Interferon‐free therapy as the cause of white matter tracts and cerebral perfusion recovery in patients with chronic hepatitis C

Bladowska, Joanna; Pawłowski, Tomasz; Fleischer‐Stępniewska, Katarzyna; Knysz, Brygida; Małyszczak, Krzysztof; Żelwetro, Agnieszka; Rymer, Weronika; Inglot, Małgorzata; Waliszewska‐Prosół, Marta; Ejma, Maria; Podgórski, Przemysław; Zimny, Anna; Sąsiadek, Marek

doi:10.1111/jvh.13069

Cited by 9 publications

(13 citation statements)

References 33 publications

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“…DTI and PWI studies in this group also revealed greater anisotropy after therapy in several association, commissural and projection tracts and lower diffusivity in several association and projection tracts that correlated with changes in the neuropsychological profile. Higher basal ganglia perfusion after therapy was also observed, but this finding did not correlate with other neuropsychiatric and DTI changes [25]. In a pilot study, improvement of working memory, visual and verbal memory and executive function after treatment with ledipasvir-sofosbuvir correlated with several inflammatory biomarkers in peripheral blood, such as tumor necrosis factor-α, IFN-γ and catechol-O-methyl-transferase [80].…”

Section: Direct-acting Antiviral Agents (Daa)mentioning

confidence: 89%

“…18 FDG-PET-Cortical anterior > posterior and cerebellar hypometabolism [17] 11 C-(R)-PK-11195-PET-Basal ganglia and thalamic microglial activation [18,19] 123 I-CIT-SPECT-Decreased dopaminergic and serotoninergic innervation [17,20] IFN-α Decreased anterior metabolism on 18 FDG-PET [21] Inhibited dopamine release in ventral striatum [22] No effect on serotoninergic innervation [23] PWI Cortical anterior > posterior reduced perfusion [24] Increased basal ganglia perfusion [24] DAA Increased basal ganglia perfusion [25]…”

Section: Nuclear Medicine Response To Treatmentmentioning

confidence: 99%

“…Reduced cortical thickness in frontal areas with [26] or without [27] occipital involvement Posterior insula and thalamic atrophy [9] Progressive amygdala and parahippocampal atrophy [9] DAA Reduced frontal cortical volumes [28] DTI Increased MD and reduced FA in global WM [15] more evident in fronto-temporal areas [29] and body of CC [9,24,30] Increased MD in external capsule [4] and fronto-occipital fasciculus [4,9,24] Decreased FA in bilateral middle cerebellar peduncles [24] and superior thalamic radiation [31] Increased FA in the basal ganglia [4] DAA Increased FA in association, commissural and projection tracts [25] Decreased MD in association and projection tract [25] fMRI Altered cortical connectivity possibly due to frontal deficit [32,33] IFN-α Reduced ventral striatum activation [22] and global network efficiency [34] MRS Decreased NAA in anterior [35][36][37] and posterior WM [4,37] Normal [18,35,[37][38][39][40][41][42] or decreased NAA in cortical GM [43] Increased Cho in frontal [35,37,38,43,44] and posterior WM…”

Section: Structural Imagingmentioning

confidence: 99%

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Neuroimaging Findings in Chronic Hepatitis C Virus Infection: Correlation with Neurocognitive and Neuropsychiatric Manifestations

Tagliapietra

Monaco

2020

IJMS

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Chronic hepatitis C virus (HCV) infection is commonly associated with neurocognitive dysfunction, altered neuropsychological performance and neuropsychiatric symptoms. Quantifiable neuropsychological changes in sustained attention, working memory, executive function, verbal learning and recall are the hallmark of HCV-associated neurocognitive disorder (HCV-AND). This constellation is at variance with the neuropsychological complex that is seen in minimal hepatic encephalopathy, which is typified by an array of alterations in psychomotor speed, selective attention and visuo-constructive function. Noncognitive symptoms, including sleep disturbances, depression, anxiety and fatigue, which are less easily quantifiable, are frequently encountered and can dominate the clinical picture and the clinical course of patients with chronic HCV infection. More recently, an increased vulnerability to Parkinson’s disease among HCV-infected patients has also been reported. The degree to which neurocognitive and neuropsychiatric changes are due to HCV replication within brain tissues or HCV-triggered peripheral immune activation remain to be determined. Without absolute evidence that clearly exonerates or indicts HCV, our understanding of the so-called “HCV brain syndrome”, relies primarily on clinical and neuropsychological assessments, although other comorbidities and substance abuse may impact on neurocognitive function, thus confounding an appropriate recognition. In recent years, a number of functional and structural brain imaging studies have been of help in recognizing possible biological markers of HCV-AND, thus providing a rationale for guiding and justifying antiviral therapy in selected cases. Here, we review clinical, neuroradiological, and therapeutic responses to interferon-based and interferon-free regimens in HCV-related cognitive and neuropsychiatric disorder.

