Title: Fluoxetine and Olanzapine for Resistant Depression
Abstract: Back to table of contents Previous article Next article Letter to the EditorFull AccessFluoxetine and Olanzapine for Resistant DepressionFRANCO BENAZZI, M.D., FRANCO BENAZZISearch for more papers by this author, M.D., Forli, ItalyPublished Online:1 Jan 2002https://doi.org/10.1176/appi.ajp.159.1.155AboutSectionsView EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: I read the article by Richard C. Shelton, M.D., et al. (1), which reported the superior efficacy of olanzapine plus fluoxetine for treating resistant nonpsychotic unipolar depression compared with either agent alone. The investigation had two main phases: a 6-week open-label trial of fluoxetine, followed by an 8-week double-blind trial in which nonresponders to fluoxetine alone were randomly assigned to receive olanzapine alone, fluoxetine alone, or fluoxetine plus olanzapine. Patients in the group receiving olanzapine alone stopped taking fluoxetine on the day of random assignment. After 1 week of treatment, fluoxetine plus olanzapine produced a marked improvement in depression symptoms, significantly much greater than that seen with olanzapine alone and with fluoxetine alone. The marked improvement persisted during the remainder of the 8-week double-blind trial and during the following 8-week open-label extension period. This interesting finding seems to me difficult to understand, because the group receiving olanzapine alone had stopped taking fluoxetine on the day of random assignment. Because fluoxetine and its active metabolite, norfluoxetine, take many weeks to disappear from the bloodstream after discontinuation (2), the group receiving olanzapine alone continued to have significant plasma levels of fluoxetine, at least during the first weeks of the double-blind trial. Therefore, the observed marked difference in response to olanzapine alone compared with the response to olanzapine plus fluoxetine during the double-blind trial seems difficult to understand because the treatments were similar.Furthermore, the small groups (N=10, 8, and 10) examined may have led to a significant difference among the groups that was caused by chance alone (3). Replication in much larger groups by using a selective serotonin reuptake inhibitor with a short half-life could produce clearer results.References1. Shelton RC, Tollefson GD, Tohen M, Stahl S, Gannon KS, Jacobs TG, Buras WR, Bymaster FP, Zhang W, Spencer KA, Feldman PD, Meltzer HY: A novel augmentation strategy for treating resistant major depression. Am J Psychiatry 2001; 158:131-134Link, Google Scholar2. Schatzberg AF, Nemeroff CB: The American Psychiatric Press Textbook of Psychopharmacology, 2nd ed. Washington, DC, American Psychiatric Press, 1998Google Scholar3. Rothman KJ, Greenland S: Modern Epidemiology, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 1998Google Scholar FiguresReferencesCited byDetailsCited ByNone Volume 159Issue 1 January 2002Pages 155-155 Metrics History Published online 1 January 2002 Published in print 1 January 2002
Publication Year: 2002
Publication Date: 2002-01-01
Language: en
Type: letter
Indexed In: ['crossref', 'pubmed']
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Cited By Count: 3
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