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)

Twelve children with chronic non-A, non-B hepatitis were entered in a pilot trial of recombinant interferon-alpha. Although all the children had hepatitis C virus RNA in serum, only five had antibodies against this virus. Children received 3 MU/m2 body surface area interferon-alpha 3 times/wk for 6 mo; they were followed for 24 mo, including the therapy period. One child was dropped from the study, so the results are from the 11 children who completed the study. At the end of the therapy period, 36% of the children had normal ALT levels; this percentage increased to 90% at mo 15 of follow-up. Thereafter, relapse occurred in five children; thus ALT normalization was observed in 5 of 11 children at the 24th month. Moreover, two different ALT patterns were found: HCV antibody-negative children had significant peaks of ALT levels with respect to the basal samples (p less than 0.05) until the third month of the therapy; these levels later decreased. In contrast, HCV antibody-positive children had slight fluctuations of ALT until normal levels were reached. At the end of treatment, three children had HCV RNA; one demonstrated a rebound in ALT levels. Finally, histological activity had decreased significantly in the second liver biopsy specimen in all children. In summary, interferon treatment in children with chronic hepatitis C may be helpful, although these results should be confirmed in controlled trials.
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PMID:Treatment of children with chronic hepatitis C with recombinant interferon-alpha: a pilot study. 132 9

To evaluate the effect of interferon-alpha treatment on the levels of serum aminotransferase (sALT) and of hepatitis C virus (HCV)-RNA, we studied 19 patients with chronic non-A, non-B (NANB) hepatitis. Before therapy, 14 patients were positive by nested polymerase chain reaction (PCR) with primers deduced from the 5'-non-coding region of the HCV genome. Serum HCV-RNA had disappeared in 12 (85.7%) of them by the end of therapy, but then reappeared 6 months later in 4 of these 12 patients. A marked improvement in sALT was seen in 5 of the 8 patients with sustained HCV-RNA disappearance, but not in the 4 patients with only transient HCV-RNA negativity. Pre-treatment levels of hepatitis C viremia, analyzed by single PCR and dot blot hybridization, ranged from 2 x 10(3) to 2 x 10(8) copies/ml, and were below 2 x 10(5) copies/ml in patients with a complete response to interferon therapy. These results suggest that this HCV-RNA assay, combined with sALT testing, may be useful for estimation of the long-term efficacy of interferon therapy in hepatitis C.
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PMID:Detection of hepatitis C virus RNA by nested polymerase chain reaction in sera of patients with chronic non-A, non-B hepatitis treated with interferon. 133 4

In a 47-year-old male patient a tonsillar swelling was pointed out in May, 1991. Lymph node biopsy revealed that he had malignant lymphoma (diffuse large cell type). He had no hepatic dysfunction on admission, but because of positive hepatitis B (HB) antigen and negative HB antibody, he was diagnosed as an asymptomatic HB carrier. The staging examination showed that he had stage IIA lymphoma. Treatment with the COP-BLAM regimen was initiated on June 8. But the level of serum GOT and GPT increased to 286 IU/l and 392 IU/l, respectively. Serum DNA polymerase also increased to 9492 cpm. Interferon-alpha (3 x 10(6) units daily) was administered intramuscularly from June 8. Serum DNA polymerase decreased to zero on September 2, and his HBe antibody became positive indicating seroconversion. COP-BLAM chemotherapy without prednisolone was initiated from September 9 and complete remission was achieved. He was discharged from our hospital on September 25. It has been frequently reported that asymptomatic HB antigen carriers developed fulminant hepatitis during the course of chemotherapy. Our case suggests that it is necessary to continue chemotherapy in order to attain seroconversion by early use of interferon-alpha, when lymphoma patients display aggravated hepatic dysfunction and increased DNA polymerase levels.
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PMID:[Successful interferon-alpha treatment of hepatitis B developing during chemotherapy of malignant lymphoma]. 143 50

We report the occurrence of autoimmune hepatitis after treatment with interferon-alpha in a patient with Philadelphia chromosome-positive chronic myeloid leukemia. Cytogenetic and molecular genetic studies of the T lymphocytes in this patient demonstrated that the T lymphocytes were not part of the leukemic clone. The role of interferon in the production of autoimmune abnormalities is reviewed.
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PMID:Interferon-alpha induced autoimmune hepatitis in a patient with Philadelphia chromosome-positive chronic myeloid leukemia with cytogenetically normal T lymphocytes. 144 68

