TO THE EDITOR
The AIDS Malignancy Consortium, a multicenter cooperative group funded by the National Cancer Institute, has enrolled 442 patients who have human immunodeficiency virus (HIV) infection and measurable Kaposi’s sarcoma in a series of therapeutic trials since 1996 (Table 1).
Table 1.
Characteristics of Patients with Kaposi’s Sarcoma Enrolled in AIDS Malignancy Consortium Trials, 1996–2007.
| Variable | Value |
|---|---|
| Total no. of patients | 442 |
| Age—yr | |
| Mean | 42 |
| Median | 40 |
| Range | 23–66 |
| CD4 count — cells per mm3 | |
| Mean ±SD | 329±379 |
| Median | 266 |
| CD4 count ≥300 per mm3 and undetectable HIV viral load — no./total no. (%) |
96/332 (28.9) |
| Therapy with protease inhibitor or non-nucleoside reverse- transcriptase inhibitor, CD4 count ≥300 per mm3, and undetectable HIV viral load — no./total no. (%) |
78/248 (31.5) |
Our data suggest that persistent Kaposi’s sarcoma despite apparently effective antiretroviral therapy is not a rare, isolated, or recent phenomenon, as suggested by Maurer and colleagues in their letter to the editor (Sept. 27 issue).1 On the contrary, our findings indicate that since the introduction of effective antiretroviral therapy, many patients with AIDS-associated Kaposi’s sarcoma have CD4 counts above the level typically associated with susceptibility to opportunistic diseases. Furthermore, although effective HIV suppression has been correlated with regression of Kaposi’s sarcoma after antiretroviral therapy,2 a substantial proportion of our patients had undetectable HIV viral loads.
These findings raise important questions about the mechanisms that control the progression of human herpesvirus 8 and Kaposi’s sarcoma. They also suggest a need for studies to identify clinically relevant correlates that can distinguish between patients whose Kaposi’s sarcoma responds to antiretroviral therapy and those who do not have such a response. These factors may include age, duration of HIV infection, human herpesvirus 8 viral load, and patterns of viral gene expression within tumors.
Contributor Information
Susan E. Krown, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, krowns@mskc.org
Jeannette Y. Lee, University of Alabama at Birmingham, Birmingham, AL 35294-3300
Dirk P. Dittmer, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7290
References
- 1.Maurer T, Ponte M, Leslie K. HIV-associated Kaposi’s sarcoma with a high CD4 count and a low viral load. N Engl J Med. 2007;357:1352–1353. doi: 10.1056/NEJMc070508. [DOI] [PubMed] [Google Scholar]
- 2.Martinez V, Caumes E, Gambotti L, et al. Remission from Kaposi’s sarcoma on HAART is associated with suppression of HIV replication and is independent of protease inhibitor therapy. Br J Cancer. 2006;94:1000–1006. doi: 10.1038/sj.bjc.6603056. [DOI] [PMC free article] [PubMed] [Google Scholar]