DETECTION OF EARLY ZONE 3 LIVER FIBROSIS IN CHRONIC ALCOHOLICS A Comparison of Four Connective Tissue Staining Methods

Author(s):  
MOGENS VYBERG ◽  
JETTE JUNGE ◽  
THOMAS HORN
2021 ◽  
Vol 19 (3) ◽  
pp. 285-293
Author(s):  
E. I. Lebedeva ◽  

Background. Angiogenesis plays a key role in the progression of liver fibrosis. However, the available data on morphological changes in the liver vascular system are insufficient and contradictory. Objective. The aim of the work is to study the morphological changes in the liver vascular system of rats under the influence of thioacetamide. Material and methods. Fibrosis and cirrhosis of the liver in Wistar rats were induced with thioacetamide given at a dose of 200 mg/kg of animal weight for 17 weeks. To study morphological changes, we used classical and immunohistochemical staining methods. Microscopic analysis was performed using OLYMPUS BX51 microscope and image analysis software ImageScope Color and cellSens Standard. Results. The introduction of a solution of thioacetamide through the stomach leads to a gradual increase in the progression of pathological changes. In addition, it permits to track all stages of cirrhosis development and morphological restructuring of the liver vascular system. Throughout the experiment there was intensive capillarization of the parenchyma sinusoids and neoangiogenesis in the portal tracts and connective tissue septa manifested by the formation of many venules and small veins. We also observed an increase in the area of interlobular veins, which in some places had reached gigantic proportions. Three morphological phenotypes of CD34-positive cells were revealed. In the interlobular arteries as well as interlobular, central and sublobular veins, these cells had an elongated shape and a rod-shaped dark-colored nucleus. During the transformation of liver fibrosis into cirrhosis CD34-positive cells of an elongated shape with light roundedelongated nuclei were observed in the sinusoids closer to the periphery of individual false nodules. Rounded cells with dark-colored nuclei were present in the connective tissue near the hepatic triads, in the connective tissue septa among the cells of the infiltrate and between the sharply increased number of bile ducts. Conclusions. The established complex phenotypic changes in sinusoidal endothelial cells prove a close connection between fibrogenesis and neoangiogenesis. They probably play a leading role in the development of fibrosis and restructuring of the venous system of the portal vein.


2006 ◽  
Vol 8 (7) ◽  
pp. 889-900 ◽  
Author(s):  
Guangming Li ◽  
Qing Xie ◽  
Yi Shi ◽  
Dingguo Li ◽  
Mingjun Zhang ◽  
...  

2009 ◽  
Vol 55 (3) ◽  
pp. 767-774 ◽  
Author(s):  
Dai Zhang ◽  
Nian-Yue Wang ◽  
Cheng-Bao Yang ◽  
Guo-Xiang Fang ◽  
Wei Liu ◽  
...  

2019 ◽  
Vol 63 (4) ◽  
pp. 549-554
Author(s):  
Katarzyna Filip-Hutsch ◽  
Tomasz Hutsch ◽  
Szymon Kolasa ◽  
Aleksander W. Demiaszkiewicz

Abstract Introduction Parafasciolopsis fasciolaemorpha is a liver fluke typically parasitising moose in Central and Eastern Europe. The aim of our studies was to describe a case of fatal moose parafasciolopsosis, with special emphasis on the histopathological changes caused in the liver tissue by around 10,000 flukes. Material and Methods A male moose, found dead in Polesie National Park, eastern Poland, was subjected to parasitological necropsy. Macroscopic and histopathological examination of the liver was performed. Results Over 10,000 flukes identified as P. fasciolaemorpha were isolated from the liver parenchyma. Histopathological examination of the liver revealed the presence of multiple cavities, which were filled with flukes and cellular detritus and encysted with a layered capsule of connective tissue. Extensive liver fibrosis with signs of incomplete septal cirrhosis was also observed. Conclusion Parafasciolopsosis with accompanying diarrhoea was the most probable reason for the moose’s death. However, it is possible that most moose are able to survive extremely intensive P. fasciolaemorpha infection by formation of extensive fibrosis, which isolates flukes from the liver parenchyma and therefore retards the failure of the organ. To the best of our knowledge, this is the first histopathological description of changes in the liver of a moose infected with P. fasciolaemorpha.


2012 ◽  
Vol 27 (7) ◽  
pp. 1023-1028 ◽  
Author(s):  
Jann‐Inn Tzeng ◽  
Mei‐Fen Chen ◽  
Hsien‐Hui Chung ◽  
Juei‐Tang Cheng

Hepatology ◽  
2009 ◽  
Vol 50 (3) ◽  
pp. 939-947 ◽  
Author(s):  
ZhenYue Tong ◽  
Ruju Chen ◽  
Daniel S. Alt ◽  
Sherri Kemper ◽  
Bernard Perbal ◽  
...  

Biomarkers ◽  
2011 ◽  
Vol 16 (5) ◽  
pp. 426-433 ◽  
Author(s):  
Efstathios Vassiliadis ◽  
Sanne S. Veidal ◽  
Henrik Simonsen ◽  
Dorthe V. Larsen ◽  
Ben Vainer ◽  
...  

2018 ◽  
pp. 62-66
Author(s):  
B. B. Osipov ◽  
A. N. Lyzikov ◽  
A. G. Skuratov ◽  
A. A. Prizentsov

Objective: to design an experimental model of liver cirrhosis in rats and to compare it with the carbon tetrachloride model of liver injury. Material and methods. White Wistar rats (n=30) were used as objects for modeling of toxic liver injury. The modeling was performed by the designed toxic-alimentary method (experimental group, n=15) and by means of the carbon tetrachloride injection (control group, n=15). The animals were sacrificed at different terms (8, 12 weeks after start of the modeling and 3 months after termination of the modeling), and the morphological and morphometric state of the liver was studied. Results. The designed toxic-alimentary model of liver injury leads to liver cirrhosis 8 weeks after start of the modeling (reproducibility - 93.3 %). The reproducibility of liver cirrhosis in case of using the carbon tetrachloride model 8 weeks after start of the modeling is 26.7%, which is proved by statistically lower thickness of connective-tissue septa in the liver in the control group in comparison with the experimental group (p=0.016, Mann Whitney U test). The designed toxic-alimentary method ensures shorter timing of the modeling of liver cirrhosis (from 12 weeks in the control group to 8 weeks in the experimental group) and also lower reversibility of liver fibrosis signs 3 months after termination of the modeling in comparison with the carbon tetrachloride model of liver injury. Conclusions. The designed toxic-alimentary model of liver injury leads to liver cirrhosis 8 weeks after start of the modeling. The developed model ensures shorter timing of the modeling of liver cirrhosis, increased reproducibility as well as lower reversibility of liver fibrosis signs 3 months after termination of the modeling in comparison with the carbon tetrachloride model of liver injury.


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