Salivary Alpha Amylase Enzyme and Salivary Cortisol Level in Depression after Treatment with Fluoxetine

Andi Jayalangkara Tanra; Hawaidah Madeali; Mayamariska Sanusi; Saidah Syamsuddin; Sonny Teddy Lisal

doi:10.3889/oamjms.2021.6278

Authors

Andi Jayalangkara Tanra Department of Psychiatry, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia
Hawaidah Madeali Department of Psychiatry, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia
Mayamariska Sanusi Department of Psychiatry, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia https://orcid.org/0000-0001-5043-4438
Saidah Syamsuddin Department of Psychiatry, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia https://orcid.org/0000-0002-4331-1680
Sonny Teddy Lisal Department of Psychiatry, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia

DOI:

https://doi.org/10.3889/oamjms.2021.6278

Keywords:

Depression, sAA enzyme, Cortisol Saliva, Fluoxetine

Abstract

BACKGROUND: Hypothalamic-pituitary-adrenal axis and its end product cortisol have been extensively investigated in patients with depressive disorders for many years. Recently, salivary alpha-amylase (sAA) had emerged as a new biomarker with non-invasive and more convenience protocol for measuring sympathetic activity which were also associated with depression. Selective Serotonin Reuptake Inhibitor is antidepressant drug extensively used to treat depression.

AIM: The aim of this study was to determine whether decrease of sAA and salivary cortisol levels could be observed in subjects with depression who were treated by fluoxetine.

METHODS: The total subjects were 25 depressed subjects and ten healthy controls. sAA was examined before therapy, and after 2, 4, and 6 weeks of fluoxetine administration using a portable cocorometer. Salivary cortisol was examined before therapy, after 4 and 6 weeks of fluoxetine administration with Elisa method. The therapeutic effect was assessed with Hamilton Depression Rating Scale (HDRS).

RESULTS: sAA and cortisol levels were significantly decreased after fluoxetine administration (p < 0.001), followed by at least 50% reduction of HDRS scores after 6 weeks of fluoxetine administration. Levels of sAA and cortisol were higher in the depression group than in the healthy control.

CONCLUSIONS: Measurement of sAA levels can be used as a potential biomarker of therapeutic response in depressed patients in addition to salivary cortisol.

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