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)

The localization of hepatitis C virus-infected hepatocytes in the human liver remains unclear despite the development of a serological assay for the antibody to hepatitis C virus. We studied their localization immunohistochemically with monoclonal antibodies to core, envelope and NS3 antigens of hepatitis C virus. We examined 48 liver biopsy samples from C100-3 antibody-positive patients with chronic liver disease (chronic persistent hepatitis, 5 cases; chronic active hepatitis, 41 cases; cirrhosis, 2 cases) and 12 liver biopsy samples from C100-3 antibody-negative patients with chronic liver disease (type B chronic hepatitis, 8 cases; alcoholic liver disease, 4 cases). In the C100-3 antibody-positive group, positive immunostaining for core antigen, envelope antigen and NS3 antigen was found in 23% (11 of 48), 24% (11 of 45) and 24% (11 of 46), respectively. Negative results were obtained in the C100-3 antibody-negative group. Hepatocytes with positive staining were scattered in the lobules, and they were found in the same regions irrespective of whether the antibody to core antigen, to envelope antigen or to NS3 antigen was used. Each positive cell was strongly stained in the cytoplasm; these decorations disappeared after absorption of the primary antibody with purified antigen. mean ALT levels in the patients with positive immunostaining for core, envelope or NS3 antigen (174.8 +/- 105.7 U/L) tended to be higher than in those with negative immunostaining (142.0 +/- 93.8 U/L). On histological evaluation of liver specimens with a scoring system of the histological activity index, intralobular inflammation and fibrosis had higher scores for samples with positive rather than negative immunostaining (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunohistochemical detection of hepatitis C virus-infected hepatocytes in chronic liver disease with monoclonal antibodies to core, envelope and NS3 regions of the hepatitis C virus genome. 137 9

There was an epidemic of non-A non-B hepatitis in a small area of a town in the central part of Japan, which began with an outbreak of several patients in 1981 and then spread extensively with the result that about one third of the inhabitants showed abnormality in serum liver function tests at the health check performed in 1985. We determined histological diagnoses on that occasion for 167 individuals of the abnormal population and recently assayed antibodies against hepatitis C virus (HCV) for most of their sera left available. Histologically, chronic active hepatitis (CAH) was the major pattern, accounting for 59.3% (99 cases) of the total. Others were chronic persistent hepatitis (CPH) (13.2%), chronic lobular hepatitis (CLH) (16.2%), liver cirrhosis (LC) (6.6%) and fatty liver (4.8%). In the serological studies, the newly developed system to detect antibodies against the viral core protein p 22 was found to be much more sensitive than the conventional system to detect anti C 100-3 antibodies. By using these two methods in combination, we found that 82% were antibody-positive, indicating strong implication of HCV in this epidemic. This was further supported by direct detection of the viral genome in patients' sera by polymerase chain reaction following reverse transcription. We further found a strong correlation between the histological inflammatory activity and the antibody prevalence, since nearly all (97.6%) of the CAH cases were antibody-positive by at least either of the antibody assays, while only about 50% were positive in the less active cases such as CPH and CLH.
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PMID:Correlation between detection of anti-viral antibody and histopathological disease activity in an epidemic of hepatitis C. 138 9

1 141 serum samples from various population groups in north China were examined for C100-3Ab by ELISA. Antibody to C100-3 antigen derived from HCV genome (C100-3A) and HBsAg were measured in 438 normal population in Beijing. The C100-3Ab positive rate was 2.1% and the HBsAg positive rate was 2.5%. There is increased occurrence with age. In 649 cases of chronic liver diseases, the HBsAg positive rate was 87.1% in chronic persistent hepatitis (CPA), 88.8% in chronic active hepatitis (CAH), 64.9% in liver cirrhosis (LC) and 67.3% in hepatocellular carcinoma (HCC). The C100-3Ab positive rate was 10.5% (CPH), 12.1% (CAH), 42.6% (LC) and 38.4% (HCC). It is noteworthy that the C100-3Ab positive rate significantly increased with disease progression from CPH to CAH, LC and HCC. Prevalence of cases positive for both C100-3Ab and HBsAg was 0% in the normal population, 6.7% in CPH, 8.4% in CAH, 31.1% in LC and 28.8% in HCC. Investigation of patients with HCV infection showed that only 36.8% had blood transfusions. HCV and HBV infection may play important pathogenic roles in CPH, CAH, LC and HCC in north China.
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PMID:Preliminary report on seroepidemiology of HCV and HBV infection in northern China. 139 40

