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 incidence of HBAg in viral hepatitis, in chronic active hepatitis and in cirrhosis has been investigated by using immunological methods and a solid-phase radioimmunoassay. RIA demonstrated as positive: 90% of 20 patients with posttransfusion hepatitis; 88% of 50 patients with acute viral hepatitis; 100% of 13 patients with chronic active hepatitis and 35% of 20 patients with cirrhosis; whereas the frequency of HBAg in the same patients appeared to be lower by AGD, CIEP and CF. The measure of antigenaemia has been obtained by use of HBAg (ad) dose response standard curve. The quantitative HBAg data of an eight-week follow-up of fully recovered 15 patients with acute hepatitis are reported. In the first week it appeared a distribution of the HBAg levels into three classes of values. The concentration of HBAg in the serum became lower week by week and in 8th week the antigen was no longer detectable. The radioimmunoquantitation of HBAg in the serum of patients suffering from chronic acitve hepatitis and cirrhosis showed wide levels of antigenaemia ranging between 17 and 5100 ng ad equivalent/ml. The use of a dose response standard curve in order to quantify HBAg in the serum represents a further increased sensitivity of RIA.
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PMID:Hepatitis B virus antigen quantitation by radioimmunoassay (RIA) in viral hepatitis and in chronic liver diseases. 80 25

The two-step direct radioimmune test RIA used to detect hepatitis B virus associated antigen (HBsAg) appeared to be more sensitive than other immunologic assays. RIA demonstrated as HBsAg positive 90% of 20 patients with posttransfusion hepatitis; 88% of 50 patients with acute viral hepatitis; 100% of 13 patients with chronic active hepatitis and 35% of 20 patients with cirrhosis; on the other hand with positivity for HBsAg in the same patients appeared to be lower by AGD, CIEP and CF. The quantitation of HBsAg by RIA has been performed with a dose response curve obtained by use of HBsAg (ad) standard. The quantitative HBsAg data of an eight week follow-up of fully recovered 15 patients with acute B-hepatitis are reported. In the first week it appeared a distribution of the HBsAg levels into three classes of values. The concentration of HBsAg in the serum became lower week by week and in the 8th week the HBsAg was no longer detectable. The radioimmunoquantitation of HBsAg in the serum of patients suffering from chronic active hepatitis and cirrhosis showed levels of antigenaemia ranging between 17 and 5100 ng ad equivalent/ml. The use of a dose response standard curve in order to quantify HBsAg in the serum represents a further increased sensitivity of RIA.
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PMID:[Radioimmunoquantization of the HBAg in clinical liver diseases]. 122 48

In 1974, Prince et al. reported the existence of posttransfusion hepatitis with a long incubation period which was not related to hepatitis B virus (HBV). These cases were named "non-A, non-B" (NANB) hepatitis. The genome of NANB hepatitis virus was discovered recently using a recombinant complementary DNA (cDNA) approach. It was termed the hepatitis C virus (HCV), and a specific diagnostic tool for the circulating HCV antibody (anti-HCV) was developed using a purified viral polypeptide derived from recombinant yeast expressing a small part of the HCV genome. HCV is believed to be the main cause of blood-borne non-A, non-B hepatitis worldwide, which frequently evolves to chronic hepatitis and cirrhosis, and which may also be involved in the development of hepatocellular carcinoma. HCV is classified as part of the flaviviridae family and contains a positive-stranded RNA molecule by approximately 10 kb nucleotides. The HCV genome encodes a large polyprotein precursor, which is processed in structural nucleocapsid and envelope proteins and in non-structural proteins (NS1-NS5). Nucleotide sequence comparisons of distinct HCV isolates have shown a significant genetic variability between the different HCV strains. At present the diagnosis of HCV infection depends on various anti-HCV tests including second generation HCV Ab. Antigenic markers for HCV are being developed but the concentrations of HCV antigens in serum are at the lower limit of detectability by existing immunoassay technology. A polymerase chain reaction has been used to detect HCV RNA in the serum and liver. Serum HCV RNA disappears from serum after effective IFN treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Fundamental studies of hepatitis C virus: a review]. 133 74

Hepatitis C virus (HCV) is the agent responsible for posttransfusion hepatitis. The incidence, timing, and clinical course of HCV positive hepatitis in liver transplant recipients are unknown. Three hundred and seventeen donor-recipient liver transplant pairs were grouped on the basis of their pretransplant HCV antibody status. The biopsy findings were examined. Four distinct groups were identified on the basis of HCV serology: group I, both were negative; group II, donor was negative and recipient was positive; group III, donor was positive and recipient was negative; group IV, both were positive. The prevalence of anti-HCV positivity in recipients was 13.6%. The rate of seroconversion was 9.2%. Histologic hepatitis not ascribable to any specific cause other than non-A, non-B (NANB) hepatitis occurred in 13.8%. The incidence of histologic chronic active hepatitis was 1.6%, and none progressed to cirrhosis. The concordance rate for a positive anti-HCV serology and NANB hepatitis was 2.8%. Of the 35 patients (group II and IV) with positive anti-HCV serology pretransplant, only 17 were positive posttransplantation. Based on these data it can be concluded that posttransplant NANB hepatitis occurred in 13.8% of liver recipients. Twenty percent of these were anti-HCV positive. Progression to histologic chronic active hepatitis occurs over a period of 1-5 years in 1.6% of cases.
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PMID:Incidence, prevalence, and clinical course of hepatitis C following liver transplantation. 161 40

