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 in situ distribution patterns of intercellular adhesion molecule-1 and human leukocyte antigen-DR antigens were studied in serial sections of 61 liver biopsy specimens from patients with hepatitis B virus infection using immunohistochemical techniques. In addition, the topographical relationship between the display of HBcAg on one hand and the expression of intercellular adhesion molecule-1 by hepatocytes on the other was analyzed with a double-staining immunohistochemical procedure in 14 selected liver biopsy samples showing chronic persistent or chronic active hepatitis and signs of active hepatitis B virus replication as reflected by the presence of variable amounts of HBcAg in a nuclear or cytoplasmic pattern of immunoreactivity. Coexpression of intercellular adhesion molecule-1 and human leukocyte antigen-DR antigens by hepatocytes correlated positively with the site and extent of the inflammatory infiltrate, which was composed of lymphocytes expressing lymphocyte function-associated antigen-1. In healthy HBsAg-positive carriers without inflammatory liver disease, no intercellular adhesion molecule-1 or human leukocyte antigen-DR expression was found on hepatocytes; in acute hepatitis, intercellular adhesion molecule-1 and human leukocyte antigen-DR were strongly expressed throughout the liver parenchyma on liver cell membranes and on sinusoidal lining cells. In chronic persistent and chronic active hepatitis and in active cirrhosis, intercellular adhesion molecule-1 and human leukocyte antigen-DR showed membranous positivity on focal clusters of hepatocytes in areas of periportal or intraacinar inflammation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatic expression of intercellular adhesion molecule-1 (ICAM-1) in viral hepatitis B. 197 79

To investigate the incidence, determinants and significance of delayed clearance of serum HBsAg in chronic hepatitis B virus infection, a prospective follow-up study was conducted in two consecutive groups of patients. Group I consisted of 984 patients (859 men and 125 women) with biopsy-proven chronic type B hepatitis, whereas group II consisted of 1,598 asymptomatic chronic carriers (998 men and 600 women) with normal serum aminotransferase activity. During a mean follow-up period of 4.0 +/- 2.3 yr, 19 patients (1.9%) of group I cleared HBsAg from their serum, whereas 35 patients (2.2%) in group II did so in a mean follow-up period of 2.7 +/- 1.4 yr. The annual incidence of delayed serum HBsAg clearance was 0.5% in group I and 0.8% in group II (p less than 0.02). The cumulative probability of HBsAg clearance was also higher in group II than in group I (p less than 0.007). Antibodies to HBsAg developed in 9 patients (47.4%) with chronic hepatitis and in 11 (31.4%) asymptomatic carriers who cleared serum HBsAg. Those who were HBeAg negative and those older than 40 at entry and those who exhibited cirrhosis during follow-up had a higher incidence of delayed HBsAg clearance. Gender, initial histological changes and hepatitis delta virus infection did not influence the occurrence of HBsAg clearance. Serum HBV DNA was not detectable by slot-blot hybridization but was still detectable by polymerase chain reaction in serum specimens collected within 1 yr of HBsAg clearance. Liver biopsy performed later in 10 patients showed no significant hepatitis activity or tissue HBV DNA, HBsAg or HBcAg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Incidence, determinants and significance of delayed clearance of serum HBsAg in chronic hepatitis B virus infection: a prospective study. 201 Jan 57

Thyroid dysfunction has long been reported in patients with liver disease, but limited information is available on thyroid gland size in cirrhosis. Most studies were carried out on small, selected series of patients, and no study has measured thyroid volume in relation to the etiology of liver disease. Thyroid volume was measured at ultrasound in 118 consecutive patients with cirrhosis of different etiology and 48 healthy subjects matched for age and sex. No subjects had evidence of overt thyroid disease. The mean volume was increased by 17% (from 16.0 [SD 5.2] ml in controls to 18.8 [7.6] in cirrhosis; P less than 0.025), and thyroid enlargement (antero-posterior diameter greater than 20 mm) was present in 38% of cases, in the presence of hormone values indicative of low-T3 syndrome. No significant differences in thyroid gland size were observed in relation to the extent of liver dysfunction or to the etiology of liver disease. The prevalence of thyroid nodules was similar in controls and in patients with cirrhosis. In only 8% of cases were laboratory values indicative of hypothyroidism, with low free triiodothyronine and raised thyroid-stimulating hormone levels; in these patients thyroid volume was decreased on average by 26%. This was mainly the case with patients with primary biliary and alcoholic cirrhosis. The largest mean thyroid volume was observed in patients with HBsAg + ve postnecrotic cirrhosis, whose thyroid volume was increased on average by 37%, and 53% of subjects had thyroid enlargement. This finding raises the question of a possible direct involvement of the thyroid in hepatitis B virus infection.
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PMID:Thyroid gland size and function in patients with cirrhosis of the liver. 205 4