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

Lectin histochemistry revealed that Kupffer cells in the normal liver bound lectins such as Concanavalin A (Con A), Ricinus communis agglutinin (RCA) and Wheat germ agglutinin (WGA), but did not bind Peanut agglutinin (PNA), Dolichos fibflorus agglutinin (DBA), Ulex europaeus agglutinin I (UEA-I) or Soybean agglutinin (SBA). Kupffer cells in viral liver diseases, however, bound the PNA lectin and the binding was specific to Kupffer cells in liver parenchyma. Computer image analysis was performed using light micrographs of sections stained with immunoperoxidase and diaminobenzidine (DAB). The dark brown area of reaction products was detected by analyzing each color component (red, green and blue) in the picture and was expressed as the percent area in the parenchyma. Quantitative analysis revealed the percent area occupied by Kupffer cells positive for the PNA lectin was as follows: acute hepatitis, 2.83 +/- 0.74; chronic persistent hepatitis, 2.51 +/- 0.88; chronic aggressive hepatitis, activity moderate and severe, 4.71 +/- 2.23 and 3.45 +/- 1.84; and liver cirrhosis, 1.96 +/- 0.99. The percent area of Kupffer cells was significantly higher in CAH2A than that in chronic persistent hepatitis or in liver cirrhosis. These results suggest that the PNA lectin could be used as a marker for activated Kupffer cells and that activated Kupffer cells were increased in volume in chronic aggressive hepatitis.
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PMID:Quantitative analysis of activated Kupffer cells in viral hepatitis: application of computer image analysis for lectin histochemistry. 140 83

The serum cholylglycine (CG), alanine aminotransferase (ALT) and total bilirubin levels were studied in 210 patients with hepatobiliary disease and in 70 healthy subjects. Serum CG concentrations in all the hepatobiliary diseases were found to be significantly higher than those of their controls. Patients with abnormal increases in ALT and bilirubin levels also showed raised CG concentrations; however, some patients with normal ALT and bilirubin levels, still had markedly elevated CG values. Patients with hepatic cirrhosis had high serum CG levels, followed, in descending order, by chronic active hepatitis and chronic persistent hepatitis. In the cholecystitis and cholelithiasis cases, their CG levels were significantly higher than those of the controls but lower than the values in hepatic disease patients; however, more cholecystitis cases had abnormally high serum bilirubin levels than CG. The results also show that serum CG concentrations vary in the different hepatobiliary diseases, and that serial CG measurements are more sensitive than measuring ALT and bilirubin levels in the diagnosis of hepatic diseases. Serum CG can be used as an index for evaluating the activity of chronic hepatitis; it can also be employed as a diagnostic tool in cholecystitis and cholelithiasis.
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PMID:A correlative study on serum cholylglycine levels in hepatobiliary disease. 142 17

Non-A, non-B hepatitis has been diagnosed in 12 blood donors in a plasmapheresis unit. The course of the disease has been symptomatic, accompanied by jaundice, fatigue, and nausea in 8 cases, and subclinical in the remaining 4 patients. Nine patients were followed-up to 2 years and only 2 patients liver biochemical tests were normalized permanently. The biopsies performed, a year after the acute phase of hepatitis period revealed chronic active disease in patients, chronic persistent hepatitis in 2 patients, acute hepatitis in one, and normal liver in one patient. Repeated liver biopsies, performed one year later, have basically shown similar lesions except one patient in whom chronic active hepatitis progressed to incipient liver cirrhosis. No symptoms of the disease have been usually noted in patients with chronic form of the disease, and liver function tests have occasionally been normal.
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PMID:[Epidemic focus of non-A, non-B viral hepatitis in a plasmapheresis unit]. 143 24

