Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/18150
Title: Depression, fatigue and neurocognitive deficits in chronic hepatitis C.
Austin Authors: Yeoh, Sern Wei;Holmes, Alex C N;Saling, Michael M ;Everall, Ian P;Nicoll, Amanda J
Affiliation: Department of Gastroenterology, Eastern Health, Box Hill, Victoria, Australia
Department of Psychiatry, University of Melbourne, Royal Melbourne Hospital, Parkville, Victoria, Australia
Melbourne School of Psychological Sciences, University of Melbourne, Parkville, Victoria, Australia
Department of Clinical Neuropsychology, Austin Health, Heidelberg, Victoria, Australia
The Florey Institute for Neuroscience and Mental Health, Parkville, Victoria, Australia
Institute of Psychiatry, Psychology and Neuroscience, Kings College London, London, UK
South London and Maudsley NHS Foundation Trust, Bethlem Royal Hospital, Beckenham, UK
Department of Gastroenterology and Hepatology, Royal Melbourne Hospital, Parkville, Victoria, Australia
Issue Date: Jul-2018
metadata.dc.date: 2018-06-21
Publication information: Hepatology international 2018; 12(4): 294-304
Abstract: Patients with chronic hepatitis C virus (HCV) infection experience a range of symptoms including depression, fatigue and neurocognitive deficits, impairing quality of life. Depression, in particular, may be reactive to increased psychosocial stress, and the physical symptoms of advanced HCV or associated comorbidities. However, even patients at an early stage of HCV infection, with minimal hepatic inflammation or comorbidities, report more depressive symptoms and fatigue than the general population. Similarly, specific neurocognitive deficits occur in early stage HCV infection and are independent of the presence of depression or encephalopathy. Therefore, intracerebral neurobiological changes associated with HCV may potentially explain these symptoms. These changes may arise from infiltration of the brain by peripherally induced cytokines, as well as direct neuropathic effects of HCV viral particles penetrating the blood-brain barrier. These phenomena parallel those reported in human immunodeficiency virus (HIV) infection. HCV-associated intracerebral changes include upregulated inflammatory responses, altered neurotransmitter levels, hormonal dysregulation, and release of neurotoxic substances. These may subsequently lead to abnormal neuronal conduction and function in areas of the brain governing affective responses, emotional processing, motivation, attention and concentration. Although direct-acting antiviral medications lead to high rates of HCV clearance, intracerebral changes may not be subsequently reversed and symptoms of depression, fatigue and neurocognitive deficits may persist. There is an ongoing role for multidisciplinary care and pharmacotherapy to manage these symptoms in HCV patients. Furthermore, there may be opportunities for future therapies to specifically target and ameliorate HCV-associated intracerebral changes.
URI: http://ahro.austin.org.au/austinjspui/handle/1/18150
DOI: 10.1007/s12072-018-9879-5
ORCID: 0000-0003-3627-4647
PubMed URL: 29931590
Type: Journal Article
Subjects: Cognition
Depression
Fatigue
Hepatitis C
Quality of life
Appears in Collections:Journal articles

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