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Risk factors for the development of depression in patients with hepatitis C taking interferon-α.

Smith KJ, Norris S, O'Farrelly C, O'Mara SM - Neuropsychiatr Dis Treat (2011)

Bottom Line: Interferon-α, currently used for the treatment of hepatitis C, is associated with a substantially elevated risk of depression.The identification of risk factors prior to treatment may allow identification of patients who will become depressed on interferon, allowing the possibility of improved treatment support and rates of treatment adherence.Here, we consolidate and review the literature on risk factors, and we discuss the potential confounds within the research examined in order to better isolate the risk factors that may be important in the development of depression in these patients and which might help predict patients likely to become depressed on treatment.

View Article: PubMed Central - PubMed

Affiliation: Trinity College Institute of Neuroscience.

ABSTRACT
Interferon-α, currently used for the treatment of hepatitis C, is associated with a substantially elevated risk of depression. However, not everyone who takes this drug becomes depressed, so it is important to understand what particular factors may make some individuals more 'at risk' of developing depression than others. Currently there is no consensus as to why interferon-induced depression occurs and the range of putative risk factors is wide and diverse. The identification of risk factors prior to treatment may allow identification of patients who will become depressed on interferon, allowing the possibility of improved treatment support and rates of treatment adherence. Here, we consolidate and review the literature on risk factors, and we discuss the potential confounds within the research examined in order to better isolate the risk factors that may be important in the development of depression in these patients and which might help predict patients likely to become depressed on treatment. We suggest that interactions between psychobehavioral, genetic, and biological risk factors are of particular importance in the occurrence of depression in patients with hepatitis C taking interferon-α.

No MeSH data available.


Related in: MedlinePlus

Cytokine-mediated pathways that influence the CNS. Diagram showing the various factors that influence the CNS. There is a complex relationship, the relationship with monoamines and the IDO–Kyn pathway, growth factors, and stress. Stressors and cytokines both increase the stress response, which is reflected by an increase in the amount of CRH, both in the CNS and peripherally, which in turn activates ACTH and cortisol (CORT) levels. CRH also has a bidirectional relationship with serotonin (5-HT) levels, and gamma aminobutyric acid acts as a mediator for this process. 5-HT levels are also influenced by the production of IDO, which favors the production of the neurotoxin KYN over 5-HT. The stressor system and IDO–KYN pathway both lead to a reduction in 5-HT. Cytokines also influence oxidative and apoptotic mechanisms, leading to a reduction in growth factors such as brain-derived neurotrophic factor, which in turn leads to impaired neuroplastic processes and decreased neurogenesis, as well as cytokines having an indirect effect on growth factor levels; stress has also been shown to have a direct effect. The culmination of these three pathways can lead to the development of major depression. Copyright © 2005, Elsevier. Adapted with permission from Hayley S, Poulter MO, Merali Z, Anisman H. The pathogenesis of clinical depression: stressor- and cytokine-induced alterations of neuroplasticity. Neuroscience. 2005;135(3):659–678.Abbreviation: CRH, corticotrophin-releasing hormone.
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f2-ndt-7-275: Cytokine-mediated pathways that influence the CNS. Diagram showing the various factors that influence the CNS. There is a complex relationship, the relationship with monoamines and the IDO–Kyn pathway, growth factors, and stress. Stressors and cytokines both increase the stress response, which is reflected by an increase in the amount of CRH, both in the CNS and peripherally, which in turn activates ACTH and cortisol (CORT) levels. CRH also has a bidirectional relationship with serotonin (5-HT) levels, and gamma aminobutyric acid acts as a mediator for this process. 5-HT levels are also influenced by the production of IDO, which favors the production of the neurotoxin KYN over 5-HT. The stressor system and IDO–KYN pathway both lead to a reduction in 5-HT. Cytokines also influence oxidative and apoptotic mechanisms, leading to a reduction in growth factors such as brain-derived neurotrophic factor, which in turn leads to impaired neuroplastic processes and decreased neurogenesis, as well as cytokines having an indirect effect on growth factor levels; stress has also been shown to have a direct effect. The culmination of these three pathways can lead to the development of major depression. Copyright © 2005, Elsevier. Adapted with permission from Hayley S, Poulter MO, Merali Z, Anisman H. The pathogenesis of clinical depression: stressor- and cytokine-induced alterations of neuroplasticity. Neuroscience. 2005;135(3):659–678.Abbreviation: CRH, corticotrophin-releasing hormone.

Mentions: However, the second theory suggests that the immune system influences secondary factors that in turn interact with the CNS.32 In the second scenario, there is a complex interplay between stressors, the IDO–KYN pathway (see Figure 2), and factors that influence neuroplasticity in the development of cytokine-induced depression (see Figure 2).57,74,75


Risk factors for the development of depression in patients with hepatitis C taking interferon-α.

