The comments of Confalonieri and Villa confirm our findings that human immunodeficiency virus (HIV)—associated autonomic dysfunction is frequent and often asymptomatic, and that in advanced HIV disease it is more serious than in early disease.1
The exact pathogenesis of HIV-related autonomic dysfunction is unknown. As Villa et al state in their recent article,2 several mechanisms are currently considered. Human immunodeficiency virus has been cultured from peripheral nerves, and thus it might act directly on neural tissue.3,4 Moreover, there is some indirect evidence that immunologic factors may play a role,5,6 including autoimmune mechanisms such as autoantibodies against peripheral nerves7 or circulating immune complexes2 as found by Confalonieri et al. In addition, nutritional factors may be involved.
We agree with Confalonieri et al that there are some rare single cases with HIV-associated autonomic neuropathy reported in the medical literature that have had favorable responses to treatment