ABSTRACT
Human immunodeficiency virus (HIV)-related vascular diseases with skin manifestations are varied. The breadth of vascular disease results, in part, from the direct effects of HIV infection and, more commonly, from indirect consequences, such as immune suppression. The pathophysiology of HIV-related vasculitis depends entirely on the mediator of inflammation. Immune-mediated vasculitis in HIV-infected patients may also occur outside the setting of opportunistic infection. HIV-positive patients tend to have more diffused cutaneous involvement than seronegative counterparts and lesions can be more severe, evolving into bullae or ulcers in some cases. Inflammation affecting large vessels has been demonstrated in HIV-infected patients, particularly involving the central nervous system. The treatment of HIV-related vasculitis, indeed vasculitis in any setting, revolves around identification and reversal of the underlying inflammatory process. Removal of the offending drug or antimicrobials targeted at infectious culprits should be pursued when appropriate.
