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Background: Interferon (IFN) - induced depression represents a major complication in antiviral treatment of chronic hepatitis C virus (HCV) infection. Aim: To evaluate in a placebo-controlled study the efficacy of a selective serotonin reuptake inhibitor (SSRI) in HCV patients with antiviral therapy and IFN-associated depression. Methods: In a randomized, double-blind, placebo-controlled study, we included 100 HCV outpatients. During interferon therapy (peginterferon alfa-2b plus ribavirin), depression was monitored using the Hospital Anxiety and Depression Scale (HADS). Patients with clinically relevant IFN-induced depression (HADS≥9) were randomly assigned to placebo or citalopram (SSRI, 20 mg/day). Results: In 28 patients (28%), HADS scores increased to ≥9 during IFN therapy. They were treated with placebo (n=14) or SSRI (n=14). HADS scores declined significantly in SSRI patients within 4 weeks of therapy (P

Background: The study objective was to determine the contribution of cytokine-induced depression to a predictive model of sustained virological response (SVR) in chronic hepatitis C. Methods: One hundred and one therapy-naïve hepatitis C virus (HCV) outpatients received treatment with peginterferon alfa-2b and ribavirin. Neuropsychiatric side effects were monitored prospectively (Hospital Anxiety and Depression Scale, DSM-IV criteria for major depression). SVR was defined as a failure to detect HCV by PCR 24 weeks after therapy. Results: SVR rate was 72.3% (73 of 101 patients). Classification data and the extent of interferon-induced depression were not significantly linked to SVR. Virus genotype (p = 0.045) and gender (p = 0.016) contributed significantly to a logistic regression model. Mean (p = 0.811) and maximum (p = 0.744) depression increases were no significant predictors of SVR. Major depression rates (DSM-IV criteria) were 12.3% (9 of 73 patients) in the subgroup with SVR and 10.7% (3 of 28) in patients without SVR. Conclusions: We found no significant association between depression and the efficacy of antiviral treatment in chronic hepatitis C. Interferon-induced depressive symptoms are important to be monitored and treated if necessary; however, they cannot be used to predict therapy success.

The trace element selenium is discussed as a chemopreventive agent in colorectal carcinogenesis. Selenocysteine-containing proteins, so-called selenoproteins, represent potential molecular targets for nutritive selenium supplementation. Due to their antioxidative potential, the selenoproteins gastrointestinal glutathione peroxidase (GI-GPx) and selenoprotein P (SePP) are considered to provide protection against reactive oxygen species (ROS), thereby reducing DNA damage and preventing development of colon cancer. GI-GPx and SePP are abundantly expressed in normal colon mucosa. Recently, we demonstrated both reduced SePP expression and increased GI-GPx expression in colorectal adenomas. In this study, we investigated the expression of SePP and GI-GPx in colorectal cancers compared with corresponding normal mucosa. Further, the occurrence of genetic alterations within the SePP and GI-GPx genes was analyzed. We observed a significant reduction or loss of SePP mRNA expression in colon cancers, whereas GI-GPx mRNA and protein expression varied between different tumor samples. In addition, we identified novel polymorphisms within the SePP and GI-GPx genes with so far unknown relevance for protein function. Our results argue against a general decrease of selenoprotein expression in colorectal carcinogenesis but imply specific differential regulation of expression of individual selenoproteins.