scholarly journals Inflammation and Liver Cell Death in Patients with Hepatitis C Viral Infection

2021 ◽  
Vol 43 (3) ◽  
pp. 2022-2035
Author(s):  
Manuela G. Neuman ◽  
Lawrence B. Cohen
Keyword(s):  
Cell Death ◽  
Chronic Hepatitis ◽  
Hepatitis C ◽  
Viral Infection ◽  
Liver Damage ◽  
Inflammatory Markers ◽  
Pathogenic Bacteria ◽  
Serum Levels ◽  
Control Group ◽  
Inflammatory Status

Hepatitis C virus (HCV)-induced liver disease contributes to chronic hepatitis. The immune factors identified in HCV include changes in the innate and adaptive immune system. The inflammatory mediators, known as “inflammasome”, are a consequence of the metabolic products of cells and commensal or pathogenic bacteria and viruses. The only effective strategy to prevent disease progression is eradication of the viral infection. Immune cells play a pivotal role during liver inflammation, triggering fibrogenesis. The present paper discusses the potential role of markers in cell death and the inflammatory cascade leading to the severity of liver damage. We aim to present the clinical parameters and laboratory data in a cohort of 88 HCV-infected non-cirrhotic and 25 HCV cirrhotic patients, to determine the characteristic light microscopic (LM) and transmission electron microscopic (TEM) changes in their liver biopsies and to present the link between the severity of liver damage and the serum levels of cytokines and caspases. A matched HCV non-infected cohort was used for the comparison of serum inflammatory markers. We compared the inflammation in HCV individuals with a control group of 280 healthy individuals. We correlated the changes in inflammatory markers in different stages of the disease and the histology. We concluded that the serum levels of cytokine, chemokine, and cleaved caspase markers reveal the inflammatory status in HCV. Based upon the information provided by the changes in biomarkers the clinician can monitor the severity of HCV-induced liver damage. New oral well-tolerated treatment regimens for chronic hepatitis C patients can achieve cure rates of over 90%. Therefore, using the noninvasive biomarkers to monitor the evolution of the liver damage is an effective personalized medicine procedure to establish the severity of liver injury and its repair.

Clinical and laboratory characteristics of patients with chronic hepatitis C and severe interferon system suppression

2021 ◽  
Vol 19 (2) ◽  
pp. 60-64
Author(s):  
Zh.B. Ponezheva ◽  
◽  
I.V. Mannanova ◽  
V.V. Makashova ◽  
A.A. Erovichenkov ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C ◽  
T Lymphocytes ◽  
Liver Fibrosis ◽  
Chronic Hepatitis C ◽  
Serum Levels ◽  
Control Group ◽  
Biochemical Activity ◽  
Duration Of Infection ◽  
Grade 3

Objective. To identify specific clinical and laboratory characteristics of patients with chronic hepatitis C (CHC) and severe interferon (IFN) system suppression. Patients and methods. This study was conducted at the Clinical Department of Infectious Pathology, Research Institute of Epidemiology, Federal Service for Surveillance on Consumer Rights Protection and Human Wellbeing. We enrolled and examined 76 patients with confirmed CHC aged 18 to 80 years who had been followed up for at least 3 years. We analyzed the level of IFN-producing T-lymphocytes, IFN status, serum levels of IFN-α, -γ and -λ depending on viral and biochemical activity, and genotype. In addition to that, we evaluated the association between the IFN system parameters and age, duration of infection, genotype, viral load, and stage of liver fibrosis. The control group comprised 30 healthy individuals who had no complaints and no clinical or laboratory changes at the time of examination. Results. We identified 3 grades of IFN system suppression: grade 1–moderate (in 21% of patients), grade 2–mild (inadequate) (in 47% of patients), and grade 3–severe (in 32% of patients). We analyzed clinical and laboratory characteristics of patients with grade 3 IFN system suppression and evaluated the IFN system depending on age, duration of infection, genotype, viral and biochemical activity. We found that severe IFN system suppression correlated with duration of infection, stage of liver fibrosis with a tendency to increased levels of T-lymphocytes expressing receptors for IFN-α and IFN-γ (CD118+, CD119+). Key words: chronic hepatitis C, genotype, interferon status

scholarly journals The Association Between Chronic Hepatitis B, Chronic Hepatitis C, Sustained Liver Damage, and Features of Increased Cardiovascular Risk

