Managing depression during hepatitis C treatment.
ABSTRACT The prevalence of hepatitis C virus (HCV) infection in Canada is estimated to be 1% and expected to increase during the next decade. Mental illness, particularly depression, is common among HCV-infected patients and remains an obstacle to interferon-alpha (IFN-alpha) treatment. We summarize the risk factors for interferon-alpha-induced major depressive disorder (IFN-alpha-MDD) in HCV patients and the evidence for antidepressant prophylaxis and symptomatic antidepressant treatment of depression.
We searched MEDLINE, EMBASE, and CINAHL for randomized controlled or quasi-experimental trials evaluating antidepressant prophylactic and symptomatic treatment approaches for depression emerging during IFN-alpha treatment. Manual searches of references listed in review articles, case series, and anecdotal reports supplemented our literature search.
A total of 9 trials involving prophylactic and symptomatic treatment approaches for IFN-alpha-MDD are summarized in our review. Antidepressant pretreatment is beneficial for patients with elevated baseline depressive symptoms and a preexisting history of IFN-alpha-MDD. Although limited evidence exists for several antidepressant agents, much of the evidence suggests that selective serotonin reuptake inhibitors (SSRIs) are safe and efficacious in treating depressive symptoms secondary to IFN-alpha therapy.
Both antidepressant pretreatment and symptomatic treatment are viable strategies for treating IFN-alpha-MDD. Improved treatment outcomes and early identification of depression during HCV treatment can be achieved using an integrated medical and mental health treatment approach.
- SourceAvailable from: Gianluca SerafiniNeurology Psychiatry and Brain Research 02/2014; 20(1):22. DOI:10.1016/j.npbr.2014.01.168 · 0.10 Impact Factor
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ABSTRACT: There is growing evidence that inflammatory mediators play a critical role in the pathophysiology of both major depression and suicidal behavior. Immunological differences have been reported in both major affective disorders and suicidal behavior. Specifically, increased levels of pro-inflammatory cytokines have been shown to correlate with the severity of depression and various cytokines have been identified as potentially important in understanding the pathophysiology of major affective disorders/suicidality. We aimed to conduct a systematic review of the current literature to investigate the association between inflammatory cytokines and suicidal behavior. Only articles from peer-reviewed journals were selected for inclusion in the present review. Most studies documented the association between suicidality and IL2, IL-6, IL-8, TNF-α and VEGF levels that have been found altered in suicidal behavior. The presence of major depressive disorder (MDD) with suicidal ideation/attempts was associated with differences in inflammatory cytokine profile when compared to that without suicidal ideation/attempts. Most suicide attempters or subjects with suicidal ideation showed an imbalance of the immune system but this does not imply the existence of a causal link. Also, not all studies demonstrated a positive correlation between inflammatory cytokines and suicidal behavior. Further additional studies should elucidate the molecular mechanisms of the immune activation pathways underlying suicidality.European neuropsychopharmacology: the journal of the European College of Neuropsychopharmacology 07/2013; 23(12). DOI:10.1016/j.euroneuro.2013.06.002 · 5.40 Impact Factor
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ABSTRACT: Neurotransmitters and hormones regulate major immune functions, including the selection of T helper (Th)1 or Th2 cytokine responses, related to cell-mediated and humoral immunity, respectively. A role of imbalance and dynamic switching of Th1/Th2 system has been proposed, with relative displacement of the immune reserve in relation to complex interaction between Th1/Th2 and neuro-hormonal balance fluctuations, in the pathogenesis of various chronic human diseases, probably also including psychiatric disorders. Components of the stress system such as norepinephrine (NE) and glucocorticoids appear to mediate a Th2 shift, while serotonin (5-HT) and melatonin might mediate a Th1 shift. Some antidepressants would occur affecting these systems, acting on neurotransmitter balance (especially the 5-HT/NE balance) and expression levels of receptor subtypes, which in turn affect cytokine production and relative Th1/Th2 balance. It could be therefore hypothesized that the antidepressant-related increase in NE tone enhances the Th2 response, while the decrease in NE tone or the increase in 5-HT tone enhances the Th1 response. However, the neurotransmitter and Th1/Th2 balance modulation could be relative, aiming to restore physiological levels a previous imbalance in receptor sensitivity and cytokine production. The considerations on neuro-immunomodulation could represent an additional aid in the study of pathophysiology of psychiatric disorders and in the choice of specific antidepressants in specific clusters of symptoms, especially in comorbidity with internal pathologies. Furthermore limited data, reviewed here, have shown the effectiveness of some antidepressants as pure immunomodulators. However, these considerations are tentative and require experimental confirmation or refutation by future studies.DNA research: an international journal for rapid publication of reports on genes and genomes 06/2012; 10(2):97-123. DOI:10.2174/157015912800604542 · 2.35 Impact Factor