Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum levels of circulating intercellular adhesion molecule-1 (cICAM-1) were measured in 23 patients with chronic hepatitis (CH), 22 with liver cirrhosis (LC) and 45 with hepatocellular carcinoma (HCC) using an ELISA. Serum samples from all patients showed significantly higher cICAM-1 levels than serum from 50 normal controls. The cICAM-1 level was significantly increased in LC or HCC when compared with CH, but no differences were noted between LC and HCC. Levels of cICAM-1 correlated well with serum bilirubin, retention rate of indocyanine green, hyaluronic acid, type IV collagen 7-S and type III procollagen peptide levels but not with tumor size or circulating tumor markers (alpha-fetoprotein and des-gamma-carboxyprothrombin). Our findings indicate that the measurement of cICAM-1 is useful for the determination of the severity of liver disease and hepatic fibrosis. HCC tissues obtained from 10 patients were immunohistochemically stained for ICAM-1. Enhanced ICAM-1 expression was found on the tumor cell membranes. Sequential measurements of cICAM-1 levels showed that they changed in a similar manner to those of alpha-fetoprotein during the course of treatment of HCC in a patient with very high pretreatment levels of both markers. These results suggest that HCC cells shed ICAM-1 into the circulation. We conclude that cICAM-1 is not a diagnostic marker for HCC, but may be useful for monitoring the response to treatment.
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PMID:Detection of circulating intercellular adhesion molecule-1 in hepatocellular carcinoma. 750 59

Serum levels of soluble forms of intracellular adhesion molecule-1 (sICAM-1) and lymphocyte function-associated antigen-3 (sLFA-3) in 122 patients with chronic liver disease including hepatocellular carcinoma (HCC) were measured by enzyme-linked immunosorbent assays. Serum levels of sICAM-1 in patients with HCC were significantly higher than those of chronic hepatitis (CH) and cirrhosis. On the other hand, serum levels of sLFA-3 in patients with HCC were almost the same as those of cirrhosis. Western blot analyses showed that molecular sizes of sICAM-1 and sLFA-3 detected in the sera were 90 kd and 50 kd, respectively, indicating that both molecules include whole extracellular domains. In patients with HCC, circulating sICAM-1 levels were significantly (P < .001) correlated with tumor volume (r = .50), total bilirubin (r = .38), serum aspartate aminotransferase levels (r = .51), and gamma-globulin (r = .63). Furthermore, serum sICAM-1 levels were significantly elevated in patients with multiple HCC (tumor number > 3) or HCC with tumor embolus in the first branch or trunk of portal vein. Survival periods were analyzed in relation to serum sICAM-1 levels in patients with HCC who had been treated by transcatheter arterial chemoembolization. The HCC patients with < 1,000 ng/mL of serum ICAM-1 showed significantly (P = .0005) longer survival than those with higher levels of the molecule. The same results were obtained when only patients with moderately differentiated HCC were analyzed (P = .02). Analyses by Cox's proportional hazard model showed that sICAM-1 is a significant (P = .032) prognostic factor for patients with HCC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum concentration of intercellular adhesion molecule-1 in patients with hepatocellular carcinoma is a marker of the disease progression and prognosis. 754 36

Soluble intercellular adhesion molecule-1 (sICAM-1) is probably released from a variety of cells, including leukocytes and endothelial cells at sites of inflammation or in the circulation, and serum levels may therefore be used to give an indication of immune activation and inflammatory processes. In the present study, an ELISA was used to measure serum ICAM-1 levels in 43 patients with chronic hepatitis C and these were correlated with histological changes in the liver and the response to interferon alpha treatment. Serum ICAM-1 levels were significantly higher in patients with chronic hepatitis C infection than in normal subjects and correlated positively with the grade of histological activity, in particular the degree of portal, periportal, and lobular inflammation, but not with the presence of lymphoid aggregates. There was also a weak but significant positive correlation between sICAM-1 and serum aspartate aminotransferase activities, and sICAM-1 levels were substantially greater in patients with than those without cirrhosis. Serum ICAM-1 levels fell significantly in 11 responders out of 19 patients treated with interferon alpha, whereas levels remained unchanged in the non-responder group. sICAM-1 levels correlate with the clinical status of patients with chronic hepatitis C infection and fall with successful interferon treatment.
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PMID:Serum intercellular adhesion molecule-1 levels in chronic hepatitis C: association with disease activity and response to interferon alpha. 773 71

