Psychiatric Symptoms in Patients With Chronic Hepatitis C Receiving Interferon Alfa-2b Therapy

Kraus, Michael R.; Schäfer, Arne; Faller, Hermann; Csef, Herbert; Scheurlen, Michael

doi:10.4088/jcp.v64n0614

Cited by 219 publications

(159 citation statements)

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“…A lower level of support was also associated with higher scores for anxiety, as measured by the HAD, more psychiatric diagnoses as listed in the medical chart, and lower psychological well-being as measured by sub-scales and summary scores of the SIP. While studies have consistently found antiviral therapy to be associated with higher levels of depression [40][41][42][43][44][45] , our crosssectional data did not show differences in the level of social support of those currently on therapy, as compared to those who were pre or post treatment. This may be surprising at first glance because of the known effects of antiviral therapy on mood.…”

Section: Discussioncontrasting

confidence: 90%

Mental and physical symptoms associated with lower social support for patients with hepatitis C

Blasiole¹,

Shinkunas²,

LaBrecque³

et al. 2006

WJG

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by others (19%). Nearly one fifth of the patients did not share information about their disease with others to avoid being stigmatized. Lower levels of social support were significantly associated with living alone, being unemployed, being excluded from antiviral therapy, having psychiatric comorbidities, contracting HCV through intravenous drug use, having high levels of anxiety and depression as measured by the HAD and negative mood state as measured by the SIP. Patients reporting lower levels of social support also noted more physical symptoms as measured by the SIP. CONCLUSION:Patients with hepatitis C often face significant social problems, ranging from social isolation to familial stress. The most common concerns reflect a limited insight of patients and their relatives and friends about the disease, the risk factors for its spread, and about potential consequences. Our data suggest that educational interventions targeting support persons and the stressors identified in our findings may lessen or alleviate the social strains patients with hepatitis C experience. INTRODUCTIONHepatitis C virus (HCV) infection, a common and slowly progressing liver disease, negatively affects quality of life. Most studies addressing the important impact of HCV focus on patients undergoing antiviral therapy [1][2][3][4][5][6] . However, even HCV-infected individuals outside of treatment have lower quality of life scores compared to uninfected controls [7][8][9] . Negative social interactions may play a unique role as a determinant of quality of life in patients with HCV, as they often face stigmatization in their professional and private environment [10][11][12] . Patients living with AIDS and stigmatizing diseases such as tuberculosis and leprosy Abstract AIM: To systematically examine the impact of the hepatitis C virus (HCV) diagnosis on patients' level of social support in a large-scale study. METHODS:Patients evaluated and treated for HCV in a tertiary referral center were enrolled in a cross-sectional study. Demographic data, functional and emotional status as measured by the Hospital Anxiety and Depression Scale (HAD) and the Sickness Impact Profile (SIP), severity of liver disease, mode of acquisition, and physical and psychiatric comorbidities were collected from patients or abstracted from the medical record. All participants completed a semi-structured interview, addressing questions of social support. RESULTS:A total of 342 patients (mean age 45.2 years; 37% women) were enrolled. Ninety-two (27%) patients described lower levels of support by family and friends. Nearly half of the participants (45%) noted the loss of at least one relationship due to the disease. Fears related to transmitting the disease (25%) were common and often associated with ignorance or even discrimination

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Section: Discussioncontrasting

confidence: 90%

Mental and physical symptoms associated with lower social support for patients with hepatitis C

Blasiole¹,

Shinkunas²,

LaBrecque³

et al. 2006

WJG

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“…52,53 Side effects of cytokine therapies A depressive syndrome including suicidal ideations is a common side effect of cytokine administration, for example, IFN-a in the therapy of hepatitis C or malignant melanoma. [54][55][56][57][58] During these therapies, IDO is activated and the tryptophan metabolism increases. The psychopathological changes seem to be closely related to the tryptophan metabolism: patients developing more severe depressive symptoms during IFN-a showed a more pronounced increase in tryptophan metabolism.…”

Section: The Inflammatory Hypothesis Of Depressionmentioning

confidence: 99%

The immune-mediated alteration of serotonin and glutamate: towards an integrated view of depression

