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 classification, clinical course, etiology and treatment of chronic hepatitis are discussed. The clinical manifestations of chronic hepatitis are of limited diagnostic use. Diagnosis must be made by liver biopsy. The disease is classified as chronic persistent or chronic active hepatitis. The prognosis for chronic persistent hepatitis is excellent, and no treatment is required. Chronic active hepatitis may progress to cirrhosis and is associated with a poor prognosis if untreated. Recognized causes of chronic active hepatitis are hepatitis-B virus infection, post-transfusion hepatitis not associated with hepatitis-B virus, and certain drugs. For drug-induced hepatitis, discontinuation of the medication is indicated. For other types of chronic active hepatitis the recommended treatment is prednisone 10 mg and azathioprine 50 mg daily.
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PMID:Drug therapy reviews: chronic hepatitis. 35 29

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

The AusRIA 2 test has been modified for HBs antibody detection. This technique is about 7 to 8 dilution steps more sensitive for antibody detection than the IPE. Using this modified radioimmunological technique investigations have been carried out on blood donors, patients with acute and chronic liver disease and on haemophiliacs. An HBs antibody incidence of 11% was found among voluntary blood donors. Intensive clinical investigation of blood donors positive for HBs antibodies by IPE demonstrated that the Serum GOT was elevated in 11% of cases and the liver biopsy showed histological changes of different severity in 16 out of 22 cases. Investigation of 22 cases of acute HBs antigen-positive hepatitis confirmed that nearly all the patients developed HBs antibodies within 10 weeks following the disappearance of HBs antigen. The HBs antibodies persist over years. The appearance of HBs antibodies after an acute HBs antigen-negative hepatitis can be taken as an indication of a hepatitis-B virus infection also in these cases. Among 22 HBs antigen-negative chronic hepatitis cases, HBs antibodies were detectable in 52%. Sera of 111 patients with HBs antigen-negative liver cirrhosis of varying aetiology showed HBs antibodies in 29.7% of cases. The incidence was higher in males. HBs antibodies were found in 98% of patients with haemophilia. These results reveal new aspects with regard to the importance of the hepatitis-B viurs, especially in chronic liver disease. Apart from a description of the newly-developed HBs antibody test and a discussion of the results obtained using this technique, a survey is given of the importance of HBs antibody determination by means of sensitive methods for clinical and epidemiological purposes.
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PMID:[Hepatitis-B-surface-antibodies (detection, incidence, clinical importance)]. 106 4

To evaluate the factors determining the severity of chronic hepatitis B virus infection and the interactions of human immunodeficiency virus and hepatitis delta virus infections, we retrospectively analyzed 260 patients, 146 of whom were followed for a mean of 31.4 +/- 1.8 mo. Human immunodeficiency virus, hepatitis B virus, and hepatitis delta virus status and aminotransferase activities, histological activity index, alcohol consumption and the prevalence of cirrhosis were investigated. The patients included 54 homosexuals, 19 parenteral drug abusers and 187 subjects with other or unidentified risk factors for exposure to hepatitis B virus. Thirty-five patients (13%) were positive for antibody to human immunodeficiency virus; 27 were homosexual and 8 were drug abusers. The mean aminotransferase activities, histological activity index and the prevalence of cirrhosis were similar in the human immunodeficiency virus-positive and human immunodeficiency virus-negative subgroups. Actuarial survival was significantly lower in the human immunodeficiency virus-negative subgroups. Actuarial survival was significantly lower in the human immunodeficiency virus-positive group than in the human immunodeficiency virus-negative subjects (p = 0.004); the cause of death was clearly related to liver failure in four of the five human immunodeficiency virus-positive patients and two of the six human immunodeficiency virus-negative subjects who died. To evaluate the factors determining the severity of liver disease, we compared homogeneous subgroups of subjects. Among the homosexual patients, the prevalence of HBeAg and hepatitis B virus DNA, aminotransferase activities and the histological activity index did not differ according to human immunodeficiency virus antibody status.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interactions between human immunodeficiency virus-1, hepatitis delta virus and hepatitis B virus infections in 260 chronic carriers of hepatitis B virus. 155 33

