BACKGROUND: This study is aim to investigate concurrent long-term psychiatric, cognitive and neurophysiological measures of alpha-IFN neurotoxicity in the treatment of chronic viral hepatitis. METHODS: Twenty patients with HCV hepatitis were enrolled while treated with alpha-IFN (3-6 MU t.i.w. for 6-12 months). Neurotoxicity was evaluated by psychiatric [Hamilton Depression Rating Scale (HAM-D), Hamilton Scale for Anxiety (HAM-A), Beck Depression Inventory (BDI) and State-Trait Anxiety Inventory (STAI-Y)], complete cognitive and neurophysiological assessments (EEG spectral analysis, P300). Patients were assessed at baseline (t0), 2 (t1) and 6 months (t2) since the beginning of therapy. RESULTS: Depression scores significantly increased (HAM-D: t0=4.4+/-2.6; t1=8.9+/-3.9, p<0.001; and t2=7.7+/-3.8, p<0.001). A concurrent increase was shown also for anxiety (HAM-A: t0=6.0+/-3.2; t1=9.6+/-4.5, p<0.005; and t2=9.1+/-4.5, p<0.005). Significant neurophysiological effects were also detected: increase of alpha power (p<0.05) in frontal derivations, reduction of the mean dominant frequency (p<0.005) and increase of theta power (p<0.05) in parietal derivations. In contrast, no significant cognitive changes occurred. LIMITATIONS: The study was performed on a relative small sample of patients mainly with observational intentions. Biological data (e.g. blood cytokines samples) are not available: they could have given useful information about biological mechanisms related to the alterations observed. CONCLUSIONS: Alpha-IFN treatment caused a time-dependent induction of symptoms of mild depression, concurrent anxiety and EEG changes. These psychiatric and neurophysiological changes can better explain the pharmacological profile of alpha-IFN and could help to address research on at risk population and, particularly, during pegylated-IFN therapy.
BACKGROUND: This study is aim to investigate concurrent long-term psychiatric, cognitive and neurophysiological measures of alpha-IFN neurotoxicity in the treatment of chronic viral hepatitis. METHODS: Twenty patients with HCV hepatitis were enrolled while treated with alpha-IFN (3-6 MU t.i.w. for 6-12 months). Neurotoxicity was evaluated by psychiatric [Hamilton Depression Rating Scale (HAM-D), Hamilton Scale for Anxiety (HAM-A), Beck Depression Inventory (BDI) and State-Trait Anxiety Inventory (STAI-Y)], complete cognitive and neurophysiological assessments (EEG spectral analysis, P300). Patients were assessed at baseline (t0), 2 (t1) and 6 months (t2) since the beginning of therapy. RESULTS:Depression scores significantly increased (HAM-D: t0=4.4+/-2.6; t1=8.9+/-3.9, p<0.001; and t2=7.7+/-3.8, p<0.001). A concurrent increase was shown also for anxiety (HAM-A: t0=6.0+/-3.2; t1=9.6+/-4.5, p<0.005; and t2=9.1+/-4.5, p<0.005). Significant neurophysiological effects were also detected: increase of alpha power (p<0.05) in frontal derivations, reduction of the mean dominant frequency (p<0.005) and increase of theta power (p<0.05) in parietal derivations. In contrast, no significant cognitive changes occurred. LIMITATIONS: The study was performed on a relative small sample of patients mainly with observational intentions. Biological data (e.g. blood cytokines samples) are not available: they could have given useful information about biological mechanisms related to the alterations observed. CONCLUSIONS: Alpha-IFN treatment caused a time-dependent induction of symptoms of mild depression, concurrent anxiety and EEG changes. These psychiatric and neurophysiological changes can better explain the pharmacological profile of alpha-IFN and could help to address research on at risk population and, particularly, during pegylated-IFN therapy.
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