scholarly journals The Difference of Hypoxic Inducible Factor-1α, Vascular Endothelial Growth Factor, and Transforming Growth Factor-β1 Based on Liver Fibrosis Severity in Patients with Chronic Hepatitis B

2021 ◽  
Vol 9 (B) ◽  
pp. 91-95
Author(s):  
Libya Husen ◽  
Gontar Alamsyah Siregar ◽  
Masrul Lubis

BACKGROUND: Hepatitis B is a global health problem. The disease damages hepatocytes and creates tissue hypoxic condition. Hypoxia triggers production of several mediators such as hypoxic inducible factor (HIF)-1α, vascular endothelial growth factor (VEGF), and transforming growth factor (TGF)-β1. The mediators act in liver fibrosis and cirrhosis, and hepatocellular carcinoma. AIM: The objective of the study was to determine the difference in serum HIF-1α, VEGF, and TGF-β1 levels based on liver fibrosis severity in patients with chronic hepatitis B. MATERIALS AND METHODS: This cross-sectional study was performed in Haji Adam Malik Hospital Medan, Indonesia, from January to July 2020. Subjects were chronic hepatitis B patients aged 18 years or older. Exclusion criteria were other chronic diseases, malignancies, or pregnancy. Liver fibrosis was determined using shear wave elastography and categorized as follow: F1, F2, F3, and F4. Serum HIF-1α, VEGF, and TGF-β1 levels were measured using enzyme-linked immunosorbent assay. Specimens were obtained from venous blood. RESULTS: A total of 63 patients were enrolled in this study with mean age of 40.3 (SD 11.69) years. Subjects were dominated by males (58.7%). There were no differences in serum HIF-1α, VEGF, and TGF-β1 levels based on liver fibrosis grading and also based on hepatitis B envelope antigen (HBeAg) status and gender. Associations between liver fibrosis grading, HBeAg, and gender were absent. There was a positive correlation between liver fibrosis severity and age (r = 0.311, p = 0.013). CONCLUSION: Serum HIF-1α, VEGF, and TGF-β1 levels were not different among chronic hepatitis B patients based on liver fibrosis severity.

2021 ◽  
Author(s):  
Ming-hui Li ◽  
Yao Lu ◽  
Fang-fang Sun ◽  
Qi-qi Chen ◽  
Lu Zhang ◽  
...  

Abstract To investigate association between immune cell-related cytokines and development of chronic hepatitis B (CHB). Patients with chronic hepatitis B virus (HBV) infection in immune tolerance (IT, n=30) and hepatitis B envelope antigen (HBeAg) positive CHB (n=250) were enrolled in the study. HBV virus, serological indicators, and plasma cytokine levels were detected at the time of enrollment. The results showed that there were significant differences in median age of patients (27 vs. 31y), alanine aminotransferase level (ALT, 29.85 vs 234.70 U/L), alanine aminotransferase level (AST, 23.40 vs. 114.90 U/L), HBsAg level (4.79 vs. 3.88 log10 IU/ml), HBeAg (1606.36 vs. 862.47 S/CO) and HBV DNA load (8.17 vs 6.71 log10 IU/ml) between IT and CHB groups (all P<0.01). The median values of Fms-like tyrosine kinase 3 ligand (FLT3-L), interferon-γ (IFN-γ), interleukin- 17A (IL-17A) and transforming growth factor- beta (TGF-β1) in IT group were significantly higher than those in CHB group (FLT3-L: 41.62 vs. 27.47 pg/ml; IFN-γ: 42.48 vs. 33.18 pg/ml; IL-17A: 15.66 vs. 8.90 pg/ml; TGF-β1: 4921.50 vs. 2234 pg/ml. All P<0.01). The median values of IFN-a2, TGF-β3 and IL-10 levels in IT group were significantly lower than those in CHB group (IFN-α2: 15.24 vs. 35.78 pg/ml, P=0.000; TGF-β3: 131.69 vs. 162.61 pg/ml, P=0.025; IL-10: 5.02 vs. 7.9 pg/ml, P=0.012). The multivariate logistic regression analysis indicated that TGF-β 1 (OR=0.999, 95% CI 0.999-1.000, P<0.001) and TGF-β2 levels (OR=1.008, 95%CI 1.004-1.012, P <0.001) were significantly associated with the incidence of CHB. The results suggest that TGF-β level might be an independent factor related to the occurrence of CHB.


