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)

To investigate clinicopathologic characteristics of hepatocellular carcinoma (HCC) in young adults, excised tumors from 21 patients younger than 45 years (young group) were compared with findings in tumors from 204 patients older than 45 (old group). In the young group HCC showed (1) a high incidence of positive hepatitis B virus surface antigen (HBsAg) (young 71.4% versus old 20.1%); (2) relatively well-preserved hepatocellular function (indocyanine green test; young 10.7 +/- 8.8% versus old 20.6 +/- 10.8%); (3) low incidence of histologically verified concomitant cirrhosis (young 52.4% versus old 78.4%); and (4) a more advanced stage of the disease in TNM classification (Stage III; young 52.4% versus old 18.1%). With respect to survival rates achieved by surgery, there was no statistically significant difference between the two groups. Thus, hepatitis B virus may relate to the occurrence of HCC in the young patients. Despite the advanced stage in the young group, survival rate after surgery was comparable with that achieved in the old group. These observations mean that a close periodic surveillance of young adults with a positive HBsAg is required to detect HCC at an early stage. Treatment of patients with HBsAg using interferon or vidarabine and hepatitis B vaccine should be made to convert HBsAg to negative in these individuals.
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PMID:Clinicopathologic features of hepatocellular carcinoma in young patients. 217 72

The efficacy of interferon treatment for Australian patients with chronic active hepatitis B (CAH-B) was assessed by a three-centre randomised controlled trial in Sydney and Brisbane. Thirty patients (29 with histologically-proven CAH-B with and without cirrhosis and one with chronic persistent hepatitis) were allocated to receive either thrice weekly intramuscular injections of recombinant human leucocyte interferon -alpha A (either 2.5, 5.0 or 10.0 million units/m2) for six months followed by 12 months of observation, or to be observed for 18 months without active treatment. Three of 23 treated patients but none of seven controls underwent clinical, biochemical and histological resolution of their disease with loss of HBsAg, HBeAg and HBV-DNA from serum. An additional six treated and two control patients underwent a sustained partial remission of their disease. This was characterised by resolution of symptoms and serum aminotransferase abnormalities in association with seroconversion from HBeAg positive to negative, loss of HBV-DNA from serum but persistent hepatitis B surface antigenaemia. In such patients, there was significant improvement in histological appearances but some necroinflammatory activity remained and fibrosis was unchanged. Although total response rates were similar in treated and control subjects, they appeared to occur earlier after interferon treatment. Treatment with interferon was associated with predictable but minor side effects that usually did not necessitate dose reduction and rarely compromised the patient's life style. Interferon is thus a feasible treatment for CAH-B. Complete responses occurred only in treated patients and partial responses appeared to occur earlier in treated than in untreated patients. However, differences in the partial response rate at 18 months were not significant and seroconversion from HBeAg positive to negative was not associated with complete histological resolution of disease activity. Hence, while interferon is a promising agent for treatment of CAH-B, efforts must continue to define more optimal treatment regimes and to identify those patients most likely to respond to this agent.
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PMID:Randomised controlled trial of recombinant human interferon -alpha A for chronic active hepatitis B. 218 91

Although there is no established therapy for the fibrogenesis of hepatic cirrhosis, many potential therapies are now emerging. The requirements for the "perfect therapy" for hepatic fibrosis can be listed: (1) the pharmacologic agent should be active only in the liver; (2) its effect should be specific for collagen (or another critical extracellular matrix component); and (3) it should not be toxic. To date no agents fulfill these criteria. Of the agents we reviewed, only colchicine appears sufficiently safe for use outside of controlled clinical trials for cirrhotic patients whose underlying disease is not otherwise treatable. However, confirmation of the efficacy of colchicine in additional well-controlled clinical trials is still required. Agents such as collagen propeptides require extensive in vitro development, while trials in animal models are required for prolyl 4-hydroxylase inhibitors, proline analogues, and prostaglandins. For more developed agents, such as malotilate and gamma-interferon, there is now a need for well-designed long-term clinical trials.
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PMID:Therapy for hepatic fibrosis. 218 90

