scholarly journals The Role of Signal Transducer and Activator of Transcription 5 and Transforming Growth Factor-β1 in Hepatic Fibrosis Induced by Chronic Hepatitis C Virus Infection in Egyptian Patients

2018 ◽  
Vol 27 (2) ◽  
pp. 115-121
Author(s):  
Mona A. Abu El Makarem ◽  
Ghada M. El-Sagheer ◽  
Moustafa A. Abu El-Ella
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C ◽  
Liver Fibrosis ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Serum Levels ◽  
Signal Transducer ◽  
Egyptian Patients ◽  
Tgf Β1

Objective: To investigate the possible role of signal transducer and activator of transcription 5 (STAT5) in the pathogenesis of liver fibrosis in Egyptian patients with chronic hepatitis C (CHC) virus infection and its relation to hepatic stellate cells (HSC). Subjects and Methods: Sixty-five patients (46 males and 19 females) were divided into 4 groups based on the severity of fibrosis as detected by Fibroscan as follows: F1, n = 15; F2, n = 21; F3, n = 13; and F4, n = 16. Twenty age- and gender-matched healthy persons volunteered as controls. The serum levels of STAT5, TGF-β1, α-smooth muscle actin (α-SMA), fasting blood sugar, and fasting insulin, as well as homeostasis model assessment of insulin resistance (HOMA-IR), were determined and compared for all groups. The usefulness of the studied serum biomarkers for predicting liver fibrosis was evaluated using a receiver operating characteristic curve. Results: Serum levels of STAT5 were significantly lower in patients compared to controls (9.69 ± 5.62 vs. 14.73 ± 6.52, p ≤ 0.001); on the contrary, TGF-β1, α-SMA, and HOMA-IR were significantly higher in patients compared to controls (mean: 1,796.04 vs. 1,636.94; 14.94 vs. 8.1; and 7.91 vs. 4.18; p ≤ 0.01 and 0.001, respectively). TGF-β1 and α-SMA showed a progressive increase with advancing severity of hepatic fibrosis (mean TGF-β1: 2,058.4 in F1-F2 and 1,583.8 in F3-F4, p ≤ 0.04; mean α-SMA: 13.59 in F1-F2 and 16.62 in F3-F4, p ≤ 0.05). STAT5 had a significant negative correlation with TGF-β1 (p ≤ 0.001), while no correlation was detected with α-SMA (p ≤ 0.8). Conclusions: STAT5 may play a significant role in hepatic fibrogenesis through the induction of TGF-β1 but not through the activation of hepatic stellate cells.

Significance of serum WFA+-M2BP level as a marker of liver fibrosis in patients with chronic hepatitis C

2020 ◽  
Vol 18 (4) ◽  
pp. 80-84
Author(s):  
N.N. Volkova ◽  
◽  
N.S. Ibadullaeva ◽  
M.U. Asilova ◽  
E.I. Musabaev ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Chronic Hepatitis ◽  
Hepatitis C ◽  
Liver Fibrosis ◽  
Antiviral Therapy ◽  
Chronic Hepatitis C ◽  
Treatment Initiation ◽  
Serum Levels ◽  
Serum Marker

Objective. To evaluate the role of dynamics of WFA+-M2BP, a serum marker of liver fibrosis, in patients with chronic hepatitis C (CHC). Patients and methods. We examined 56 CHC patients who received antiviral therapy. The severity of liver fibrosis was assessed using indirect elastometry. There were 8 patients with F0 fibrosis, 17 patients with F1 fibrosis, 6 patients with F2 fibrosis, 12 patients with F3 fibrosis, and 13 patients with F4 fibrosis. The level of WFA+-M2BP was measured prior to treatment initiation, then 1 month after treatment initiation, and 3 months after treatment completion. Results. We found that both CHC patients and patients with HCV-induced liver cirrhosis demonstrated a decrease in the serum level of WFA+-M2BP in response to antiviral therapy. Mean levels of WFA+-M2BP in individuals with F3 and F4 fibrosis were significantly higher than those in patients with F0 fibrosis (p < 0.01). Conclusion. Higher grades of liver cirrhosis were associated with higher serum levels of WFA+-M2BP, while antiviral therapy led to a decrease in the concentration of this biomarker. The assessment of WFA+-M2BP dynamics will help to detect early stages of liver fibrosis and also to monitor it in patients receiving antiviral therapy. Key words: chronic hepatitis C, liver cirrhosis caused by HCV, biomarker, WFA+-M2BP, liver fibrosis, antiviral therapy

scholarly journals Reelin expression in human liver of patients with chronic hepatitis C infection

2017 ◽  
Author(s):  
Simone Carotti ◽  
Giuseppe Perrone ◽  
Michelina Amato ◽  
Umberto Vespasiani Gentilucci ◽  
Daniela Righi ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C ◽  
Liver Fibrosis ◽  
Liver Injury ◽  
Hepatic Stellate Cells ◽  
Human Liver ◽  
Critical Role ◽  
Adaptor Protein ◽  
Stellate Cells ◽  
Functional Protein