The aim of this work was to detect, in patients with chronic hypertransaminasemia (CH), the factors associated with the changes of ALT serum levels after one year of 10 mg/Kg/die ursodeoxycholic acid (UDCA). One hundred and twenty two consecutive patients with ALT values more than twice the normal upper limit for at least six months were admitted to the study. At the liver biopsy 82 patients were affected by liver cirrhosis (LC), 7 by chronic persistent hepatitis (CPH), and 14 by chronic active hepatitis (CAH). Nineteen patients were classified as unspecified chronic liver disease (UCLD) due to biopsy refusal. Five patients (4 LC and 1 UCLD) did not finish the study. Before and after the beginning of the treatment ALT and the other routine tests of liver function were determined in serum by routine laboratory methods. In all the diagnosis a decrease of ALT was observed after one year UDCA therapy. Particularly, in cirrhotic patients a reduction of 40% in the ALT serum levels was detected (baseline m +/- ds 98 +/- 55 UI, one year transaminase decrease -39 UI with 95% C.I. -27 UI to -52 UI). Furthermore in liver cirrhosis there was an increase of serum albumin (baseline m +/- ds 3.5 +/- 0.6, one year albumin increase +0.2 gr with 95% I.C. +0.1 gr to +0.3 gr). The decrease of ALT showed an inverse association (p < 0.05) with the presence of antibodies to hepatitis C virus and with diagnosis of CAH, and a direct one with the basal values of ALT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Factors influencing the effect of ursodeoxycholic acid therapy in chronic hypertransaminasemia]. 143 11

Anti-HCV assay with ORTHO kits was done in 100 blood donors and recipients and 374 cases of viral hepatitis, including 65 cases of fulminant, subacute and chronic hepatic failure. None of the 100 blood donors and recipients showed positive anti-HCV response. Anti-HCV was positive in 7.6% of the patients with chronic persistent hepatitis, 9.7% of the patients with chronic active hepatitis and 23.1% of the patients with liver cirrhosis. High prevalence of anti-HCV was observed in subacute hepatic failure (60.8%) and chronic hepatic failure (53.9%). Fifty-two (83.9%) of 62 anti-HCV positive cases were infected concurrently with HBV. The incidence of HBV replicating marker in patients with HCV or co-infected with HBV was lower than that of those with HBV alone. It is suggested that HCV might inhibit the replication of hepatitis B virus. The mortality rate of patients with anti-HCV positive hepatic failure was higher than that of those with HBV infection. Therefore, anti-viral therapy for anti-HCV positive hepatic failure should be considered.
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PMID:Prevalence of antibodies to hepatitis C virus in Chinese patients with viral hepatitis and hepatic failure. 145 57

In order to evaluate if oral lichen planus (OLP) may be regarded as a marker of even unknown liver disease, 96 incident OLP cases were screened through anamnestic, laboratory, instrumental investigations and gastroenterology consultation. The frequency of hepatopathies was 23/96 (24%): 7 had cirrhosis, 3 had chronic active hepatitis, 2 had chronic persistent hepatitis, 10 steatosis and 1 had undetermined liver disease. Eleven of these 23 patients (48%) had unknown hepatopathies, although five of them had severe liver disorders (cirrhosis, chronic hepatitis). Forty-four of 73 patients without definite liver disorders (60%) had at least one abnormal liver parameter. This results confirm frequent association of OLP with hepatic damage and moreover it shown that OLP may be an important clinical sign of symptomless hepatopathies.
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PMID:[Oral lichen planus and liver pathology. I. The prevalence of liver damage in a case load of 96 patients with oral lichen planus]. 146 Dec 42


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