Aberrant expression of the cell surface marker CD30 in systemic B-cell HIV-related NHL other than anaplastic large cell lymphoma (ALCL) has been reported. CD30 is a member of the tumor necrosis factor (TNF) family of receptors, and activation of CD30 mediates cell cycle regulation in preclinical models. The outcome of AIDS-related lymphoma (ARL) patients (pts) has improved dramatically in recent years with good control of HIV infection and the ability to intensify chemotherapy appropriate to the lymphoma. To determine whether CD30+ systemic ARL might have different clinical outcome and require a tailored approach to therapy, we performed a retrospective clinical-pathological correlation in pts seen at St. Paul’s Hospital in Vancouver, Canada (SPH) and focused on 39 B-cell lymphoma (BCL) pts since 1992. Clinical and HIV-related data were abstracted by chart review and from the CFE data-base. Stored biopsy material diagnostic of BCL was sectioned and stained for CD30 expression by immunohistochemistry. Median age was 41 (range 20–64) years and 37 pts were male. 16 pts had diffuse large B-cell lymphoma (DLBCL), 17 other B-cell NHL excluding ALCL, and 6 Hodgkin’s Lymphoma (HL); 29 were advanced stage. HIV risk was sexual in 31 and injection drug use (IDU) in 8. Median CD4 at diagnosis was 140 (10–770) cells/ul and 20 pts received HAART. Lymphoma therapy was administered according to era and histology: CHOP-like ± Rituximab (R) n=28; ABVD-like n= 6; CODOX-M/IVAC-R n=1; HAART alone n=1; resection n=1; declined therapy n= 2. 8 pts received added R and 4 added radiation therapy. 20 were CD30+ and 19 CD30−; the only baseline characteristic that differed significantly according to CD30 status was histology p<0.02 (6 of 6 HL were CD30+), no other HIV or lymphoma related characteristics differed by CD30 expression. In a Kaplan-Meier analysis, there was a trend toward improved overall survival (OS) in pts with CD30+ NHL; median survival (MS) was 16.3 (2.7–74.3) months (mo) for CD30+ vs. 5.9 (0–50) mo for CD30− (p<0.09). However, OS for HL was 100% at 11–66 mo vs. 7.2 (2.5–48) mo for DLBCL and 7.4 (0–74.3) mo for other NHL (p<0.04); when HL were removed from the analysis there was no difference in OS according to CD30 status (p<0.09), however progression-free survival (PFS) for all pts was; CD30+, 5.4 (0.8–20) mo and CD30−, 3.9 (0.03–6.2) mo (p<0.05). PFS for pts with a CD4 count at NHL Dx was; CD4<100, 3.3 (0–8.8) mo and CD4 ≤100, 5.9 (2.1–20) mo (p<0.04). PFS by CD4 count and CD30 status were as follows: CD4<100 and CD30+, 3.3 (0.8–8.8) mo; CD4<100 and CD30−, 2.0 (0.03–6.0) mo; CD4 ≤100 and CD30+, 6.7 (5.4–20) mo; CD4 ≤100 and CD30−, 4.5 (2.1–6.2) mo, (p<0.07). In conclusion, in this retrospective analysis, there was a trend toward improved PFS in pts with CD30+ B-cell NHL, particularly in pts with a CD4 count of at least 100. These data suggest that non-ALCL CD30+ NHL patients do not require intensified lymphoma therapy and underscores the importance of adequate control of HIV infection in the outcome of HIV-related lymphoma.

This study was supported by a grant from the Saint Paul’s Hospital Foundation.

Disclosure: No relevant conflicts of interest to declare.

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