypercholesterolaemia (59%), corticosteroids (55%), hypertriglyceridaemia (45%), smoking (45%), alcohol (27%) and CD4 <200 cells/μL (23%). 9% were idiopathic. AVN is an important musculoskeletal manifestation of HIV and may be multi-focal with multi-factorial aetiology. Preventative strategies should focus on risk factor modification. When investigating joint pain in HIV-infected patients, clinicians should maintain a high index of suspicion for AVN. Unexplained AVN, particularly if multi-focal, should prompt consideration of HIV testing.
Avascular necrosis (AVN) is an emerging complication of HIV infection. The incidence of AVN in HIV patients is greater than the general population. Although the incidence has increased in the HAART era, the aetiology remains unclear. We report our experience of AVN from our tertiary referral HIV centre and evaluate risk factors for its development. Review of MRI reports of HIV-positive patients between 2007 and 2010 identified 22 patients with AVN (19 men, 3 women). Case notes and electronic records were reviewed. Twenty-two patients developed AVN, among 6,487 HIV patients attending our centre (0.34% incidence; 95% CI, 0.2-0.48%). 68% of patients had multi-joint involvement. The median nadir CD4 count was 52 cells/μL. 73% of patients had more than two risk factors including HAART (91%), protease inhibitors (68%), hypercholesterolaemia (59%), corticosteroids (55%), hypertriglyceridaemia (45%), smoking (45%), alcohol (27%) and CD4 <200 cells/μL (23%). 9% were idiopathic. AVN is an important musculoskeletal manifestation of HIV and may be multi-focal with multi-factorial aetiology. Preventative strategies should focus on risk factor modification. When investigating joint pain in HIV-infected patients, clinicians should maintain a high index of suspicion for AVN. Unexplained AVN, particularly if multi-focal, should prompt consideration of HIV testing.
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