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Promoter Polymorphisms of the Interferon-α Receptor Gene and Development of Interferon-Induced Depressive Symptoms in Patients with Chronic Hepatitis C: Preliminary Findings

Yoshida K.a, b · Alagbe O.a · Wang X.a, † · Woolwine B.a · Thornbury M.a · Raison C.L.a · Miller A.H.a
aDepartment of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Ga., USA; bDepartment of Psychiatry, Akita University School of Medicine, Akita, Japan Neuropsychobiology 2005;52:55–61 (DOI:10.1159/000086605)


Background: Interferon (IFN)-α treatment frequently induces depression, which can impair quality of life and reduce treatment adherence. Defining relevant risk factors for IFN-α-induced depression is essential for designing preventative treatment strategies. Objective: The purpose of the present study was to determine whether promoter polymorphisms of –408C/T, –3C/T and GT repeat dinucleotide microsatellite in the IFN-α/β receptor 1 (IFNAR1) gene are associated with the development of IFN-induced depression. Method: Fifty patients with chronic hepatitis C were treated with pegylated IFN α-2b plus a standard or weight-based dose of ribavirin. Severity of depression was assessed using the Zung Self-Rating Depression Scale (SDS) at baseline and at 4, 8, 12 and 24 weeks of treatment. Result: The baseline to maximum difference in the SDS index score of neurovegetative/somatic symptoms was higher in patients with the 5/14 genotype of the GT repeat dinucleotide microsatellite polymorphism than in those patients with other genotypes (p = 0.0084). Conclusion: This preliminary result suggests that the promoter GT repeat dinucleotide microsatellite polymorphism of the IFNAR1 gene may represent a risk factor for the development of depressive symptoms during IFN-α therapy for hepatitis C and other conditions.


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