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

Clinical and experimental data show that beta-IFN enhances the effect of tamoxifen on advanced breast cancer. There is a similarity between breast and liver as far as the proliferating effect on normal and neoplastic tissue of estrogen and progestin receptors is concerned. The authors tested this pharmacological association in unresectable liver neoplasms. They considered 76 (not randomized) patients affected with HCC; 38 were treated by trans-arterial chemoembolization (TACE) and 38 to beta-INF and tamoxifen (the 2 groups were comparable according to age, sex, Child-Pugh score, Okuda and TNM stages, cirrhosis etiology). The treatment response (positive when a tumor diameter decreased or stabilization was observed) was similar in the two groups; in the TACE group, the presence of a peritumoral capsula had a significant influence on survival (p < 0.02); on the other hand, in the patients treated with beta-INF and tamoxifen important factors for a better prognosis were the TNM stage (I and II, p < 0.02) and a symptom-free condition (p < 0.04). The authors believe the beta-INF and tamoxifen treatment could represent an effective alternative in the management of unresectable HCC. A better knowledge of the presence and meaning of estrogen and progestin receptors in the neoplastic tissue may allow a better selection of patients.
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PMID:[The palliative treatment of hepatocarcinoma: chemoembolization vs. the combination of tamoxifen plus beta-interferon]. 751 97

The indication and the evaluation of IFN treatment for chronic hepatitis type C has been discussed. Good response to IFN depend on the level of HCV RNA just before the treatment. The patients who has low level of HCV RNA (less than 1 Meq/ml by DNA probe assay) could be able to estimate the response more than 80%. On the contrary, it is less than 10% for the patients with high level of HCV RNA. The evaluation of IFN treatment for chronic hepatitis were divided into 3 groups. Cure was defined as the continuous normalization of serum ALT and disappearance of HCV RNA during 12 month or more after the treatment. Partial response was defined as continuous normalization of ALT level but positive for HCV RNA. The others were defined as non responder. First and second group should be evaluated for the IFN treatment. Final purpose for IFN treatment should be prevent to develop liver cirrhosis or hepatocellular carcinoma.
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PMID:[The indication and the evaluation of IFN treatment of chronic hepatitis C]. 752 17

Possible effects of IFN and SNMC combination therapy for active liver cirrhosis were described. 28 patients with active liver cirrhosis were treated with natural IFN alpha 3-6 MU TIW for 3-17 months (mean, 8 +/- 6). 8 of 28 patients received combination therapy of SNMC (40 ml iv, TIW). 8 (29%) of 28 patients sustained normal ALT levels with no relapse (complete response) which involved 6 patients with persistent lack of serum HCV RNA sequences after IFN therapy. In those 8 patients, 4 had been received combination of SNMC. There were 4 (14%) patients with relative response. Patients with genotype III or IV had significantly higher response to IFN therapy than the patients with genotype II. In active liver cirrhosis, determination of HCV genotype and HCV RNA levels thought to be significant for the indication of IFN therapy, and that combination of SNMC may provide beneficial effect to IFN therapy for active liver cirrhosis.
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PMID:[Long-term interferon (IFN), neominophagen C (SNMC) combination therapy of active liver cirrhosis type C]. 752 34

Chronic hepatitis B virus (HBV) infection is a serious problem because of its world wide distribution and possible adverse chronic sequalae such as cirrhosis and hepatocellular carcinoma. Over the past 20 years, many antiviral or immunomodulatory agents, or both, have been used in patients with chronic HBV infection. Among immunomodulatory agents, levamisole, BCG, picibanil and interleukin-2 have been shown to be ineffective. Corticosteroid therapy is also ineffective and can cause deleterious effects in chronic HBV infection. Thymosin-alpha 1 therapy is currently in phase III clinical trial. Among antiviral agents, acyclovir, dideoxynucleosides, suramin, zidovudine and ganciclovir have been shown to be ineffective and have intolerable side effects. While adenine arabinoside (Ara-A) and its monophosphate derivative (Ara-AMP) are effective agents if the treatment course is long enough, they have been withdrawn from investigative use because of their substantial neuromuscular toxicity. Interferon-alpha may directly inhibit HBV replication and enhance hepatocyte HLA class I antigen expression with subsequent increase of T-cell mediated cytotoxicity. Randomized, controlled clinical trials have shown that 25% to 50% of adult patients with elevated alanine transaminase (ALT) levels lost HBeAg and HBV-DNA when treated with IFN-alpha at a dose of 5MU daily or 10 MU three times a week for 3 to 6 months. In view of the fact that the response rate is far from satisfactory, particularly in Asian patients, combination therapies including interferon alpha with Ara-AMP, acyclovir, didoxynucleoside or interferon-gamma have been studied. Most forms of combination therapy have been shown to be of limited effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Drug therapy in patients with chronic type B hepatitis]. 754 84