Thirty-three patients with chronic hepatitis C/non-A, non-B were included in a randomized controlled study of interferon-alpha 2b (IFN-alpha 2b) treatment, 3 x 10(6) U three times weekly for 36 weeks. Using an immunoperoxidase technique, frozen liver biopsy specimens were examined with MoAbs for the presence of T helper cells (CD4), T suppressor/cytotoxic cells (CD8), total T cells (CD2) and B cells (CD22) before and after treatment. beta 2-microglobulin (beta 2-MG) expression on hepatocytes was semiquantified using a scoring system on sections from paraffin-embedded biopsy specimens. Serum levels of beta 2-MG were analysed with a radioimmunoassay technique. Intralobular T helper and T suppressor/cytotoxic cells declined significantly in the treated patients but not in the controls. The portal CD4/CD8 ratio did not change. Before treatment, serum beta 2-MG levels and hepatocyte beta 2-MG expression were significantly higher in patients with chronic active hepatitis compared to patients with chronic persistent hepatitis. Serum beta 2-MG levels increased significantly in responders during IFN treatment, with a maximum after 12 weeks. However, in the liver, the hepatocyte beta 2-MG expression was significantly decreased after treatment. Thus, IFN-alpha treatment does not seem to induce an increased HLA class I antigen hepatocyte expression in chronic non-A, non-B hepatitis, which favours the hypothesis that its anti-viral effects are more important in modulating the disease activity.
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PMID:Lymphocyte subsets and beta 2-microglobulin expression in chronic hepatitis C/non-A, non-B. Effects of interferon-alpha treatment. 154 20

A total of eight patients with chronic active HBsAg-positive hepatitis was treated with recombinant interferon-alpha 2b for 12 months and serum aspartate aminotransferase, alanine aminotransferase, gamma-globulin and prolyl hydroxylase concentrations were determined every 3 months. Liver biopsies after 12 months' treatment revealed a significant (P less than 0.05) reduction in the histological activity score. After 6 months, alanine aminotransferase (P less than 0.01) and aspartate aminotransferase (P less than 0.05) concentrations fell significantly compared with baseline concentrations. Serum prolyl hydroxylase concentrations declined significantly (P less than 0.05) after 15 months and remained depressed. It is concluded that interferon-alpha 2b therapy reduced fibrogenetic activity in chronic active hepatitis B.
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PMID:Modifications in the serum concentrations of prolyl hydroxylase in patients with chronic hepatitis B during and after interferon therapy. 169 25

We investigated the effects of interferon therapy on hepatocyte human leukocyte antigen class I and class II antigen expression and intrahepatic lymphocyte subsets in patients with chronic viral hepatitis B (n = 11) and C (n = 10). Interferon-alpha was administered intramuscularly in doses ranging from 3 to 18 million international units daily for 4 wk. Liver biopsy specimens were obtained just before and immediately after treatment, and the specimens were stained by the indirect immunoperoxidase method for evaluation of human leukocyte antigen expression and lymphocyte subsets. Before therapy, no significant difference was noted between hepatitis B and C in human leukocyte antigen class I antigen expression on hepatocytes or in the lymphocyte subsets in the intralobular and portal areas. After interferon-alpha treatment, hepatocyte expression of human leukocyte antigen class I antigens and serum beta 2-microglobulin levels were virtually unchanged in chronic viral hepatitis C patients, but both were increased in chronic viral hepatitis B patients. Human leukocyte antigen class II antigens were not expressed during treatment. The mean number of intralobular CD3+ and CD8+ cells and the mean serum ALT level decreased significantly in chronic viral hepatitis C patients (p less than 0.05) but not in chronic viral hepatitis B patients. The mean number of intralobular CD4+ cells was unaffected by interferon therapy in both groups. In all 21 patients, the changes in CD8+ cell numbers paralleled the changes in serum ALT levels. Our findings suggest that T-cell cytotoxicity may play an important role in hepatocyte damage in both chronic viral hepatitis C and chronic viral hepatitis B and that the response to interferon-alpha differs in these two types of hepatitis.
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PMID:Effects of interferon on intrahepatic human leukocyte antigens and lymphocyte subsets in patients with chronic hepatitis B and C. 171 Oct

