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)

A clinical, biochemical, and pathological study was performed in 38 chronic HBsAg carriers. The study group is a part of 393 carriers found among 117 705 voluntary blood donors at the National Blood Bank, Hospital del Salvador, Santiago, Chile. None of the 38 carriers had a past history of illicit drug abuse, hepatitis, or work involving a high risk of hepatitis B virus infection. Ten individuals had a normal liver biopsy, 17 reactive non-specific hepatitis, one fatty changes, four chr onic persistent hepatitis, one aggressive hepatitis, two post-necrotic cirrhosis, and three alcoholic cirrhosis. There was not a close correlation between liver function test and liver histology. The most significant laboratory finding was the postivity of alpha fetoprotein in two cases. During the follow-up the two alpha fetoprotein patients presented a hepatocarcinoma 12 and 14 months after admission to the study.
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PMID:Clinical and pathological study of asymptomatic HBsAg carriers in Chile. 68 May 91

In order to assess the frequency of significant liver disease in hepatitis B surface antigen carriers with normal liver tests, 54 such individuals were identified and prospectively followed for 4 to 48 months with monthly liver tests. Upon testing, 4 were found to carry e antigen and 14 carried e antibody (anti-e). During follow-up, only 4 patients, none of whom were e antigen-positive, developed persisting abnormalities in liver tests. Of the 23 patients who underwent percutaneous liver biopsies, normal histologies were found in 2, nonspecific changes (ground glass hepatocytes, focal necrosis, fatty changes, etc.) in 18, and chronic persistent hepatitis (with or without other nonspecific changes) in 3. Chronic active hepatitis and/or cirrhosis, lesions which may carry more serious prognostic implications, were not seen in any biopsies. Two of the 4 e antigen-positive patients consented to biopsy, both of whom had chronic persistent hepatitis. All 6 patients with anti-e who underwent biopsy had ground glass hepatocytes, which were found in only about 50% of the remaining patients. It is concluded that hepatitis B surface antigen carriers should be followed with serial liver tests, and those whom tests remain normal should not be considered for liver biopsy.
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PMID:Hepatitis B surface antigen carriers--to biopsy or not to biopsy. 70 Mar 27

Circulating complete and defective hepatitis B virus forms, as represented by full, DNA polymerase-positive and empty, DNA polymerase-negative Dane particles, respectively, were investigated in sera from patients with chronic hepatitis B virus infection and related to the presence of e antigen and antibody and to the histological findings on liver biopsy. Complete hepatitis B virus particles were detected in the serum of all patients postive for e antigen, their percentage ranging from 15 to 61% of the total Dane particle population. Although most of these cases had chronic persistent or chronic active hepatitis, complete viral particles were also found in serum of 3 healthy carriers of hepatitis B surface antigen who had e antigen. These results indicate that e antigen is a marker of active virus replication and support its association with infectivity. It is also associated with liver damage because production of complete virus is a feature of chronic hepatitis. In the presence of anti-e, detection of Dane particles in serum appeared to be related to the histological findings. Most of the healthy carriers had no Dane particles in serum, whereas 80% of the cases with chronic liver disease had circulating Dane particles. However, in contrast to the cases with e antigen, 98 to 100% of Dane particles in these cases appeared to be defective in nucleic acid material on electron microscopy after positive staining. All of the patients with chronic active hepatitis in this group had progressed to cirrhosis and it is possible that production of complete virus particles is reduced in the later stages of the illness.
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PMID:Full and empty Dane particles in chronic hepatitis B virus infection: relation to hepatitis B e antigen and presence of liver damage. 70 Mar 29

Hepatitis type B is hyperendemic in Greenland with serologic evidence of infection in 54% of adults and a hepatitis B surface antigen (HBsAg) carrier rate of 7--25%. The impact of this infection rate on the occurrence of cirrhosis and primary liver cancer (PLC) was studied. Mortality rates for cirrhosis were obtained from official mortality statistics, 1951--1975. PLC was identified by a study of all biopsy and necropsy material taken in the study area during the same period. Neither cirrhosis nor PLC was found to be a more prevalent cause of death in this population than in Northern Europe where hepatitis B is at least 10-fold less prevalent. It is concluded that hepatitis B infection per se does not contribute significantly to the development of cirrhosis or to PLC, at least in the Eskimo population of Greenland.
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PMID:Occurrence of cirrhosis and primary liver cancer in an Eskimo population hyperendemically infected with hepatitis B virus. 70 73

Immunosuppressive treatment with prednisolone and/or azathioprine has been assessed in three chronic liver diseases with immunological features, namely chronic active hepatitis, cryptogenic cirrhosis and primary biliary cirrhosis. In chronic active hepatitis, controlled prospective clinical trials have shown clinical, biochemical and hepatic histological improvement when prednisolone with or without azathioprine is employed. Azathioprine alone has no advantage over placebo tablets. Cirrhosis is probably not prevented. Selection of patients for treatment, the response and therapeutic regimes are discussed. Patients with hepatitis B surface antigen positive chronic active hepatitis have a worse therapeutic response than those patients with chronic active hepatitis who are HBsAg negative. In primary biliary cirrhosis, corticosteroid treatment is contra-indicated on account of bone thinning. Azathioprine has been used in controlled clinical trials and is of only marginal benefit.
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PMID:Immunosuppressive therapy in chronic liver disease. 71 60

