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)

51 cases of chronic hepatitis were followed up by serial liver biopsies. 6 cases, all of which were of the active type, showed transition to liver cirrhosis within 5 to 10 months after the initial biopsy which had indicated chronic hepatitis. In 109 cases of liver cirrhosis, the antecedent acute hepatitis had been found within a relatively short period, usually 2 to 3 years before the establishment of the diagnosis of liver cirrhosis. Whether these cases which showed rapid transition to liver cirrhosis after acute hepatitis should be included in the group of chronic hepatitis or in another group remains to be settled.
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PMID:Chronic hepatitis: a follow-up study. 96 19

To document the sequelae of acute hepatitis among recipients of commercial and volunteer blood and to assess factors influencing the development of chronic hepatitis (CH), 47 patients with post-transfusion hepatitis were followed prospectively from the time they received their transfusions. Twenty-nine had prolongation of at least 2-fold serum glutamic pyruvic transaminase (T) elevations for more than 20 weeks, and were classified as CH. When the patients with CH were compared to those with only acute hepatitis (abnormal T for less that 20 weeks), no difference was found with respect to age, sex, number of units transfused, incubation period, presence or absence of symptoms, occurrence of jaundice, maximum T, receipt or development of hepatitis B surface antigen or antibody, underlying illness, or area of the hospital where the patient was treated. Liver biopsies in 15 of the 29 revealed chronic-active hepatitis in 9, chronic persistent hepatitis in 2, unresolved hepatitis in 4. Five of the 9 patients with chronic active hepatitis were without symptoms. None of these died or have developed cirrhosis. Because chronic liver disease frequently developed after acute post-transfusion hepatitis among multiply transfused hepatitis B surface antigen negative blood recipients, close follow-up, including liver biopsy, is warranted in such patients with prolonged transaminase elevations.
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PMID:Post-transfusion chronic liver disease. 96 71

A radioimmunoassay for human alpha1-acid glycoprotein has been developed. 97.8% of 125I-alpha1-acid glycoprotein prepared for the assay were immunoprecipitable with specific anti-sera against the protein. alpha1-acid glycoprotein concentration in sera from normal adults was found to range between 70 and 114 mg/100 ml, with a mean of 93. Fulminant hepatitis, liver cirrhosis or chronic active hepatitis with sublobular necrosis caused a significant lowering of alpha1-acid glycoprotein concentration. Sera obtained from patients with acute hepatitis in convalescence, chronic inactive hepatitis or primary biliary cirrhosis gave normal concentration of the glycoprotein.
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PMID:Serum glycoproteins in the liver diseases. II. Radioimmunoassay of alpha-1 acid glycoprotein. 101 93

Serum samples from 103 HBsAg positive and 69 negative patients were examined in Ouchterlony double diffusion in agarose for the presence of e antigen and anti-e antibody. e antigen was found in 66% of the cases of active chronic hepatitis, 18% of those of active cirrhosis, and 12% of those of acute hepatitis. Anti-e antibody was found only in asymptomatic chronic carriers; it occurred in 56% of HBsAg-positive individuals with normal livers at biopsy. No e reactivity was found in 6 subjects with inactive disease and in 3 with chronic persistent hepatitis. The e system seems a valuable diagnostic tool utilizing the presence of the antigen to differentiate patients with chronic progressive disease from healthy carriers who, in contrast, often have circulating anti-e antibodies; its clinical value, however, is at present limited by the low sensitivity of the technique used for antigen detection. A significant association between e antigen and the intrahepatic expression of the core determinant of the HB virus was observed inthis study, suggesting they have a similar role in pathogenicity and infectivity; the association between anti-e antibody and HBsAg appeared uncertain, HBsAg being present in the liver irrespective of e reactivity.
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PMID:The e antigen and antibody in the serum of patients with HBsAg-positive liver disease and in asymptomatic carriers. 102 47

Sera of altogether 282 patients with different forms of hepatitis and cirrhosis were screened for cold reacting complement dependant auto-lympho-cytotoxins (CoCoCy). These antibodies are 19S-IgM-immunoglobins and have no HLA-antigen-specificity. CoCoCy occurred in 48% of the patients with chronic aggressive hepatitis (CAH), in 14% of the patients with chronic persistent hepatitis (CPH) and in intermediate rates in the sera of patients with acute hepatitis. No correlations was found between CoCoCy and hepatitis B-antigen (HB-Ag). CoCoCy could be demonstrated also in 20% of the sera of a HB-Ag-positive and in 6% of a HB-Ag-negative control group. The serum concentration of CoCoCy is low. CoCoCy seems to be of T-cell-specificity and to reflect the overall-immunoreactivity without relation to the specificity of the antigenic stimulus. Thus demonstration of CoCoCy may be of pathogeneic and pathodynamic rather than of diagnostic interest.
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PMID:[Autolymphocytotoxins (CoCoCy) in different forms of hepatitis and cirrhosis (author's transl)]. 108 62

