Disease relevance of Liver Cirrhosis

• Patients with chronic hepatitis or liver cirrhosis develop HCC, and when this occurs, some patients exhibit autoantibodies of new specificities [1].
• An increased prevalence of the C3 F allele has been reported in patients with partial lipodystrophy, IgA nephropathy, and Indian childhood hepatic cirrhosis [2].
• This model of hepatic fibrosis results from an inflammatory granulomatous host response to Schistosoma mansoni ova in portal tracts, rather than from direct lover cell injury as with carbon tetrachloride-induced liver fibrosis [3].
• Liver disease may develop with subsequent end-stage liver cirrhosis in patients with intestinal failure as a consequence of both underlying digestive disease and unadapted parenteral nutrition [4].
• Prevalence of antibodies to hepatitis C virus in Spanish patients with hepatocellular carcinoma and hepatic cirrhosis [5].

Psychiatry related information on Liver Cirrhosis

• Furthermore, chronic use of antiretroviral therapy containing PI together with reduction of alcohol consumption and maintenance of high CD4 count could have a beneficial impact on liver fibrosis progression in HIV/HCV coinfected patients [6].
• Permanent alcohol abuse may lead to chronic liver injury with deleterious sequelae such as liver cirrhosis and hepatocellular carcinoma [7].

High impact information on Liver Cirrhosis

• Thus, the mouse quantitative trait gene led to the identification of an unknown gene underlying human susceptibility to liver fibrosis, supporting the idea that C5 has a causal role in fibrogenesis across species [8].
• Theophylline disposition in patients with hepatic cirrhosis [9].
• Administering Fas siRNA beginning one week after initiating weekly ConA injections protected mice from liver fibrosis [10].
• Endocannabinoids acting at vascular CB1 receptors mediate the vasodilated state in advanced liver cirrhosis [11].
• Hepatocyte growth factor gene therapy of liver cirrhosis in rats [12].

Chemical compound and disease context of Liver Cirrhosis

• In murine liver fibrosis models using dimethylnitrosamine, mice with haploinsufficiency of the SOCS1 gene (SOCS1(-/+) mice) developed more severe liver fibrosis than did wild-type littermates (SOCS1(+/+) mice) [13].
• We examined the expression of HSP47 mRNA during the progression of carbon tetrachloride (CCl4)-induced liver fibrosis in rats [14].
• Insulin resistance and glucose intolerance are a major feature of patients with liver cirrhosis [15].
• Downregulation of the male-specific hepatic microsomal steroid 16 alpha-hydroxylase, cytochrome P-450UT-A, in rats with portal bypass. Relevance to estradiol accumulation and impaired drug metabolism in hepatic cirrhosis [16].
• Reduced peripheral conversion of thyroxine to triiodothyronine in patients with hepatic cirrhosis [17].

Biological context of Liver Cirrhosis

• Nitric oxide (NO) has been implicated in the arterial vasodilation and associated vascular hyporesponsiveness to vasoconstrictors observed in liver cirrhosis [18].
• Because the liver plays a key role in plasma lysophosphatidylcholine removal and biotransformation and because virtually nothing is known of these processes in a diseased organ, the hepatobiliary metabolism of lysophosphatidylcholine was investigated in rats with carbon tetrachloride-induced liver cirrhosis [19].
• Although it has no apparent antiviral activity, IL-10 normalizes serum ALT levels, improves liver histology, and reduces liver fibrosis in a large proportion of patients receiving treatment [20].
• RESULTS: In the mouse model of DDC-induced liver fibrosis, natural killer cell activation by polyinosinic-polycytidylic acid induced cell death to activated hepatic stellate cells and attenuated the severity of liver fibrosis [21].
• The -2518 promotor polymorphism in the MCP-1 gene is not associated with liver cirrhosis in chronic hepatitis C virus infection [22].

Anatomical context of Liver Cirrhosis

• Furthermore, in these animals, accentuated increases in procollagen alpha 1(I) and TGF beta 1 mRNA levels were found in both liver tissues and freshly isolated hepatic stellate cells, perisinusoidal cells believed to be a major source of extracellular matrices in liver fibrosis [23].
• METHODS: The effect of 2 TZD (pioglitazone or rosiglitazone) was tested on liver fibrosis induced in rats by either toxin administration (dimethylnitrosamine or carbon tetrachloride) or bile duct ligation [24].
• Seven patients with compensated liver cirrhosis and esophageal varices, all with a base line wedge hepatic vein pressure greater than 20 cm H2O, received 1-mg doses of vasopressin hormonogen (tGLVP) intravenously [25].
• Furthermore, CMV antigenaemia and enhanced plasma TNF occurred in many patients with liver cirrhosis, common variable immunodeficiency, and B-cell chronic lymphocytic leukaemia [26].
• Fatty liver, alcoholic hepatitis, liver cirrhosis, acute and chronic gastritis, deranged structure and function of the small intestine, acute and chronic pancreatitis, and pancreatic lithiasis are some of the sequelae of ethanol abuse [27].

Gene context of Liver Cirrhosis

• Thus, HGF gene therapy may be potentially useful for the treatment of patients with liver cirrhosis, which is otherwise fatal and untreatable by conventional therapy [12].
• SOCS1 is a suppressor of liver fibrosis and hepatitis-induced carcinogenesis [13].
• The mean mRNA ratio of group II PLA2/GAPDH was increased in liver tissue by 126% (P < 0.001) and in kidney tissue by 263% (P < 0.006) following induction of liver cirrhosis [28].
• In addition, only 1 of 20 patients with hepatitis plus liver cirrhosis displayed elevated levels of serum GPC3 [29].
• Smad7 prevents activation of hepatic stellate cells and liver fibrosis in rats [30].

Analytical, diagnostic and therapeutic context of Liver Cirrhosis

• The cellular distribution and temporal expression of transcripts from transforming growth factor-beta 1 (TGF-beta 1) and procollagen alpha 1(I), alpha 1(III), and alpha 1(IV) genes were studied in carbon tetrachloride (CCl4)-induced rat liver fibrosis by using in situ hybridization technique [31].
• METHODS: Liver cirrhosis or fibrosis was induced by intraperitoneal injections of dimethylnitrosamine or porcine serum into rats [32].
• The neu oncoprotein level in the stored serum was measured by an enzyme-linked immunosorbent assay for 27 cases of newly developed hepatocellular carcinoma (HCC), 12 liver cirrhosis cases, and 40 healthy controls [33].
• By the radioimmunoassay for the KM-2 antigen, the antigen was detected in sera of 72 (47%) of 154 patients with HCC and 3 (3%) of 102 patients with liver cirrhosis; it was not detected in 96 patients with chronic hepatitis or in 100 healthy control individuals [34].
• Plasma levels of pipecolic acid, which is a minor metabolite of lysine, were determined by high-performance liquid chromatography in 22 patients with chronic liver disease, composed of 6 patients with chronic active hepatitis, 11 with liver cirrhosis and 5 with hepatocellular carcinoma [35].

References