To study the influence of chronic hepatitis on intercellular adhesion molecule-1 serum concentration, we measured intercellular adhesion molecule-1 in the serum of 84 patients with chronic liver disease (17 chronic persistent hepatitis, 42 chronic active hepatitis and 25 active cirrhosis) caused by hepatitis B virus (n = 46), hepatitis C virus (n = 10) and autoimmunity (n = 28). Furthermore, 20 patients with acute viral hepatitis (16 hepatitis B virus and 4 hepatitis A virus) and 6 patients with acute drug-induced hepatitis were included. Sera from 20 healthy persons were used as control. Follow-up examinations were performed during immunosuppressive therapy in 20 patients with autoimmune chronic liver disease (13 chronic active hepatitis and 7 active cirrhosis). Intercellular adhesion molecule-1 serum concentration was significantly increased in patients with acute viral hepatitis, drug-induced hepatitis, chronic active hepatitis and active cirrhosis compared with healthy controls and with patients with chronic persistent hepatitis. Intercellular adhesion molecule-1 was also significantly increased in severe chronic active hepatitis and active cirrhosis compared with moderate chronic active hepatitis and moderate active cirrhosis. Serum concentration of intercellular adhesion molecule-1 decreased significantly in patients with autoimmune chronic liver disease after 2 mo of immunosuppression when remission was present. A close correlation between aspartate aminotransferase and intercellular adhesion molecule-1 serum levels was found. We conclude the following: (a) in chronic liver disease intercellular adhesion molecule-1 serum concentration may represent, at least in part, hepatocellular damage; and (b) intercellular adhesion molecule-1 serum level does not differentiate between chronic autoimmune and chronic viral hepatitis.
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PMID:Intercellular adhesion molecule-1 concentration in sera of patients with acute and chronic liver disease: relationship to disease activity and cirrhosis. 810 56

Sialyl-Lewisa antigen (SLe(a)), the immune determinant of carbohydrate antigen 19-9 (CA 19-9), is the ligand of E-selectin. To verify the possibility of an association between nonspecific elevation of CA 19-9 and adhesion molecules, sera from 12 patients with acute hepatitis, 55 with non-cirrhotic chronic liver disease, 33 with cirrhosis and 25 with hepatocellular carcinoma, were tested for common liver function tests. Besides, CA 19-9 and soluble forms of E-selectin, VCAM-1 and ICAM-1 were measured immunoenzymatically. One-way analysis of variance demonstrated that mean CA 19-9 concentration differed among groups (F 15.27, P < 0.0001) with the highest values found in patients with acute hepatitis. By univariate analysis, the strongest correlation of CA 19-9 was with soluble ICAM-1, which by stepwise multiple regression analysis was the only independent predictor of elevated CA 19-9 (multiple R 0.560). The association between ICAM-1 and CA 19-9 might originate in the biliary cells where they might be simultaneously overexpressed during inflammatory processes.
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PMID:Non-specific increase of serum carbohydrate antigen 19-9 in patients with liver disease associated with increased circulating levels of adhesion molecules. 874 11

Soluble intercellular adhesion molecule-1(ICAM-1) is probably released from a variety of cells, including leukocytes and endothelial cells at sites of inflammation or in the circulation, and serum levels may therefore be used to give an indication of immune activation and inflammatory processes. In the present study, an ELISA was used to measure serum ICAM-1 levels in forty patients with endemic chronic liver diseases and these were correlated with histological changes in the liver and with liver functions. Serum ICAM-1 levels were significantly higher in patients with chronic active liver diseases than in normal subjects and correlated positively with the grade of histological activity. Furthermore, serum levels of ICAM-1 were substantially greater in patients with cirrhosis than in those without cirrhosis. There was also a significant positive correlation between serum levels of ICAM-1 and serum alanine aminotransferase activities. It is concluded that, in chronic liver disease, intercellular adhesion molecule-1 serum concentration seems to represent hepatocellular damage. The authors suggest that serum ICAM-1 may prove worthy in the investigation, diagnosis and therapeutic monitoring of various inflammatory conditions of the liver.
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PMID:Circulating intercellular adhesion molecule-1 in endemic chronic liver diseases. 909 39

Bacterial lipopolysaccharide (LPS) stimulates Kupffer cells and participates in the pathogenesis of alcohol-induced liver injury. However, it is unknown whether LPS directly affects hepatic stellate cells (HSCs), the main fibrogenic cell type in the injured liver. This study characterizes LPS-induced signal transduction and proinflammatory gene expression in activated human HSCs. Culture-activated HSCs and HSCs isolated from patients with hepatitis C virus-induced cirrhosis express LPS-associated signaling molecules, including CD14, toll-like receptor (TLR) 4, and MD2. Stimulation of culture-activated HSCs with LPS results in a rapid and marked activation of NF-kappaB, as assessed by in vitro kinase assays for IkappaB kinase (IKK), IkappaBalpha steady-state levels, p65 nuclear translocation, NF-kappaB-dependent luciferase reporter gene assays, and electrophoretic mobility shift assays. Lipid A induces NF-kappaB activation in a similar manner. Both LPS- and lipid A-induced NF-kappaB activation is blocked by preincubation with either anti-TLR4 blocking antibody (HTA125) or Polymyxin B. Lipid A induces NF-kappaB activation in HSCs from TLR4-sufficient (C3H/OuJ) mice but not from TLR4-deficient (C3H/HeJ) mice. LPS also activates c-Jun N-terminal kinase (JNK), as assessed by in vitro kinase assays. LPS up-regulates IL-8 and MCP-1 gene expression and secretion. LPS-induced IL-8 secretion is completely inhibited by the IkappaB super repressor (Ad5IkappaB) and partially inhibited by a specific JNK inhibitor, SP600125. LPS also up-regulates cell surface expression of ICAM-1 and VCAM-1. In conclusion, human activated HSCs utilize components of TLR4 signal transduction cascade to stimulate NF-kappaB and JNK and up-regulate chemokines and adhesion molecules. Thus, HSCs are a potential mediator of LPS-induced liver injury.
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PMID:Toll-like receptor 4 mediates inflammatory signaling by bacterial lipopolysaccharide in human hepatic stellate cells. 1271 78