The relative sensitivities of counterimmunoelectrophoresis (CIE) and haemagglutination assays for the detection of hepatitis B surface antigen (HB(s)Ag) and antibodies (anti-HB(s)) were compared. Twelve scientists from ten countries in Asia, Africa and the Pacific region participated in the study. The participants provided serum samples from 15 953 subjects comprising patients with acute and chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC), as well as blood donors and other normal individuals. For the detection of HB(s)Ag in a reference panel serum, immune adherence haemagglutination (IAHA) was slightly more sensitive than passive haemagglutination inhibition (PHI); CIE was the least sensitive. Mean HB(s)Ag frequencies in patients with acute hepatitis, chronic hepatitis, cirrhosis, and HCC were significantly higher than in healthy controls. Passive haemagglutination (PHA) was more sensitive than CIE for the detection of anti-HB(s). The frequency of anti-HB(s) in patients with HCC was significantly lower than that in the other groups. Mean anti-HB(s) frequencies in patients with acute hepatitis, chronic hepatitis, and cirrhosis were not significantly different from that in normal subjects. Subtyping of HB(s)Ag was performed by PHI. Among asymptomatic carriers the predominant HB(s)Ag subtype in northeast Asia was adr.In India, ayw predominated in carriers, with the demarcation between adr and ayw occurring west of Burma. In West Africa the only subtype detected was ayw, but in East Africa the majority subtype was adw. The r subtype was found only in Asian populations east of India and in Western Pacific populations. In Papua New Guinea all four subtypes were identified. With one possible exception, the subtypes of HB(s)Ag-positive patients with liver disease reflected the predominant type in each geographic location.
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PMID:Hepatitis B antigen, antigen subtypes, and hepatitis B antibody in normal subjects and patients with liver disease. 108 99

This study concerns hepatitis B antigen and antibody, (HBAg and HBAb) auto-antibodies and liver disease in a renal haemodialysis and transplantation unit between February, 1970 and December, 1972. Fourteen per cent of patients on maintenance haemodialysis, 25% of renal transplant recipients, and 5% of the staff were HBAg positive during this period. Three family members of antigen positive patients developed hepatitis; all were either antigen or antibody positive. Both immuno-electro-osmo-phoresis and radio-immuno-assay were used to detect HBAg. No additional carriers were identified among the dialysis or transplant patients by applying the more sensitive technique, although two persons with hepatitis were positive only by RIA. None of the staff members who developed antigen positive hepatitis died, and no one became a carrier. Dialysis patients who had icteric hepatis also cleared the antigen from the serum. Clinical hepatitis did not occur in immunosuppressed graft recipients who were carriers of the ay subtype of the antigen, nor was there histological evidence of liver disease in 18 of 19 of such carriers studied. Moreover, there was no association between long term carriage of the antigen and the presence of the auto-antibodies characteristic of chronic active hepatitis. Rapid reduction of immunosuppression was followed by acute hepatitis in one carrier, while another, whose antigen was of the ad subtype, developed micro-nodular cirrhosis.
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PMID:Hepatitis B antigen, auto-antibodies and liver disease in a haemodialysis and transplantation unit. 110 68

In clinical pathologic correlations, including the potential effect of the virus on the liver, the morphologic features of the various stages of viral hepatitis are the firm information available today. With acute hepatitis being an inflammatory reaction to cell injury and necrosis, and chronic hepatitis being sustained inflammation, correlation with clinical features and functional defects is good in acute hepatitis and less so in the chronic stages. The pathogenesis of the diseases-including cell necrosis, inflammation, fibrosis, and cirrhosis formation-is reasonably well understood, and this knowledge assists both in prognosis and in monitoring of therapy. The localization of the components of the hepatitis B antigen and their effects, including the nature of the immune response, is the most exciting aspect of the clinical pathologic problem. Today's interpretations offer, at best, a working hypothesis promising further understanding of the evolution of the disease.
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PMID:Clinical pathologic correlation in viral hepatitis. The effect of the virus on the liver. 110 67

A retrospective analysis has been made of 57 patients with subacute hepatic necrosis demonstrated on a liver biopsy obtained during the course of an episode of acute hepatitis. Fourteen patients have been lost to follow-up. One patient died acutely with massive hepatic necrosis, while 8 have developed chronic active liver disease. Two of nine biopsies subsequently performed on patients who had shown complete clinical and biochemical resolution revealed an inactive postnecrotic cirrhosis. The incidence of these complications developing in patients with subacute hepatic necrosis was approximately 30%. These findings add qualitative support to the position that liver biopsy findings bear important prognostic value in patients with acute hepatitis.
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PMID:Prognostic significance of subacute hepatic necrosis in acute hepatitis. 111 53

Large amounts of bile acid sulfate were found in the urine of patients with hepatobiliary diseases. In patients with acute hepatitis, daily excretion of bile acid into urine was 68.24 plus or minus 51.80 mumoles per day, and the percentage of sulfated bile acid was 83.4 plus or minus 16.7%. In patients with chronic hepatitis and cirrhosis, a slight increase of urinary bile acid was observed (2.89 plus or minus 2.69 and 5.27 plus or minus 4.28 mumoles per day, respectively), and the percentage of sulfated bile acid was 73.9 plus or minus 28.6 and 44.6 plus or minus 30.4%, respectively. In patients with obstructive jaundice, a moderate increase of urinary bile acid was found (32.62 plus or minus 18.35 mumoles per day), and the percentage of sulfated bile acid was 58.3 plus or minus 22.6%. In patients with hepatobiliary diseases, the elevation of both levels of sulfated and nonsulfated bile acids in serum was observed. The percentage of sulfated bile acid was 9% in normal serum, and varied from zero to 82.8% in pathological sera. A remarkable increase of sulfated bile acid was found in patients with obstructive juandice and acute hepatitis, while a slight elevation was found in patients with chronic hepatitis and cirrhosis. Sulfated bile acid in bile was nonexistent or below 0.5% of total bile acid. According to these findings, the increased bile acid in serum of patients with hepatobiliary diseases might be more easily excreted into the urine as sulfated bile acid.
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PMID:Sulfated and nonsulfated bile acids in urine, serum, and bile of patients with hepatobiliary diseases. 111 56


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