Syndecan 1 (CD138) serum levels: a novel biomarker in predicting liver fibrosis stage in patients with hepatitis C

2009 ◽  
Vol 29 (2) ◽  
pp. 208-212 ◽  
Author(s):  
Isabel Zvibel ◽  
Phillipe Halfon ◽  
Sigal Fishman ◽  
Guillaume Penaranda ◽  
Moshe Leshno ◽  
...  
2021 ◽  
Vol 19 (2) ◽  
pp. 60-64
Author(s):  
Zh.B. Ponezheva ◽  
◽  
I.V. Mannanova ◽  
V.V. Makashova ◽  
A.A. Erovichenkov ◽  
...  

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


Author(s):  
Zehra Öksüz ◽  
Enver Üçbilek ◽  
Mehmet Sami Serin ◽  
Serkan Yaraş ◽  
Gülhan Örekici Temel ◽  
...  

2018 ◽  
Vol 27 (2) ◽  
pp. 115-121
Author(s):  
Mona A. Abu El Makarem ◽  
Ghada M. El-Sagheer ◽  
Moustafa A. Abu El-Ella

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.


Pathogens ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 57
Author(s):  
Momen Askoura ◽  
Hisham A. Abbas ◽  
Hadeel AlSadoun ◽  
Wesam H. Abdulaal ◽  
Amr S. Abu Lila ◽  
...  

Hepatitis C virus (HCV) is one of the most epidemic viral infections in the world. Three-quarters of individuals infected with HCV become chronic. As a consequence of persistent inflammation, a considerable percentage of chronic patients progress to liver fibrosis, cirrhosis, and finally hepatocellular carcinoma. Cytokines, which are particularly produced from T-helper cells, play a crucial role in immune protection against HCV and the progression of the disease as well. In this study, the role of interleukins IL-33, IL-17, and IL-25 in HCV patients and progression of disease from chronicity to hepatocellular carcinoma will be characterized in order to use them as biomarkers of disease progression. The serum levels of the tested interleukins were measured in patients suffering from chronic hepatitis C (CHC), hepatocellular carcinoma (HCC), and healthy controls (C), and their levels were correlated to the degree of liver fibrosis, liver fibrosis markers and viral load. In contrast to the IL-25 serum level, which increased in patients suffering from HCC only, the serum levels of both IL-33 and IL-17 increased significantly in those patients suffering from CHC and HCC. In addition, IL-33 serum level was found to increase by liver fibrosis progression and viral load, in contrast to both IL-17 and IL-25. Current results indicate a significant role of IL-33 in liver inflammation and fibrosis progress in CHC, whereas IL-17 and IL-25 may be used as biomarkers for the development of hepatocellular carcinoma.


PLoS ONE ◽  
2018 ◽  
Vol 13 (12) ◽  
pp. e0209481
Author(s):  
Neven Papic ◽  
Snjezana Zidovec Lepej ◽  
Lana Gorenec ◽  
Ivana Grgic ◽  
Slavko Gasparov ◽  
...  

2017 ◽  
Vol 16 (5) ◽  
pp. 742-748 ◽  
Author(s):  
Laura A. Azevedo ◽  
Ursula Matte ◽  
Themis R. Silveira ◽  
Jacqueline W. Bonfanti ◽  
Juliana P. Bruch ◽  
...  

2020 ◽  
Vol 18 (4) ◽  
pp. 80-84
Author(s):  
N.N. Volkova ◽  
◽  
N.S. Ibadullaeva ◽  
M.U. Asilova ◽  
E.I. Musabaev ◽  
...  

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


Sign in / Sign up

Export Citation Format

Share Document