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TIMOTHY E. Wilens, MD
Pediatric Psychopharmacology Unit (ACC 725) Massachusetts General Hospital Boston, MA 02114

Joseph Biederman, MD; Ross J. Baldessarini, MD; Stephen P. McDermott, MD
Patricia R. Puopolo

James G. Flood, PhD
Boston, Mass

Arch Gen Psychiatry. 1992;49(9):752.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

We read with interest the article by Nelson et al¹ on the treatment of depression with fluoxetine and desipramine, particularly regarding effects of fluoxetine on serum levels of desipramine and its major active metabolite, 2-hydroxydesipramine. Fluoxetine can elevate blood concentrations and the risk of toxic effects of tricyclic antidepressants unless their dose is greatly restricted.^2,3 This interaction probably reflects competition for enzymatic oxidation.⁴ Although ring-hydroxylation to 2-hydroxydesipramine is a major route of metabolism of desipramine, assessment of effects of fluoxetine on 2-hydroxydesipramine is very limited.^2-4

In a retrospective comparison of 14 adults with depression given desipramine and fluoxetine and 52 patients given desipramine alone, Nelson et al¹ found serum desipramine levels to be similar in both groups despite an approximate reduction of 30% in desipramine dose with fluoxetine. In their data, we find (eg, at 4 weeks of fixed-dose treatment) lower mean . . . [Full Text PDF of this Article]

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