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)

Five hundred patients with the isomorphic pattern of the isoenzymes of serum lactate dehydrogenase (LDH) were surveyed. The isomorphic pattern of LDH isoenzymes is defined as a significant increase of total LDH with normal or low percentage of individual fractions, but with the LDH1:2 ratio less than unity. Diagnoses were, in descending order of frequency, cardiorespiratory diseases, malignancy, fracture, diseases of the central nervous system, infection/inflammation, hepatic cirrhosis and/or alcoholism, trauma without fracture, infectious mononucleosis, hypothyroidism, uremia, necrosis, pseudomononucleosis, viremia and intestinal obstruction. Incidence of increased serum activity in individuals without evidence of disease or drug explanation was 3 percent. Low PaO2 was observed in 88 percent of the 67 patients in whom it was measured.
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PMID:Clinical significance of the isomorphic pattern of the isoenzymes of serum lactate dehydrogenase. 90 Aug 65

Sera from 103 patients were tested for hepatitis C virus RNA by nested polymerase chain reaction assay. Using primers from the highly conserved 5'-untranslated region, we detected hepatitis C virus RNA in 67 (88.2%) of 76 patients positive for antibody to hepatitis C virus by both second-generation and neutralization enzyme immunoassays. Hepatitis C virus RNA was detected in 93% of patients who had been infected for 10 yr or less and in 89% of those who had been infected for longer than 10 yr. Hepatitis C virus RNA was detected in all patients with chronic hepatitis, active cirrhosis or hepatocellular carcinoma and in 50% of those with nonspecific reactive hepatitis or inactive cirrhosis. Hepatitis C virus RNA was not detected in sera from 22 patients negative for antibody to hepatitis C virus or in 5 patients positive for antibody to hepatitis C virus by second-generation but not by neutralization enzyme immunoassay. Using primers from the less conserved nonstructural region 4, we detected hepatitis C virus RNA at a lower frequency, in 66% of patients who were positive for antibody to hepatitis C virus by both second-generation and neutralization enzyme immunoassays. The detection rate was higher in patients with frequent parenteral exposure. Our study showed that hepatitis C viremia can be detected in most patients with hepatitis C virus infection, including those with long-standing infection or advanced liver disease.
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PMID:Hepatitis C viremia in patients with hepatitis C virus infection. 131 37

To examine the postliver transplant recurrence of hepatitis C virus (HCV) infection in patients with pretransplant infection, as well as its acquisition in patients without prior infection, we used the polymerase chain reaction to amplify HCV RNA in serum and/or liver samples of 89 patients with alcoholic and cryptogenic cirrhosis undergoing liver transplantation. Results were correlated with histologic findings from posttransplant liver biopsies. Ninety-five percent of patients with pretransplant infection had posttransplant viremia. In contrast, 35% of patients without pretransplant infection acquired the virus (P less than 0.0001). Pretransplant HCV infection predisposed patients to hepatitis in the new graft. HCV RNA was present in serum of 96% of patients with posttransplant hepatitis. Fifty-six percent of patients with posttransplant HCV infection had no evidence of liver damage at least 1 year posttransplant. However, of those patients with histologic hepatitis, chronic active hepatitis was common. It is concluded that although HCV infection recurs posttransplant in almost all infected patients, acquisition of the HCV infection with transplant is common. Pretransplant HCV infection is an independent risk factor for the development of posttransplant hepatitis. HCV infection accounts for the majority of posttransplant hepatitis not due to cytomegalovirus, and although many patients with posttransplant viremia have little evidence of histologic hepatitis, significant hepatic damage may occur.
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PMID:Recurrent and acquired hepatitis C viral infection in liver transplant recipients. 137 43

Seven carriers of the Hepatitis B surface antigen who had acquired a form of chronic hepatitis D in the recent past were treated with lymphoblastoid alpha interferon (IFN) (10 MU three times weekly for 4 months, 6 MU three times weekly for other 8 months, with a 12 month follow-up after treatment). At the beginning of the study, these patients had a chronic active hepatitis with intrahepatic hepatitis D antigen but without signs of cirrhosis. By the end of therapy, five had normal amino-transferases and no trace of HDV-RNA in the serum. In two patients the liver enzymes and viremia relapsed during follow up; biochemical and virologic remission persisted after discontinuation of therapy in the other three patients. In the early non-cirrhotic stage of chronic hepatitis D, IFN may play a more consistent therapeutic role than in the average advanced case of the disease. Cytokine should be used as soon as a diagnosis of progressive hepatitis D is reached.
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PMID:Treatment of early chronic delta hepatitis with lymphoblastoid alpha interferon: a pilot study. 156 48