We conducted a prospective, randomized trial to study the efficacy and tolerance of long-term versus short-term treatment with recombinant interferon alfa-2a in patients with chronic hepatitis B. Ten patients were randomly assigned to a 6-month interferon regimen, and 10 patients were assigned to a 3-week interferon trial. Eleven patients (five assigned to long-term treatment and six to short-term treatment) did not complete interferon therapy: eight had either severe thrombocytopenia or neutropenia; one had pronounced fatigue in relationship to administration of interferon; one had spontaneous bacterial peritonitis and sepsis and died; and one had a massive fatal variceal hemorrhage during interferon therapy. Most of the serious hematologic complications occurred in patients with cirrhosis and hypersplenism. In one patient, seroconversion to hepatitis B virus DNA negativity occurred before the onset of treatment. Four of the five patients able to complete the 6-month interferon regimen and only one of four patients able to complete the 3-week trial had seroconversion to hepatitis B virus DNA negativity. Thus, we conclude that the therapeutic response was better among patients who were able to complete a 6-month interferon trial. In patients with cirrhosis and hypersplenism, development of either severe thrombocytopenia or leukopenia associated with interferon therapy precluded completion of treatment.
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PMID:Long-term versus short-term treatment with recombinant interferon alfa-2a in patients with chronic hepatitis B: a prospective, randomized treatment trial. 221 80

We have measured natural killer (NK) cell activity in patients with hepatocellular carcinoma (HCC) and have examined the effects of in vitro and in vivo administration of alpha-interferon (IFN) on NK cell activity. The NK cell cytotoxicity of HCC patients was significantly lower than that of patients with cirrhosis or healthy controls. Reduced NK cell cytotoxicity in HCC did not correlate significantly with either the serum alpha-foetoprotein concentration or the patient WHO performance grade. NK cell cytotoxicity in all groups could be increased by prior incubation of effector cells with IFN, but this was significant only in HCC patients, in whom 10 IU/ml of IFN increased NK cell cytotoxicity from 37 +/- 10% to 53 +/- 8% (effector to target ratio, 50:1, mean +/- SEM; p less than 0.05). Further increases in IFN concentration failed to increase NK cell activity further. NK cell cytotoxicity was measured immediately before and 24 h after 2.5 x 10(6) IU/m2 of IFN was given subcutaneously to four HCC patients. NK cell cytotoxicity rose from 27 +/- 9% to 61 +/- 5% (effector to target ratio, 50:1, mean +/- SEM; p = 0.05).
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PMID:Natural killer cell activity in hepatocellular carcinoma. In vitro and in vivo responses to interferon. 244 65

It was previously thought that two distinct types of chronic hepatitis B virus (HBV) infection existed. However recent evidence suggests that these are in fact phases in a continuous spectrum which evolves with time. Immediately after infection there is active viral replication. In patients infected in adult life, particularly in Europe and the USA, this is associated with varying degrees of liver damage. In those infected at birth, particularly in the Far East, there is initially much less inflammation with normal liver function. In succeeding years, viral replication decreases and liver damage increases with more deranged liver function test results. Eventually viral replication ceases and liver inflammation decreases, resulting in seroconversion with a loss of HBeAg and appearance of anti-HBe. Unfortunately, cirrhosis has already developed in some adults, with the increased risk of the later development of primary hepatocellular carcinoma. It is likely that there is a favourable window during the natural history of the infection when interferon is effective, probably in the few years immediately before spontaneous seroconversion.
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PMID:The natural history of hepatitis B virus infection. 247 May 21

We measured activities of alpha- and gamma-interferon simultaneously in 198 sera of 70 patients with acute and chronic viral hepatitis using specific and sensitive enzyme immunoassay and immunoradiometric assay. The results were compared with those in patients with influenza and in healthy controls. Twelve out of 28 patients with acute viral hepatitis showed positive alpha-IFN and/or gamma-IFN activities. alpha-IFN was detectable throughout the clinical course while gamma-IFN levels rose in the convalescent phase regardless of etiology. Conversely, in patients with influenza, both alpha-IFN and gamma-IFN levels of initial samples tended to be higher than those of late samples. Six out of 12 patients with chronic active type B hepatitis showed increased alpha-IFN and/or gamma-IFN values during acute deterioration with marked elevation of serum alanine aminotransferase. However, the two interferons did not always appear simultaneously, although either was detectable in both acute and chronic hepatitis. Enhanced alpha-IFN or gamma-IFN activity was not found in asymptomatic chronic hepatitis B carriers or in patients with chronic persistent hepatitis and liver cirrhosis with chronic hepatitis B virus infection, with the exception of 2 cases. Our results indicated that circulating multiple IFN species were present during the clinical course in some patients with acute and chronic viral hepatitis.
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PMID:Serum levels of alpha-interferon and gamma-interferon in patients with acute and chronic viral hepatitis. 249 28

