Disease relevance of Liver Diseases

• Chronically infected patients with active liver disease carry a high risk of developing cirrhosis and hepatocellular carcinoma [1].
• METHODS: With the polymerase chain reaction, we searched for HBV DNA in liver and serum samples from 200 HBsAg-negative patients with hepatitis C virus (HCV)-related liver disease (147 with chronic hepatitis, 48 with cirrhosis, and 5 with minimal histologic changes) [2].
• We made direct noninvasive magnetic measurements of hepatic iron stores with a specially designed superconducting quantum-interference-device (SQUID) susceptometer in 20 normal subjects and in 110 patients with liver disease, iron deficiency, hereditary hemochromatosis, or transfusional iron overload [3].
• Plasma endothelin immunoreactivity in liver disease and the hepatorenal syndrome [4].
• The progressive familial intrahepatic cholestases (PFIC) are a group of inherited disorders with severe cholestatic liver disease from early infancy [5].

Psychiatry related information on Liver Diseases

• Visual event-related P300 potentials, conventional visual evoked potentials, and psychometric tests were applied to patients with noncirrhotic chronic liver disease and to clinically nonencephalopathic and encephalopathic cirrhotics to compare their diagnostic efficacy in detecting early portosystemic encephalopathy (PSE) [6].
• An increase in GGT concentration has been regarded as a marker of alcohol consumption or liver disease [7].
• Modest weight loss and physical activity in overweight patients with chronic liver disease results in sustained improvements in alanine aminotransferase, fasting insulin, and quality of life [8].
• The whole-body BMC status of 106 children with various diseases (42 cystic fibrosis [CF], 29 juvenile dermatomyositis [JDM], 15 liver disease [LD], 6 Rett syndrome [RS], and 14 human immunodeficiency virus [HIV]) was evaluated [9].
• The purpose of this study was to determine the prevalence of vitamin E deficiency in adults with chronic cholestatic liver disease and to quantify the association between their psychomotor performance and vitamin E status [10].

High impact information on Liver Diseases

• Keratin 8 mutations in patients with cryptogenic liver disease [11].
• Methotrexate therapy and liver disease [12].
• Homozygous disruption of the murine mdr2 P-glycoprotein gene leads to a complete absence of phospholipid from bile and to liver disease [13].
• Conjugated estrogen for platelet dysfunction associated with liver disease [14].
• We conclude that cocaine intoxication can cause acute rhabdomyolysis with acute renal failure, severe liver dysfunction, and disseminated intravascular coagulation and that the mortality rate among patients with this syndrome is high [15].

Chemical compound and disease context of Liver Diseases

• Peptic ulcer, prednisone and serum gastrin in chronic active liver disease [16].
• A total of 230 patients (90 percent with alcoholism and 46 percent with a Child-Pugh grade C classification) with large esophageal varices without previous bleeding were randomly assigned to receive either propranolol (n = 118) or placebo (n = 112), after they had been divided into two groups according to the severity of their liver disease [17].
• In 25 patients in whom one or more of the conventional tests for liver disease showed abnormal results, fasting-state levels of conjugated cholic acid were increased in 20, but plasma disappearance of cholyglycine was delayed in all [18].
• Patients with other liver diseases and persons recently exposed to halothane without adverse effects did not differ from healthy controls [19].
• These results indicate that liver disease is prenatal in hereditary tyrosinemia and that therapy aimed at reduction of the elevated tyrosine level is unlikely to be of fundamental value [20].
• This review outlines recent findings on the progression of liver disease, including our knowledge of the role of apoptotic processes, with an emphasis on the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) [21].
• Factors independently associated with liver disease at baseline were history of meconium ileus, pancreatic insufficiency, chronic colonization with Burkholderia cepacia and the number of IV antibiotic courses per year [22].

Biological context of Liver Diseases

• The CD95 system mediates apoptosis and has been demonstrated to be involved in liver disease [23].
• Transgene expression resulted in obstruction of NF-kappaB activation, yet produced no signs of liver dysfunction, even when implemented over 15 months [24].
• We conclude that the neonatal lethal and liver dysfunction phenotype of the alf/hsdr-1 deletion is entirely attributable to loss of Fah [25].
• We examined SOCS1 gene methylation in >200 patients with chronic liver disease and found that the severity of liver fibrosis is strongly correlated with SOCS1 gene methylation [26].
• In addition, dysfunction of the ASGR or altered N-linked glycosylation, but not O-glycans, that affects recognition by this receptor may account for the elevated serum IgA seen in liver disease and IgA nephropathy [27].

Anatomical context of Liver Diseases

• Liver repopulation with bone marrow-derived hepatocytes (BMHs) can cure the genetic liver disease fumarylacetoacetate hydrolase (Fah) deficiency [28].
• Localization of T and B cells and alpha fetoprotein in hepatic biopsies from patients with liver disease [29].
• Erythrocyte porphobilinogen deaminase activity in liver disease [30].
• Manganese deposition in basal ganglia structures results from both portal-systemic shunting and liver dysfunction [31].
• CONCLUSIONS: Severe liver disease is characterized by significant reductions in body fat and body cell mass, most class A patients have a significant reduction in some nutritional compartments, and the pattern of tissue loss may reflect mechanisms of tissue wasting [32].

Gene context of Liver Diseases

• On the other hand, PXR agonists may prove useful in the treatment of diseases in which toxic metabolites accumulate, such as cholestatic liver disease [33].
• In man, genetically determined FAH deficiency is the primary defect in tyrosinemia type I, a fatal liver disease of infants [34].
• Mice homozygous for the c14CoS albino deletion die as neonates as a result of liver dysfunction [25].
• These studies indicate that MCP-1 secreted by FSC is stimulated by proinflammatory cytokines and that MCP-1 gene expression is upregulated in chronic inflammatory liver disease [35].
• Ctsb inhibition may be therapeutic in liver diseases [36].

Analytical, diagnostic and therapeutic context of Liver Diseases

• Liver transplantation for advanced liver disease with alpha-1-antitrypsin deficiency [37].
• A bile acid tolerance test, which measures the plasma disappearance rate of injected cholyglycine by radioimmunoassay, was studied in 36 patients with biopsy-proved chronic liver disease and compared to fasting-state levels of conjugated cholic acid and other conventional liver tests [18].
• Splanchnic transplantation. An approach to the infant dependent on parenteral nutrition who develops irreversible liver disease [38].
• The hepatoprotection seen in these animal models by the synthetic FXR agonist suggests FXR agonists may be useful in the treatment of cholestatic liver disease [39].
• Cohort study of internal malignancy in genetic hemochromatosis and other chronic nonalcoholic liver diseases [40].

References