Liver transplantation remains a problem for end stage liver disease due to chronic viral hepatitis, in contrast to the success with fulminant hepatitis B, D and C in which recurrence of viraemia is relatively rare. Following transplantation for chronic HCV disease recurrence of hepatitis C is infrequent and does not appear to be an important clinical problem. The complete picture will only be described when a suitable HCV-RNA test becomes routinely available. Patients with cirrhosis due to hepatitis B, with low levels of viraemia, or patients with hepatitis D are less likely to develop reinfection than those with high levels of HBV viraemia. The use of hepatitis B immunoglobulin in high doses for prolonged periods delays rather than prevents recurrence. It is a very expensive ancillary treatment. Patients with chronic hepatitis D related cirrhosis in whom levels of hepatitis B replication are suppressed, have a low recurrence rate even without immunoglobulin prophylaxis although HDAg remains in the liver. Hepatitis only reoccurs with recurrence of HBV infection. Unfortunately transplantation of HBV DNA and HBeAg positive patients has many shortcomings, and reinfection of the engrafted liver and subsequent development of hepatitis B is common. Survival rates are reduced in this latter group. At present there are no firm recommendations that can be given to prevent recurrence: HBIG in large doses and for prolonged periods would appear to be insufficient to prevent reinfection and these patients often die of recurrent disease. A major challenge for transplant groups will be the prevention of viral reinfection particularly in this latter group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Liver transplantation for chronic viral hepatitis. 174 98

A 44-year-old man with chronic hepatitis B virus infection and cirrhosis was treated with recombinant human interferon alfa for 67 days immediately before orthotopic liver transplantation and immunoprophylaxis with hyperimmune globulin to hepatitis B virus in the peritransplant period. Dot blots for hepatitis B virus DNA demonstrated marked reduction in viremia after 41 days of interferon alfa treatment. Southern analysis for hepatitis B virus in liver showed a pronounced decrement in actively replicating forms in the explant, although hepatic infection was still detectable. After liver transplantation, tests for serum hepatitis B virus DNA and hepatitis B surface antigen remained negative. The patient died 32 days after transplantation of causes unrelated to hepatitis B virus. DNA isolated from liver and other visceral organs at autopsy showed infection of the engrafted liver and the persistence of monomeric relaxed circular forms of hepatitis B virus DNA in pancreas, kidney, and spleen. Thus, graft reinfection occurred despite aggressive antiviral therapy and immunoprophylaxis combined with liver transplantation. Existing viral serological markers appear insufficiently sensitive to assess residual infectivity.
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PMID:Persistent hepatitis B virus following interferon alfa therapy and liver transplantation. 198 31

To elucidate the biologic significance of hepatocyte HBsAg, its expression patterns were correlated with virus replication and liver pathology in 578 liver biopsies taken from chronic HBsAg carriers aged 1 to 80 years. Five major patterns of hepatocyte HBsAg were identified: homogeneous [intense and discrete, (Pattern A), faint and discrete, (Pattern B) and faint and grouped (Pattern C)]; globular or spotty (Pattern D), and marginal (Pattern E). Pattern A was always associated with viremia and also very frequently with membrane HBsAg expression, but rarely with active liver disease. It occurred most commonly in HBeAg-positive carrier children and young adults, reflecting an early immune tolerance phase with active virus replication. Pattern B was also usually associated with viremia, but very commonly associated with active disease (70%), reflecting active virus replication with enhanced immune response. Pattern E (marginal HBsAg), which was always in group distribution resembling a clonal expansion, predominated the HBeAg-negative phase and was associated with absence of viremia and occurred mostly in older adults with inactive bipolar disease spectrum (normal liver/mild disease or cirrhosis/hepatocellular carcinoma); this reflects a late phase of inactive virus replication or integration. Patterns C and D did not correlate well with viremia, but also tended to have inactive diseases as did Pattern E. These findings suggest that hepatocyte HBsAg expression is closely related to the natural course of chronic hepatitis B virus infection.
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PMID:Correlation of hepatocyte HBsAg expression with virus replication and liver pathology. 339 3