Smith KJ, Norris S, O'Farrelly C, O'Mara SM - Neuropsychiatr Dis Treat (2011)

Cytokine-mediated pathways that influence the CNS. Diagram showing the various factors that influence the CNS. There is a complex relationship, the relationship with monoamines and the IDO–Kyn pathway, growth factors, and stress. Stressors and cytokines both increase the stress response, which is reflected by an increase in the amount of CRH, both in the CNS and peripherally, which in turn activates ACTH and cortisol (CORT) levels. CRH also has a bidirectional relationship with serotonin (5-HT) levels, and gamma aminobutyric acid acts as a mediator for this process. 5-HT levels are also influenced by the production of IDO, which favors the production of the neurotoxin KYN over 5-HT. The stressor system and IDO–KYN pathway both lead to a reduction in 5-HT. Cytokines also influence oxidative and apoptotic mechanisms, leading to a reduction in growth factors such as brain-derived neurotrophic factor, which in turn leads to impaired neuroplastic processes and decreased neurogenesis, as well as cytokines having an indirect effect on growth factor levels; stress has also been shown to have a direct effect. The culmination of these three pathways can lead to the development of major depression. Copyright © 2005, Elsevier. Adapted with permission from Hayley S, Poulter MO, Merali Z, Anisman H. The pathogenesis of clinical depression: stressor- and cytokine-induced alterations of neuroplasticity. Neuroscience. 2005;135(3):659–678.Abbreviation: CRH, corticotrophin-releasing hormone.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3101888&req=5

f2-ndt-7-275: Cytokine-mediated pathways that influence the CNS. Diagram showing the various factors that influence the CNS. There is a complex relationship, the relationship with monoamines and the IDO–Kyn pathway, growth factors, and stress. Stressors and cytokines both increase the stress response, which is reflected by an increase in the amount of CRH, both in the CNS and peripherally, which in turn activates ACTH and cortisol (CORT) levels. CRH also has a bidirectional relationship with serotonin (5-HT) levels, and gamma aminobutyric acid acts as a mediator for this process. 5-HT levels are also influenced by the production of IDO, which favors the production of the neurotoxin KYN over 5-HT. The stressor system and IDO–KYN pathway both lead to a reduction in 5-HT. Cytokines also influence oxidative and apoptotic mechanisms, leading to a reduction in growth factors such as brain-derived neurotrophic factor, which in turn leads to impaired neuroplastic processes and decreased neurogenesis, as well as cytokines having an indirect effect on growth factor levels; stress has also been shown to have a direct effect. The culmination of these three pathways can lead to the development of major depression. Copyright © 2005, Elsevier. Adapted with permission from Hayley S, Poulter MO, Merali Z, Anisman H. The pathogenesis of clinical depression: stressor- and cytokine-induced alterations of neuroplasticity. Neuroscience. 2005;135(3):659–678.Abbreviation: CRH, corticotrophin-releasing hormone.
Mentions: However, the second theory suggests that the immune system influences secondary factors that in turn interact with the CNS.32 In the second scenario, there is a complex interplay between stressors, the IDO–KYN pathway (see Figure 2), and factors that influence neuroplasticity in the development of cytokine-induced depression (see Figure 2).57,74,75

Bottom Line: Interferon-α, currently used for the treatment of hepatitis C, is associated with a substantially elevated risk of depression.The identification of risk factors prior to treatment may allow identification of patients who will become depressed on interferon, allowing the possibility of improved treatment support and rates of treatment adherence.Here, we consolidate and review the literature on risk factors, and we discuss the potential confounds within the research examined in order to better isolate the risk factors that may be important in the development of depression in these patients and which might help predict patients likely to become depressed on treatment.

View Article: PubMed Central - PubMed

Affiliation: Trinity College Institute of Neuroscience.

ABSTRACT
Interferon-α, currently used for the treatment of hepatitis C, is associated with a substantially elevated risk of depression. However, not everyone who takes this drug becomes depressed, so it is important to understand what particular factors may make some individuals more 'at risk' of developing depression than others. Currently there is no consensus as to why interferon-induced depression occurs and the range of putative risk factors is wide and diverse. The identification of risk factors prior to treatment may allow identification of patients who will become depressed on interferon, allowing the possibility of improved treatment support and rates of treatment adherence. Here, we consolidate and review the literature on risk factors, and we discuss the potential confounds within the research examined in order to better isolate the risk factors that may be important in the development of depression in these patients and which might help predict patients likely to become depressed on treatment. We suggest that interactions between psychobehavioral, genetic, and biological risk factors are of particular importance in the occurrence of depression in patients with hepatitis C taking interferon-α.

No MeSH data available.


Related in: MedlinePlus