It has recently been suggested that the hepatitis C virus may play a significant role in chronic liver diseases, such as autoimmune chronic active hepatitis, which are usually attributed to non-viral causes. We tested for antibodies to hepatitis C virus (anti-HCV) in sera from 140 patients with well characterised "non-viral" chronic liver diseases as well as sera from 51 patients thought to have chronic non-A, non-B (NANB) hepatitis (acting as positive controls) and 25 patients with non-hepatic autoimmune disorders. As expected, 45 of 51 patients (88%) diagnosed as having chronic NANB hepatitis were anti-HCV seropositive. Among 26 patients with cryptogenic cirrhosis, 8 were anti-HCV seropositive; in 5 patients (22%) there was no apparent risk factor for parenteral transmission. In the remaining 114 patients with chronic liver disease, 10 patients (9%) were seropositive for anti-HCV. However, 5 of these patients had a significant risk factor for parenteral transmission of hepatitis C virus, leaving only 5 of 106 (4.7%) with unexplained positive anti-HCV test results. Among patients with high titres of circulating autoantibodies but no liver disease, no positive results occurred. It is concluded that hepatitis C virus infection may account for some cases of cryptogenic cirrhosis. Although anti-HCV occurs more commonly in patients with other "non-viral" chronic liver diseases than has been reported in the community (0.5%-1.2%), the low prevalence of the antibodies indicates that hepatitis C virus infection is unlikely to be important in the aetiology or pathogenesis of autoimmune chronic active hepatitis and other poorly understood chronic liver diseases.
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PMID:Does hepatitis C virus play a role in "non-viral" chronic liver disease? 211 23

Case-control studies were initiated to investigate possible risk factors (life style, etc.) for hepatocellular carcinoma (HCC) and liver cirrhosis (LC). One hundred and fifty-four patients with HCC and 97 patients with LC who had no evidence of HCC were compared with frequency-matched 298 control subjects. Chronic hepatitis B virus infection and histories of blood transfusion and familial liver diseases were highly and significantly associated with both HCC and LC. Heavy drinkers in their younger years showed about 2 to 3 times risk increase for HCC or LC as compared with non-drinkers. Smoking was suspected as a risk factor, but a dose-response relationship was not clear, and further investigations are needed. To study the factors in the development of HCC from LC, 120 HCC patients with LC were compared with LC patients. No significant factors were observed. Ex-drinkers among LC patients experienced a slightly decreased risk for HCC in contrast to some belief that ex-drinkers with LC have higher risk for HCC.
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PMID:[Case-control studies of hepatocellular carcinoma and liver cirrhosis in relation to life style and other risk factors]. 215 92

As part of a larger study designed to investigate the interaction of factors such as cirrhosis and hepatitis B virus infection as aetiological agents in the development of hepatocellular carcinoma, we investigated the status of hepatic HBV-DNA sequences in 156 cirrhotic patients. Forty-one were HBsAg seropositive and 18 (44%) of these had HBV-DNA sequences detectable in their livers. There are also 26 subjects who showed markers of a previous HBV infection (anti-HBs/anti-HBc), only one (4%) of whom had demonstrable hepatic HBV-DNA sequences. No sequences were found in any of the remaining 89 patients who were seronegative for all markers. Thus, liver HBV-DNA was only detected in the presence of a serum marker, usually HBsAg.
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PMID:Frequency of hepatic HBV-DNA in patients with cirrhosis and hepatocellular carcinoma: relation to serum HBV markers. 216 37

Two major aetiological factors have been definitively incriminated in the pathogenesis of HCC: these are chronic hepatitis and hepatic cirrhosis. Chronic infection with hepatotropic viruses may account for the majority of cases of hepatocellular carcinoma in high incidence areas, and a varying prevalence of human hepatitis B and hepatitis C virus infection appears to determine the differing geographical prevalence of hepatocellular carcinoma in high and low incidence areas of the world. Patients with advanced hepatocellular carcinoma have a grave prognosis. However, at-risk groups have been characterized, and recent advances in hepatic imaging and tumour marker testing have made screening for asymptomatic primary liver cancer feasible. It it not clear, however, whether screening for small hepatocellular carcinoma improves the prognosis. Lipiodol has been shown to serve as a useful vehicle for diagnosis of small, centimetre sized nodules of tumour, and for delivery of cancer chemotherapeutic or radioactive agents to HCC. The combination of early diagnosis, and coupled medical and surgical treatments including targeted lipiodol or monoclonal antibody conjugates and hepatic resection or transplantation may lead to an improved outlook for viral-associated hepatocellular carcinoma.
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PMID:Hepatocellular carcinoma associated with chronic viral hepatitis. Aetiology, diagnosis and treatment. 216 44