Hepatitis B and Non-A-non-B infections often become chronic and proceed to cirrhosis associated with a shortened life expectancy. Both infections are transmitted by parenteral or sexual routes. New insights in the structure of the hepatitis B virus (HBV) as well as in the immune response mechanism of the organism permit by serological testing a clear definition of the replicative state of the virus. Together with the parameters of inflammation (e.g. transaminases, liver histology) it is possible to determine the activity of the hepatitis. The most effective treatment of chronic HBV-infection today is the therapy with alpha- or beta-interferon. The aim of this treatment is the inhibition of HBV replication and accellerated elimination of the virus, indicated by seroconversion of HBEAg to anti-HBEAg. The most significant advance in the knowledge of percutaneous Non-A-non-B hepatitis is the identification of the responsible virus and the development of a diagnostic test for its serological detection. Since this type of hepatitis becomes chronic in 50-60% of the cases, therapy is urgently required. Clinical studies showed that also for Non-A-non-B virus infection alpha-interferon is most effective. Currently the optimal dosage, duration and point in time for interferon treatment is being evaluated.
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PMID:[Epidemiology and clinical aspects of chronic hepatitis B and non-A, non-B virus infections]. 250 33

Alpha-interferon (IFN-alpha) has been shown to be beneficial in the treatment of chronic active hepatitis occurring as a consequence of hepatitis B virus (HBV) infection. Therefore, it has been used to reduce the high rate of allograft infection in clinical liver transplantation of HBV-positive individuals. This study was performed to evaluate the effect of IFN-alpha on lymphocyte subsets as well as the HLA-DR antigen expression in liver tissue. The resected livers obtained from two groups of patients who received liver transplants between 1983 and 1987 at the University of Pittsburgh were examined: group A consisted of 11 patients who were not treated (controls), and group B consisted of 10 patients (experimental group) who were treated with IFN-alpha for 29.4 +/- 5.6 days prior to transplantation. No differences between the two groups existed in terms of a variety of demographic and clinical characteristics. Both groups had cirrhosis as a result of chronic HBV infection. Monoclonal antibodies to cell-surface antigens unique to different lymphocyte populations and the HLA-DR antigens were used in conjunction with the avidin-biotin-immunoperoxidase technique to identify cells in tissue sections. The number of HLA-DR-positive lymphocytes in the liver was increased (P less than 0.005) within the portal areas in rIFN-alpha-treated group as compared to that seen in the untreated group (84.4 +/- 13.6/HPF vs 33.3 +/- 4.8/HPF). Moreover, the intensity of the HLA-DR antigen expression in the portal areas (P less than 0.02) and in the hepatic lobule (P less than 0.05) was greater in the treated group than in untreated group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alpha-interferon. Its effect upon lymphocyte subpopulations and HLA-DR expression within the liver. 253 Oct 67

Lymphokine-activated killer activity and natural killer activity in hepatocellular carcinoma patients were assessed. Maximum lymphokine-activated killer activity was induced at 3 to 5 days of incubation, and lymphokine-activated killer activity tended to increase in a manner dose dependent of recombinant interleukin-2. However, the maximum increase of lymphokine-activated killer activity in hepatocellular carcinoma was not as high as that of normal subjects or liver cirrhosis patients. Lymphokine-activated killer activity was impaired in hepatocellular carcinoma as compared to that in normal subjects. Hepatocellular carcinoma seemed to consist of two groups: i.e. a high-lymphokine-activated killer activity group and a low-lymphokine-activated killer activity group. Reduction of natural killer activity was also observed in hepatocellular carcinoma as compared with that in normal subjects and patients with liver cirrhosis. No correlation could be demonstrated between natural killer activity and lymphokine-activated killer activity in normal subjects, liver cirrhosis patients and hepatocellular carcinoma patients. With regard to the presence of HBsAg or alpha-fetoprotein concentration in the sera, there was no significant difference in natural killer and lymphokine-activated killer activity in hepatocellular carcinoma patients. Patients with a small mass lesion showed a low lymphokine-activated killer activity, and depressed lymphokine-activated killer activity was not necessarily related to tumor size. In comparison with the high-lymphokine-activated killer group, the low-lymphokine-activated killer group showed a significant decrease in gamma-interferon production and a preserved function of indocyanine green clearance.
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PMID:Defective function of lymphokine-activated killer cells and natural killer cells in patients with hepatocellular carcinoma. 253 90


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