Controversy surrounds the indication of liver transplantation in patients with hepatitis B virus infection. The major problem is the very high risk of infection of the graft. Some investigators have suggested that the presence of HBsAg is a contraindication to liver transplantation. Between February 1975 and December 1990, 178 HBs positive patients were transplanted at Paul Brousse Hospital in Professor H. Bismuth's Department, 137 for post hepatitis cirrhosis and 41 for fulminant hepatitis. Since April 1984 we have decided long term immunoprophylactic therapy for all patients with HBs infection. But only from August 1987 our supply of purified anti HBs immunoglobulin has been adequate to treat all our patients according to the following protocol: 10.000 IU during the peroperative phase, 10.000 IU immediately after intervention, 10.000 IU every day for the first 6 days, 10.000 IU when the anti HBs levels were under 150 IU/l. One hundred thirty-nine patients were treated by this method. 110 cleared HBs antigen from their sera and their liver were biologically and histologically free of B virus infection. 29 patients showed reappearance of HBs antigen in their sera and nearly all of them developed objective, histologically confirmed, graft lesions. These lesions are those of classical infection: acute hepatitis, active chronic hepatitis and cirrhosis. So 79% of patients were successfully treated with a follow up of 45 months to 6 months. We also studied the prognostic factors under treatment. The study shows: in the case of fulminant hepatitis, 93% success versus 77% in post hepatitis cirrhosis; in the case of Delta superinfection, 94% success versus 66% with pure B infection; in the absence of HBVDNA in the patient's sera before transplantation, 92% success versus 20% in the presence of HBVDNA. For a better understanding of the overall results, the two following parameters have to be considered: some patients relapsed after stopping their treatment, some other patients, despite repositivation of HBs antigen in their sera showed a paradoxal good evolution. These considerations enable us to obtain HBVDNA positive patients: 10% success, HBVDNA negative patients: Fulminant hepatitis: 100% success B Delta post hepatitis cirrhosis: 100% success B post hepatitis cirrhosis: 92% success.
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PMID:[Relapse prevention in liver transplant patients treated for liver involvement due to hepatitis B virus]. 163 19

Serum samples (1,428) from 1,149 patients with chronic liver diseases and polytransfused subjects were tested for antibody to hepatitis C virus by first-generation enzyme immunoassays. Antibody to hepatitis C virus was detected in 87% of patients with transfusion-related chronic non-A, non-B hepatitis; 17.6% of patients with nonmalignant, chronic hepatitis B virus infection; 37.3% of patients with hepatocellular carcinoma; 14.3% of patients with alcoholic liver diseases; 22.2% of patients with cryptogenic cirrhosis; 76% of intravenous drug abusers; 16.4% of patients on hemodialysis; 1.8% of patients on peritoneal dialysis; 6.2% of kidney transplant recipients; and 3.1% of normal subjects. A high frequency of weakly positive results was found in "aged" samples: 61.9% of antibody to hepatitis C virus-positive patients whose sera had been stored for more than 2 yr had optical densities less than two times the cut-off values in contrast to 7.9% of those whose sera had been stored for less than 2 yr (p less than 0.0001). A significantly lower proportion of patients who had optical densities less than two times the cut-off values were reactive in subsequent samples, 27.5% vs. 87.5% (p less than 0.0001). On retests, only 70% and 56% of sera that were initially positive for antibody to hepatitis C virus remained antibody to hepatitis C virus positive using second-generation enzyme immunoassays and neutralization enzyme immunoassays, respectively. Our results suggest that retrospective studies on stored sera may have overestimated the prevalence of antibody to hepatitis C virus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Overestimation of the prevalence of antibody to hepatitis C virus in retrospective studies on stored sera. 165 51