2007

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Beside the well-known deficiency in serotonergic neurotransmission as pathophysiological correlate of major depression (MD), recent evidence points to a pivotal role of increased glutamate receptor activation as well. However, cause and interaction of these neurotransmitter alterations are not understood. In this review, we present a hypothesis integrating current concepts of neurotransmission and hypothalamus-pituitary-adrenal (HPA) axis dysregulation with findings on immunological alterations and alterations in brain morphology in MD. An immune activation including increased production of proinflammatory cytokines has repeatedly been described in MD. Proinflammatory cytokines such as interleukin-2, interferon-c, or tumor necrosis factor-a activate the tryptophan-and serotonin-degrading enzyme indoleamine 2,3-dioxygenase (IDO). Depressive states during inflammatory somatic disorders are also associated with increased proinflammatory cytokines and increased consumption of tryptophan via activation of IDO. An enhanced consumption of serotonin and its precursor tryptophan through IDO activation could well explain the reduced availability of serotonergic neurotransmission in MD. An increased activation of IDO and its subsequent enzyme kynurenine monooxygenase by proinflammatory cytokines, moreover, leads to an enhanced production of quinolinic acid, a strong agonist of the glutamatergic N-methyl-D-aspartate receptor. In inflammatory states of the central nervous system, IDO is mainly activated in microglial cells, which preferentially metabolize tryptophan to the NMDA receptor agonist quinolinic acid, whereas astrocytes -counteracting this metabolism due to the lack of an enzyme of this metabolism -have been observed to be reduced in MD. Therefore the type 1/type 2 immune response imbalance, associated with an astrocyte/microglia imbalance, leads to serotonergic deficiency and glutamatergic overproduction. Astrocytes are further strongly involved in re-uptake and metabolic conversion of glutamate. The reduced number of astrocytes could contribute to both, a diminished counterregulation of IDO activity in microglia and an altered glutamatergic neurotransmission. Further search for antidepressant agents should take into account anti-inflammatory drugs, for example, cyclooxygenase-2 inhibitors, might exert antidepressant effects by acting on serotonergic deficiency, glutamatergic hyperfunction and antagonizing neurotoxic effects of quinolinic acid. Molecular Psychiatry (2007) 12, 988-1000; doi:10.1038/sj.mp.4002006; published online 24 April 2007 Keywords: major depression; psychoneuroimmunology; IDO; glutamate; immune system; serotonin Glutamate in depressionGlutamatergic neurotransmission is involved in depression and interacts with the serotonergic and noradrenergic systems The common therapeutic mechanism of antidepressant drugs is the enhancement of serotonergic and/or noradrenergic neurotransmission. On the basis of this pharmacological profile of antidepressant drugs, neurochemical research on major depression ...

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“…Two types of studies have been conducted -one concerning patient populations and the second involved experiments utilizing healthy adult subjects. In studies involving patient populations, cytokine immunotherapy for the treatment of such disorders as AIDS, cancer and hepatitis C have shown that such therapy increased aggressive behavior as determined by measures of anger, hostility and irritability [12,51,67]. In one study, it was demonstrated that experimentally induced enhancement of proinflammatory cytokines was correlated with increases in hostility scores [92].…”

Section: Cytokines and Aggressionmentioning

confidence: 99%

The Neurobiological Bases for Development of Pharmacological Treatments of Aggressive Disorders

Siegel

Bhatt²,

Bhatt³

et al. 2007

123

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Violence and aggression are major causes of death and injury, thus constituting primary public health problems throughout much of the world costing billions of dollars to society. The present review relates our understanding of the neurobiology of aggression and rage to pharmacological treatment strategies that have been utilized and those which may be applied in the future. Knowledge of the neural mechanisms governing aggression and rage is derived from studies in cat and rodents. The primary brain structures involved in the expression of rage behavior include the hypothalamus and midbrain periaqueductal gray. Limbic structures, which include amygdala, hippocampal formation, septal area, prefrontal cortex and anterior cingulate gyrus serve important modulating functions. Excitatory neurotransmitters that potentiate rage behavior include excitatory amino acids, substance P, catecholamines, cholecystokinin, vasopressin, and serotonin that act through 5-HT2 receptors. Inhibitory neurotransmitters include GABA, enkephalins, and serotonin that act through 5-HT1 receptors. Recent studies have demonstrated that brain cytokines, including IL-1 and IL-2, powerfully modulate rage behavior. IL-1 exerts its actions by acting through 5-HT2 receptors, while IL-2 acts through GABAA or NK1 receptors. Pharmacological treatment strategies utilized for control of violent behavior have met with varying degrees of success. The most common approach has been to apply serotonergic compounds. Others included the application of antipsychotic, GABAergic (anti-epileptic) and dopaminergic drugs. Present and futures studies on the neurobiology of aggression may provide the basis for new and novel treatment strategies for the control of aggression and violence as well as the continuation of existing pharmacological approaches.

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Psychiatric Symptoms in Patients With Chronic Hepatitis C Receiving Interferon Alfa-2b Therapy

Cited by 219 publications

References 0 publications

Mental and physical symptoms associated with lower social support for patients with hepatitis C

Mental and physical symptoms associated with lower social support for patients with hepatitis C

The immune-mediated alteration of serotonin and glutamate: towards an integrated view of depression

The Neurobiological Bases for Development of Pharmacological Treatments of Aggressive Disorders

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