To evaluate the effect of interferon alfa (IFN-alpha) on the hepatic extracellular matrix, we investigated the changes in serum N-terminal propeptide of type III procollagen during and after 4 months of INF-alpha treatment in 178 treated and 45 nontreated patients with chronic hepatitis C. Serum pretreatment levels in nonresponders were significantly higher than those in long-term and short-term responders, but those levels were not different in the latter two groups. Serum propeptide levels decreased significantly during and after IFN-alpha therapy in the treated patients, although those levels were unchanged in the nontreated patients. This decrease was sustained for 12 months after IFN-alpha was completed not only in long-but also in short-term responders and nonresponders. Serum propeptide levels decreased in those with elevated pretreatment levels, but not in those with normal initial levels, whereas serum transaminase levels decreased similarly in both groups. The changes in serum propeptide levels during and after treatment were more closely correlated with the initial levels compared with those in serum transaminase levels. These results suggested that IFN-alpha treatment induces the long-term suppression of active fibrogenesis in chronic hepatitis C independent of antiviral and anti-necroinflammatory effects, thus preventing progression to cirrhosis.
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PMID:Long-term decrease in serum N-terminal propeptide of type III procollagen in patients with chronic hepatitis C treated with interferon alfa. 763 9

Hepatitis C virus infection is a common disease with a high propensity to progress towards chronicity. Alpha interferon has been proposed to halt progression of the disease and prevent the development of more severe liver diseases such as cirrhosis and hepatocellular carcinoma. Unfortunately, less than 20% of treated patients show a long-lasting ALT normalization and HCV-RNA negativity. Factors which might be predictive of a long term response to interferon are debated. Univariate analysis of data collected in randomized clinical studies, has shown that IFN dose, age, duration of disease, cirrhosis and early response (primary) to IFN were all predictors of a sustained response to IFN, but with differences in different studies. When data were analyzed by a multivariate analysis, short duration of the disease and absence of cirrhosis were found to predict long-term response to interferon. Finally, many evidences indicate that response rates to therapy may be better in patients with low pretreatment levels of HCV-RNA measured either by polymerase chain reaction (PCR) or the branched-DNA assay (b-DNA).
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PMID:Alpha interferon treatment of chronic hepatitis C. 764 81

Antibody against the recombinant protein Y19 deriving from non-structural region 3 (NS3) of the hepatitis C virus (HCV) genome was measured in the serum from 300 patients with nonA-nonB chronic liver disease including serial serum samples from these patients by using an enzyme linked immuno-sorbent assay. Simultaneously, antibodies to a synthetic core peptide (AR142) and the recombinant peptide of NS 3-4 region (C-100) were tested. Anti-Y19 antibody was detected in 83.3%, 65.2% and 76.6% of patients with nonA-nonB chronic hepatitis (n = 144), liver cirrhosis (n = 46) and hepatocellular carcinoma (n = 43), respectively. In sera of other chronic liver disease, the detection rate of anti-Y19 antibody was significantly low comparing to nonA-nonB chronic liver disease. Positive rates of the patients for AR142 antibody and C-100 antibody were similar to the one for Y19 antibody. Patients positive for Y19 antibody have a tendency to be positive for C-100 antibody. Serum Y19 antibody level during and after treatment with natural interferon alpha (IFN-alpha; 5MU, 24 weeks) was studied in 33 patients with chronic hepatitis C. The effectiveness of IFN therapy did not correlate with the Y19 antibody level before the treatment. In most cases Y19 antibody level decreased relating to the improvement of the serum ALT level during the treatment. Y19 antibody level declined not only during IFN treatment but after the treatment in Responder group (as assessed by normal ALT for 6 months after the treatment; n = 14). Whereas, in Non-responder group (the rest of Responder group; n = 16) Y19 antibody level was maintained to the level at the end of the treatment or elevated again to the level before the treatment. In Responder group, 6 of 7 cases in whose serum HCV-RNA disappeared at 6 months after the treatment, had decrease of Y19 antibody to less than 20% of the pretreatment level and Y19 antibody became undetectable in 4 cases at 6 months after the treatment. One case in whom Y19 antibody did not decrease by the treatment had an increase of serum ALT level and a relapse of the disease at 12 months after the treatment. 5 of 6 cases in "Responder" group that HCV-RNA remained positive had more than 20% of Y19 antibody level of the pretreatment level at 6 months after the treatment. Therefore the decrease of Y19 antibody level was closely related to the efficacy in terms of serum ALT level and HCV-RNA level.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Clinical significance of antibody to Y19 protein in nonA and nonB chronic liver disease]. 768 28

