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)

Consumption coagulopathy was developed in three cases of liver cirrhosis and a case of haemophilia B upon administration of Factor IX preparations which had been tested by the manufacturers for the absence of active clotting factors according to the Japanese Minimum Requirements for Biological Products. By employing the TGT determination, however, active clotting factor(s) could be detected in some of the preparations used in these cases. Accordingly, it was found necessary to modify the current test method in the Minimum Requirements by introducing calcium ion into the test medium. There was no correlation between the clotting activitiy detected by our modified test method and the Factor IX potency of the product. Addition of heparin did not significantly influence the results in our modified method.
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PMID:A test method for the absence of thrombogenicity in factor IX complex. 54 93

Chronic liver disease is not often reported in patients with haemophilia. Although a high incidence of abnormal liver function tests has been reported, the clinical significance of these findings and their relation to chronic liver disease cannot be established without a liver biopsy. The results of this procedure, carried out in 11 patients with severe haemophilia A and B, in whom SGOT had been persistently raised for three years, are reported. Five patients had chronic active hepatitis, four had chronic persistent hepatitis, one had cirrhosis, and one alcoholic hepatitis. No haemorrhagic complication followed the biopsy procedure, which was carried out in patients given prophylactic clotting factor concentrates. These results suggest that duration of abnormal liver function tests is likely to represent liver disease in haemophiliacs, and that biopsy should be considered to establish the diagnosis and plan a suitable therapeutic programme.
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PMID:A clinicopathological study of liver disease in haemophiliacs. 69 Feb 43

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

A simple modification of the radioimmunoassay Ausria I 125 was employed for detecting anti-HBs using the inhibition of a constant amount of HBs Ag. Anti-HBs was demonstrated in up to 82% of follow-up patients recovering from viral hepatitis B and in 79% of hemophilia patients. The antibody was found in 3.4% of healthy blood donors and in 10% of family contacts of patients with acute HBs Ag-positive viral hepatitis. The frequency of anti-HBs in 44 patients with HBs Ag-negative chronic aggressive hepatitis or cryptogenic liver cirrhosis (23%) did not differ significantly as compared with the occurrence of anti-HBs in 58 patients with chronic rheumatoid arthritis (16%). These findings give further support to the suggestion that the hepatitis B virus does not contribute to the aetiology of HBs Ag-negative chronic active hepatitis.
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PMID:Detection of antibody to hepatitis Bs-antigen in patients with acute and chronic hepatitis as measured by a modified procedure of the radioimmunoassay Ausria I 125. 119 21

A simple modification of the radioimmunoassay Ausria I and Ausria II was employed for detecting anti-HGsAg using the inhibition of a constant amount of HBsAg. The highest incidence of anti-HGsAg was demonstrated in follow-up patients recovering from viral hepatitis B (82%) and in hemophilia patients (79%). Lower frequencies were observed in patients with chronic aggressive hepatitis or liver cirrhosis (23%), patients with chronic rheumatoid arthritis (16%), family contacts of patients with viral hepatitis B (10%) and blood donors (3.4%). No difference in sensitivity for the presence of anti-HBsAg was found between the Ausria I and the Ausria II test.
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PMID:Anti-HBsAg assay using the Ausria system with standard antigen dilutions. 120 48

Since the detection of hepatitis B virus (HBV) in the 1960s and hepatitis A virus in the 1970s, a considerable proportion of infections of (probably viral) hepatitis could not be classified. About 90% of transfusion-related hepatitis was identified as non-A/non-B. In 1988 investigators from the Chiron Company (USA) detected the non-A, non-B agent and named it hepatitis C virus (HCV). An anti-HCV antibody assay (ELISA) and subsequently confirmation tests (immunoblot and polymerase chain reaction) were developed. HCV infection results in a chronic carrier state of the virus in about 80%. Almost all HCV carriers have, irrespective of their liver function tests, histologic signs of chronic hepatitis and/or liver cirrhosis. Chronic HCV infection is, like HBV, also associated with the development of hepatocellular carcinoma. Most HCV carriers are infected by parenteral routes (intravenous drug use, blood transfusion, tattooing). Intravenous drug users and haemophilia patients have the highest risk (80-90%) of becoming infected. Sexual and perinatal transmission does not play an important role in spreading the infection. Antiviral therapy (alpha-interferon) in patients with chronic hepatitis C will normalize liver function tests in about 25% of the cases, but it is unclear if the HCV carrier state will disappear and if liver cirrhosis will be prevented. At present no specific immunoglobulin or vaccine preparations are available to prevent the HCV infection.
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PMID:New developments in hepatitis C. 129 54