Twelve patients on haemodialysis for 6 months to 3 years contracted AgHBs positive hepatitis, 9 being also Ag e positive. They continued to carry the same antigens. Histological surveillance was begun from the 6th month of the disease onwards, with 2 to 4 repeated biopsies in 1,5 to 3,5 years in 9 patients, the last 3 having only one biopsy between the 8th and the 15th month. In 6 patients, the first biopsy revealed chronic persistent hepatitis (CPH) and in other 6 (5 male and 1 female) chronic aggressive hepatitis (CAH). Subsequent biopsies revealed cirrhosis in a patient treated with alphamethyldopa (Ag e +), the absence of any changes in 7 other patients (4 CPH including 3 Ag e + and 3 CAH including 2 Ag e +), and an improvement in the last. Long term surveillance of hepatitis B by repeated biopsies in haemodialysed patients reveals that histological lesions are stable at 2 years, that certain drugs may have an aggravating role and that Ag e has no prognostic value.
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PMID:[B virus chronic hepatitis in the haemodialysed uraemic patient. Correlation between hepatic lesions and the presence of antigen e in 12 patients (author's transl)]. 71 64

Sera of 184 patients were examined to determine the incidence of hepatitis B surface antigen (HBsAg). Ninety-two patients had primary liver cancer (PLC) and there were 92 matched controls. Thirty-one of the 92 patients with PLC and 8 of the 92 patients with no clinical evidence of liver disease had radio-immunoassay-positive tests for HBsAg. The difference was significant (P less than 0,01). In 56 of the patients with PLC it was possible to assess the nature of associated liver disease histologically. HBsAg was found in the sera of 66,6% of patients with postcollapse cirrhosis and in 22,2% of patients with chronic Budd-Chiari syndrome. It is likely that the role played by hepatitis B infection in the pathogenesis of PLC varies according to local circumstances in different geographical areas.
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PMID:Hepatitis B surface antigen and primary liver cancer. 71 32

329 patients with acute ouvert viral hepatitis which occurred in the Hannover area 1975 were classified according to virological data. The proportions of type A and type non A - non B hepatitis were each approximately 20 percent of the total cases (n = 60). Viral hepatitis B was the most frequent type of viral hepatitis (n = 209). 174 individuals of the 329 hepatitis patients were reexamined serologically two years after the onset of the acute disease. 7 out of 105 patients with hepatitis B (6,7%) and 5 out of 40 patients with hepatitis non A - non B (12,5%) revealed a serological pattern compatible with chronic hepatitis. In contrast none of 29 patients with hepatitis A indicated chronic liver disease. The frequency of anti-HAV was also determined in 41 patients with HBsAg positive and HBsAg negative histologically proven chronic hepatitis or liver cirrhosis. All patients were under 35 years of age. An equal proportion of anti-HAV was found in both groups. These results suggest that hepatitis A practically never results in chronic hepatitis, while hepatitis non A - non B can run a chronic course with a frequency similar to that of hepatitis B.
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PMID:[Chronic hepatitis as sequela of acute viral hepatitis A and hepatitis non A - non B (author's transl)]. 74 46

The clinical course is reported in 17 patients in whom the histological picture of subacute hepatic necrosis ("bridging hepatitis") was found on needle liver biopsy or at autopsy. The patients' ages ranged from 10-71 years, 12 patients being less than 40 years old. Ten patients were males. Jaundice lasted 2-4 months in nine cases and over six months in two, one of the latter having developed cirrhosis. In five patients a relapse of jaundice occurred within three months. Hepatitis B antigen was found in one of 13 patients tested. Two patients died in fulminant hepatic failure, one developed cirrhosis. These three patients and an additional two received prednisone therapy. Twelve of the remaining patients were followed for periods of 8-81 months; an additional two patients' follow-up was incomplete. None developed clinical evidence of chronic liver disease, and laboratory data at the last examination were normal except for slight elevation of alkaline phosphatase in six cases. Repeat biopsies showed persistent hepatitis in one case, slight portal fibrosis in one, cirrhosis in one and at autopsy in a patient who died of unrelated causes two years after hepatitis no evidence of chronic liver disease was found. This relatively good outome of subacute hepatic necrosis is probably due to the young average age of the patients, and the low incidence of B hepatitis in this series.
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PMID:The clinical course of subacute hepatic necrosis. 74 11

Our knowledge of the cellular changes that lead to liver cell carcinoma in humans is limited by proper and necessary ethical restriction on clinical research. We know rather more about risk factors, the most important of which is cirrhosis, it seems that both the causative agent and the time of duration of the cirrhotic process are relevent to the magnitude of this risk. According to present knowledge, alpha1-antitrypsin deficiency, alcoholism, naturally occurring carcinogens, drugs, and the hepatitis B virus seem to carry the greatest risk of cancer developing in a cirrhotic patient. Cirrhosis, however, is not an essential prerequisite, and some or possibly all of these agents can also induce cancer without cirrhosis. Bile duct carcinoma commonly follows infestation with liver flukes. Cirrhosis is usually absent but duct epithelial hyperplasia is present prior to the development of cancer. Many cellular changes have been observed in patients and among populations considered to be at risk from liver cancer. Of these, liver cell dysplasia is the most striking and studies of its prevalence, natural history, and association with cirrhosis suggest that it is a precancerous change.
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PMID:Precursor lesions for liver cancer in humans. 77 94


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