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Query: UMLS:C0239946 (liver fibrosis)
 8,268 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The validity of monoamine oxidase (EC 1.4.3.4) activity in serum for the diagnosis of fibroproliferative liver disorders was assessed by measuring the specificity, sensitivity and positive and negative predictive values of the enzyme. Enzyme activity was measured in sera of 567 patients including those with biochemically and/or histologically verified non-fibrotic liver diseases (n = 64), liver fibrosis (n = 45), and liver cirrhosis (n = 51). The fraction of liver cirrhotic subjects with pathologically elevated monoamine oxidase activity (greater than 630 U/1) was 0.61, whereas only 0.16 of the cases with liver fibrosis and 0.11 of those with non-fibrotic liver diseases had abnormally high enzyme activities. Among the various categories of diseases tested, significantly increased enzyme activities were confined to liver cirrhosis and chronic active hepatitis. For liver cirrhosis, sensitivities and specificities were calculated as functions of various cut-off (critical) values of monoamine oxidase activity in serum, and with respect to a reference population of healthy men and non-cirrhotic subjects. The predictive value of the positive test result (enzyme activity higher than 720 U/1) at a prevalence of liver cirrhosis of maximum 0.033 (estimated incidence of chronic liver diseases in West Germany) is 0.68 if tested against healthy persons and less than 0.30 if tested against patients with non-liver cirrhotic diseases. It is concluded that monoamine oxidase is probably not helpful in the early diagnosis of fibroproliferative liver dysfunctions but may provide a parameter of complications of cirrhosis, e.g. portal-systemic collateral circulation (portal hypertension).
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PMID:Validity of monoamine oxidase in serum for diagnosis of liver cirrhosis: estimation of predictive values, sensitivities and specificities. 713 Sep 9

1. Activated hepatic lipocytes are central to the pathogenesis of liver fibrosis as the principal source of both interstitial collagens and matrix-degrading metalloproteinases. In progressive fibrosis there is a failure to degrade interstitial collagens with a reported decrease in collagenase activity. In these studies we investigate expression of the potent collagenase inhibitor, tissue inhibitor of metalloproteinase-1, and interstitial collagenase in end-stage autoimmune chronic active hepatitis and activated human hepatic lipocytes in culture. 2. Messenger RNA transcripts for interstitial collagenase and tissue inhibitor of metalloproteinase-1 in explanted human liver were quantified by ribonuclease protection assay and densitometric analysis. This indicated that tissue inhibitor of metalloproteinase-1 and interstitial collagenase expression in autoimmune chronic active hepatitis were also coordinately up-regulated. 3. Using Northern analysis of RNA from human lipocytes in primary culture on plastic, mRNA for interstitial collagenase could not be detected in unstimulated cells but was present after stimulation with tumour necrosis factor alpha. Tissue inhibitor of metalloproteinase-1 mRNA was present in unstimulated lipocytes and up-regulated fivefold in response to tumour necrosis factor alpha. Using activity assay of serum-free conditioned media, interstitial collagenase could not be detected in unstimulated primary cultures, primary cultures stimulated with tumour necrosis factor alpha or transforming growth factor beta-1 (n = 3 and n = 4 respectively) or in passaged lipocytes (n = 6). In contrast, free tissue inhibitor of metalloproteinase-1 activity was present in unstimulated and passaged cultures and this was increased in response to tumour necrosis factor alpha and transforming growth factor beta-1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tissue inhibitor of metalloproteinase-I and interstitial collagenase expression in autoimmune chronic active hepatitis and activated human hepatic lipocytes. 767 71

Liver fibrosis determines the course and prognosis of alcoholic liver disease. Evaluation of serum concentration of procollagen-III peptides (sPIIIP) is considered a biochemical test useful for evaluating a fibrotic process. We have investigated 30 healthy subjects and 53 patients with alcoholic liver disease, histologically diagnosed by percutaneous liver biopsy in four clusters: steatosis (11), fibrosteatosis (11), chronic active hepatitis (11) and cirrhosis (20). SPIIIP levels were increased in patients with cirrhosis and chronic active hepatitis; while they were regular in patients with steatosis and fibrosteatosis. Evaluation of serum concentration of sPIIIP by radioimmunoassay seems to be an useful test for identifying patients with alcoholic liver disease with a good prognosis and patients in progress to cirrhosis and it is an useful test for control the course and evolution of chronic liver disease.
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PMID:[The procollagen-III peptide in the clinical surveillance of alcoholic hepatopathy and other chronic hepatopathies]. 793 73

No report has been found on comparison of pre- and post-treatmental liver biopsies for chronic active hepatitis (CAH) caused liver fibrosis. The aim of this paper was to study the effects of a heavy dosage of Radix Paeoniae rubra to the reabsorptive action of liver collagen fibres. The patients were suffering from CAH or CAH with liver cirrhosis confirmed by liver biopsies. By the end of 3 months, the second liver biopsy was carried out. The results showed that among 4 patients with liver cirrhosis, the false lobules disappeared; and that 6 patients with CAH only, the interlobular collagen fibres of 4 patients were completely reabsorbed. The effective rate reached 77.8%. It was concluded that a heavy dosage of Paeonia rubra was effective in arresting the development of liver fibrosis, and in promoting the reabsorption of collagen fibres.
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PMID:[Comparison of pre- and post-treatmental hepatohistology with heavy dosage of Paeonia rubra on chronic active hepatitis caused liver fibrosis]. 795 Jan 94

Hepatic fibrogenesis is a dynamic process which characterizes the course of chronic hepatitis. It has stimulated interest in the possible effect of interferon therapy on liver fibrosis. We have evaluated a panel of serum markers of fibrogenesis, namely N-terminal procollagen III peptide (PII-INP), C-terminal procollagen I peptide (PICP), laminin and hyaluronate in 35 patients with chronic hepatitis type C, before, during and after interferon treatment. Before treatment, PIIINP was elevated in 8.5%, 44% and 71% of patients with chronic persistent hepatitis, chronic active hepatitis and cirrhosis, respectively, while the corresponding figures for PICP were 0%, 50% and 46%, and for laminin 16.5%, 70% and 71%; hyaluronate was elevated in only five out of seven patients with cirrhosis. Patients with high PIIINP levels at presentation and a persistent response to treatment showed persistent normalization of this parameter, which was not observed in non-responders. In contrast, the other markers showed no significant correlation with interferon response. These results indicate that PIIINP correlates with interferon response in chronic hepatitis type C.
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PMID:Serum markers of hepatic fibrogenesis in chronic hepatitis type C treated with alfa-2A interferon. 799 85

Serum concentrations of laminin and hyaluronate were assayed in 138 patients of liver disease with an enzymoimmunological method. There was a mild increase of hyaluronate level in patients with acute hepatitis (P < 0.05) and a significant increase of both serum laminin and hyaluronate concentrations in patients with chronic hepatic diseases, as compared with those in healthy controls (P < 0.001). Serum laminin and hyaluronate reached the highest levels in patients with liver cirrhosis. Comparing the results from a group of patients with liver cirrhosis with those from a reference group of patients with chronic active hepatitis, we obtained values for specificity, sensitivity, and diagnostic efficiency of 0.90, 0.90 and 0.90 respectively. The results suggested that quantification of serum laminin and hyaluronate may be a useful test to assess the degree of chronic liver injury and to diagnose liver fibrosis.
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PMID:[The extracellular matrix and liver disease: a study with enzymoimmunological assay]. 807 Feb 90

