Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0239946 (liver fibrosis)
8,268 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The morphologic type of cirrhosis that is followed most frequently by hepatocellular carcinoma is posthepatitic cirrhosis. Furthermore, HB AG is detected in a high rate among cases with hepatocellular carcinoma suggesting the intimate causal relationship between hepatitis b virus and hepatocellular carcinoma. It has been considered that hepatocellular carcinoma might develop during destruction and regeneration of fully developed liver cirrhosis. However, hepatocellular carcinoma is combined with not only liver cirrhosis but also with mild liver fibrosis. An attempt was made to determine HBs Ag in the liver tissue of liver fibrosis with hepatocellular carcinoma. HBs Ag was found in non-cancerous liver tissue of 40 percent of those cases. Therefore, it may be concluded that, at least some of those fibrosis is caused by chronic viral hepatitis and hepatocellular carcinoma may develop not only on posthepatitic cirrhosis but also on chronic persistent hepatitis. This evidence also suggests the carcinogenicity of hepatitis B virus.
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PMID:Hepatocellular carcinoma and chronic persistent hepatitis. 20 57

We present pathologic findings for 52 livers (51 autopsy specimens and one wedge biopsy specimen) from patients with systemic lupus erythematosus (SLE). Hepatic congestion was the most common disease (40 livers), followed by fatty liver (38), arteritis (11), cholestasis (nine), peliosis hepatis (six), chronic persistent hepatitis (six), nonspecific reactive hepatitis (five), cholangiolitis (four), nodular regenerative hyperplasia of the liver (three), and hemangioma (three). The data obtained here suggest that arteritis of the SLE liver is more common than has been recognized previously. One patient had hepatic infarction complications induced by arteritis. On the basis of the findings in the present study and a review of the literature, we suggest that hepatic infarction resulting from arteritis is rare in SLE. On the other hand, while occurrence of nodular regenerative hyperplasia of the liver in SLE patients has been considered to be rare, our findings suggest that it may be more common than has been recognized previously. Although congestion and cholestasis may be acute terminal illnesses, fatty change is considered to be specific to the SLE liver. Statistical analysis indicates that exposure to a large dosage of glucocorticoids is a significant factor in the etiology of severe fatty liver. In addition, our review of Japanese autopsy registry data for 1,468 patients with SLE indicates that the incidence of chronic liver diseases in SLE autopsy cases is as follows: chronic hepatitis, 2.4%; cirrhosis, 1.1%; and liver fibrosis, 0.8%.
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PMID:The liver in systemic lupus erythematosus: pathologic analysis of 52 cases and review of Japanese Autopsy Registry Data. 139 43

Liver fibrosis determines the course and prognosis of chronic liver disease. Histological examination of liver biopsy is essential for diagnosing hepatic disease. Evaluation of serum concentration procollagen III peptides (sPIIIP) by radioimmunoassay (RIA) is a biochemical test useful for evaluating a fibrotic process. We have investigated 20 healthy subjects and 50 patients with chronic liver disease, histologically diagnosed by percutaneous liver biopsy: steatosis (8), fibrosteatosis (7), chronic persistent hepatitis (10), chronic active hepatitis (7), cirrhosis (18). SPIIIP levels were increased in patients with cirrhosis and chronic active hepatitis and in these groups of patients such levels were well correlated with histological activity of hepatic disease. Evaluation of serum concentration of PIIIP by RIA seems to be a useful test for evaluating a fibrotic process in chronic liver diseases evolving towards cirrhosis.
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PMID:[Determination of serum procollagen-III peptide in chronic liver diseases. Clinical usefulness]. 146 42

We evaluated the prevalence of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection in 78 Italian patients with hereditary hemochromatosis as well as the relation between HCV antibody (anti-HCV) status, hepatitis B surface antigen (HBsAg) and liver histology. None of the patients had been transfused or ever consumed more than 60 g of alcohol per day. Eighteen showed histological signs of chronic hepatitis, active cirrhosis was present in 12, chronic active hepatitis in 4 and chronic persistent hepatitis in 2. Liver fibrosis or cirrhosis without inflammatory activity was observed in 31 subjects, whereas liver histology was normal except for iron overload in 18. The prevalence of HBsAg in the whole series was 5% and of anti-HCV was 20.5%. The prevalence of HBsAg and anti-HCV was significantly higher in the chronic hepatitis group than in the fibrosis/cirrhosis (p = 0.01) and the normal groups (p < 0.01). Fourteen of 18 hereditary hemochromatosis patients with chronic hepatitis were HBsAg (4) or anti-HCV (10) positive and all the latter subgroup had HCV-RNA in their serum as shown by the polymerase chain reaction. Although most of the patients with associated chronic hepatitis had cirrhosis, their serum ferritin levels and amount of mobilizable iron were significantly lower than those of the fibrosis/cirrhosis group (p < 0.01). This indicates that hepatitis viral infection acts synergistically with iron in accelerating the development of liver damage.
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PMID:Liver damage in Italian patients with hereditary hemochromatosis is highly influenced by hepatitis B and C virus infection. 148 15

