title: Vulnerability to somatic symptoms of depression during interferon-alpha therapy for hepatitis C: a 16-week prospective study.
abstract: OBJECTIVE
  This study evaluated the distinctive clinical and biological manifestations of depressive symptom subtypes (i.e., cognitive-affective and somatic) in Veterans with hepatitis C viral infection (HCV) before and during interferon-alpha (IFN) based antiviral therapy.
  
  
  METHODS
  Thirty-two Veterans with HCV and no prior history of IFN therapy were followed prospectively during the first 16weeks of therapy to evaluate depressive symptoms and to determine if baseline cytokine and serotonin levels predicted subsequent changes in depressive scores.
  
  
  RESULTS
  IFN therapy resulted in a significant increase in total depressive symptoms from baseline (week 0) to week 16, with neurovegetative and somatic symptoms of depression including loss of appetite, fatigue and irritability increasing within the first two weeks of therapy and continuing to increase throughout IFN therapy. When depressive symptoms were evaluated using a two-factor (i.e., Cognitive-Affective and Somatic) model, the Cognitive-Affective factor score did not change significantly following IFN therapy initiation, while the Somatic factor score showed a significant increase from week 0 to week 16. Veterans with the largest increases in somatic symptoms from week 0 to week 2 had significantly higher levels of tumor necrosis factor-alpha (TNF-α) and lower levels of serotonin at baseline, as compared to Veterans with minimal or no increase in somatic symptoms.
  
  
  CONCLUSIONS
  Somatic symptoms of depression can be significantly exacerbated during IFN therapy and may be predicted by higher TNF-α levels and lower serotonin levels at baseline.
authors.affiliation: Research & Development Service, Portland VA Medical Center, Portland, OR, USA. Jennifer.loftis2@va.gov
authors.forename: Jennifer M
authors.initials: JM
authors.lastname: Loftis
authors.forename: Alexander L
authors.initials: AL
authors.lastname: Patterson
authors.forename: Clare J
authors.initials: CJ
authors.lastname: Wilhelm
authors.forename: Henry
authors.initials: H
authors.lastname: McNett
authors.forename: Benjamin J
authors.initials: BJ
authors.lastname: Morasco
authors.forename: Marilyn
authors.initials: M
authors.lastname: Huckans
authors.forename: Timothy
authors.initials: T
authors.lastname: Morgan
authors.forename: Shira
authors.initials: S
authors.lastname: Saperstein
authors.forename: Aliya
authors.initials: A
authors.lastname: Asghar
authors.forename: Peter
authors.initials: P
authors.lastname: Hauser
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000009:adverse effects* / Q000627:therapeutic use*; D003866:Depressive Disorder / Q000139:chemically induced* / Q000175:diagnosis / Q000276:immunology / Q000523:psychology; D003865:Major Depressive Disorder / Q000139:chemically induced / Q000175:diagnosis / Q000276:immunology / Q000523:psychology; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D005260:Female; D019698:Hepatitis C, Chronic / Q000188:drug therapy* / Q000276:immunology; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000009:adverse effects* / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011092:Polyethylene Glycols / Q000009:adverse effects* / Q000627:therapeutic use*; D011446:Prospective Studies; D011994:Recombinant Proteins / Q000009:adverse effects / Q000627:therapeutic use; D012307:Risk Factors; D012701:Serotonin / Q000097:blood; D013001:Somatoform Disorders / Q000139:chemically induced* / Q000175:diagnosis / Q000276:immunology / Q000523:psychology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014728:Veterans / Q000523:psychology*
chemical_list: D000998:Antiviral Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D012701:Serotonin; D011092:Polyethylene Glycols; C417083:peginterferon alfa-2b; C100416:peginterferon alfa-2a