To examine the clinical significance of serum level of tissue inhibitor of metalloproteinases (TIMP) in chronic liver disease and in hepatocellular carcinoma, we measured serum TIMP concentration by a sandwich enzyme immunoassay in 79 patients with chronic liver disease and 49 patients with hepatocellular carcinoma. Serum TIMP concentration was 164 +/- 20 ng/ml in healthy controls, and was 10% higher than control in chronic persistent hepatitis, 36% higher in chronic active hepatitis, 62% higher in liver cirrhosis and 30% higher in primary biliary cirrhosis. Serum TIMP level was closely correlated with serum level of type IV collagen 75 domain and with the histological degree of liver fibrosis in chronic liver disease. Serum TIMP level in hepatocellular carcinoma was increased 2.3-fold compared with that in controls, and was significantly higher than in liver cirrhosis. Serum TIMP level increased with tumor size, and significantly correlated with serum alpha-fetoprotein level. Gel filtration on Sephadex G-75 showed that the TIMP in serum was present as an enzyme-complexed form. These results suggest that the measurement of serum TIMP concentration is useful in the clinical assessment of liver fibrosis in chronic liver disease and of the development of hepatocellular carcinoma.
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PMID:Serum tissue inhibitor of metalloproteinases in patients with chronic liver disease and with hepatocellular carcinoma. 829 19

Persistent hepatitis B virus (HBV) infection is epidemiologically closely associated with the development of human hepatocellular carcinoma (HCC). A molecular mechanism that would explain the strong epidemiological link of persistent HBV infection with HCCs is still open to debate. Among HBV carriers, HCC develops only in patients with chronic liver disease, such as chronic active hepatitis, liver fibrosis, or liver cirrhosis. In other words, hepatitis-related proliferative changes, which are mainly sustained by repeating cycles of cell death and regeneration either immunologically or through virus infection, appear important for HBV hepatocarcinogenesis. The same mechanism may also be present in human hepatitis C virus-related hepatocarcinogenesis. In this article, I reviewed animal models of HBV-related hepatocarcinogenesis. It is important to evaluate and check whether the animal models are fit with human HBV hepatocarcinogenesis or not.
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PMID:[Hepatitis and hepatocarcinogenesis in the transgenic mice]. 846 65

We report for the first time the measurement of the serum concentration of the carboxy-terminal cross-linked telopeptide of type I collagen in patients with various liver diseases. This breakdown product of type I collagen, which is the major collagen type found in fibrotic liver, was measured by a radioimmunoassay in the serum of 149 patients with various liver diseases and in 67 controls. Its concentration is significantly elevated (P < 0.05) above reference intervals in sera from patients with liver diseases, except in patients with chronic active hepatitis of unknown origin and in patients with acute hepatitis A. In the 143 patients with liver fibrosis, the serum level of the carboxy-terminal telopeptide of type I collagen is correlated with the extent of fibrosis, as assessed by a histological scoring system (r = 0.3899, P < 0.0001), but not with inflammation and necrosis.
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PMID:The carboxy-terminal cross-linked telopeptide of type I collagen (ICTP) is a potential serum marker of ongoing liver fibrosis. 874 May 82

Erythrocyte membrane Na+,K+: Ca2+ ATP ase activities, cholesterol (CH) phospholipid (PL) composition and erythrocyte glutathione (GSH) contents were determined in controls, in patients with chronic active hepatitis and liver cirrhosis. NA+,K+ ATP ase activities were significantly (P < 0.0001) less in patients with chronic active hepatitis and liver cirrhosis (n = 8, 0.102 +/- 0.02 mumol P/mg protein/hour; n = 8, 0.081 +/- 0.02 mumol P/mg protein/hour) than in controls (n = 10, 0.219 +/- 0.05). Histopathological analysis of liver sections obtained from patients with chronic active hepatitis (n = 3) and liver cirrhosis (n = 2) correlated well with erythrocyte biochemical findings. There was a significant negative correlation between Na+,K+ ATP ase activity and portal fibrosis (P < 0.05, r = -8680). However, further experiments performed on larger study populations are needed to better elucidate this correlation. Therefore, NA+K+ ATP ase activity measurement can be reliable assessment of liver fibrosis.
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PMID:Erythrocyte membrane Na+,K+ ATP ase activity can be a marker of liver histopathology. 895 35


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