Dataset Information

Vulnerability to somatic symptoms of depression during interferon-alpha therapy for hepatitis C: a 16-week prospective study.

ABSTRACT: 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.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.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-?) and lower levels of serotonin at baseline, as compared to Veterans with minimal or no increase in somatic symptoms.Somatic symptoms of depression can be significantly exacerbated during IFN therapy and may be predicted by higher TNF-? levels and lower serotonin levels at baseline.

SUBMITTER: Loftis JM

PROVIDER: S-EPMC4408920 | biostudies-literature | 2013 Jan

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Vulnerability to somatic symptoms of depression during interferon-alpha therapy for hepatitis C: a 16-week prospective study.

Loftis Jennifer M JM Patterson Alexander L AL Wilhelm Clare J CJ McNett Henry H Morasco Benjamin J BJ Huckans Marilyn M Morgan Timothy T Saperstein Shira S Asghar Aliya A Hauser Peter P

Journal of psychosomatic research 20121121 1

<h4>Objective</h4>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.<h4>Methods</h4>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 ...[more]

PMID: 23272989

Similar Datasets

Project description:Patients with heart failure (HF) have high rates of cognitive impairment and depressive symptoms. Depressive symptoms have been associated with greater cognitive impairments in HF; however, it is not known whether particular clusters of depressive symptoms are more detrimental to cognition than others.The aim of this study was to identify whether somatic and/or nonsomatic depressive symptom clusters were associated with cognitive function in persons with HF.Participants were 326 HF patients (40.5% women, 26.7% non-white race-ethnicity, aged 68.6 ± 9.7 years). Depressive symptoms were measured using a depression questionnaire commonly used in medical populations: the Patient Health Questionnaire-9. Somatic and nonsomatic subscale scores were created using previous factor analytic results. A neuropsychological battery tested attention, executive function, and memory. Composites were created using averages of age-adjusted scaled scores. Regressions adjusting for demographic and clinical factors were conducted.Regressions revealed that Patient Health Questionnaire-9 total was associated with attention (? = -.14, P = .008) and executive function (? = -.17, P = .001). When analyzed separately, the nonsomatic subscale, but not the somatic symptoms subscale (P values ? .092), was associated with attention scores (? = -.15, P = .004) and memory (? = -.11, P = .044). Both nonsomatic (? = -.18, P < .001) and somatic (? = -.11, P = .048) symptoms were related to executive function. When included together, only the nonsomatic symptom cluster was associated with attention (? = -.15, P = .020) and executive function (? = -.19, P = .003).Greater overall depressive symptom severity was associated with poorer performance on multiple cognitive domains, an effect driven primarily by the nonsomatic symptoms of depression.These findings suggest that screening explicitly for nonsomatic depressive symptoms may be warranted and that the mechanisms underlying the depression-cognitive function relationship in HF are not solely related to sleep or appetite disturbance. Thus, interventions that target patients' somatic symptoms only (eg, poor appetite or fatigue) may not yield maximum cognitive benefit compared with a comprehensive treatment that targets depressed mood, anhedonia, and other nonsomatic symptoms.

Project description:Importance: The high incidence of major depressive episodes during interferon-α (IFN-α) therapy is considered the most powerful supportive evidence for the inflammation theory of depression. As the kynurenine pathway plays an important role connecting inflammation and depression, it is plausible to investigate this pathway for predictive genetic markers for IFN-α-induced depression. Methods: In this prospective case-control study, we assessed 291 patients with chronic hepatitis C viral infection taking IFN-α therapy and analyzed the single nucleotide polymorphisms (SNPs) in genes in the kynurenine pathway. Our case group contained patients who developed IFN-α-induced depression during the treatment, and others were defined as the control group. Genomic DNA was extracted from leukocytes in the peripheral blood and analyzed by Affymetrix TWB array. We first tested allelic, dominant, and recessive models on each of our SNPs using Fisher's exact test. We then conducted 5000 gene-wide max(T) permutations based on the best model of each SNP to provide strong gene-wide family-wise error rate control. Finally, we preformed logistic regression for the significant SNPs acquired in previous procedures, with sex and education level as covariates to build predictive models. Additional haplotype analyses were conducted with Haploview 4.2 to investigate the combining effect of multiple significant SNPs within a gene. Results: With sex and education level as covariates, rs8082252 (p = 0.0015, odds ratio = 2.716), rs8082142 (p = 0.0031, odds ratio = 2.499) in arylformamidase (AFMID), and rs12477181 (p = 0.0004, odds ratio = 0.3478) in kynureninase (KYNU) were significant in logistic regression models with dominant modes of inheritance. Haplotype analyses showed the two significant SNPs in AFMID to be in the same haploblock and highly correlated (r2 = 0.99). There were two significant haplotypes (by the sequence of rs8082252, rs8082142): AT (χ2 = 7.734, p = 0.0054) and GC (χ2 = 6.874, p = 0.0087). Conclusions: This study provided supportive evidence of the involvement of the kynurenine pathway in IFN-α-induced depression. SNPs in this pathway were also predictive of this disease.

Dataset Information

Vulnerability to somatic symptoms of depression during interferon-alpha therapy for hepatitis C: a 16-week prospective study.

Publications

Vulnerability to somatic symptoms of depression during interferon-alpha therapy for hepatitis C: a 16-week prospective study.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets