Plasma concentrations of zinc, copper, interleukin-6 and interferon-γ, and plasma dipeptidyl peptidase IV activity in chronic hepatitis C

Grüngreiff,

doi:10.3892/mmr_00000062

Cited by 11 publications

(15 citation statements)

References 21 publications

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“…21 TNF-dependent processes are up regulated and activated in CHC, and TNF-α mRNA is ubiquitously expressed in hepatocytes, Kupffer cells, and infiltrating mononuclear cells at higher levels in CHC patients than in healthy controls. 22,23 31 Falasca et al 32 Helaly et al 33 Khan et al 34 Migita et al 36 Zekri et al 37 Malaguarnera et al 38 Costantini et al 39 Capone et al 40 Oyanagi et al 41 Lapinski et al 42 Lecube et al 43 Sandler et al 44a Grungreiff et al 46a Cotler et al 48a Hung et al 49 Antonelli et al 50 Shive et al 52 Cua et al 53 Grungreiff et al 54 Lee et al 84 Mishra et al 87 Sousa et al 91 Tsui et al 35 Zuwała-Jagiełło et al 57 Mourtzikou et al 58 Han et al 85 Müller et al 92…”

Section: Biomarkers Of Inflammationmentioning

confidence: 99%

Inflammatory and cardiovascular diseases biomarkers in chronic hepatitis C virus infection: A review

Babiker

Hassan

Muhammed

et al. 2019

Clinical Cardiology

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Hepatitis C virus (HCV) infects 180 million people worldwide and over 4 million people in the United States. HCV infection is a major cause of chronic liver disease and is recognized as a risk factor for clinical cardiovascular disease (CVD). Many studies have shown increased prevalence of cardiac and inflammatory biomarkers in patients with chronic HCV infection (CHC), and though these markers may be used to risk stratify people for cardiac disease in the general population their role in the HCV population is unknown. Patients with CHC have elevated cardiac and inflammatory biomarkers compared to noninfected controls which may play a role in CVD risk stratification. We undertook a systematic review of inflammatory and cardiac biomarkers in people with HCV infection with a focus on the effect of CHC on serum levels of these markers and their utility as predictors of CVD in this population. Medline, EMBASE, and Cochrane databases were searched for relevant articles until June 2019. A total of 2430 results were reviewed with 115 studies included. Our review revealed that HCV infection significantly alters serum levels of markers of inflammation, endothelial function, and cardiac dysfunction prior to HCV treatment, and some of which may change in response to HCV therapy. Current risk stratification tools for development of CVD in the general population may not account for the increased inflammatory markers that appear to be elevated among HCV‐infected patients contributing to increased CVD risk.

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Section: Biomarkers Of Inflammationmentioning

confidence: 99%

Inflammatory and cardiovascular diseases biomarkers in chronic hepatitis C virus infection: A review

Babiker

Hassan

Muhammed

et al. 2019

Clinical Cardiology

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“…Hepatitis C viral sequences and proteins have been found in brain macrophage/microglia cells, and activation of these brain cells in HCV+ patients is associated with higher expression of messenger ribonucleic acid (mRNA) transcripts for key immune activation cytokines (e.g., IL-1 and TNF-a) than in HCVÀ control patients (Wilkinson et al 2010). When analyzing a small panel of one or several blood immune factors, previous studies have revealed significantly increased levels of specific blood immune factor levels, including IL-6, IL-18, IL-10, IL-4, TNF-a, and RANTES, in untreated HCV+ adults compared with uninfected (HCVÀ) controls (Abayli et al 2003;Vecchiet et al 2005;Falasca et al 2006;Grungreiff et al 2009;Tawadrous et al 2012). Moreover, in two small studies, peripheral immune factor levels were shown to be significantly associated with neuropsychiatric impairments in untreated HCV+ adults.…”

Section: Introductionmentioning

confidence: 99%

Multi‐analyte profile analysis of plasma immune proteins: altered expression of peripheral immune factors is associated with neuropsychiatric symptom severity in adults with and without chronic hepatitis C virus infection

