Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied 145 children with acute lymphocytic leukemia (ALL) in remission who had been off chemotherapy for at least 2 years, to assess the prevalence of hepatitis delta virus (HDV) infection, and to determine whether HDV infection was associated with more severe chronic liver disease. The prevalence of chronic HBV infection was 41.5% (60/145). The prevalence of HDV infection among these patients with chronic HBV infection was 50% (30/60). Eighty-five patients were HBsAg-negative. There was evidence that HDV-infected children had more severe chronic liver disease than did HBsAg-positive, anti-HDV-negative patients: (1) their serum ALT levels were significantly more likely to be elevated at long-term follow-up (27/30 vs. 10/26, p = 0.0001); (2) their mean ALT levels were significantly higher 3 years after the cessation of chemotherapy (128 vs. 84 IU/L, p = 0.001); and (3) they were more likely to have either chronic acute hepatitis or cirrhosis when liver biopsy was done (18/23 vs. 6/18, p = 0.0038). Children who were HBsAg-negative had the lowest alanine aminotransferase (ALT) levels and were least likely to have chronic active hepatitis or cirrhosis (3/31). We conclude that infection with HDV in children with ALL is associated with serious chronic liver disease. In long-term survivors, HDV infection is a major cause of morbidity and an adverse prognostic factor in terms of leukemia-free survival.
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PMID:Delta virus and childhood leukemia. 202 65

The frequency and clinical features of acute hepatitis B virus (HBV) infection with and without a hepatitis D virus (HDV) co-infection was investigated retrospectively in the Stockholm region during two different time periods, September 1977-October 1978 and November 1984-October 1986. Totally, 31/229 (14%) patients with acute HBV infection had a HDV co-infection. No change in the frequency of co-infections, 12% and 15%, respectively, was observed between the 1970s and 1980s. Among the 31 HDV co-infected patients 74% were intravenous drug addicts. Totally 23/66 (35%) intravenous drug addicts with acute HBV infection had HDV co-infection. Clinically a biphasic rise of the serum levels of alanine aminotransferase and bilirubin was noted among 63% of the HDV co-infected patients but only among 8% of the solely HBV infected patients (p less than 0.001). A clinically more severe hepatitis was seen significantly more often among the HDV co-infected patients than among the solely HBV infected.
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PMID:Acute hepatitis B and hepatitis D co-infection in the Stockholm region in the 1970s and 1980s--a comparison. 207 8

The aim of the study was to evaluate the safety and effectiveness of interferon alfa-2b, alone and following prednisone withdrawal, in patients with chronic type B hepatitis. Thirty-five patients (27 men and eight women) were randomly allocated to two treatment groups. Group I (n = 17) received 6 weeks of prednisone followed by interferon alfa-2b (INTRON A, Schering-Plough Corporation) 10 million units subcutaneously, three times a week for 16 weeks. Group II (n = 18) was used as an untreated control group for 24 weeks, after which they received 16 weeks of treatment with the same dose of interferon as Group I. Both groups were followed up for 24 weeks after treatment. In Group I, 10/17 patients (58.8%) eliminated hepatitis B e antigen; 8/17 (47.1%) developed antibodies to hepatitis B e antigen; 9/17 (52.9%) became hepatitis B virus DNA negative and 1/17 (5.9%) was hepatitis B surface antigen negative at the end of follow up. In Group II, during the control phase, 1/18 (5.5%) became hepatitis B e antigen negative. When treated with interferon, 7/15 (46.7%) eliminated the e antigen, and 6/15 (40%) developed antibodies to hepatitis B e antigen and were hepatitis B virus DNA negative at the end of follow up. Serum alanine aminotransferase reached normal levels in all seroconverted patients. Liver biopsies showed a marked reduction of inflammation and disappearance of hepatitis B core antigen in liver cell nuclei in almost all cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recombinant interferon alfa-2b following prednisone withdrawal in the treatment of chronic type B hepatitis. 207 67