We have evaluated the clinical and histopathological outcomes of patients who contracted chronic non A, non B hepatitis as a result of transfusions administered during heart surgery at the National Institutes of Health. Posttransfusion hepatitis developed in 65 of 1,070 (6.1%) patients and became chronic in 45 (69%) of those cases. Antibody to hepatitis C virus was detectable in 53 patients (82%) with posttransfusion non A, non B hepatitis. Thirty-three patients with chronic non A, non B hepatitis agreed to liver biopsy (group 1). In addition, six other patients with chronic posttransfusion non A, non B hepatitis were evaluated (group 2). These 39 patients were followed between 1 and 24 yr (mean = 9.7 yr). Cirrhosis developed in 8 patients (20%) between 1.5 and 16 yr after blood transfusion. Of the 33 patients in group 1, 11 (33%) died during follow-up. In two cases (6%), this was related to liver failure. At this writing, two additional patients (6%) have decompensated cirrhosis and one (3%) had debilitating fatigue. Twenty of 33 patients (61%) with histological evidence of chronic active hepatitis or cirrhosis are asymptomatic and have no clinical evidence of liver disease. Thus chronic non A, non B posttransfusion hepatitis appeared to be due to hepatitis C virus infection in most cases. It was associated with the development of cirrhosis in approximately 20% of cases and end-stage liver disease in 12% of patients followed prospectively. Most patients with histological evidence of cirrhosis or chronic active hepatitis, however, had minimal clinical evidence of liver disease within the time frame of this study.
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PMID:Long-term clinical and histopathological follow-up of chronic posttransfusion hepatitis. 195 84

Serum levels of the aminoterminal propeptide of type III procollagen (PIIINP) and hyaluronan were analysed before and during the acute, recovery and chronic phases of non-A, non-B (NANB) posttransfusion hepatitis (PTH) in 13 patients. All patients were discovered during a prospective study on NANB PTH in patients undergoing open-heart surgery. 7/13 (54%) patients resolved their hepatitis within 6 months after onset, whereas 6/13 (46%) went on to chronic hepatitis. In 5 of these 6 patients a liver biopsy during the chronic phase of the hepatitis showed chronic active hepatitis in 2 and chronic persistent hepatitis in 3. During the acute NANB PTH phase the mean serum PIINP level rose significantly as compared to prehepatitis levels and to levels in a reference group not developing hepatitis. Neither PIIINP levels nor hyaluronan levels, however, could differentiate patients with resolving from patients with nonresolving hepatitis. These markers should, however, be further evaluated as potential markers for development of fibrosis/cirrhosis during chronic hepatitis.
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PMID:Serum levels of the aminoterminal propeptide of type III procollagen and hyaluronan during resolving and nonresolving posttransfusion non-A, non-B hepatitis. 210 89

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

Ninety-two patients with biopsy-proven chronic non-A, non-B hepatitis after blood transfusions, illicit self-injections or sporadically were followed clinically for an average of nearly 5 years. In the posttransfusion hepatitis group, which comprised 37 patients with a mean age of 54 years (range 18-83 years), 59% developed chronic active hepatitis (CAH) and 46% also showed signs of early cirrhosis (eCi) or manifest cirrhosis (Ci). In the illicit self-injection group, comprising 33 patients with a mean age of 26 years (range 17-63 years), 39% manifested CAH and 18% eCi or Ci. In the sporadic group, which consisted of 22 patients with a mean age of 32 years (range 16-62 years), 41% showed CAH and 23% eCi. Thus, in all, 44/92 (48%) of the patients with chronic non-A, non-B hepatitis developed CAH and 28/92 (30%) signs of early or manifest cirrhosis. Patients greater than or equal to 30 years of age displayed CAH and signs of cirrhosis more often than patients less than 30 years of age (p less than 0.01). Chronic non-A, non-B hepatitis is a slowly progressive disease with a high incidence of cirrhosis, especially in patients greater than or equal to 30 years of age and when caused by blood transfusion.
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PMID:Chronic non-A, non-B hepatitis developed after transfusions, illicit self-injections or sporadically. Outcome during long-term follow-up--a comparison. 249 81

Non-A non-B (NANB) hepatitis has at least two distinct causative agents. NANB hepatitis can lead to chronic liver disease, cirrhosis, and hepatocellular carcinoma. No definitive policy exists to exclude this disease as a cause of posttransfusion hepatitis. Delta agent is epidemiologically linked to hepatitis B virus (HBV) infection, either as a coinfection or as a superinfection in chronic hepatitis B surface antigen carriers. Recognition of hepatitis due to delta agent will probably increase as testing for this agent becomes more available and its presence becomes more generally well known throughout the medical profession.
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PMID:Hepatitis in clinical practice. 2. Non-A non-B and delta hepatitis. 308 83

We have followed up 69 patients who developed non-A, non-B posttransfusion hepatitis in 1972-1978. Chronic hepatitis, defined by biochemical criteria, was observed in 46 patients (67%), the majority of whom subsequently failed to resolve the abnormalities. Chronic hepatitis was a sequela of non-A, non-B posttransfusion hepatitis less often after the blood bank changed to a policy of all volunteer donors. (However, this association may be explained by other coexistent factors.) The alanine aminotransferase level was more likely to be abnormal than the aspartate aminotransferase level during the chronic phase of non-A, non-B posttransfusion hepatitis. By actuarial means it was calculated that the probability of developing normal enzymes after 6-10 yr was 0.47. However, in spite of this high incidence of biochemical disease, virtually all of the patients have remained asymptomatic. Histologic evidence of cirrhosis has been obtained in 4 of these patients, but in only 2 patients at most has clinical evidence of hepatic failure supervened.
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PMID:Non-A, non-B posttransfusion hepatitis--a decade later. 392 Jan 12


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