Lysyl oxidase was partially purified from serum by a diethylaminoethyl batch procedure in the presence of 6 mol/L urea and dialyzed against 3 mol/L KSCN. Using this method, we determined serum lysyl oxidase activity in 52 patients with liver disease and in 14 healthy controls, and we examined usefulness of serum lysyl oxidase in assessing liver fibrogenesis. For this purpose, serum lysyl oxidase activity in chronic liver disease was compared with serum levels of prolyl hydroxylase and laminin P1. As compared with controls, serum lysyl oxidase activity increased 1.6-fold in chronic persistent hepatitis, 4.4-fold in chronic active hepatitis and 11.8-fold in cirrhosis, indicating an increase in concert with the development of liver fibrosis. In hepatocellular carcinoma, the serum activity, although significantly increased, was lower than that in cirrhosis. Serum prolyl hydroxylase was significantly increased in chronic active hepatitis, in liver cirrhosis and in hepatocellular carcinoma. Serum laminin P1 was significantly increased in chronic active hepatitis, in cirrhosis and in hepatocellular carcinoma. Serum lysyl oxidase activity did not correlate significantly with serum levels of prolyl hydroxylase and laminin P1 in any subject or in any subgroup. The magnitude of the increase and the abnormal percentage of serum lysyl oxidase activity were larger than those for serum prolyl hydroxylase and laminin P1. These results suggest that serum lysyl oxidase activity is a more sensitive indicator of liver fibrosis than serum prolyl hydroxylase and laminin P1.
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PMID:Serum lysyl oxidase activity in chronic liver disease in comparison with serum levels of prolyl hydroxylase and laminin. 168 40

To assess the significance of serum basement membrane- and type III procollagen-related antigens in reflecting the degree of liver fibrosis, we measured radioimmunologically the concentrations of 7S collagen, laminin fragment P1, and the aminoterminal propeptide of type III procollagen (P-III-P) in serum from 48 patients with chronic viral liver disease: chronic persistent hepatitis (9), chronic active hepatitis (13), chronic active hepatitis with lobular disorganization (17), and liver cirrhosis (9). Concentrations of 7S collagen, laminin P1, and P-III-P in serum were increased in respectively 92%, 69%, and 77% of the patients with both chronic active hepatitis with lobular disorganization and liver cirrhosis. Concentrations of 7S collagen and laminin P1 in serum correlated well (r = 0.65, P less than 0.001, and r = 0.55, P less than 0.001, respectively) with the histological grade of liver fibrosis, whereas P-III-P correlated only weakly (r = 0.33, P less than 0.05). Evidently, measurement of serum 7S collagen is a reliable noninvasive test for detection of fibrosis in chronic viral liver disease.
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PMID:Basement membrane-related and type III procollagen-related antigens in serum of patients with chronic viral liver disease. 231 Dec 24

To evaluate the diagnostic significance of the collagen Type III (Col 1-3) N-terminal propeptide of procollagen Type III, with respect to activity and degree of liver fibrosis, Col 1-3 serum concentrations were measured in 111 patients with chronic liver diseases and in 60 patients were correlated with liver histology and morphometry. Col 1-3 was measured by a specific radioimmunoassay. Biopsies were read without knowledge of diagnosis. Periportal and intralobular lesions were assessed semiquantitatively by allocating 1 of 4 severity grades to each parameter. All portal areas were measured morphometrically. Compared to 27 normal controls, Col 1-3 concentrations were significantly elevated in patients with untreated chronic active hepatitis, cirrhosis and primary biliary cirrhosis, but not in chronic persistent hepatitis or fatty liver. Morphometrically measured portal tract area significantly correlated with Col 1-3 plasma levels. Among the semiquantitatively measured periportal lesions, the number of fibroblasts exhibited the closest relationship with Col 1-3 levels; there was no relationship between Col 1-3 levels and intralobular lesions. These data suggest that Col 1-3 serum levels reliably reflect the activity and degree of liver fibrosis and are useful along with liver biopsy in follow-up of patients with chronic liver disease.
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PMID:The N-terminal propeptide of collagen type III in serum reflects activity and degree of fibrosis in patients with chronic liver disease. 647 51

To evaluate the diagnostic and prognostic significance of the N-terminal propeptide of collagen Type III (Col 1-3) in chronic liver disease, the peptide level was measured in the serum of 4 patients with primary biliary cirrhosis, 5 with chronic persistent hepatitis, 12 with chronic active hepatitis, and 1 with autoimmune hepatitis, for a period of 2 to 10 years and compared with liver function and histology. In primary biliary cirrhosis, Col 1-3 peptide levels were always elevated, regardless of medical therapy; however, after liver transplantation in one patient, the Col 1-3 peptide level decreased. In chronic persistent hepatitis, the peptide level fluctuated around the upper limit of normal. Among patients with chronic active hepatitis, the Col 1-3 peptide level normalized in 2 patients during remission, but was elevated in 7 patients who developed cirrhosis. Only in a patient with autoimmune hepatitis was the Col 1-3 peptide level normal, although the patient developed cirrhosis during prednisone therapy. When prednisone was withdrawn, the Col 1-3 peptide level increased. The data suggest that the serum Col 1-3 peptide may estimate the course of liver fibrosis in chronic liver disease and has prognostic value, particularly in chronic active hepatitis. Persistent elevation suggests ongoing fibrosis and development of cirrhosis; normalization suggests remission.
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PMID:Long-term follow-up of serum N-terminal propeptide of collagen type III levels in patients with chronic liver disease. 647 52

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

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


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