scholarly journals Restoring Inflammatory Mediator Balance after Sofosbuvir-Induced Viral Clearance in Patients with Chronic Hepatitis C

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Geórgia Nascimento Saraiva ◽  
Natalia Fonseca do Rosário ◽  
Thalia Medeiros ◽  
Paulo Emílio Côrrea Leite ◽  
Gilmar de Souza Lacerda ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Liver Disease ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Transient Elastography ◽  
Sustained Virological Response Rate ◽  
Disease Status ◽  
Control Group ◽  
Viral Control ◽  
Immune Biomarkers

This study aimed at analyzing circulating levels of inflammatory and profibrogenic cytokines in patients with hepatitis C virus (HCV) chronic infection undergoing therapy with direct-acting antiviral agents (DAA) and correlating these immune biomarkers with liver disease status. We studied 88 Brazilian monoinfected chronic hepatitis C patients receiving interferon- (IFN-) free sofosbuvir-based regimens for 12 or 24 weeks, followed-up before therapy initiation and three months after the end of treatment. Liver disease was determined by transient elastography, in addition to APRI and FIB-4 indexes. Analysis of 30 immune mediators was carried out by multiplex or enzymatic immunoassays. Sustained virological response rate was 98.9%. Serum levels of cytokines were increased in HCV-infected patients when compared to control group. CCL-2, CCL-3, CCL-4, CXCL-8, CXCL-10, IL-1β, IL-15, IFN-γ, IL-4, IL-10, TGF-β, FGFb, and PAI-1 decreased significantly after antiviral therapy, reaching values similar to noninfected controls. TGF-βand suPAR levels were associated with fibrosis/cirrhosis. Also, we observed amelioration in hepatic parameters after DAA treatment. Together, our results suggest that viral control induced by IFN-free DAA therapy restores inflammatory mediators in association with improvement in liver function.

Chronic Hepatitis C Virus Infections in Leukemia Survivors: Prevalence, Viral Load, and Severity of Liver Disease

Blood ◽  
1999 ◽  
Vol 93 (11) ◽  
pp. 3672-3677 ◽  
Author(s):  
Ian M. Paul ◽  
Jeffrey Sanders ◽  
Francesca Ruggiero ◽  
Thomas Andrews ◽  
David Ungar ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Liver Disease ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Screening Tests ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Hcv Rna ◽  
Rna Levels

The natural history of chronic hepatitis C (HCV) infections in long-term leukemia survivors has not been well characterized. We studied the prevalence of HCV infections, measured HCV RNA levels, and evaluated the severity of liver disease in patients with leukemia who achieved long-term remissions after intensive chemotherapy or bone marrow transplantation (BMT). HCV antibody tests were performed by the enzyme-linked immunosorbent assay (ELISA) and positive tests confirmed by the recombinant immunoblot assay (RIBA). HCV RNA levels were measured by the branched DNA (bDNA) assay. Seventy-five leukemia survivors with 25 or more blood donor exposures were identified. Nine (12%) were anti-HCV positive. All were infected before 1992 when second generation HCV screening tests were implemented. Mean HCV RNA levels were 10.3 ×106 eq/mL versus 3.2 × 106 eq/mL (P = .056) in a control group of 20 anti-HCV positive immunocompetent individuals of comparable age who were infected twice as long (17.8 ± 6.5 years v 9.0 ± 4.4 years in leukemia survivors, P = .001). Liver biopsies were performed on six of the nine anti-HCV positive leukemia survivors. All showed at least moderate portal inflammation and half had evidence of bridging fibrosis. We conclude that viral loads in anti-HCV positive leukemia survivors are markedly higher than in immunocompetent controls. Our results suggest that long-term leukemia survivors with chronic HCV may have more rapidly progressive liver disease than has been previously recognized.