et al. 2013

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BackgroundThe purpose of this study was to characterize hepatitis C virus (HCV)-associated differences in the expression of 47 inflammatory factors and to evaluate the potential role of peripheral immune activation in HCV-associated neuropsychiatric symptoms—depression, anxiety, fatigue, and pain. An additional objective was to evaluate the role of immune factor dysregulation in the expression of specific neuropsychiatric symptoms to identify biomarkers that may be relevant to the treatment of these neuropsychiatric symptoms in adults with or without HCV.MethodsBlood samples and neuropsychiatric symptom severity scales were collected from HCV-infected adults (HCV+, n = 39) and demographically similar noninfected controls (HCV−, n = 40). Multi-analyte profile analysis was used to evaluate plasma biomarkers.ResultsCompared with HCV− controls, HCV+ adults reported significantly (P < 0.050) greater depression, anxiety, fatigue, and pain, and they were more likely to present with an increased inflammatory profile as indicated by significantly higher plasma levels of 40% (19/47) of the factors assessed (21%, after correcting for multiple comparisons). Within the HCV+ group, but not within the HCV− group, an increased inflammatory profile (indicated by the number of immune factors > the LDC) significantly correlated with depression, anxiety, and pain. Within the total sample, neuropsychiatric symptom severity was significantly predicted by protein signatures consisting of 4–10 plasma immune factors; protein signatures significantly accounted for 19–40% of the variance in depression, anxiety, fatigue, and pain.ConclusionsOverall, the results demonstrate that altered expression of a network of plasma immune factors contributes to neuropsychiatric symptom severity. These findings offer new biomarkers to potentially facilitate pharmacotherapeutic development and to increase our understanding of the molecular pathways associated with neuropsychiatric symptoms in adults with or without HCV.

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“…DPP IV affects the immune system through HCV-specific T-cell activation and various chemokine modifications, including IP-10 [ 9 , 23 , 24 ]. Patients with HCV infection show increased serum DPP IV expression [ 25 , 26 ]. High baseline sDPP IV is related to poor treatment response [ 11 ].…”

Section: Discussionmentioning

confidence: 99%

Association between CXCL10 and DPP4 Gene Polymorphisms and a Complementary Role for Unfavorable IL28B Genotype in Prediction of Treatment Response in Thai Patients with Chronic Hepatitis C Virus Infection

et al. 2015

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Pretreatment serum levels of interferon-γ-inducible protein-10 (IP-10, CXCL10) and dipeptidyl peptidase-4 (DPP IV) predict treatment response in chronic hepatitis C (CHC). The association between functional genetic polymorphisms of CXCL10 and DPP4 and treatment outcome has not previously been studied. This study aimed to determine the association between genetic variations of CXCL10 and DPP4 and the outcome of treatment with pegylated interferon-α (PEG-IFN-α) based therapy in Thai patients with CHC. 602 Thai patients with CHC treated using a PEG-IFN-α based regimen were genotyped for CXCL10 rs56061981 G>A and IL28B rs12979860 C>T. In addition, in patients infected with CHC genotype 1, DPP4 (rs13015258 A>C, rs17848916 T>C, rs41268649 G>A, and rs 17574 T>C) were genotyped. Correlations between single nucleotide polymorphisms, genotype, and treatment response were analyzed. The rate of sustained virologic response (SVR) was higher for the CC genotype of IL28B rs12979860 polymorphisms than for non-CC in both genotype 1 (60.6% vs. 29.4%, P < 0.001) and non-genotype 1 (69.4% vs. 49.1%, P < 0.05) CHC. SVR was not associated with the CXCL10 gene variant in all viral genotypes or DPP4 gene polymorphisms in viral genotype1. Multivariate analysis revealed IL28B rs12979860 CC genotype (OR = 3.12; 95% CI, 1.72–5.67; P < 0.001), hepatitis C virus RNA < 400,000 IU/ml (OR = 2.21; 95% CI, 1.22–3.99, P < 0.05), age < 45 years (OR = 2.03; 95% CI, 1.11–3.68; P < 0.05), and liver fibrosis stage 0–1 (OR = 1.64; 95% CI, 1.01–2.65, P < 0.05) were independent factors for SVR. Unfavorable IL28B rs12979860 CT or TT genotypes with the CXCL10 rs56061981 non-GG genotype were associated with a higher SVR than GG genotype (66.7% vs. 33.0%, P = 0.004) in viral genotype 1. In Thai CHC genotype 1 infected patients with an unfavorable IL28B rs12979860 CT/TT genotype, the complementary CXCL10 polymorphism strongly enhances prediction of treatment response.

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Plasma concentrations of zinc, copper, interleukin-6 and interferon-γ, and plasma dipeptidyl peptidase IV activity in chronic hepatitis C

Cited by 11 publications

References 21 publications

Inflammatory and cardiovascular diseases biomarkers in chronic hepatitis C virus infection: A review

Inflammatory and cardiovascular diseases biomarkers in chronic hepatitis C virus infection: A review

Multi‐analyte profile analysis of plasma immune proteins: altered expression of peripheral immune factors is associated with neuropsychiatric symptom severity in adults with and without chronic hepatitis C virus infection

Association between CXCL10 and DPP4 Gene Polymorphisms and a Complementary Role for Unfavorable IL28B Genotype in Prediction of Treatment Response in Thai Patients with Chronic Hepatitis C Virus Infection

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