Neurologic Manifestations of Hepatitis C Virus Infection

Iriana, Sentia; Curry, Michael P.; Afdhal, Nezam H.

doi:10.1016/j.cld.2017.03.008

Cited by 29 publications

(28 citation statements)

References 38 publications

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“…These changes are seen even in the absence of cirrhosis, decompensated liver disease, hepatic encephalopathy or previous history of abuse of psychoactive substances, suggesting an effect of the viral infection on the central nervous system. HCV locally induced inflammation and the passage of systemic pro-inflammatory cytokine through the blood-brain barrier could also impair neurologic functioning [ 14 , 15 ]. The neurocognitive disturbances may be documented long before the beginning of interferon-based antiviral therapy, which is a well-known cause of neurocognitive, mood and psychiatric dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…However, no clear correlation between HCV viral load and cognitive impairment could be demonstrated [ 12 ]. Despite HCV infection itself within the brain causing local inflammation and neurocognitive disturbances, another hypothesis suggest these disturbances, including depression, could be in part a result of elevated systemic cytokine levels due to chronic HCV activation of the immune system [ 13 – 15 ]. Putative inflammatory cytokines are interleukin-1, 4, and 6, tumor necrosis factor-α and interferon-α, that can cross the blood-brain barrier and impact brain functioning [ 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

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Hepatitis C virus eradication improves immediate and delayed episodic memory in patients treated with interferon and ribavirin

et al. 2017

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BackgroundChronic hepatitis C virus (HCV) infection is associated with impairment of cognitive function and mood disorders. Our aim was to evaluate the impact of sustained virological response (SVR) on cognitive function and mood disorders.MethodA prospective exploratory one arm study was conducted. Adult clinically compensated HVC patients were consecutively recruited before treatment with interferon and ribavirin for 24 to 48 weeks, according to HCV genotype. Clinical, neurocognitive and mood assessments using the PRIME-MD and BDI instruments were performed at baseline, right after half of the expected treatment has been reached and 6 months after the end of antiviral treatment. Exclusion criteria were the use of illicit psychotropic substances, mental confusion, hepatic encephalopathy, hepatocellular carcinoma, severe anemia, untreated hypothyroidism, Addison syndrome and major depression before treatment.ResultsThirty six patients were enrolled and 21 completed HCV treatment (n = 16 with SVR and n = 5 without). Regardless of the viral clearance at the end of treatment, there was a significant improvement in the immediate verbal episodic memory (p = 0.010), delayed verbal episodic memory (p = 0.007), selective attention (p < 0.001) and phonemic fluency (p = 0.043). Patients with SVR displayed significant improvement in immediate (p = 0.045) and delayed verbal episodic memory (p = 0.040) compared to baseline. The baseline frequency of depression was 9.5%, which rose to 52.4% during treatment, and returned to 9.5% 6 months after the end of treatment, without significant difference between patients with and without SVR. Depressive symptoms were observed in 19.1% before treatment, 62% during (p = 0.016) and 28.6% 6 months after the end of treatment (p = 0.719).ConclusionsEradication of HCV infection improved cognitive performance but did not affect the frequency of depressive symptoms at least in the short range.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hepatitis C virus eradication improves immediate and delayed episodic memory in patients treated with interferon and ribavirin

et al. 2017

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“…Some groups have argued that cognitive deficits in HCV are due to interferon treatment (Asnis and Migdal, 2005 ; Capuron et al, 2005 ; Reichenberg et al, 2005 ), but cognitive deficits persist despite successful antiviral (interferon) therapy (Thein H. H. et al, 2007 ; Weissenborn et al, 2009 ; Cattie et al, 2014 ; Kuhn et al, 2017 ). Although the literature is heterogeneous and characterized by cross-sectional rather than longitudinal assessments of relatively small and select cohorts, neurocognitive deficits reported in HCV include compromised attention, memory, and psychomotor speed (Forton et al, 2002 ; Hilsabeck et al, 2002 ; Capuron et al, 2005 ; Iriana et al, 2017 ) with fewer reports of deficits in executive functioning (Córdoba et al, 2003 ; Weissenborn et al, 2004 ), fine-motor coordination (Vigil et al, 2008 ), and presence of peripheral neuropathy (Adinolfi et al, 2015 ; Mathew et al, 2016 ).…”

Section: Neuropsychological and Motor Effects Of Hiv And Comorbiditiementioning

confidence: 99%

The Aging Brain With HIV Infection: Effects of Alcoholism or Hepatitis C Comorbidity

Zahr

2018

Front. Aging Neurosci.

