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Blood, 1 November 2004, Vol. 104, No. 9, pp. 2943-2946. Prepublished online as a Blood First Edition Paper on July 6, 2004; DOI 10.1182/blood-2004-05-1747. This Article Full Text (PDF) All Versions of this Article: 2004-05-1747v1 104/9/2943    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Bower, M. Articles by Stebbing, J. Search for Related Content PubMed PubMed Citation Articles by Bower, M. Articles by Stebbing, J. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted May 11, 2004 Accepted June 17, 2004 Protease inhibitors potentiate chemotherapy-induced neutropenia Mark Bower*, Neil McCall-Peat, Natalie Ryan, Liz Davies, Anne Marie Young, Srirupa Gupta, Mark Nelson, Brian Gazzard, and Justin Stebbing Departments of Oncology and HIV Medicine, The Chelsea and Westminster Hospital, London, United Kingdom * Corresponding author; email: m.bower{at}imperial.ac.uk. Pharmacokinetic interactions between chemotherapy and highly active anti-retroviral therapy (HAART) are described but there are few data on their clinical relevance. Patients with systemic AIDS-related non-Hodgkin's lymphoma (ARL) were treated with concomitant HAART and infusional cyclophosphamide-doxorubicin-etoposide (CDE) chemotherapy. We compared neutropenia according to whether patients received protease inhibitor (PI) based HAART or non-PI regimens. Differences in survival, response rates, immunologic and virologic parameters were also investigated. The day 10 (Mann Whitney U test p=0.012) and day 14 (p=0.025) neutrophil counts were significantly lower in patients receiving PIs, although there were no differences in the number of days of G-CSF administered between groups (p=0.16). Grade 3 or 4 infections requiring hospitalisation were recorded for a total of 58/190 (31%) cycles of CDE: 23/48 (48%) when prescribed PIs and 35/142 (25%) with concomitant PI sparing HAART (2 p = 0.0025). There were no statistically significant differences in the response rates, relapse free survival and disease free survival between individuals receiving a PI and those not receiving PIs. PI based HAART appears to significantly potentiate the myelotoxicity of CDE chemotherapy. This may be a consequence of microsomal enzyme inhibition reducing metabolism of cytotoxics in this regimen. 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