Clinical Pearls & Morning Reports
HIV-2 is prevalent in West Africa. Read the NEJM Case Records of the Massachusetts General Hospital here.
A: The differential diagnosis for brain lesions in people with HIV and AIDS is quite broad. Brain lesions may be mass or nonmass lesions, and they may or may not have contrast enhancement. Mass lesions of the brain may be caused by Toxoplasma gondii encephalitis; tuberculosis with central nervous system (CNS) involvement (tuberculoma); primary CNS lymphoma, which is associated with Epstein–Barr virus infection; Cryptococcus neoformans infection with CNS involvement (cryptococcoma); brain abscess due to bacterial or fungal infection; neurocysticercosis; or Treponema pallidum infection (syphilitic gumma). Progressive multifocal leukoencephalopathy, due to JC virus and HIV encephalopathy, does not typically cause mass lesions.
A: It should be noted that, among patients with HIV-2 infection, immune reconstitution associated with antiretroviral therapy (ART) is slower than it is among patients with HIV-1 infection and immune reconstitution inflammatory syndrome has been observed only rarely.
A: A patient who has cerebral toxoplasmosis in addition to HIV and AIDS should be treated with antiparasitic therapy along with the prompt initiation of ART. Initial antiparasitic therapy consists of sulfadiazine and pyrimethamine; leucovorin is also administered to counteract the myelosuppressive effects of the treatment. In the United States, pyrimethamine has unfortunately become prohibitively expensive in many instances because of a large price increase by the company that acquired the marketing rights to the drug. If pyrimethamine cannot be obtained because of cost or lack of availability, then trimethoprim–sulfamethoxazole should be used instead of sulfadiazine and pyrimethamine.
A: It should be noted that no ART drugs have been approved by the Food and Drug Administration for the treatment of HIV-2 infection. The off-label use of drugs is based on their approved indication for the treatment of HIV-1 infection. There have been no randomized, controlled trials of ART for HIV-2 infection, although one such trial is under way. Nonnucleoside reverse-transcriptase inhibitor–based regimens should be avoided because HIV-2 is intrinsically resistant to these drugs. If a protease inhibitor is used, then one with sufficient activity against HIV-2, such as boosted darunavir or lopinavir, should be chosen, since many of the HIV-1 protease inhibitors have reduced activity against HIV-2.