Abstract
Background: Depression is among the commonest of psychiatric disorders, and inflammatory mechanisms have been suggested to play a role in its pathophysiology. Interferons are a superfamily of proinflammatory cytokines that play a role in host defence mechanisms. Interferons are used in the treatment of a variety of autoimmune (e.g. multiple sclerosis), viral (e.g. chronic hepatitis B and C), and malignant (e.g. malignant melanoma, hairy cell leukemia) disorders; depression, however, is a notable and clinically troublesome adverse effect.
Objective: This article seeks to present a simple explanation and update for the reader about what interferons are, how interferons are classified, the clinical conditions in which interferons are used, the occurrence of depression as a clinical adverse effect of interferon therapy, possible mechanisms that explain interferon-related depression, the treatment of interferon-related depression, and the prevention of interferon-related depression.
Methods: A qualitative literature review is presented.
Results and Conclusions: Irrespective of the indication for IFN therapy, IFNs are associated with a 30- 70% risk of treatment-emergent depression. This risk could be due to the IFN, or to an interaction between the IFN and the indication for which it was prescribed. Various neurohormonal, neurochemical, neurohistological, and other mechanisms have been put forth to explain IFN-related depression. Prophylactic treatment with antidepressants reduces the risk of IFN-related depression; antidepressants also effectively treat the condition. Recent alternatives to IFNs have shown to decrease the risk of treatment-emergent depression.
Keywords: Adverse effect, classification, depression, interferon, mechanism, prevention.
Current Neuropharmacology
Title:Interferon-Related Depression: A Primer on Mechanisms, Treatment, and Prevention of a Common Clinical Problem
Volume: 14 Issue: 7
Author(s): Ekta Franscina Pinto and Chittaranjan Andrade
Affiliation:
Keywords: Adverse effect, classification, depression, interferon, mechanism, prevention.
Abstract: Background: Depression is among the commonest of psychiatric disorders, and inflammatory mechanisms have been suggested to play a role in its pathophysiology. Interferons are a superfamily of proinflammatory cytokines that play a role in host defence mechanisms. Interferons are used in the treatment of a variety of autoimmune (e.g. multiple sclerosis), viral (e.g. chronic hepatitis B and C), and malignant (e.g. malignant melanoma, hairy cell leukemia) disorders; depression, however, is a notable and clinically troublesome adverse effect.
Objective: This article seeks to present a simple explanation and update for the reader about what interferons are, how interferons are classified, the clinical conditions in which interferons are used, the occurrence of depression as a clinical adverse effect of interferon therapy, possible mechanisms that explain interferon-related depression, the treatment of interferon-related depression, and the prevention of interferon-related depression.
Methods: A qualitative literature review is presented.
Results and Conclusions: Irrespective of the indication for IFN therapy, IFNs are associated with a 30- 70% risk of treatment-emergent depression. This risk could be due to the IFN, or to an interaction between the IFN and the indication for which it was prescribed. Various neurohormonal, neurochemical, neurohistological, and other mechanisms have been put forth to explain IFN-related depression. Prophylactic treatment with antidepressants reduces the risk of IFN-related depression; antidepressants also effectively treat the condition. Recent alternatives to IFNs have shown to decrease the risk of treatment-emergent depression.
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Cite this article as:
Pinto Franscina Ekta and Andrade Chittaranjan, Interferon-Related Depression: A Primer on Mechanisms, Treatment, and Prevention of a Common Clinical Problem, Current Neuropharmacology 2016; 14 (7) . https://dx.doi.org/10.2174/1570159X14666160106155129
| DOI https://dx.doi.org/10.2174/1570159X14666160106155129 |
Print ISSN 1570-159X |
| Publisher Name Bentham Science Publisher |
Online ISSN 1875-6190 |
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