In this pilot study, 12 patients with chronic delta hepatitis were studied. The diagnosis was based on the presence of antibodies to the hepatitis delta antigen in the serum and hepatitis delta virus RNA and hepatitis delta antigen in the serum and liver. All patients were also positive for hepatitis B surface antigen. The infection was presumed to have been transmitted by intravenous drug abuse in six of the patients, blood transfusion in one and by sexual contact in four (two had antibodies to human immunodeficiency virus in their serum, but did not show signs of acquired immunodeficiency syndrome). In one further patient, the source of infection was unknown. Interferon alfa-2b (INTRON A, Schering-Plough Corporation) was initiated at 5 million units per day subcutaneously for at least 4 months, being reduced by half if side effects occurred. Serum alanine aminotransferase levels, hepatitis delta virus RNA and hepatitis delta antigen were measured at monthly intervals for up to 12 months in some patients. Interferon therapy resulted in decreased serum levels of these three markers. On cessation of therapy, most patients experienced a relapse over 6 months, but alanine amino transferase levels could be normalized once more by restarting interferon therapy. In conclusion, interferon decreased hepatic inflammation by the inhibition of hepatitis delta virus replication, although relapse occurred when interferon was stopped and long-term therapy is required to achieve permanent control of the disease. Care will be required when treating patients with advanced or decompensated liver disease.
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PMID:Therapy of chronic delta hepatitis with interferon alfa-2b. 207 75

Liver biopsies from 52 patients with chronic hepatitis B were investigated for the presence and distribution of HBcAg and the results were compared with the status of hepatitis B virus deoxyribonucleic acid (HBV-DNA). The patients consisted of 37 men and 15 women, aged 16-55 years (mean = 34 years). Serum alanine aminotransferase (ALT) was elevated in 50 patients (range: 18-969 U/L; mean = 290 U/L). Serological testing showed HBsAg in all, HBeAg in 45 (87%), and HBV-DNA in 28 (54%). Liver biopsies demonstrated HBcAg in 35 (67%) patients. HBcAg was not only present in 31 of 45 (69%) patients who were seropositive for HBeAg, but also in four of seven (57%) with antibody to HBeAg (anti-HBe). In 28 of 35 (80%) patients with HBcAg in the liver, serum HBV-DNA was detected. However, no serum HBV-DNA was detected in 17 patients who had no detectable HBcAg in the liver. The distribution of HBcAg in the liver was rather cytoplasmic and nuclear than nuclear alone. Among 33 patients with cytoplasmic HBcAg in the liver, 15 (45%) had an evidence of acute exacerbation of hepatitis with marked ALT elevation (range: 168-894 U/L; mean = 385 U/L) and nine patients showed severe chronic active hepatitis and confluent necrosis, histologically. These results indicate that the presence of HBcAg in the liver correlates with the amount of circulating hepatitis B virus as quantified by serum level of HBV-DNA. The predominant cytoplasmic HBcAg in the liver may suggest the possibility of multiple episodes of acute exacerbation and more severe ongoing hepatitis during the clinical course.
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PMID:Significance of hepatitis B core antigen in the liver in patients with chronic hepatitis B and its relation to hepatitis B virus DNA. 210 4

In a survey carried out from 1985 through 1986, volunteer blood donors to The Greater New York Blood Program were tested for two surrogate markers for non-A, non-B hepatitis--elevation of alanine aminotransferase level and presence of antibody to hepatitis B core antigen. Stored serum samples from selected donors were also recently tested for antibody to hepatitis C virus (anti-HCV). Anti-HCV was detected in 0.9% to 1.4% of donors and was higher in black and Hispanic donors than in white donors. Anti-HCV prevalence increased with increasing age through the fourth decade of life, but decreased thereafter, possibly reflecting the disappearance of detectable antibody with time. Anti-HCV correlated with both alanine aminotransferase level and the presence or absence of antibody to hepatitis B core antigen. These associations suggest that donor screening for elevation of alanine aminotransferase level and presence of antibody to hepatitis B core antigen was, as expected, at least partially effective in preventing transfusion-associated non-A, non-B hepatitis. The detection of anti-HCV in donors who have neither an elevation of alanine aminotransferase level nor presence of antibody to hepatitis B core antigen suggests that donor screening for anti-HCV will further reduce the risk of transfusion-associated hepatitis.
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PMID:Epidemiology of hepatitis C virus. A preliminary study in volunteer blood donors. 210 48