The influence of hepatitis B virus infection, alcohol consumption, tobacco smoking and use of oral contraceptives on the risk of hepatocellular carcinoma (HCC) was evaluated in a hospital-based case-control study in Catalonia, in the Mediterranean coastal area of north-eastern Spain. A total of 96 HCC cases (86.5% of them with associated liver cirrhosis) and 190 age- and sex-matched controls were studied. The odds ratio of HCC and 95% confidence interval among hepatitis B surface antigen (HBsAg) carriers was 4.9 (1.3-21.9). The OR was not significantly elevated in smokers, and a marginally significant increased risk was found among users of oral contraceptives based on 6 female cases. There was a significant dose-response relationship between alcohol consumption and risk of HCC (chi 2 for trend: 24.3, p less than 0.001). Although hepatitis B infection was strongly associated with HCC, alcohol abuse leading to cirrhosis appears to be one of the main causes of HCC in this region.
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PMID:Risk factors for hepatocellular carcinoma in Catalonia, Spain. 216 42

To clarify the role of hepatitis B virus infection in HBsAg-seronegative patients with chronic liver disease and hepatocellular carcinoma in Taiwan, we examined the hepatitis B virus DNA in liver biopsy tissues of 112 patients by Southern blot analysis. The patients studied included 43 patients with nonalcoholic chronic liver disease, 21 patients with hepatocellular carcinoma and 48 control patients with other hepatobiliary and gastrointestinal diseases. To confirm the specificity of the intrahepatic hepatitis B virus DNA signal and to understand the structure of the integrated viral sequences, molecular cloning and DNA sequencing of an integrated hepatitis B virus DNA were done in one patient. Among 13 patients without serological evidence of previous hepatitis B virus infection, no hepatitis B virus sequences were found in the liver. In other HBsAg-negative patients with evidence of previous hepatitis B virus exposure, a substantial positive rate of intrahepatic hepatitis B virus DNA was found (7%). The intrahepatic hepatitis B virus DNA was all in integrated form. The positive rate among patients with nonalcoholic chronic hepatitis and cirrhosis (2%) was not different from that of the control group with other hepatobiliary and gastrointestinal diseases (4%). However, the positive rate of integrated hepatitis B virus DNA between hepatocellular carcinoma patients and nonhepatocellular carcinoma patients was statistically significant (19% vs. 3%, p less than 0.05). Molecular cloning and sequencing of a 3.0 kb EcoRI fragment of an integrated hepatitis B virus DNA from an anti-HBs-positive patient revealed that it was a partial copy of the hepatitis B virus genome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Identification and characterization of intrahepatic hepatitis B virus DNA in HBsAg-seronegative patients with chronic liver disease and hepatocellular carcinoma in Taiwan. 216 54

To clarify the relationship between hepatitis C virus infection and the development of hepatocellular carcinoma as sequelae of non-A, non-B posttransfusion hepatitis, 231 patients with chronic non-A, non-B hepatitis (96 with chronic hepatitis, 81 with cirrhosis and 54 with hepatocellular carcinoma) were analyzed for antibody to hepatitis C virus and were compared with 125 patients with chronic hepatitis B (50 with chronic hepatitis, 46 with cirrhosis and 29 with hepatocellular carcinoma). Antibody to hepatitis C virus was detected in 89.6%, 86.4% and 94.4% of patients with non-A, non-B hepatitis-related chronic hepatitis, cirrhosis and hepatocellular carcinoma, respectively, compared with 6%, 17.4% and 34.5% with similar diseases related to hepatitis B. A history of transfusion was documented in 52%, 33% and 42% of anti-hepatitis C virus-positive cases of chronic hepatitis, cirrhosis and hepatocellular carcinoma. The mean intervals between the date of transfusion and the date of diagnosis of anti-hepatitis C virus-positive chronic hepatitis, cirrhosis and hepatocellular carcinoma were 10, 21.2 and 29 yr, respectively. In 21 patients with transfusion-associated hepatocellular carcinoma, anti-hepatitis C virus was present in each serial sample available for testing, including samples obtained up to 14 yr before the diagnosis of hepatocellular carcinoma. These data suggest the slow, sequential progression from acute hepatitis C virus-related non-A, non-B hepatitis through chronic hepatitis and cirrhosis to hepatocellular carcinoma and support a causal association between hepatitis C virus and hepatocellular carcinoma.
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PMID:Interrelationship of blood transfusion, non-A, non-B hepatitis and hepatocellular carcinoma: analysis by detection of antibody to hepatitis C virus. 217 Feb 65


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