IL6-174G > C genetic polymorphism influences antidepressant treatment outcome. (17th February 2017)

• Record Type: Journal Article
• Authors: Carvalho, Serafim; Santos, Marlene; Lima, Luís; Mota-Pereira, Jorge; Pimentel, Paulo; Maia, Dulce; Correia, Diana; Gomes, Sofia; Cruz, Agostinho; Medeiros, Rui
• Is Part Of: Nordic journal of psychiatry. Volume 71:Number 2(2017)
• Page Start: 158
• Page End: 162
• Publication Date: 2017-02-17
• Subjects: IL6 -- genetic polymorphisms -- antidepressants -- treatment resistant depression; Psychopharmacology -- Periodicals; Psychotherapy -- Periodicals; Psychiatry -- Periodicals; Psychiatry -- Scandinavia -- Periodicals; 616.89
• DOI: 10.1080/08039488.2016.1242650
• Languages: English
• ISSNs: 0803-9488

Abstract

Abstract: Background: Major depressive disorder is a condition associated with dysregulated cytokine levels; among these, IL6. Furthermore, genetic variations within cytokine genes have been proposed to predict antidepressant treatment outcome. Objectives: This study aims to evaluate the role of IL6-174G > C and IL6R D358A A > C functional polymorphisms in antidepressant treatment phenotypes, specifically remission, relapse, and treatment resistant depression (TRD). Methods: The referred polymorphisms were genotyped in 80 MDD patients followed at Hospital Magalhães Lemos, Portugal, within a period of 27 months. Results: It was found that patients carrying IL6-174 GC genotype present a protection towards the development of TRD (OR = 0.242; 95% CI = 0.068–0.869; p = .038), when compared with GG genotype. Additionally, carriers of IL6-174 CC genotype remit earlier than patients with IL6-174 GG/GC genotypes, with a median time to remission of 6 weeks for CC carriers and 15 weeks for GG or GC carriers ( p = .030, Log-rank test). No association was found between IL6R D358A genetic polymorphism and any of the treatment phenotypes evaluated. Conclusions: The IL6-174G > C polymorphism influences antidepressant treatment outcome in this sub-set of MDD patients, providing a putative mechanistic link for the dysregulated IL-6 levels described in the literature in patients with TRD.