Author(s):  
Yostila Derosa ◽  
Nasrul Zubir ◽  
Raveinal Arnelis

Background: Hepatitis B is acute or chronic liver inflammation caused by hepatitis B viral and can progress to hepatic chirrosis or liver cancer. Chronic hepatitis B has a high risk for liver fibrosis. Chronic inflammation and liver fibrosis are interrelated processes. This study aimed to determine the differences in T-regulator cells, Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) between chronic hepatitis B patients with and without liver fibrosis.Method: This study used a cross-sectional method for patients diagnosed with chronic hepatitis B in the Inpatient and Outpatient Department of the Internal Medicine Department  DR. M. Djamil Padang and other hospitals in Padang city for 6 months. Samples were selected by consecutive sampling according to inclusion and exclusion criteria. Liver fibrosis is identified by fibroscan. Data were analyzed by SPSS 21.0.Results: thirty-two patients were diagnosed with chronic hepatitis B and 50% had liver fibrosis. The levels of T-regulator cells in chronic hepatitis B patients without liver fibrosis were 2.08% and liver fibrosis 2.25%, but this difference was not statistically significant (p 0.05). Mean ALT levels in the group without fibrosis were 19 IU/L (7IU/L-71IU/L) and liver fibrosis 61 IU / L (13IU/L-625IU/L). The mean AST level in the group without fibrosis were 15.5 IU/L (10IU/L-32IU/L) and liver fibrosis 35.5 IU/L (10IU/L-476IU/L). The difference between ALT and AST in the two groups was significant (p 0.05). Hepatitis B patients with liver fibrosis had higher ALT and AST levels than without fibrosis.Conclusion: There were differences levels of T-regulator cells in the two groups, but it was not statistically significant. ALT and AST levels were higher in the liver fibrosis group and statistically significant.


2008 ◽  
Vol 13 (2) ◽  
pp. 62-68 ◽  
Author(s):  
Shinichi Kakumu ◽  
Yuji Ito ◽  
Masahiro Takayanag ◽  
Kentaro Yoshioka ◽  
Takaji Wakita ◽  
...  

2020 ◽  
Vol 7 (1) ◽  
pp. e000543
Author(s):  
Ta-Wei Liu ◽  
Chung-Feng Huang ◽  
Ming-Lun Yeh ◽  
Pei-Chien Tsai ◽  
Tyng-Yuan Jang ◽  
...  

Background and aimsChronic hepatitis B patients in Taiwan with no or limited liver injury are not reimbursed for antiviral treatment by the Taiwan National Health Insurance (NHI). Innovative fibrosis marker, age-adjusted Fibrosis-4 Index (FIB4-AA), was implemented to evaluate the tendency of liver fibrosis in these patients.MethodsThe FIB-4 indices of 256 antiviral treatment-naïve chronic hepatitis B patients at Kaohsiung Medical University Hospital from 2003 to 2019 were reviewed. The difference in initial FIB-4 and last FIB4-AA was treated as a categorical variable, representing the tendency of liver fibrosis in each individual aside from ageing. Logistic regression was implemented to evaluate the three parameters most dependent on increment of FIB4-AA: e seroconversion, body mass index (BMI) and initial FIB-4 index.ResultsThe yearly FIB-4 growth rate of an individual without chronic hepatitis was lower than that of the study group (0.0237 vs 0.0273 for males, 0.02 vs 0.0288 for females). Patients undergoing or completing e seroconversion were less prone to increment of FIB4-AA (p=0.036, OR 0.524). Logistic regression revealed that BMI ≥25 kg/m2 significantly less increment of FIB4-AA (p=0.001, OR 0.383, 95% CI 0.212 to 0.690), while patients with initial FIB-4 <1.29 were prone to increasing liver FIB4-AA (p=0.000, OR 3.687, 95% CI 1.999 to 6.797).ConclusionChronic hepatitis B patients not meeting the reimbursement criteria of the Taiwan NHI are prone to increment of liver fibrosis marker. Overweight is associated with less increment of fibrosis marker, while initial FIB-4 <1.29 is associated with increasing fibrosis marker.


2021 ◽  
pp. 1-10
Author(s):  
Yong Guo ◽  
Chunxue Li ◽  
Rongrong Zhang ◽  
Yating Zhan ◽  
Jinglu Yu ◽  
...  

BACKGROUND: Long non-coding RNA-growth arrest specific transcript 5 (lncRNA-GAS5) plays a suppressive role in activated hepatic stellate cells (HSCs). LncRNAs could circulate in the blood in a cell-free form and serve as promising biomarkers for various human diseases. Herein, we investigated the feasibility of using serum GAS5 as a biomarker for liver fibrosis in chronic hepatitis B (CHB) patients and whether promoter methylation was responsible for GAS5 down-regulation. METHODS: Serum GAS5 levels were quantified using quantitative real-time PCR in CHB patients and healthy controls. GAS5 promoter methylation was examined in LX-2 cells and cirrhotic tissues. RESULTS: Compared with the sera from healthy controls, lower GAS5 levels were found in the sera from CHB patients. Receiver operating characteristic curve analysis indicated that serum GAS5 had a significant diagnostic value for liver fibrosis in CHB patients. Serum GAS5 negatively correlated with HAI scores as well as ALT values in CHB patients. GAS5 was additionally reduced in cirrhotic tissues, associated with its hypermethylation promoter. In LX-2 cells, transforming growth factor-β1 treatment led to a reduction in GAS5 expression and an increase in promoter methylation. Hypermethylation of GAS5 was blocked down by DNA methyltransferase (DNMT) inhibitor and restored GAS5 inhibited HSC activation including proliferation and collagen production. Further studies confirmed that GAS5 methylation was mediated by DNMT1. CONCLUSION: We demonstrate that epigenetically-regulated serum GAS5 could serve as a potential biomarker in CHB patients. Loss of GAS5 is associated with DNMT1-mediated promoter methylation.


Sign in / Sign up

Export Citation Format

Share Document