Previously unrecognized advanced liver disease unveiled by transient elastography in patients with Haemophilia and chronic hepatitis C

Haemophilia ◽  
2011 ◽  
Vol 17 (6) ◽  
pp. 938-943 ◽  
Author(s):  
B. K. MOESSNER ◽  
E. S. ANDERSEN ◽  
N. WEIS ◽  
A. L. LAURSEN ◽  
J. INGERSLEV ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Liver Disease ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Transient Elastography ◽  
Advanced Liver Disease

Chronic Hepatitis C Virus Infections in Leukemia Survivors: Prevalence, Viral Load, and Severity of Liver Disease

Blood ◽  
1999 ◽  
Vol 93 (11) ◽  
pp. 3672-3677 ◽  
Author(s):  
Ian M. Paul ◽  
Jeffrey Sanders ◽  
Francesca Ruggiero ◽  
Thomas Andrews ◽  
David Ungar ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Liver Disease ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Screening Tests ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Hcv Rna ◽  
Rna Levels

Abstract The natural history of chronic hepatitis C (HCV) infections in long-term leukemia survivors has not been well characterized. We studied the prevalence of HCV infections, measured HCV RNA levels, and evaluated the severity of liver disease in patients with leukemia who achieved long-term remissions after intensive chemotherapy or bone marrow transplantation (BMT). HCV antibody tests were performed by the enzyme-linked immunosorbent assay (ELISA) and positive tests confirmed by the recombinant immunoblot assay (RIBA). HCV RNA levels were measured by the branched DNA (bDNA) assay. Seventy-five leukemia survivors with 25 or more blood donor exposures were identified. Nine (12%) were anti-HCV positive. All were infected before 1992 when second generation HCV screening tests were implemented. Mean HCV RNA levels were 10.3 ×106 eq/mL versus 3.2 × 106 eq/mL (P = .056) in a control group of 20 anti-HCV positive immunocompetent individuals of comparable age who were infected twice as long (17.8 ± 6.5 years v 9.0 ± 4.4 years in leukemia survivors, P = .001). Liver biopsies were performed on six of the nine anti-HCV positive leukemia survivors. All showed at least moderate portal inflammation and half had evidence of bridging fibrosis. We conclude that viral loads in anti-HCV positive leukemia survivors are markedly higher than in immunocompetent controls. Our results suggest that long-term leukemia survivors with chronic HCV may have more rapidly progressive liver disease than has been previously recognized.

scholarly journals Protein C Deficiency in Chronic Hepatitis C

2016 ◽  
Vol 23 (1) ◽  
pp. 72-77 ◽  
Author(s):  
Aida Saray ◽  
Rusmir Mesihovic ◽  
Nenad Vanis ◽  
Mehmedović Amila
Keyword(s):  
Chronic Hepatitis ◽  
Liver Disease ◽  
Hepatitis C ◽  
Chronic Liver Disease ◽  
Chronic Hepatitis C ◽  
Protein C ◽  
Chronic Liver ◽  
Fibrosis Stage ◽  
Coagulation System ◽  
Control Group

There is accumulating evidence that the coagulation system is involved in the process of fibrogenesis in chronic liver disease. Recent studies postulated a possible connection between plasmatic hypercoagulability and progression of fibrosis. The aim of the study was to investigate disorders of the coagulation system in patients with chronic hepatitis C having different extent of hepatic fibrosis well defined by liver histology. A total of 62 patients with chronic hepatitis C were recruited and categorized into 2 groups according to their histological fibrosis stage : mild/moderate fibrosis group (F0-F3 group, n = 30) and extensive fibrosis/cirrhosis group (F4-F6 group, n = 32). The control group consisted of 31 healthy individuals. The following hemostatic assays were evaluated: antithrombin III (AT), protein C (PC) activity, activated partial thromboplastin time, prothrombin time, plasma fibrinogen as well as conventional liver function test. The PC level exhibited a significant reduction in both patient groups when compared to the normal control group (89.25% ± 10.05% and 48.33% ± 15.86% vs 111.86 ± 10.90; P < .001 and P < .001). The PC was found to be the strongest associated factor to histological fibrosis stage ( r = –.834; P < .0001). Univariate and multivariate analysis showed that AT ( P = .003) and PC ( P = .0001) were the most important factors associated with advanced fibrosis. The PC ( P = .001) was found to be the only predictor of mild fibrosis. In conclusion, PC deficiency occurs in an early stage of liver fibrosis. The severity of deficiency is proportional to extent of fibrosis. The PC may have a key role in linking hypercoagulability with hepatic fibrogenesis in chronic liver disease.

scholarly journals Status of liver stiffness following directly acting antiviral treatment in patients with chronic hepatitis C: A Nepalese study