The gamma interferon (gamma-IFN) concentration and the adenosine deaminase (ADA) activity were evaluated in 30 patients with tuberculous peritonitis, 21 patients with ascites due to a malignant disorder, and 41 patients with cirrhosis. The gamma-IFN concentrations were significantly higher (p < 0.0001) in tuberculous peritonitis patients (mean: 6.70 U/ml) than in the malignant (mean: 3.10 U/ml) and cirrhotic (mean: 3.08 U/ml) groups. Use of a cut off value of > or = 3.2 U/ml gave the assay a sensitivity of 93% (25 of 27), a specificity of 98% (54 of 55), positive (P+) and negative (P-) predictive values of 96% and a test accuracy of 96%. The ADA activity was significantly (p < 0.0001) higher in the tuberculous peritonitis group (mean: 101.84 U/l) than in the control groups (cirrhosis (mean: 13.49 U/l) and malignancy (mean: 19.35 U/l)). A cut off value of > 30 U/l gave the ADA test a sensitivity of 93% (26 of 28) a specificity of 96% (51 of 53), a (P+) value of 93%, a (P-) value of 96%, and a test accuracy of 95%. There was a significant (p < 0.0001) correlation (r = 0.72) between ADA activity and gamma-IFN values in patients with tuberculous peritonitis. These results show that a high concentration of gamma-IFN in ascitic fluid is as valuable as the ADA activity in the diagnosis of tuberculous peritonitis. Both are rapid non-invasive diagnostic tests for tuberculous peritonitis.
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PMID:Ascitic fluid gamma interferon concentrations and adenosine deaminase activity in tuberculous peritonitis. 769 2

Cytokines constitute a complex network of molecules involved in the regulation of the inflammatory response and the homeostasis of organ functions. Cytokines coordinate physiologic and pathologic processes going on in the liver, such as liver growth and regeneration, inflammatory processes including viral liver disease, liver fibrosis and cirrhosis. Liver growth and regeneration are regulated by several cytokines. The platelet-derived hepatocyte growth factor, in particular, delivers a strong mitogenic stimulus for hepatocyte regeneration. The cell-mediated immune response plays a central role in hepatocellular necrosis and in the immunopathogenetic mechanisms involved in viral clearance and persistence in liver disease of viral etiology. In this context, cytokines modulate the immune system and exert direct antiviral activity by cytopathic and non-cytopathic mechanisms, as demonstrated in a transgenic mouse model. IL-6, TNF-alpha, IL-1 and IL-2 increase in acute fulminant viral hepatitis; in fact, they have pro-inflammatory and cytotoxic effects. Reduced IL-2 and IFN-alpha synthesis and increased serum levels of IL-1 and IL-2 soluble receptor (IL-2R) have been observed in HBV chronic liver disease. In HCV chronic hepatitis, IL-2R increases as well, while IFN-gamma and IL-2 decrease. In personal experimental observations, intra-hepatic messenger RNA expression of several cytokines was measured in liver specimens of patients with chronic HBV and HCV infections: patients with HCV chronic liver disease had higher levels of IL-2, IL-6, IL-10, and IFN-gamma. These data are in accordance with immunological studies showing a vigorous cell-mediated immune response in HCV chronic liver disease and a deficient immune response in HBV chronic hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cytokine mediators in acute inflammation and chronic course of viral hepatitis]. 772 1

We have demonstrated that patients with ovarian carcinoma have higher levels of soluble intercellular adhesion molecule-1 (ICAM-1) in their serum and ascitic fluids than serum from normal individuals and non-neoplastic gynaecological disease or ascites from patients with cirrhosis. In order to investigate the source of the ICAM-1, and to study the mechanisms which regulate ICAM-1 release in ovarian carcinoma, we have employed the nude mouse model system. Three different human ovarian carcinoma (HOC) cell lines were grown as ascitic tumours in the peritoneal cavity of nude mice. HOC xenografts harvested from nude mice expressed comparable levels of ICAM-1 on their cell surface. Human ICAM-1 was detected, with a species-specific ELISA, in serum and ascitic fluid of tumour-bearing mice, confirming that the tumours were the source of the ICAM-1. The three HOC xenografts showed different levels of ICAM-1 release, but within each xenograft model the level of ICAM-1 in serum and ascitic fluid correlated with the tumour burden. The level of ICAM-1 released by the HOC xenografts could be increased by in vivo treatment with interferon gamma (IFN-gamma). Interleukin 1 (IL-1), tumour necrosis factor (TNF) and IFN gamma increased the cell surface expression of ICAM-1 and caused the release of soluble ICAM-1 from HOC cells established in vitro. The nude mouse provides a useful system in which to study the effects of modulating ICAM-1 release on the progression of ovarian carcinoma and suggests that measuring ICAM-1 levels in the blood or ascites of patients may provide an indication of tumour burden.
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PMID:Soluble intercellular adhesion molecule-1 (ICAM-1) is released into the serum and ascites of human ovarian carcinoma patients and in nude mice bearing tumour xenografts. 788 Jun 19


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