Pre-treatment waking cortisol response and vulnerability to interferon α induced depression

Eccles, Jessica; Lallemant, Camille; Mushtaq, Farrah; Greenwood, Matthew; Keller, Majella; Golding, Bruno; Tibble, Jeremy; Haq, Inam; Whale, Richard

doi:10.1016/j.euroneuro.2012.03.009

Cited by 8 publications

(5 citation statements)

References 24 publications

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“…Promising findings from studies awaiting replication include genetic polymorphisms coding for phospholipase A2, cyclooxygenase 2 [15] and the serotonin transporter protein 5-HTTLPR [16]. Additionally we recently reported an enhanced baseline reactivity of the hypothalamicpituitary-adrenal axis, as measured by waking salivary cortisol secretion, to be associated with later MDD emergence during IFNα treatment [17]. This is consistent with preliminary findings in non-iatrogenic depression.…”

Section: Introductionsupporting

confidence: 63%

Psychomotor retardation and vulnerability to interferon alpha induced major depressive disorder: Prospective study of a chronic hepatitis C cohort

Whale

Fialho

Rolt

et al. 2015

Journal of Psychosomatic Research

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Section: Introductionsupporting

confidence: 63%

Psychomotor retardation and vulnerability to interferon alpha induced major depressive disorder: Prospective study of a chronic hepatitis C cohort

Whale

Fialho

Rolt

et al. 2015

Journal of Psychosomatic Research

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“…Recently Huckans et al also reported increased symptoms of depression during interferon therapy in a cohort of 33 HCV infected patients, which decreased or remitted following treatment discontinuation [ 42 ]. Eccles et al have demonstrated that hypothalamic-pituitary-adrenal axis hyperactivity prior to interferon based therapy evaluated through measurement of the waking salivary cortisol response was associated to depression during treatment [ 43 ]. Whale et al showed recently that younger age, previous history of major depression disorder, higher baseline psychomotor retardation and somatic symptoms item scores using the Hamilton Depression Rating Scale and HCV genotype 2 were implicated in depression during IFN treatment [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Hepatitis C virus eradication improves immediate and delayed episodic memory in patients treated with interferon and ribavirin

et al. 2017

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BackgroundChronic hepatitis C virus (HCV) infection is associated with impairment of cognitive function and mood disorders. Our aim was to evaluate the impact of sustained virological response (SVR) on cognitive function and mood disorders.MethodA prospective exploratory one arm study was conducted. Adult clinically compensated HVC patients were consecutively recruited before treatment with interferon and ribavirin for 24 to 48 weeks, according to HCV genotype. Clinical, neurocognitive and mood assessments using the PRIME-MD and BDI instruments were performed at baseline, right after half of the expected treatment has been reached and 6 months after the end of antiviral treatment. Exclusion criteria were the use of illicit psychotropic substances, mental confusion, hepatic encephalopathy, hepatocellular carcinoma, severe anemia, untreated hypothyroidism, Addison syndrome and major depression before treatment.ResultsThirty six patients were enrolled and 21 completed HCV treatment (n = 16 with SVR and n = 5 without). Regardless of the viral clearance at the end of treatment, there was a significant improvement in the immediate verbal episodic memory (p = 0.010), delayed verbal episodic memory (p = 0.007), selective attention (p < 0.001) and phonemic fluency (p = 0.043). Patients with SVR displayed significant improvement in immediate (p = 0.045) and delayed verbal episodic memory (p = 0.040) compared to baseline. The baseline frequency of depression was 9.5%, which rose to 52.4% during treatment, and returned to 9.5% 6 months after the end of treatment, without significant difference between patients with and without SVR. Depressive symptoms were observed in 19.1% before treatment, 62% during (p = 0.016) and 28.6% 6 months after the end of treatment (p = 0.719).ConclusionsEradication of HCV infection improved cognitive performance but did not affect the frequency of depressive symptoms at least in the short range.

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“…Often it is not so much the possible somatic side effects such as thyroid dysfunction, headache and anemia but frequent psychic side effects that impair the health-related quality of life of those affected. Many patients develop a IFN-α-induced depressive symptomatology that usually appears within three months after the start of IFN-α treatment [ 5 , 9 – 13 ].…”

Section: Introductionmentioning

confidence: 99%

Quinolinic Acid Responses during Interferon-α-Induced Depressive Symptomatology in Patients with Chronic Hepatitis C Infection - A Novel Aspect for Depression and Inflammatory Hypothesis

et al. 2015

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BackgroundThe aim of this exploratory study is to gain for the first time a more comprehensive picture of the impact of changes of quinolinic acid concentrations on depressive symptomatology during and after IFN-α therapy.MethodsThe quinolinic acid concentrations of 35 HCV patients are examined in a prospective survey over the entire period of IFN-α treatment as well as three months later at six different times (baseline, one, three, six and nine months after the beginning of IFN-α treatment, and after the end of treatment).ResultsDuring IFN-α treatment Hamilton Depression Rating Scale scores rise significantly. At the same time there is greater activity of indoleamine 2,3-dioxygenase, with a resulting increase in plasma kynurenine concentrations. Compared to baseline values quinolinic acid concentrations increase significantly during therapy, reflecting an increased neurotoxic challenge. In addition, patients with higher scores in the Hamilton Depression Rating Scale at six and nine months after starting therapy show significantly higher levels of quinolinic acid concentration.ConclusionsThe increase of quinolinic acid during IFN-α therapy might contribute to depressive symptomatology through the neurotoxic challenge caused by quinolinic acid. Subsequently, our exploratory study results support the inflammatory hypothesis of depression. The awareness of relevant risk factors of IFN-α treatment-induced depression is essential to develop preventative treatment strategies.

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Pre-treatment waking cortisol response and vulnerability to interferon α induced depression

Cited by 8 publications

References 24 publications

Psychomotor retardation and vulnerability to interferon alpha induced major depressive disorder: Prospective study of a chronic hepatitis C cohort

Psychomotor retardation and vulnerability to interferon alpha induced major depressive disorder: Prospective study of a chronic hepatitis C cohort

Hepatitis C virus eradication improves immediate and delayed episodic memory in patients treated with interferon and ribavirin

Quinolinic Acid Responses during Interferon-α-Induced Depressive Symptomatology in Patients with Chronic Hepatitis C Infection - A Novel Aspect for Depression and Inflammatory Hypothesis

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