The hepatitis D virus (HDV) infection plays a major role in severe liver damage caused by hepatitis. To establish the prevalence of HDV infection in haemophilic patients and patients without haemophilia, 87 patients with chronic hepatitis B virus (HBV) infection were examined for serological evidence of delta hepatitis. In addition HBV, HDV and human immunodeficiency virus type 1 (HIV) infection markers were compared to clinical and histopathological outcome of hepatitis. Out of 46 haemophiliacs 30 (65%) were anti-HD-seropositive; 10 out of 30 anti-HD-positive patients (33%) had pathological liver function tests compared to 2 out of 16 anti-HD-negative haemophiliacs (13%). The rate of HIV infection did not differ between the HDV infected and the non-HDV infected individuals with haemophilia (17/27 anti-HD-positive patients versus 12/16 anti-HD-negative patients). Two haemophilic anti-HD-positive patients underwent liver biopsy, in both cases hepatitis D antigen (HDAg) was detected in the biopsies. Only 2 out of 41 patients without haemophilia were anti-HD-positive. Both had pathological liver function tests; chronic active hepatitis and cirrhosis, respectively, were diagnosed and HDAg was found in the liver biopsies. Out of 39 anti-HD-seronegative patients without haemophilia, 26 (67%) were hepatitis B e antigen positive; in the sera of 20 patients (51%) HBV-DNA was demonstrated, but only 6 patients (15%) had pathological liver function tests. In conclusion a high seroprevalence of HDV infection was found in haemophilic patients treated with non-pasteurized commercial clotting factor concentrates. An endemic spreading of HDV infection in patients without haemophilia with chronic HBV infection could not be detected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Correlation of hepatitis B virus, hepatitis D virus and human immunodeficiency virus type I infection markers in hepatitis B surface antigen positive haemophiliacs and patients without haemophilia with clinical and histopathological outcome of hepatitis. 153 69

A questionnaire-based survey involving 11,801 hemophiliacs from 54 hemophilia centers in the USA and Europe documented the occurrence of hepatocellular carcinoma (HCC) in 10 patients. The crude rate of HCC was 3.2/100,000 patients/year, at least 30 times higher than the background incidence of this tumor in the countries of origin of the patients. All patients were Caucasians with hemophilia A, 39 to 74 years of age, and had liver cirrhosis. All had one or more risk factor for cirrhosis and HCC: 5 were positive for serum hepatitis B surface antigen, 4 had the antibody to hepatitis C virus, and 4 had histories of alcohol abuse. Serum alpha-fetoprotein, measured in 6 patients, was significantly elevated in 4 (range: 807-1399 ng/ml), and only moderately elevated in 2 (25 and 171 ng/ml). The onset of HCC was asymptomatic in 5 patients, whereas it was accompanied by jaundice, abdominal pain, or ascites in the remaining patients. Thus, HCC seems to be a more important secondary disease for hemophiliacs than formerly recognized. Since HCC is often asymptomatic, screening hemophiliacs with chronic liver disease with periodic ultrasound scans might increase the changes of detecting HCC at a stage amenable to surgical treatment.
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PMID:Hepatocellular carcinoma in hemophilia. 165 Jan 34

The occurrence of a portal vein thrombosis in a haemophilia A patient is reported. The patient, a 53 year old male, had been followed by us for the past 20 years in our out-patient Clinic. He was hospitalized recently for a suspected hepatic cirrhosis. Severe ascites, hepato-splenomegaly together with weight loss and mild fever were present. During the hospitalization, an ultrasound and CT scan of the liver confirmed the cirrhotic pattern and showed the presence of a portal vein thrombosis. There were no changes in the underlying coagulation defect, in fact, the patient had recurrent haemarthrosis. Furthermore, with the ultrasound examination, some focal hepatic lesions--probably due to a hepatocellular carcinoma--were also observed. The patient died because of massive haematemesis due to rupture of oesophageal varices.
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PMID:Portal vein thrombosis in a patient with severe haemophilia A and post-hepatitis liver cirrhosis. 166 75

Laser Nephelometry is a technique which allows the evaluation of the concentration of several serum proteins and clotting factors. By means of this technique it is also possible to study the kinetic of the reaction between antigen and antibody. In a few instances the method was also applied in the characterization of abnormal molecules. We developed assays for the measurement of Factor IX antigen and the results were compared with those obtained by conventional immunological methods such as rocket immunoelectrophoresis. Plasmas from patients with haemophilia B, on coumarin treatment, with liver cirrhosis were studied. A standard reference curve was obtained using pooled normal plasma. The factor IX levels obtained by laser nephelometer correlated fairly well with those obtained by electroimmunoassay.
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PMID:Laser nephelometer evaluation of factor IX. 171 91


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