2021 ◽  
Vol 69 (1) ◽  
pp. 23-30
Author(s):  
Jacek Czepiel ◽  
Marek Rajzer ◽  
Grzegorz Bilo ◽  
Gianfranco Parati ◽  
Grażyna BIesiada ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Cardiovascular Risk ◽  
Hepatitis C ◽  
Hepatitis B ◽  
Chronic Hepatitis C ◽  
Chronic Hepatitis B ◽  
Liver Damage ◽  
Multivariable Analysis ◽  
Control Group ◽  
Cvd Risk

It is thought that chronic liver disease affects a person's risk of cardiovascular disease (CVD) development. The aim of this study was to assess the effect of Chronic Hepatitis B (HBV) infection, Chronic Hepatitis C (HCV) infection, and liver damage on cardiovascular risk and selected vascular parameters contributing to CVD risk. This case-control study included a group of 114 patients composed of 34 patients with HBV, 35 patients with HCV, and 45 patients as the control group. Cardiovascular risk was assessed by analyzing classic risk factors, and the SCORE system. The following arterial properties were analyzed using applanation tonometry with SphygmoCor Vx technology: central systolic blood pressure (cSBP), central pulse pressure, augmentation pressure, augmentation index, and carotid-femoral pulse wave velocity (PWV). Asymmetric dimethyloarginine (ADMA) blood levels were analyzed using ELISA as a marker of vascular function. In a univariable analysis we found no significant differences between the hepatitis B, hepatitis C, and control groups in terms of PWV (respectively: median 7.2 [Q25-Q75 6.4-8.5], 7.3 [6.9-8.7], 7.8 [6.5-8.9]), cSBP (115 [109-126], 118 [107-123], 116 [107-129]), ADMA (0.52 [0.47-0.60], 0.53 [0.45-0.62], 0.58 [0.51-0.63]), SCORE (0 [0-1], 0 [0-2], 0 [0-2]). No significant differences in cardiovascular variables were observed between cirrhotic and non-cirrhotic patients. A multivariable analysis confirmed the above findings. (PWV, p=0 . 29; cSBP, p=0.26; ADMA, p=0.19). We concluded that chronic hepatitis B or C was not independently associated with an adverse cardiovascular risk profile nor with an unfavorable pattern of vascular parameters contributing to CVD risk in our study population, even in the case of liver cirrhosis. The same was true for blood ADMA levels.

scholarly journals Modern clinical laboratory aspects of chronic hepatitis C

2021 ◽  
pp. 37-42
Author(s):  
O. N. Sumlivaia ◽  
M. S. Nevzorova ◽  
A. T. Sayfitova ◽  
S. A. Vysotin
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C ◽  
Viral Hepatitis ◽  
Chronic Hepatitis C ◽  
Clinical Examination ◽  
Liver Damage ◽  
Clinical Laboratory ◽  
Diagnostic Value ◽  
Control Group ◽  
Viral Hepatitis C

Aim. Assess the current diagnostic value of clinical laboratory markers of liver damage in chronic viral hepatitis C. Materials and methods. Comprehensive clinical examination of 194 patients with the diagnosis chronic hepatitis C and 73 almost healthy faces was conducted. Results. According to the clinical examination, 91% of patients have hepatomegaly. According to the results of elastography, the subgroup without fibrosis F0 49 (25%) people, with fibrosis of stages F1-F3-145 (75%) patients. The occurrence of HCV genotypes was: HCV-1-33%, HCV-2-12% and HCV-3-55%. The virusemia indicator showed large variations of values. During the research it was established that indirect indicators of a fibrosis of a liver: levels of AST and ALT, GGTP, a direct and general bilirubin, the APRI index are authentically exceeded by indexes of control group while the level of thrombocytes and de Ritis’s coefficient authentically decrease. Conclusions. The current course of chronic hepatitis C occurs with hepatomegalia, often associated with gastrointestinal and cardiovascular damage. The most common virus among patients is the HVC-3 genotype virus. When examining indirect markers of fibrosis in viral hepatitis C, the APRI test is an early predictor and has high predictive value. Platelet levels decrease with viral liver damage. As a consequence, the APRI index increases and the de Ritis ratio decreases.

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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