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As successfully treated individuals with Human Immunodeficiency Virus (HIV)-infected age, cognitive and health challenges of normal aging ensue, burdened by HIV, treatment side effects, and high prevalence comorbidities, notably, Alcohol Use Disorders (AUD) and Hepatitis C virus (HCV) infection. In 2013, people over 55 years old accounted for 26% of the estimated number of people living with HIV (~1.2 million). The aging brain is increasingly vulnerable to endogenous and exogenous insult which, coupled with HIV infection and comorbid risk factors, can lead to additive or synergistic effects on cognitive and motor function. This paper reviews the literature on neuropsychological and in vivo Magnetic Resonance Imaging (MRI) evaluation of the aging HIV brain, while also considering the effects of comorbidity for AUD and HCV.

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“…Psychiatric diseases such as anxiety, depression, bipolar disorder, post-traumatic stress disorder, and personality disorders are also common in patients with HCV regardless of active or prior psychiatric diseases (19)(20)(21). Particularly, all of these conditions may affect the neurocognitive status on measurements of concentration, attention, and processing speed (16).…”

Section: Discussionmentioning

confidence: 99%

Modification of Serum Brain-Derived Neurotrophic Factor Levels Following Anti-HCV Therapy with Direct Antiviral Agents: A New Marker of Neurocognitive Disorders

et al. 2020

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Background: A large number of central nervous system impairments occur in subjects with chronic HCV infection regardless of liver disease. Brain-derived neurotrophic factor (BDNF) plays an essential role in the adult brain concerning its development and proper functioning. Our study aimed at contributing to the discussion on the involvement of BDNF in neurocognitive disorders associated with HCV infection. Objectives: We aimed to evaluate the prevalence of neurocognitive disorders in a cohort of HCV-infected subjects, to measure serum BDNF levels in the same cohort according to the degree of neurocognitive disorders, and to evaluate serum BDNF level modification in HCV-infected patients after direct antiviral agents (DAA) therapy. Methods: We enrolled patients scheduled for DAA therapy in January 2018 from three infectious disease units in Eastern Sicily. Each participant was evaluated for neurocognitive status with MoCA score at baseline and 12 and 24 weeks after the end of therapy. Moreover, we measured serum BDNF levels at baseline and 12 weeks after the end of therapy. Results: Of 70 HCV-infected patients, 42 (60%) were males. The average age was 57 ± 19 years and the average ALT level was 79 ± 24 UI/mL; 38 (54.3%) individuals had HCV genotype 1 infection and 23 (32.8%) and 25 (35.7%) individuals had F1 and F2 fibrosis stages, respectively. Moreover, 67 (95.7%) individuals achieved sustained virological response. The MoCA score at baseline identified four groups of patients. Higher MoCA scores 24 weeks after the end of therapy highlighted the improvement of neurocognitive status in all groups. Serum BDNF levels in the same four groups, measured 12 weeks after the end of DAA therapy, appeared significantly modified compared to baseline serum BDNF levels, matching the improvement of MoCA score results obtained 24 weeks after DAA therapy. Conclusions: The serum BDNF level may represent a useful marker of cognitive dysfunction in patients with HCV infection and a useful index for assessing the post-therapy follow-up.

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Neurologic Manifestations of Hepatitis C Virus Infection

Cited by 29 publications

References 38 publications

Hepatitis C virus eradication improves immediate and delayed episodic memory in patients treated with interferon and ribavirin

Hepatitis C virus eradication improves immediate and delayed episodic memory in patients treated with interferon and ribavirin

The Aging Brain With HIV Infection: Effects of Alcoholism or Hepatitis C Comorbidity

Modification of Serum Brain-Derived Neurotrophic Factor Levels Following Anti-HCV Therapy with Direct Antiviral Agents: A New Marker of Neurocognitive Disorders

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