In order to assess the sequential changes of liver pathology after interferon therapy, 70 liver biopsy specimens, collected from 23 HBeAg-positive patients with chronic hepatitis B and 12 patients with chronic non-A, non-B hepatitis, were studied using a numerical scoring system proposed by Knodell et al. The biopsy specimens were obtained immediately prior to the administration of interferon and within one week following the termination of interferon therapy. Three patients with chronic hepatitis B were negative for DNA-polymerase (DNA-P) prior to the interferon administration. Ten patients (50%) lost DNA-P activity. HBeAg became negative in 8 patients (34.8%), of whom 2 seroconverted to anti-HBe. Serum alanine aminotransferase levels normalized in 9 patients with chronic hepatitis B, and non-A, non-B hepatitis. The total Histological Activity Index (HAI) scores in both patients with chronic hepatitis B, and non-A, non-B decreased significantly (P less than 0.001 and P less than 0.005, respectively) after interferon treatment. There was also a significant improvement (0.02 less than P less than 0.001) in each histological category except for fibrosis. When the changes of the HAI scores in patients with chronic hepatitis B were correlated to the outcome in the DNA-P and HBeAg/anti-HBe system after treatment, the histological improvement did not significantly correlate to the outcome of these serological parameters.
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PMID:Histological improvement of chronic hepatitis B, and non-A, non-B with interferon treatment: application of a numerical scoring system for evaluating sequential morphologic changes. 210 67

Liver wedge biopsies were obtained from chimpanzees during the acute phase of experimental non-A, non-B hepatitis infections. Primary chimpanzee hepatocytes were maintained for over 4 weeks in vitro with a serum-free medium supplemented with growth factors and hormones. The de novo synthesis and secretion of plasma proteins characteristic for differentiated primate hepatocytes were sustained under these culture conditions. Immunocytochemical staining for a non-A, non-B hepatitis-associated antigen revealed expression of this cytoplasmic marker during the culture period, indicating a persistence of the infection in vitro. Tissue culture medium derived from the hepatocyte cultures was used to inoculate a nonimmune chimpanzee. The animal subsequently displayed an increase in the serum levels of alanine aminotransferase, the development of histopathologic alterations indicative of viral hepatitis, and the appearance of liver cell cytoplasmic tubules diagnostic for non-A, non-B hepatitis. Concentrated tissue culture medium examined by electron microscopy contained virus-like particles with an average diameter of 39-46 nm, which exhibited an envelope and inner 37-nm core structure.
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PMID:Expression of infectious viral particles by primary chimpanzee hepatocytes isolated during the acute phase of non-A, non-B hepatitis. 211 39

Sera from 172 intravenous drug users were tested for the presence of antibodies to hepatitis C virus (anti-HCV). The results were analysed in relation to aspects of the history of drug use and evidence of liver disease. The presence of anti-HCV was strongly associated with duration of intravenous drug use. Two-thirds of patients were anti-HCV seropositive within two years of commencing regular intravenous drug use, and there was 100% seropositivity among people injecting drugs for more than eight years. Seropositivity for hepatitis C virus closely paralleled exposure to hepatitis B virus, which was also endemic in this population. In contrast, only one patient tested positive for antibodies to the human immunodeficiency virus. The presence of anti-HCV correlated poorly with biochemical markers of hepatitis. About half the patients with anti-HCV had normal serum levels of alanine aminotransferase, whereas an abnormal liver biochemistry was frequently observed in anti-HCV seronegative subjects. Previous studies of non-A, non-B hepatitis that have used abnormal liver biochemistry as a marker have underestimated the prevalence of chronic hepatitis among intravenous drug users; the use of a specific screening test reveals that infection with hepatitis C virus is very common in this population.
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PMID:Hepatitis C virus in intravenous drug users. 804 44

The purpose of this study was to determine whether the response of serum alanine aminotransferase (ALT) to recombinant alpha-interferon was related to the presence or absence of antibodies to hepatitis C virus (anti-HCV) in patients with chronic non-A,non-B hepatitis. A group of 65 patients with chronic non-A, non-B hepatitis was studied. The source of contamination was blood transfusion or administration of blood products in 32, intravenous drug addiction in 14 and unknown in 19. The patients received 1, 3 or 5 MU of recombinant alpha-interferon, three times a week, for 6 months. A complete response was defined as normal ALT by the end of recombinant alpha-interferon treatment. Sera collected before treatment were tested for anti-HCV with an enzyme immunoassay. The overall percentage of anti-HCV positive patients in the study group was 75%. There was no difference between the anti-HCV positive and the anti-HCV negative patients before the treatment with respect to age, sex ratio, source of contamination, serum albumin, prothrombin, bilirubin, ALT or prevalence of cirrhosis. In the anti-HCV positive and the anti-HCV negative groups, there was no difference in the proportion of patients receiving the 1, 3 or 5 MU dosage. The percentage of patients with complete response was not different in anti-HCV positive patients (48%) and in anti-HCV negative patients (50%). There was also no difference in the kinetics of the decrease of mean serum ALT levels between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is the response to recombinant alpha interferon related to the presence of antibodies to hepatitis C virus in patients with chronic non-A, non-B hepatitis? 164 37


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