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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We characterized the structural and immunohistological changes of sinusoidal endothelial cells that occur during cirrhosis in rats made cirrhotic with thioacetamide. Thioacetamide (200 mg/kg body wt) was injected intraperitoneally three times a week into male Wistar rats. Two, 4, 6 and 12 wk later, rat livers were observed under transmission and scanning electron microscopy and regular microscopy and immunostained with laminin and von Willebrand factor (factor VIII-related antigen) antibodies. The diameters and numbers of sinusoidal endothelial fenestrations did not change significantly after 2 wk in the thioacetamide-treated rats; however, they decreased within 4 wk after thioacetamide treatment. A basement membranelike structure in Disse's space was noted 6 wk after thioacetamide treatment. Laminin was detected in Disse's space after 4 wk. In vitro, in cultured sinusoidal endothelial cells, the diameter of sinusoidal endothelial fenestrations was significantly lower at 6 wk in thioacetamide-treated rats. von Willebrand factor was detected in the cytoplasm as granular fluorescence after 6 wk of thioacetamide treatment. These results suggest that as fibrosis develops in cirrhosis, the structural and immunohistochemical characteristics of sinusoidal endothelial cells change.
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PMID:Defenestration of the sinusoidal endothelial cell in a rat model of cirrhosis. 824 83

We characterized the structural changes of sinusoidal endothelial cells in chronic ethanol-fed rats and rats with cirrhosis induced by thioacetamide. The phenotypic changes of sinusoidal endothelial cells in fibrotic rats induced by thioacetamide and the reversibility of these changes were also investigated under transmission and scanning electron microscopy, regular microscopy and by immunohistochemistry with laminin and von Willebrand factor antibodies. The diameter and porosity of sinusoidal endothelial fenestrations were increased in chronic ethanol-fed rats without liver fibrosis, however, they decreased within 4 weeks of the cessation of thioacetamide treatment. A basement membrane-like structure in Disse's space was noted 6 weeks after thioacetamide treatment. Laminin was detected in Disse's space after 4 weeks and von Willebrand factor was detected in the cytoplasm as granular fluorescence after 6 weeks of thioacetamide treatment. Reversibility of the phenotypic changes of the sinusoidal endothelial cells was demonstrated in fibrotic liver of rats that received thioacetamide for 6 weeks after long-term discontinuation of thioacetamide administration. These results indicate that the structural and immunohistochemical characteristics of sinusoidal endothelial cells change in chronic ethanol-fed rats and fibrotic rats and these changes are reversible.
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PMID:Role of sinusoidal endothelial cells in liver disease. 858 39

The immunohistochemical expression of CD34 (human hematopoietic stem cell and endothelial cell marker) and laminin were studied in chronic liver diseases and hepatocellular carcinoma (HCC) to elucidate whether their expression reflected phenotypic differences between non-cancerous sinusoids and sinusoid-like tumor vessels. In normal liver, hepatic sinusoids were always negative for CD34 and laminin. In chronic hepatitis and cirrhosis, the two antigens were sparsely expressed in capillarized sinusoids at periportal and perinodular area. In advanced HCC, CD34 was strongly and diffusely expressed by the endothelial lining of sinusoid-like tumor vessels. However, early-stage HCC showed a wide spectrum of CD34 expression from negative to focal and diffuse, strongly positive staining in sinusoid-like vessels. Laminin was strongly expressed in advanced HCC but not in early-stage HCC. The results indicate that the enhanced expression of CD34 by sinusoidal endothelial cells may reflect the phenotypic change of endothelial cells in chronic liver diseases and HCC, and that the expression may correlate with the processes of angiogenesis induced by hepatocarcinogenesis.
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PMID:Enhanced CD34 expression of sinusoid-like vascular endothelial cells in hepatocellular carcinoma. 891 44