The 2'-5' oligoadenylate synthetase (2-5 AS) activity of peripheral blood mononuclear cells and serum was measured in 23 patients with chronic non-A, non-B hepatitis during interferon therapy, 16 of whom were found to have antibody to hepatitis C virus (anti-HCV). Patients received a daily dose of either 1 million, 3 million or 6 million units of human interferon-alpha or -beta for 4 to 6 weeks. Before treatment, the 2-5 AS activity was not significantly different from that in normal control subjects or patients with chronic hepatitis B. However, during treatment the 2-5 AS activity increased 2- to 41-fold from the initial level. Alanine aminotransferase (ALT) levels normalized promptly after the start of treatment in 15 (65.2%) of the 23 patients, but remained elevated in the remaining 8 (34.8%). Six (40%) of the 15 patients showed consistently normal ALT levels for 6 to 30 months after the end of treatment. There was no significant difference between the responders and non-responders in the pattern of change of 2-5 AS activity, but pretreatment activity levels in peripheral blood mononuclear cells were significantly higher (P less than 0.001) in the patients whose ALT levels did not normalize during treatment. The frequency of patients with a positive anti-HCV was significantly higher (P less than 0.05) in the group in which ALT levels normalized. Therefore, these findings suggest that the pretreatment 2-5 AS activity and the detection of anti-HCV may be useful parameters for predicting the response to interferon therapy.
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PMID:2',5' Oligoadenylate synthetase activity in peripheral blood mononuclear cells and serum during interferon treatment of chronic non-A, non-B hepatitis. 175 91

We measured thyrotropin receptor antibodies in serum obtained from 2 groups of patients participating in clinical trials of recombinant interferon-alpha 2b for viral hepatitis. Group I: Patients with hepatitis B (N = 8), received interferon 5 x 10(6) units thrice weekly for 4 months. Group II: Patients with non-A, non-B hepatitis (N = 16) were randomized to receive interferon in a dose of either 0.25 x 10(6) or 3 x 10(6) U thrice weekly for 6 months and then crossed over to receive the other dosage schedule for a further 6 months. None of the patients developed thyrotoxicosis. Thyrotropin receptor antibody activity was detectable within the "normal range" (less than 10 U/l) in 6 patients prior to treatment. In Group I, thyrotropin receptor antibodies became detectable in 6 patients on treatment, in 4 of whom it was 10 U/l. In Group II, thyrotropin receptor antibody activity was unchanged on low-dose interferon, but on the higher dose became detectable in 9 patients, in 7 of whom it was greater than 10 U/l. We conclude that treatment with interferon is associated with the development of thyrotropin receptor antibodies in a large proportion of patients. It is possible that in some patients treated with higher doses of interferon the increase in thyrotropin receptor antibody activity may be sufficient to induce hyperthyroidism.
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PMID:Thyrotropin receptor antibodies following treatment with recombinant alpha-interferon in patients with hepatitis. 175 38

Reinfection of the graft with hepatitis B virus (HBV) and hepatitis delta virus (HDV) is a potential complication in patients undergoing orthotopic liver transplantation (OLT). Therefore, we added recombinant interferon-alpha (rIFNa) to the standard immunosuppressive regimen in 11 patients who received transplants following liver failure attributed to cirrhosis B (n = 10, with HDV co-infection in four cases) or fulminant hepatitis B (n = 1). Patients were treated with rIFNa for periods ranging from 2 to 3 months between the first and the 13th month after OLT. All patients received immunosuppressive treatment with low-dose corticosteroids, azathioprine and cyclosporine. Anti-HBs hyperimmune globulin was also administered. None of the patients showed evidence of severe allograft rejection. Seven patients suffered HBV reinfection of the graft with histological signs of acute hepatitis in five cases and transition to chronic hepatitis in one patient. Treatment with rIFNa did not prevent or reduce HBV replication. Reinfection of the graft with HDV was demonstrated by PCR in four patients co-infected with HDV. During treatment with rIFNa liver biopsy specimens from three reinfected patients were transiently negative for HDV antigen but not for HDV RNA, and the sera from two patients were transiently negative for HDV RNA. The data indicate that rIFNa can reduce HDV replication in reinfected liver allografts.
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PMID:Follow-up of recurrent hepatitis B and delta infection in liver allograft recipients after treatment with recombinant interferon-alpha. 180 26


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