BACKGROUND AND OBJECTIVE: Anetoderma has been reported in patients with HIV-1 disease. In patients with autoimmune disease, anetoderma has been associated with increased levels of antiphospholipid antibodies (APL) that include anticardiolipin antibodies (ACA) and lupus anticoagulant (LA). This has led to speculation that the autoimmune phenomena seen in HIV-1 disease and the immune dysregulation induced by HIV-1 disease may play a role in the development of these lesions. We have seen both primary and secondary lesions of anetoderma in patients followed for HIV-1 disease. In this study, we wanted to determine whether there was an association in the development of anetoderma and elevated anticardiolipin antibodies (ACA) in HIV-1 patients. METHODS: Quantitative ACA levels were measured in eight HIV-1-infected patients with anetoderma and four HIV-1-infected patients without anetoderma. RESULTS: Anticardiolipin antibodies were moderately elevated in seven of eight patients with lesions and were borderline in the four HIV-1-positive patients without lesions of anetoderma. CONCLUSIONS: There appears to be a correlation between increased ACA and the development of cutaneous lesions of anetoderma in HIV-1 disease. Patterns of immune dysregulation, including APL, may predispose to the development of lesions of anetoderma in HIV-1-positive patients. Although some of the lesions appear to represent primary anetoderma, the majority of our patients develop lesions in areas secondary to well characterized eruptions.
BACKGROUND AND OBJECTIVE:Anetoderma has been reported in patients with HIV-1 disease. In patients with autoimmune disease, anetoderma has been associated with increased levels of antiphospholipid antibodies (APL) that include anticardiolipin antibodies (ACA) and lupus anticoagulant (LA). This has led to speculation that the autoimmune phenomena seen in HIV-1 disease and the immune dysregulation induced by HIV-1 disease may play a role in the development of these lesions. We have seen both primary and secondary lesions of anetoderma in patients followed for HIV-1 disease. In this study, we wanted to determine whether there was an association in the development of anetoderma and elevated anticardiolipin antibodies (ACA) in HIV-1patients. METHODS: Quantitative ACA levels were measured in eight HIV-1-infectedpatients with anetoderma and four HIV-1-infectedpatients without anetoderma. RESULTS: Anticardiolipin antibodies were moderately elevated in seven of eight patients with lesions and were borderline in the four HIV-1-positivepatients without lesions of anetoderma. CONCLUSIONS: There appears to be a correlation between increased ACA and the development of cutaneous lesions of anetoderma in HIV-1 disease. Patterns of immune dysregulation, including APL, may predispose to the development of lesions of anetoderma in HIV-1-positivepatients. Although some of the lesions appear to represent primary anetoderma, the majority of our patients develop lesions in areas secondary to well characterized eruptions.