Liver fibrosis in chronic liver disease refers to the body’s repair response to sustained repeated necrosis or inflammation of liver cells, which results in fibrosis accompanied by relative or absolute lack of fiber degradation and deposition of extracellular matrix in the liver. Early and timely diagnosis and treatment of hepatic fibrosis are of great importance to patients with liver disease. A rational and complete diagnostic model of liver fibrosis should involve clinical pathology and histology, imaging, and serum biochemical markers. Liver biopsy has been regarded as the "gold standard" for the diagnosis of liver fibrosis and as a reference standard for other non-invasive diagnostic tests of liver fibrosis. Since it is invasive, liver biopsy is difficult to implement in clinical practice and a second liver biopsy is even more difficult. As for the non-invasive diagnosis of liver fibrosis, clinical symptoms and signs are not specific. The sensitivity and specificity of individual serum biochemical markers are still very weak, and imaging studies also lack specificity. The mathematical model “FibroTest” of serum biochemical markers has better diagnostic accuracy, but the calculation is complicated, making it difficult to achieve widespread use. There is insufficient evidence to suggest that the "gold standard" of liver biopsy can be replaced. Therefore, further research is needed to investigate how best to balance the benefits and harms of different tests, to identify the best combination, to simplify any calculation steps, to reduce costs, to avoid liver biopsy, and to find new, more specific and sensitive markers.
Objective To review the current status of magnetic resonance imaging (MRI) techniques in the evaluation of hepatic fibrosis. Methods The application and recent advances of various kinds of MRI techniques in evaluating hepatic fibrosis were summarized by literature review. Results The state-of-the-art of MRI evaluating of hepatic fibrosis included common contrast-enhanced MRI, double contrast-enhanced MRI, and various functional MRI techniques. Common contrast-enhanced MRI could detect morphological changes of the liver, but little value in phasing. Double contrast-enhanced MRI markedly increased the contrast to noise ratio. Except diagnosis liver fibrosis, functional MRI also could phase it by its serverity. Conclusion MRI techniques, especially those functional MRI techniques, are advancing very fast and have very great potentiality in both the diagnosis and severity assessment of hepatic fibrosis.
Objective To find a new specific marker that can be used to early diagnose hepatic fibrosis by detecting the change of serum protein in patients with hepatic fibrosis. Methods This research adopted 50 SD rats (25 males and 25 females), and from which 6 rats were selected randomly (3 males and 3 females) as control group, last 44 rates were divided into four groups according to four pathological stages as hepatic fibrosis model group (experimental group). Distinct proteins in serum were detected by surface-enhanced laser desorption/ionization-time of flight-mass spectra (SELDI-TOF-MS). Radioimmunoassay was used to measure four parameters of hepatic fibrosis which were hyaluronidase (HA), precollagen Ⅲ (PCⅢ), laminin (LN) and collagen Ⅳ (Ⅳ-C). Results Distinct proteins in serum were detected in 8 cases of stage Ⅰ of hapatic fibrosis, 5 cases of stage Ⅱ, 5 cases of stage Ⅲ, 6 cases of stage Ⅳ, and 5 cases of control by SELDI-TOF-MS. Three protein peaks were found (M/Z: 4 203, 4 658, and 7 400). The peaks of M/Z 4 658 and 4 700 proteins were obviously increased in the stage Ⅰ of hepatic fibrosis （Plt;0.05）, while the changes of hepatic fibrosis four parameters appeared in stage Ⅳ of hepatic fibrosis. Conclusion This method shows great potential for early diagnosing of hepatic fibrosis and finding better biomarkers to hepatic fibrosis.
ObjectiveTo observe the survival, migration, and effect of human amniotic epithelial cells (hAECs) on hepatic fibrosis in immune rats so as to provide the experimental theory for the clinical treatment with hAECs. MethodsSixty-four 10-week-old male Sprague Dawley rats (weighing, 220-280 g) were randomly divided into 4 groups, sixteen rats in each group. Rat hepatic fibrosis model was induced in groups A, B, and C; hepatic fibrosis rats were injected with 4×106 hAECs in group A, and with normal saline in group B, and no treatment was given in group C; group D served as control group. After 2 weeks of transplantation, the expression of human Alu gene repeat sequence was detected by DNA-PCR method and human leucocyte antigen G (HLA-G) by immunohistochemical staining in heart, liver, spleen, kidney, lung, and brain in group A, and then the percentage of positive expression was compared between organs except spleen. Semi-quantitative analysis was done for liver fibrosis with HE staining according to Chevallier semi-quantitative histological liver fibrosis scoring system, and immunohistochemical staining for TGF-β1 was used to record immunohistochemical score (ISH), the concentrations of aspartate transaminase (AST), alanine aminotransferase (ALT), and albumin (ALB) were determined to analyze hepatic fibrosis. ResultsAlu gene repeat sequence and HLA-G could be detected in liver, heart, brain, lung, and kidney in group A, the percentage of positive expression in the liver was significantly higher than that in the other organs (P<0.05). The histological semi-quantitative score of group A (10.47±3.20) was significantly lower than that of groups B and C[(13.84±3.46) and (13.85±3.16)](P<0.05), but no significant difference was found between groups B and C (P>0.05). The ISH scores in groups A, B, C, and D were 3.60±1.50, 5.38±2.60, 5.50±2.40, and 1.87±1.36, respectively; groups A, B, and C were significantly higher than group D, and group A was significantly lower than groups B and C (P<0.05), but there was no significant difference between groups B and C (P>0.05). The concentrations of ALT and AST in groups A, B, and C were significantly higher than those in group D, and group A was significantly lower than groups B and C (P<0.05), but there was no significant difference between groups B and C (P>0.05). The concentration of ALB in groups A, B, and C was significantly lower than that in group D, and group A was significantly higher than groups B and C (P<0.05), but there was no significant difference between groups B and C (P>0.05). ConclusionhAECs can survive in immune rats by intrasplenic transplantation and migrate to liver, heart, brain, lung, and kidney, and the liver shows the largest migration. The transplantation of hAECs in immune rat with cirrhosis can alleviate hepatic fibrosis and improve the serum indexes of liver function.
ObjectiveTo investigate the expressions of type Ⅰ and type Ⅲ collagen protein in hepatic alveolar echinococcosis tissues, and to explore its relationship with the biological behavior in progress of hepatic alveolar echinococcosis (HAE). MethodsTwenty samples of normal liver tissues and liver tissues at the edge of the lesion with HAE in our hospital from Jan. 2012 to Dec. 2014 were collected, and HE and Masson staining were performed. The pathological changes and the degree of fibrosis of liver tissues around HAE lesion were observed under light microscope. The expressions of type Ⅰ and type Ⅲ collagen protein in liver tissues were detected by immunohistochemical staining. ResultsThe degree of liver fibrosis of liver tissues at the edge of the lesion with HAE was grade Ⅱ, and the degree of fibrosis of normal liver tissues was grade 0, the difference between the two was statistically significant (P < 0.05). The color index of type Ⅰand type Ⅲ collagen protein in the liver tissues at the edge of the lesion with HAE was 7.45±1.85 and 8.00±1.62, respectively, which were higher than those of normal liver tissues (3.10±1.02 and 3.50±0.89), the difference were statistically significant (t=-9.21, P=0.001;t=-10.88, P=0.001). ConclusionsThere is liver fibrosis around the lesion in the patients with HAE. HAE may promote the expressions of type Ⅰ and type Ⅲ collagen and then induce the occurrence of liver fibrosis.