To determine serum thyroxine-binding globulin (TBG) levels, we used radioimmunoassay, and compared the results obtained with other tests in 231 patients with chronic hepatitis B virus infection to evaluate its clinical implications. All of these patients were hepatitis B surface antigen (HBsAg)-positive. Among them, 38 patients had hepatocellular carcinoma (HCC), 18 had chronic persistent hepatitis, 70 had chronic lobular or active hepatitis (grouped as CAH), 31 had active cirrhosis (AC), 25 had inactive cirrhosis, 20 had decompensated cirrhosis, and 29 were "healthy" HBsAg carriers. Twenty-seven patients with acute hepatitis, 12 with cancer metastasis to the liver, and 81 normal adults served as disease or normal controls. The results showed that serum TBG level increased significantly in patients with CAH, AC, or HCC. Serum TBG did not correlate with albumin or bilirubin level, but correlated with alanine aminotransferase (ALT) positively in patients with CAH (p less than 0.001) and negatively in patients with HCC (p less than 0.01) (slope difference p less than 0.05). Serial determination of serum TBG and ALT also showed parallel changes in 15 patients with CAH, but not in nine patients with HCC. In contrast, the fall and rise of serum TBG levels in patients with HCC coincided with tumor resection and recurrence. The data suggest that serum TBG elevation in patients with hepatitis activity is the result of hepatocellular damage, whereas that in patients with HCC is due to increased synthesis. Whether serum TBG elevation without concomitant rise of ALT could be used as a marker of HCC awaits further study.
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PMID:Thyroxine-binding globulin in patients with chronic hepatitis B virus infection: different implications in hepatitis and hepatocellular carcinoma. 168 51

To determine the intrahepatic production of tumour necrosis factor alpha (TNF alpha) in chronic liver disease three monoclonal antibodies were used against TNF alpha in immunohistochemical studies of liver tissue sections from patients with chronic liver disease. All three monoclonal antibodies stained infiltrating mononuclear cells. Monoclonal antibody II 7C2 also stained the cytoplasm or nucleus, or both, of a varied number of hepatocytes from nine patients with chronic hepatitis B virus infection, suggesting that the antigenic epitope related to hepatitis B core antigen (HBcAg) crossreacted with II7C2. The other two monoclonal antibodies, III2F3 and IV3E5, stained significantly larger numbers of mononuclear cells in cases of chronic active hepatitis B than in chronic persistent hepatitis B, or hepatitis B related liver cirrhosis. III2F3 stained significantly larger numbers of mononuclear cells in non-A, non-B chronic active hepatitis than in chronic persistent hepatitis B or hepatitis B related liver cirrhosis. These results indicate that TNF alpha is produced and secreted by infiltrating mononuclear cells in focal inflammatory areas of the liver, and suggest that TNF alpha may have a role in the inflammatory activity of chronic liver disease.
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PMID:Immunohistochemical studies of intrahepatic tumour necrosis factor alpha in chronic liver disease. 169 47

Antiviral therapy for chronic hepatitis B virus infection can result in clearance of replicating virus from the liver and prevention of progression to cirrhosis in a substantial proportion of patients. Adenosine arabinoside monophosphate, a potent inhibitor of HBV replication, is of limited usefulness because it causes significant neuromuscular toxicity. Acyclovir alone is relatively nontoxic, but is clinically ineffective in eliminating HBV from the liver. Lymphoblastoid or recombinant alpha-interferons are the best option at present and offer up to a 50% chance of long-term inhibition of HBV replication (with only minor side-effects) in patients who acquire the infection in adulthood. However alpha-interferon therapy alone is not effective when infection is acquired from birth. In this latter group of patients, prednisolone pre-treatment followed by alpha-interferon is currently under evaluation.
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PMID:Antiviral therapy: hepatitis B. 169 58

Three-hundred forty-one HBsAg-positive family members of 152 patients with chronic hepatitis B virus infection (47 asymptomatic carriers, 59 with chronic hepatitis, 17 with cirrhosis and 29 with hepatocellular carcinoma) were prospectively studied to determine the morbidity and mortality from chronic hepatitis B virus infection in the family members of patients with malignant and nonmalignant hepatitis B virus-related chronic liver diseases. Most of the family members had no history of acute hepatitis, were asymptomatic and were unaware of their carrier status. However, 5.3% had stigmata of chronic liver disease, 6% had serum ALT levels that exceeded two times the upper limit of normal and 78% of those who had biopsies had chronic hepatitis with or without cirrhosis. During a follow-up period of 12 to 90 mo (median = 39 mo), 3% had symptoms of chronic liver disease; 24% had transient, recurrent or persistent elevation in serum ALT levels, 1.4% had cirrhosis and 1% had hepatocellular carcinoma. Neither hepatocellular carcinoma in the index patient nor a previous history of hepatocellular carcinoma in the family was associated with an increase in the morbidity and mortality from chronic hepatitis B virus infection in the HBsAg-positive family members.
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PMID:Morbidity and mortality from chronic hepatitis B virus infection in family members of patients with malignant and nonmalignant hepatitis B virus-related chronic liver diseases. 170 10


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