2017 ◽  
Vol 13 (3) ◽  
pp. 302-305 ◽  
Author(s):  
Dilip Sharma ◽  
Sudhamshu KC ◽  
Ananta Shrestha ◽  
Bikash Jaishi
Keyword(s):  
Chronic Hepatitis ◽  
Liver Disease ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Associated Factors ◽  
Transient Elastography ◽  
Antiviral Treatment ◽  
Liver Stiffness ◽  
End Of Treatment ◽  
Excellent Accuracy

Background & Objectives:Chronic hepatitis C is one of the leading causes of chronic liver disease in our country. With the introduction of directly acting antivirals, many patients are benefitted these days. Transient elastography is one of the newer technologies for measuring liver stiffness and quantifying liver fibrosis and has excellent accuracy for the diagnosis of fibrosis in patients with chronic hepatitis C. Our study analyzes changes of liver stiffness and its associated factors in patients with chronic hepatitis C treated with directly acting antivirals (DAAs).Materials & Methods: One hundred and seven patients with chronic hepatitis C, who were treated with DAAs (Sofosbuvir 400 mg and velpatasvir 100mg) and have significant fibrosis (>7.0 kPa) at baseline were included. Liver stiffness was measured at the time of enrollment, and after completion of DAAs with fibroscan and changes of stiffness and its associated factors were analyzed.  Results:The study showed significant decrease in liver stiffness at the end of treatment, which continued after treatment only in patients who achieved a sustained virological response.Conclusion: Liver stiffness decreased following 12 weeks of successful DAAs therapy in patients with chronic hepatitis C at the end of treatment who achieved sustained virological response. 

scholarly journals Intrahepatic TLR3 and IFNL3 Expressions Are Associated with Stages of Fibrosis in Chronic Hepatitis C

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1103
Author(s):  
Keyla Santos Guedes de Sá ◽  
Ednelza da Silva Graça Amoras ◽  
Simone Regina Souza da Silva Conde ◽  
Maria Alice Freitas Queiroz ◽  
Izaura Maria Vieira Cayres-Vallinoto ◽  
...  
Keyword(s):  
Immune Response ◽  
Chronic Hepatitis ◽  
Viral Load ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Control Group ◽  
Gene Expressions ◽  
Healthy Control ◽  
Advanced Stages ◽  
Chronic Hcv

An inefficient immune response against the hepatitis C virus (HCV), combined with viral evasion mechanisms, is responsible for the chronicity of infection. The need to evaluate the innate mechanisms of the immune response, such as TLR3 and IFN-λ3, and their relationship with the virus–host interaction is important for understanding the pathogenesis of chronic hepatitis C. The present study aimed to investigate the gene expressions of TRL3 and IFNL3 in liver tissue, seeking to evaluate whether these could be potential biomarkers of HCV infection. A total of 23 liver biopsy samples were collected from patients with chronic HCV, and 8 biopsies were collected from healthy control patients. RNA extraction, reverse transcription and qPCR were performed to quantify the relative gene expressions of TLR3 and IFNL3. Data on the viral load; AST, ALT, GGT and AFP levels; and the viral genotype were collected from the patients′ medical records. The intrahepatic expression of TLR3 (p = 0.0326) was higher in chronic HCV carriers than in the control group, and the expression of IFNL3 (p = 0.0037) was lower in chronic HCV carriers than in the healthy control group. The expression levels of TLR3 (p = 0.0030) and IFNL3 (p = 0.0036) were higher in the early stages of fibrosis and of necroinflammatory activity in the liver; in contrast, TLR3 and IFNL3 expressions were lower in the more advanced stages of fibrosis and inflammation. There was no correlation between the gene expression and the serum viral load. Regarding the initial METAVIR scale scores, liver transaminase levels were lower in patients with advanced fibrosis when correlated with TLR3 and IFNL3 gene expressions. The results suggest that in the early stages of the development of hepatic fibrosis, TLR3 and IFN-λ3 play important roles in the antiviral response and in the modulation of the tolerogenic liver environment because there is a decrease in the intrahepatic expressions of TLR3 and IFNL3 in the advanced stages of fibrosis, probably due to viral evasion mechanisms.

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