Neuroendocrine (HPA axis) and clinical correlates during fluvoxamine and amitriptyline treatment

Rota, Eugenia; Broda, Roberta; Cangemi, Luigi; Migliaretti, Giuseppe; Paccotti, Piero; Rosso, Carlo; Torre, Eugenio; Zeppegno, Patrizia; Portaleone, Paolo

doi:10.1016/j.psychres.2003.12.030

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Volume 133, Issue 2 , Pages 281-284, 28 February 2005

Neuroendocrine (HPA axis) and clinical correlates during fluvoxamine and amitriptyline treatment

Eugenia Rota
- Department of Neuroscience, University of Turin, Via Cherasco 15, Turin 10126, Italy
- Corresponding author. Tel.: +39 11 6636327, +39 11 6335423; fax: +39 11 6963487.
Roberta Broda
- Department of Psychiatry, Amedeo Avogadro University, Novara, Italy
Luigi Cangemi
- Department of Anatomy, Pharmacology and Forensic Medicine, University of Turin, Turin, Italy
Giuseppe Migliaretti
- Department of Public Health and Microbiology, Statistical Unit, University of Turin, Turin, Italy
Piero Paccotti
- Department of Clinical and Biological Sciences, University of Turin, Turin, Italy
Carlo Rosso
- Department of Anatomy, Pharmacology and Forensic Medicine, University of Turin, Turin, Italy
Eugenio Torre
- Department of Psychiatry, Amedeo Avogadro University, Novara, Italy
Patrizia Zeppegno
- Department of Psychiatry, Amedeo Avogadro University, Novara, Italy
Paolo Portaleone
- Department of Anatomy, Pharmacology and Forensic Medicine, University of Turin, Turin, Italy

Received 15 September 2003; accepted 22 December 2003.

Abstract

The effect of amitriptyline on hypothalamic–pituitary–adrenocortical (HPA) axis activity was compared with that of fluvoxamine in 38 patients suffering from DMS-IV major depressive disorder. Basal plasma adrenocorticotropic hormone and cortisol levels were determined in the so-called “observation window” of an hour (08:00–09:00 h), and cortisol levels were determined again at 20:00 h. Clinical and biochemical assessments were performed before therapy (T₀), at day 14 (T₁₄), and at day 42 (T₄₂) of the course of antidepressant treatment. At T₀, neuroendocrine parameters did not differ in patients from those in controls, except for the ratio between cortisol levels at 20:00 h and the mean level of the “window” (ratio F₂₀/F₈), which was significantly higher, suggesting a dysregulation of the circadian pattern of cortisol. Although a decrease in the ratio F₂₀/F₈ was already apparent at T₁₄ of both treatments, the repeated measures analysis of variance failed to demonstrate a significant variation with time (T₀, T₁₄, and T₄₂) and with treatment (amitriptyline and fluvoxamine) for any hormonal measure. At T₄₂, both treated groups showed a similar level of clinical improvement. Our results did not demonstrate any effect of antidepressant therapy on the cortisol circadian rhythm abnormality.