Reelin is a secreted extracellular glycoprotein that plays a critical role during brain development. Several studies have described Reelin expression in hepatic stellate cells of the human liver. In order to investigate the possible role of Reelin in the process of hepatic fibrogenesis, in this study we investigated Reelin expression in the liver tissue of patients infected with the Hepatitis C Virus (HCV). On this basis, Reelin expression was analysed by immunohistochemistry during liver biopsies of 81 patients with HCV-related chronic hepatitis. A Knodell score was used to stage liver fibrosis. Hepatic stellate cells/myofibroblast immunohistochemical markers (CRBP-1, alpha-SMA) were also evaluated. As further confirmed by co-localization experiments (Reelin +CRBP-1), Reelin protein was expressed by hepatic stellate cells/myofibroblasts, and a significant positive correlation was found between Reelin expression and the stage of liver fibrosis (P=0.002). Moreover, Reelin correlated with CRBP-1 positive cells (P=0.002), but not with alpha-SMA, suggesting that Reelin should not be regarded as a marker of hepatic stellate cells/myofibroblasts differentiation but rather as a functional protein expressed during some phases of liver fibrosis. Furthermore, Disabled-1 (Dab1), a Reelin adaptor protein, was expressed in cells of ductular reaction suggesting a paracrine role for Reelin with regards these elements. In conclusion, Reelin was expressed by human hepatic stellate cells/myofibroblasts and the number of these cells increased significantly in the lobule as the liver fibrosis progressed, suggesting a role for Reelin in the activation of hepatic stellate cells/myofibroblasts during liver injury. Reelin may potentially be incorporated into liver injury evaluations in combination with other histological data.

The role of ITPA and ribavirin transporter genes polymorphisms in prediction of ribavirin-induced anaemia in chronic hepatitis C Egyptian patients

2017 ◽  
Vol 44 (9) ◽  
pp. 965-968 ◽  
Author(s):  
Ehab S El Desoky ◽  
Alaa T Abdelhafez ◽  
Jessica Cusato ◽  
Sherif I Kamel ◽  
Abeer MR Hussein ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Egyptian Patients

scholarly journals Association of TM6SF2 rs58542926 with Hepatic and Extrahepatic Alterations in Chronic Hepatitis C Patients

2021 ◽  
Author(s):  
Mohi I. Mohammed Abdul ◽  
Adriana Vitiello ◽  
Hanieh Ghassabian ◽  
Heba M. Eltahir ◽  
Elham Ahmed Hassan ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C ◽  
Liver Fibrosis ◽  
Chronic Hepatitis C ◽  
Biochemical Analysis ◽  
Complete Blood Count ◽  
Minor Allele ◽  
Chronic Hepatitis C Patients ◽  
Severe Fibrosis

Abstract Human genetic variants play major roles in predicting and prognosis of several diseases. The effect of rs58542926 variant in transmembrane 6 superfamily member 2 (TM6SF2) gene on liver fibrosis among patients with chronic hepatitis C (CHC) is still debatable. The aim of this study is to investigate the possible effects of this variant in CHC patients. The study comprised 351 subjects: 250 CHC patients with different fibrosis stages (F0-F4) and 101 healthy volunteers. TM6SF2 (rs58542926) genotype was determined for all subjects. Blood samples were collected for complete blood count and biochemical analysis and cohort subjects were genotyped for the variant TM6SF2 rs58542926. Fibrosis staging was performed using Fibrotest and Fibroscan standard tests. The presence of the minor allele was significantly associated with severe liver fibrosis, as well as thrombocytopenia as an extrahepatic alteration. In addition, there was a significant association between the minor allele and lower thrombopoietin levels. The association of TM6SF2 genotype with thrombocytopenia was explored by measuring plasma thrombopoietin (TPO) levels for CHC patients. The results showed an association with extrahepatic alteration (thrombocytopenia) through its effect on plasma TPO level, and consequently on platelets production, which raises questions about the role of this variant in HCV treatment outcome. In conclusion, the occurrence of the minor allele of the variant rs58542926 can be linked to severe fibrosis stages as well as thrombocytopenia, enabling this variant to be used as a diagnostic pharmacogenetic marker for predicting the risk of fibrosis onset in CHC patients.

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 Role of DDAH/ADMA pathway in TGF-β1-mediated activation of hepatic stellate cells

2017 ◽  
Author(s):  
Zhenguo Liu ◽  
Juan Wang ◽  
Wu Xing ◽  
Yingqiong Peng ◽  
Yan Huang ◽  
...  
Keyword(s):  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Tgf Β1

Expression of large tenascin-C splice variants by hepatic stellate cells/myofibroblasts in chronic hepatitis C

2007 ◽  
Vol 46 (4) ◽  
pp. 664-673 ◽  
Author(s):  
Amro El-Karef ◽  
Masahiko Kaito ◽  
Hideaki Tanaka ◽  
Kazuo Ikeda ◽  
Tomohiro Nishioka ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Hepatic Stellate Cells ◽  
Splice Variants ◽  
Stellate Cells ◽  
Tenascin C
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