© 2004 by Oxford University Press
© 2004 Oxford University Press
CORRESPONDENCE |
Re: Active Tamoxifen Metabolite Plasma Concentrations After Coadministration of Tamoxifen and the Selective Serotonin Reuptake Inhibitor Paroxetine
Affiliations of authors: Hormone Laboratory (EAL), Department of Pharmacology (PMU), Department of Oncology (PEL), Haukeland University Hospital, Bergen, Norway
Correspondence to: Ernst A. Lien, MD, Hormone Laboratory, Haukeland University Hospital, Jonas Liesvei 65, 5021 Bergen, Norway (e-mail: ernst.lien{at}helse-bergen.no)
In a recent study by Stearns et al. (1), the authors identified the tamoxifen metabolite 4-hydroxy-N-desmethyl-tamoxifen. The authors stated that this active metabolite had not been previously recognized, and they named it endoxifen. However, 4-hydroxy-N-desmethyl-tamoxifen was observed in human breast tumor tissue by Mauvais-Jarvis et al. (2) and termed desMeOHTAM in 1986. This compound was already known to have a high affinity toward the estrogen receptor in 1982 (3).
We reported in 1989 that 4-hydroxy-N-desmethyl-tamoxifen could be found in human biologic fluids and tissues and demonstrated that aminoglutethimide, a first-generation aromatase inhibitor, decreased its formation (4–6). Because 4-hydroxy-tamoxifen was designated metabolite B and N-desmethyl-tamoxifen was designated metabolite X (7), we called 4-hydroxy-N-desmethyl-tamoxifen metabolite BX.
We believe that the introduction of an additional name (i.e., endoxifen) for 4-hydroxy-N-desmethyl-tamoxifen will lead to confusion and propose, therefore, that the abbreviation 4OHNDtam should be used in the future.
REFERENCES
1 Stearns V, Johnson MD, Rae JM, Morocho A, Novielli A, Bhargava P, et al. Active tamoxifen metabolite plasma concentrations after coadministration of tamoxifen and the selective serotonin reuptake inhibitor paroxetine. J Natl Cancer Inst2003;95:1758–64.
2 Mauvais-Jarvis P, Baudot N, Castaigne D, Banzet P, Kuttenn F. Trans-4-hydroxytamoxifen concentration and metabolism after local percutaneous administration to human breast. Cancer Res1986;46:1521–5.
3 Robertson DW, Katzenellenbogen JA, Long DJ, Rorke EA, Katzenellenbogen BS. Tamoxifen antiestrogens. A comparison of the activity, pharmacokinetics, and metabolic activation of the cis and trans isomers of tamoxifen. J Steroid Biochem1982;16:1–13.[CrossRef][Web of Science][Medline]
4 Lien EA, Solheim E, Lea OA, Lundgren S, Kvinnsland S, Ueland PM. Distribution of 4-hydroxy-N-desmethyltamoxifen and other tamoxifen metabolites in human biological fluids during tamoxifen treatment. Cancer Res1989;49:2175–83.
5 Lien EA, Anker G, Lonning PE, Solheim E, Ueland PM. Decreased serum concentrations of tamoxifen and its metabolites induced by aminoglutethimide. Cancer Res1990;50:5851–7.
6 Lien EA, Solheim E, Ueland PM. Distribution of tamoxifen and its metabolites in rat and human tissues during steady-state treatment. Cancer Res1991;51:4837–44.
7 Robinson SP, Jordan VC. Metabolism of steroid-modifying anticancer agents. Pharmacol Ther1988;36:41–103.[Medline]
Related Correspondence
CiteULike 
Connotea 
Del.icio.us What's this?
J Natl Cancer Inst 2004 96: 883.
J Natl Cancer Inst 2004 96: 883-884.
J Natl Cancer Inst 2004 96: 884-885.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||