Blood, 1 June 2002, Vol. 99, No. 11, pp. 4250-4251
CORRESPONDENCE
To the editor:
Systemic non-Hodgkin lymphoma in
HIV-infected patients in the era of highly active
antiretroviral therapy
We recently read with interest Kirk et al's paper
"Non-Hodgkin lymphoma in HIV-infected patients in the era of highly
active antiretroviral therapy." 1 The authors analyzed
the incidence and clinical characteristics of HIV-infected patients
with primary central nervous system non-Hodgkin lymphoma
(PCNS-NHL) and 3 categories of systemic non-Hodgkin lymphoma (S-NHL)
according to their history of highly active antiretroviral therapy
(HAART). The authors concluded that there was a significant decline in
the incidence of PCNS-NHL and all 3 subtypes of S-NHL. Two issues could
be raised about the data upon which this conclusion is based. First, it
is important to point out that 47% (46 of 97) of the S-NHL cases in
HIV-infected patients receiving HAART were categorized as
"other/unknown." This makes it difficult to determine the incidence
of the different histologic types of S-NHL in this group of patients.
Second, the median CD4 count and plasma HIV RNA viral load in patients
with S-NHL receiving HAART were 108 cells/µL (range, 33 cells/µL to 223 cells/µL) and 4.0 log10 copies/mL, respectively. These data lead
to the suggestion that S-NHL may be the result of stimulation and
proliferation of B lymphocytes due to sustained HIV replication in
these patients.
In contrast, a recent study of S-NHL among HIV-infected patients
receiving HAART during the period of 1996-2000 at our community program
located in Houston, Texas indicated that S-NHL is associated with
higher CD4 cell counts.2 But no significant difference in
the histologic types of this malignancy was observed among patients
naive to antiretroviral drugs, as compared with those receiving HAART.
More importantly, the analysis of HIV-infected patients with S-NHL who
were receiving HAART indicated that 35% (12 of 34) had both HIV RNA
viral load below the level of detection (< 400 copies/mL) and higher
CD4 cell counts (median, 301 cells/µL; range, 46 cells/µL to 667 cells/µL). Such findings support the hypothesis that factors
promoting the development of lymphoma may not be related to
immunodysfunction or may be associated with processes not
affected by HAART. Further studies are required to clarify the
incidence and the pathogenesis of S-NHL in HIV-infected patients
receiving HAART. Although the goal of antiretroviral therapy is the
complete suppression of HIV replication,3,4 failure to
achieve this goal is common in clinical practice, occurring at a rate
of 40% to 70%.5-7 Furthermore, it is believed that the
efficacy of present antiretroviral therapy may allow more persons with
HIV infection to survive with long-term mild-to-moderate immunosuppression and some degree of continuing B-cell stimulation, thereby placing such patients at risk for the development of S-NHL.
Regis A. Vilchez, Jeffrey L. Jorgensen, and Michael H. Kroll
Correspondence: Regis A. Vilchez, Department of Medicine,
Section of Infectious Diseases, Baylor College of Medicine, One Baylor
Plaza, BCM 286, Room N1319, Houston, TX 77030; e-mail:
rvilchez{at}bcm.tmc.edu
References
1.
Kirk O, Pedersen C, Cozzi-Lepri A, et al.
Non-Hodgkin lymphoma in HIV-infected patients in the era of highly active antiretroviral therapy.
Blood.
2001;98:3406-3412[Abstract/Free Full Text].
2.
Vilchez RA, Kozinetz CA, Jorgensen JL, Kroll MH, Butel JS.
AIDS-related systemic non-Hodgkin's lymphoma at a large community program.
AIDS Research and Human Retroviruses.
2002;18:241-246.
3.
Guidelines for the use of antiretroviral agents in HIV-infected adults and adolescents.
MMWR Morb Mortal Wkly Rep.
1998;47:619.
4.
Carpenter CC, Cooper DA, Fischl MA, et al.
Antiretroviral therapy in adults: updated recommendations of the International AIDS Society-USA Panel.
JAMA.
2000;283:381-390[Abstract/Free Full Text].
5.
Ledergerber B, Egger M, Opravil M, et al.
Clinical progression and virological failure on highly active antiretroviral therapy in HIV-1 patients: a prospective cohort study.
Lancet.
1999;353:863-868[CrossRef][Medline]
[Order article via Infotrieve].
6.
Deeks SG, Barbour JD, Martin JN, Swanson MS, Grant RM.
Sustained CD4+ T cell response after virologic failure of protease inhibitor based regimens in patients with human immunodeficiency virus infection.
J Infect Dis.
2000;181:946-953[CrossRef][Medline]
[Order article via Infotrieve].
7.
Lucas GM, Chaisson RE, Moore RD.
Highly active antiretroviral therapy in a large urban clinic: risk factors for virologic failure and adverse drug reactions.
Ann Intern Med.
1999;131:81-87[Abstract/Free Full Text].