Individuals with chronic hepatitis C (CHC) progress to cirrhosis and hepatic cancer. Individuals with advanced CHC are coagulopathic and can manifest fibrinolysis. The coagulopathy is a consequence of hepatocytic dysfunction. The fibrinolysis represents a response to local endothelial cell injury, and is of a low-grade. Based upon this hypothesis, the effect of the infusion of recombinant human factor VIIa (rh-FVIIa) on endothelial cell inflammatory integrins and measures of endothelial stress were determined in 17 individuals with advanced CHC. Immediately prior to the infusion of rh-FVIIa, the plasma levels of tissue factor (TF), Thrombomodulin (TM), human soluble ICAM-1 (hs-ICAM-1), human soluble VCAM-1 (hs-VCAM-1), human soluble L-Selectin (hs-L-Selectin), the prothrombin time and the activated partial thromboplastin time were determined. The same parameters were assayed at 5, 10, 30, 120, 240 and 360 min after infusion. TF and TM levels were very high at baseline consistent with a vascular endothelial stress response. Similarly hs-ICAM-1, hs-VCAM-1 as well as L-Selectin levels were increased. Thirty minutes after the infusion, a marked reduction in ICAM-1 and VCAM-1 and to a lesser degree L-Selectin levels was observed. This reduction persisted for 360 min. No change in measures of fibrinolysis [plasminogen activator inhibitor-1 (PAI-1), total tissue factor pathway inhibitor (t-TFPI), activated tissue factor pathway inhibitor (TFPIa), d-dimers (DD), FSP and fibrinogen levels] occurred. In addition, no change in plasma Annexin-V was observed. Based upon these data it can be concluded that: (1) rh-FVIIa corrects the coagulopathy seen in advanced CHC; (2) reduces endothelial cell injury and/or stress as evidenced by the TF, TM, hs-ICAM-1 and hs-VCAM-1 levels in plasma; (3) these changes in coagulation occurred without inducing a propagated vascular thrombosis.
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PMID:Modulation of endothelial cell inflammatory integrins and stress markers with rh-factor VIIa in patients with advanced chronic hepatitis C. 1282 99

This study was to evaluate the effects of thalidomide on expression of adhesion molecules in liver cirrhosis. The cirrhosis was induced in Wistar rats by intraperitoneal injection of CCl(4), and thalidomide (10 mg/kg/day or 100 mg/kg/day) was given by intragastric administration for 8 weeks. Liver histopathology and immunohistochemistry were significantly improved and the expressions of ICAM-1, VCAM-1, E-selectin, and TNF-alpha mRNA and protein were decreased significantly in rats treated with a high dose of thalidomide. Close positive correlation was observed in the expression of the TNF-alpha mRNA and that of ICAM-1, VCAM-1, and E-selectin mRNA, respectively. These results indicate that thalidomide exerts its effect on the downregulation of adhesion molecules via TNF-alpha signaling pathway to inhibit liver fibrosis.
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PMID:Effects of thalidomide on the expression of adhesion molecules in rat liver cirrhosis. 1704 96

Intercellular adhesion molecule-1 (ICAM-1) plays an important role in the pathogenesis of viral hepatitis B. Several inflammatory diseases are associated with distinct polymorphisms of the ICAM-1 gene. The aims of this study were to analyse the association of ICAM-1 polymorphisms G241R and K469E with susceptibility to active decompensated cirrhosis in chronic hepatitis B virus (HBV) carriers. The polymorphisms at codons G241R and K469E of ICAM-1 were analysed by sequence-specific primer polymerase chain reaction (PCR-SSP) in 572 unrelated chronic HBV carriers and 157 unrelated healthy HBV non-infected blood donors. There were significantly increased frequencies of R at codon 241 and E at codon 469 in patients with active decompensated cirrhosis (38.3% and 58.3%), compared with patients with chronic hepatitis B (CHB; 21.9% and 46.5%) and chronic asymptomatic HBV carriers (AsC; 12.6% and 40.3%). The frequencies of R241-E469 haplotype and genotypes carrying at least one R241-E469 haplotype were significantly higher in patients with active decompensated cirrhosis than those in patients with CHB (38.3% and 63.3%vs 21.9% and 36.7%), and significantly higher in patients with CHB than those in AsC (21.9% and 36.7%vs 12.6% and 23.3%). The ICAM-1 polymorphisms at codons G241R and E469K were associated with the disease susceptibility, and susceptibility to active decompensated cirrhosis is significantly increased in chronic HBV carriers carrying at least one R241-E469 haplotype.
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PMID:Susceptibility to active decompensated cirrhosis is associated with polymorphisms of intercellular adhesion molecule-1 (ICAM-1) in chronic HBV carriers. 1823 90


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