Five Swedish patients with chronic hepatitis C were prospectively followed until hepatocellular carcinoma (HCC) developed. Hepatitis C virus (HCV) antibodies were analysed by a second generation anti-HCV ELISA and a recombinant immunoblot assay (RIBA-2) and viraemia by detection of serum HCV RNA by polymerase chain reaction. Four patients had post transfusion hepatitis and in one patient the source of infection was unknown. HCC developed after 8 to 23 years of mostly asymptomatic disease and all patients died. Four of them were repeatedly biopsied during follow-up and all had chronic active hepatitis. When HCC was diagnosed, cirrhosis was present in all 5. In 4 patients with available sera, anti-HCV was positive and confirmed with RIBA-2, whereof 2 were reactive only to the c-22 and c-33c epitopes. HCV-RNA was present in all sera when HCC was diagnosed. Thus, after prolonged disease duration these patients were still viraemic.
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PMID:Hepatitis C virus infection with progression to hepatocellular carcinoma: a report of five prospectively followed patients in Sweden. 750 21

One hundred renal transplant recipients were studied for antibodies to hepatitis C virus (HCV), and to HCV RNA in serum by reverse transcription+nested polymerase chain reaction (RT-PCR). Presence of antibody to HCV confirmed by recombinant immunoblot assay II was considered evidence of HCV infection, and detection of HCV RNA by RT-PCR was considered evidence for active viremia. On pretransplant sera, 18 patients were RT-PCR positive and an additional 3 had antibody evidence of HCV infection. At 1-year follow-up, all of these patients were RT-PCR positive and an additional 7 patients became RT-PCR positive. Clinical diagnosis of non-A, non-B hepatitis underestimated the prevalence of HCV infection (5/28 cases, 18%). Serum alanine aminotransferase (ALT) elevations were neither sensitive nor specific. An isolated pretransplant ALT elevation predicted a 52% chance of being RT-PCR positive for HCV. An ALT elevation greater than 2 months after transplant predicted a 45% chance of HCV positivity; however, 18% of patients who never had any ALT abnormality were also HCV positive. Sixty-eight patients had an early postoperative rise in ALT, but there was no correlation with HCV status. After an average follow-up of over 4 years, 3/28 HCV-positive patients developed cirrhosis. HCV infection in the renal transplant population is common and underdiagnosed by clinical and biochemical parameters. HCV appears not to cause aggressive liver disease in the early posttransplant period, but longer follow-up is needed to define the natural history of HCV in the renal transplant population.
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PMID:Non-A, non-B hepatitis and elevated serum aminotransferases in renal transplant patients. Correlation with hepatitis C infection. 750 51

In testing for antibodies to the hepatitis C virus (anti-HCV) in 112 patients with primary hepatocellular carcinoma, 10 of 33 white patients (30%) and 15 of 79 Asian patients (19%) had a positive response to the antibody. The antibody profile to individual hepatitis C viral antigens and the presence of circulating hepatitis C viral RNA were determined in the 25 patients. The anti-HCV antibodies most frequently detected were toward the antigens from the core (C22) and NS3 regions. Serum hepatitis C viral RNA was present in 17 of the 25 patients (68%), and these patients tended to have serum levels of alanine and aspartate aminotransferases higher than those patients without viremia (136 +/- 22 U per liter versus 64 +/- 11 U per liter and 161 +/- 26 U per liter versus 79 +/- 14 U per liter, respectively, both P < .05). Of the 15 Asian patients with hepatocellular carcinoma and anti-HCV, 4 (27%) had coexisting hepatitis B surface antigen (HBsAg) and 13 (87%) had antibodies to either hepatitis B core or surface antigen. Of the 10 white patients with anti-HCV, however, only 1 (10%) had hepatitis B virus antibodies (P < .01). Among 4 Asian patients with coexisting anti-HCV and HBsAg, 1 was found to have serum hepatitis B viral DNA and the other 3 had hepatitis C viral RNA. A history of blood transfusion was obtained from 12 of the 25 patients with anti-HCV (48%); 20 (80%) had coexisting cirrhosis. Our findings support the hypothesis that hepatitis C virus is an important etiologic agent in the development of primary hepatocellular carcinoma in both white and Asian patients in the United States.
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PMID:Evidence for hepatitis C viral infection in patients with primary hepatocellular carcinoma. 751 78


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