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Correspondence

HIV-Associated Kaposi's Sarcoma with a High CD4 Count and a Low Viral Load

N Engl J Med 2007; 357:1352-1353September 27, 2007

Article

To the Editor:

Kaposi's sarcoma associated with HIV infection has been decreasing in incidence and severity since the introduction of antiretroviral therapy.1 These reductions have been attributed to improved immune function directly related to such therapy. Patients with Kaposi's sarcoma typically have a low CD4 cell count (<150 cells per cubic millimeter) and a high viral load (>10,000 copies per milliliter).1,2 In the majority of patients, the regression of Kaposi's sarcoma lesions has been reported to occur within 8 months after the initiation of antiretroviral therapy, paralleling the increase in the CD4 cell count and decrease in the viral load that mark successful therapy.3 Likewise, progression of Kaposi's sarcoma has been associated with a high viral load, a low CD4 cell count, and concomitant opportunistic infections.2,3

We report on a cluster of unusual cases of cutaneous, unremitting HIV-associated Kaposi's sarcoma occurring in nine patients with sustained CD4 cell counts of more than 300 cells per cubic millimeter and suppression of the viral load to a value below 300 copies per milliliter for at least 2 years. These patients presented between November 2004 and January 2006. All were receiving antiretroviral regimens containing at least one protease inhibitor or non-nucleoside reverse-transcriptase inhibitor. The median age was 51 years (range, 41 to 74), the median time since the onset of HIV infection was 18 years (range, 4 to 25), and the median duration of antiretroviral therapy was 7 years (range, <1 to 19). The median nadir CD4 cell count was 340 (range, 90 to 455). None of the patients had a history of opportunistic infections. The patients have had a relatively indolent course of Kaposi's sarcoma, with no eruptive cutaneous lesions, visceral involvement, or other AIDS-defining illnesses.

This cluster of cases of persistent HIV-associated Kaposi's sarcoma in patients with HIV viral suppression and good immune-system function (as measured by the viral load and CD4 cell count) is important for three reasons. First, although there have been sporadic reports of similar patients,4 it is possible that we are seeing a greater number in San Francisco because of the high number of aging patients who are infected with both HIV and human herpesvirus 8. This hypothesis raises questions about the immune system's integrity and ability to control certain viruses in patients with long-standing HIV infection.5 Second, it has been postulated that drug regimens containing protease inhibitors are preferable in the treatment of Kaposi's sarcoma because of their antitumorigenic and antiangiogenic effects. In our series, seven patients have been receiving protease inhibitors without improvement in their Kaposi's sarcoma. Finally, these patients present a clinical and prognostic conundrum in that they are receiving maximal antiretroviral therapy yet have persistent Kaposi's sarcoma. This phenomenon may increase in frequency as the HIV-infected population ages, and we recommend that physicians monitor this group carefully.

Toby Maurer, M.D.
Maya Ponte, Ph.D.
Kieron Leslie, M.D.
University of California at San Francisco, San Francisco, CA 94110

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