Pharmacopsychiatry 2016; 49(05): 210-212
DOI: 10.1055/s-0042-103968
Letter to the Editor
© Georg Thieme Verlag KG Stuttgart · New York

A Prospective Study of Serotonin and Norepinephrine Transporter Genes and the Response to Desvenlafaxine Over 8 Weeks in Major Depressive Disorder

C. H. Ng
1   Professorial Unit, The Melbourne Clinic, Department of Psychiatry, University of Melbourne
,
C. Bousman
2   Florey Institute for Neuroscience and Mental Health, Parkville, Australia
3   Department of General Practice, The University of Melbourne, Melbourne, Australia
4   Melbourne Neuropsychiatry Centre, Department of Psychiatry, University of Melbourne
5   Centre for Human Psychopharmacology, Swinburne University of Technology, Melbourne, Victoria, Australia.
,
D. J. Smith
1   Professorial Unit, The Melbourne Clinic, Department of Psychiatry, University of Melbourne
,
N. Dowling
1   Professorial Unit, The Melbourne Clinic, Department of Psychiatry, University of Melbourne
,
K. Byron
6   Healthscope Advanced Pathology, Melbourne, Victoria, Australia
,
J. King
1   Professorial Unit, The Melbourne Clinic, Department of Psychiatry, University of Melbourne
,
J. Sarris
1   Professorial Unit, The Melbourne Clinic, Department of Psychiatry, University of Melbourne
5   Centre for Human Psychopharmacology, Swinburne University of Technology, Melbourne, Victoria, Australia.
› Author Affiliations
Further Information

Publication History

Publication Date:
29 March 2016 (online)

Abstract

No studies to date have evaluated SLC6A2 and SLC6A4 genetic polymorphisms influencing antidepressant response to desvenlafaxine. We conducted an 8-week, open-label, prospective pilot study in 35 patients with major depressive disorder to assess the effects of genetic variations in SLC6A2 and SLC6A4 on both efficacy and side effect profile of desvenlafaxine. Results revealed that homozygotes for the SLC6A4 HTTLPR S allele showed a 33% HDRS reduction compared to a 58% reduction for L allele carriers (p=0.037). No results survived adjustments for covariates or multiple comparisons. While these results need to be interpreted cautiously, they provide preliminary support for the SLC6A4 HTTLPR polymorphism as potential modifier of desvenlafaxine efficacy.

 
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