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Section: Direct-acting Antiviral Agents (Daa)mentioning

confidence: 89%

Section: Nuclear Medicine Response To Treatmentmentioning

confidence: 99%

Section: Structural Imagingmentioning

confidence: 99%

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Neuroimaging Findings in Chronic Hepatitis C Virus Infection: Correlation with Neurocognitive and Neuropsychiatric Manifestations

Tagliapietra

Monaco

2020

IJMS

View full text Add to dashboard Cite

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“…Bladowska et al used magnetic resonance diffusion tensor and perfusion weighted imaging of white matter tracts to demonstrate significant changes in the microstructure and perfusion after DAA induced HCV eradication. This was believed to indicate white matter recovery 35 . On the functional level, Kleefeld et al found cognitive function improvement in visual memory/learning, executive functions, verbal fluency, processing speed and motor skills but not in verbal learning and attention/working memory after DAA treatment 36 …”

Section: Discussionmentioning

confidence: 99%

Hepatitis C related cognitive impairment: Impact of viral and host factors and response to therapy

Bar

Levy

Deutsch

et al. 2021

Journal of Viral Hepatitis

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Chronic hepatitis C virus (HCV) infection is associated with cognitive impairment via several suggested mechanisms including direct neurotoxicity and minimal hepatic encephalopathy. The prevalence of HCV‐related cognitive impairment and whether it is reversed by anti‐viral therapy is unknown. We aimed to assess predictors and reversibility of cognitive impairment of HCV‐infected patients after successful treatment. Consecutive HCV patients treated during the EMERALD study (AbbVie 3D regimen for protease inhibitors failure) underwent neuropsychological (number connection test A [NCTA] and digital symbol test [DST]) and neurophysiological (critical flicker frequency [CFF]) tests at baseline and at 12 weeks post‐treatment. Patient self‐reported outcomes (PROs) were prospectively collected. Patients with a history of hepatic encephalopathy were excluded. Thirty‐two patients underwent the cognitive tests at baseline. Seven of them had abnormal CFF test findings. Twenty‐five (25/32, 78%) patients had repeated evaluations 3 months post‐treatment. High viral loads were significantly associated with abnormal CFF across fibrosis levels (area under the ROC curve 0.817). CFF results significantly improved following viral eradication, from 40.9 (interquartile range 38.6–42.9) at baseline to 41.5 (39.8–44), p = .042, at follow‐up. Both NCTA and DST results improved, but not significantly. There was improvement in the PROs of general health perception and vitality. The NCTA and DST results were more significantly associated with PROs than CFF. This prospective interventional study showed greater cognitive impairment in HCV patients with high viral load and demonstrated partial reversibility of HCV neurotoxicity and subsequent improvement in PROs following treatment.

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“…The direct-acting antiviral agents (DAAs) are a set of medications used to treat patients infected by the HCV. The summary of study characteristics and quality assessment of the 12 [29][30][31][32][33][34][35][36][37][38][39][40] included studies are presented in Table 2. Two of them were considered high quality, whilst the remaining ten others had ratings ranging from 4 to 6 stars, suggesting moderate quality.…”

Section: Significance Statementmentioning

confidence: 99%

Neuropsychological effects of direct‐acting antiviral treatment for Hepatitis C virus subjects: A systematic review

Santos-Lima

Souza-Marques

Vieira

et al. 2021

Journal of Viral Hepatitis

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Chronic Hepatitis C is a disease related to the Hepatitis C virus (HCV), associated with adverse extrahepatic manifestations on the Central Nervous System, with neurological and neuropsychological effects, 1 induction of depression, fatigue, sleep disturbances 2-4 and worse health-related quality of life-HRQoL. 5 These neuropsychiatric and neurocognitive changes have been reported in cases of non-cirrhotic infection, 6 in minimal hepatic encephalopathy 7,8 and in more severe cases of hepatic encephalopathy.Interferon based-treatment (IFN) for HCV is related to a decrease of neuropsychological functions, such as executive function and attention, 9-11 as well as neuropsychiatric dysfunction involving depression, anxiety, fatigue and deterioration of HRQoL. 12,13

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Interferon‐free therapy as the cause of white matter tracts and cerebral perfusion recovery in patients with chronic hepatitis C

Cited by 9 publications

References 33 publications

Neuroimaging Findings in Chronic Hepatitis C Virus Infection: Correlation with Neurocognitive and Neuropsychiatric Manifestations

Neuroimaging Findings in Chronic Hepatitis C Virus Infection: Correlation with Neurocognitive and Neuropsychiatric Manifestations

Hepatitis C related cognitive impairment: Impact of viral and host factors and response to therapy

Neuropsychological effects of direct‐acting antiviral treatment for Hepatitis C virus subjects: A systematic review

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