The aim of this study was to follow semiquantitatively by immunohistochemical means the alterations of the expression of the hepatic glycoproteins tenascin, fibronectin, and laminin in two different models of chronic liver injury, i.e. thioacetamide-induced liver cirrhosis and fibrosis after bile duct ligation. The tenascin distribution pattern observed during cholostasis-induced liver fibrosis showed some similarities, but also some differences in comparison with the results obtained after TAA intoxication. Most importantly, the data show that tenascin staining was detectable in almost all areas of the chronically injured livers up to 3 and 6 months in bile duct-ligated and chemically-injured livers, respectively. Thus, tenascin does not seem to play only a transient role in the fibrogenetic process as previously suggested. Laminin was strongly stained in proliferating ductules, whereas only a weak continuous distribution was observed along the sinusoidal wall. Furthermore, our findings confirm the role of fibronectin as a pacemaker of fibrosis. Regional differences in the kinetics of the expression of the glycoproteins may reflect local differences in their production by parenchymal or non parenchymal cells or regional patterns of proteolytic activity.
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PMID:Expression of tenascin, fibronectin, and laminin in rat liver fibrogenesis--a comparative immunohistochemical study with two models of liver injury. 978 3

49 patients with viral hepatitis were studied on the correlationship between liver fibrosis and the level of serum precollagen type III (PC III), pre-collagen III pre-peptide (P III P), Laminin (LN), hyaluronic acid (HA) and collagen type IV (IV-C), as well as relationship between them and the expression of LN, IV-C, a-smooth muscle actin (a-SMA) and cytokeration (CK) in the liver tissues examined by immunohistochemistry. Results showed that the level of PC III, P III P, LN, HA and IV-C in the groups of liver cirrhosis and chronic severe hepatitis were higher than that in the groups of acute and chronic hepatitis. High correlation was found between the level of these markers (especially the level of the IV-C) and the degree of fibrosis in the group of chronic hepatitis. So were the expression of LN, IV-C, a-SMA and CK in the liver tissue. The results also showed that the liver fibrosis correlated with inflammatory reaction in the liver. So the authors suggested that more attention should be paid to the inflammatory reaction of the liver for prevention and treatment of liver fibrosis.
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PMID:[Clinical and pathological study on liver fibrosis in viral hepatitis]. 1561 38

Laminin levels in ascitic fluid have been proposed as a marker for neoplastic ascites. We compared the concentration of laminin in serum and in ascitic fluid from patients with hepatic cirrhosis and peritoneal carcinomatosis and assessed the diagnostic value of serum laminin levels in differentiating neoplastic from benign ascites. Laminin concentrations were determined by ELISA with antibodies against laminin extracted from the human placenta, in patients with ascites due to peritoneal carcinomatosis (N = 20) and hepatic cirrhosis (N = 33). Patients with infected or hemorrhagic ascites were excluded. The receiver operating characteristic curve was used to determine the sensitivity and specificity of serum laminin for the diagnosis of neoplastic ascites. When compared to the group with cirrhosis, the carcinomatosis group presented significantly higher mean laminin levels in serum (3.3 +/- 0.5 vs 2.1 +/- 0.4 microg/ml, mean +/- SD, P < 0.05) and ascites (2.8 +/- 0.5 vs 1.6 +/- 0.4 microg/ml, P < 0.05). Although laminin concentration was higher in serum than in ascites, the laminin serum/ascites ratio and serum-ascites gradient did not differ between the studied groups. A significant correlation (r = 0.93, P < 0.0001) was observed between the serum and ascites laminin values. Serum laminin levels >2.25 microg/ml showed 100% sensitivity and 73% specificity for the diagnosis of neoplastic ascites. Serum concentration seems to be the main determinant of laminin levels in ascitic fluid and its values can be used as a diagnostic parameter in the study of neoplastic ascites.
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PMID:Laminin concentration in ascites of patients with hepatic cirrhosis and peritoneal carcinomatosis. 1578 39


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