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)

To elucidate the role played by interferon-alpha (IFN alpha) in the pathogenesis of autoimmune endocrine disease, we determined the autoantibody status, thyroid function test results, hemoglobin-A1c levels, and clinical symptoms of 58 patients who received IFN alpha for treatment of chronic active type C hepatitis. Each patient was treated for 6 months with a total dose of 391 +/- 140 x 10(6) U (mean +/- SD). Thyroid microsomal and/or thyroglobulin antibodies newly appeared or were increased in titer in 6 patients, 2 of whom developed hypothyroidism during IFN alpha therapy. Neither islet cell antibodies nor insulin-dependent diabetes mellitus developed during IFN alpha therapy, although hemoglobin-A1c levels were increased in 2 patients. One patient became positive for antimitochondrial antibodies, and another patient with preexisting antimitochondrial antibodies also manifested deterioration in liver function test results. Parietal cell antibodies and smooth muscle cell antibodies were the most frequent newly developed antibodies in 7 patients. Adrenal medullary cell antibodies and nuclear antibodies newly developed in 2 and 1 patients, respectively. At least 1 of 8 autoantibodies newly appeared in 19 patients (32.8%) and hypothyroidism developed in 2 patients (3.4%) during IFN alpha therapy. On the other hand, in 19 age- and sex-matched patients who did not receive IFN alpha, no autoantibody appeared, and no autoimmune disease developed during a follow-up period of 3 months. These findings suggest that IFN alpha acts as an immunomodulatory agent, inducing autoantibody production and the development of autoimmune disease in susceptible patients. Special attention should be paid to the development of hypothyroidism during IFN alpha therapy.
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PMID:Autoimmune endocrine disease induced by recombinant interferon-alpha therapy for chronic active type C hepatitis. 788 51

Following a three-week administration of alpha-interferon (IFN-alpha), a 62-year-old woman with chronic hepatitis C manifested fever and dyspnea and showed diffuse infiltrative opacities on chest roentgenograms. Her laboratory data included results of anemia with reticulocytosis, a decreased complement level and hepatitis with elevated ALP, LDH and gamma-GTP. Because laboratory data also revealed a positive lymphocyte stimulation test for IFN-alpha, this cytokine was considered to be responsible for the development of interstitial pneumonia, hemolytic anemia and cholestatic liver dysfunction due to its immunomodulatory effects. Although these three disorders have been reported to develop singly after IFN-alpha therapy, this is the first report of a patient in whom these disorders occurred simultaneously.
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PMID:A patient with chronic hepatitis C who simultaneously developed interstitial pneumonia, hemolytic anemia and cholestatic liver dysfunction after alpha-interferon administration. 791 19

In the present paper we described the first case report of silent thyroiditis following alpha-interferon (IFN-alpha) treatment for chronic type C hepatitis in Japan. A 51-year-old woman with chronic type C hepatitis was treated with 6 million units of IFN-alpha three times a week for 24 weeks. Thyroid function was within normal limits and thyroid autoantibodies were negative before IFN therapy. Sixteen weeks after initiation of the treatment, she complained of increasing fatigue, palpitation and losing 7 kg in weight. Thyroid function tests at that time revealed an increase in serum T3, T4, free T3 and free T4 and a markedly suppressed TSH concentration. Both antithyroglobulin antibody (TgAb) and antimicrosomal antibody (McAb) were positive in a dilution of 1: 400. The computed tomographic (CT) scan of the thyroid showed a decrease in the CT number (Hounsfield unit; H.U.) to 58 H.U. (normal, 95-167 H.U.). The 24-h thyroid uptake of 123I was 0.75%. Aspiration biopsy specimens from a nodule in the right lobe and the remaining struma disclosed papillary adenocarcinoma and Hashimoto thyroiditis, respectively. Thyroid function spontaneously returned to normal two months after the onset of thyrotoxicosis through the subclinical hypothyroid stage. After recovery of thyroid function, patient had an operation of papillary cancer without any complications. These clinical features and laboratory findings led to the diagnosis of silent thyroiditis developing in the course of the long-term IFN therapy, which, to our knowledge, has not been reported before in Japan.
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PMID:An episode of silent thyroiditis in a patient with chronic thyroiditis and papillary adenocarcinoma following alpha interferon treatment for hepatitis C. 792 Aug 83

Chronic hepatitis due to putative non-A, non-B, non-C hepatitis occurring in an individual who is negative for HBV and HCV markers has been identifiable only recently. Little or nothing is known about its natural history or response to interferon therapy. In the present study, 13 subjects with chronic non-A, non-B, non-C hepatitis were treated with interferon for 6 months (5 million units, three times per week). Prior to and after 6 months of therapy and again 6 weeks after discontinuing interferon therapy, each subject underwent a liver biopsy. These tissues were used to define the histopathology, the character of the cellular infiltrate within the liver, and the changes in histopathology and inflammatory infiltrate achieved in response to interferon therapy and withdrawal. No differences for age, gender, initial AST, bilirubin, histopathology, or Knodell score were evident between responders (n = 7) and non-responders (n = 6). Only the number of NK cells was altered significantly as a result of IFN treatment and distinguished responders from non-responders. These data demonstrate that: (1) chronic non-A, non-B, non-hepatitis can be treated with interferon; (2) interferon activates NK cells and enhances hepatocyte expression of Class II MHC antigens; and (3) interferon also increases the number of CD3, CD4, and CD8 cells found within the liver but these changes do not distinguish between responders and non-responders.
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PMID:Treatment of putative non-A, non-B, non-C hepatitis with alpha interferon: a preliminary trial. 793 74

The polymerase chain reaction (PCR) was used to examine expression of interferon-alpha (IFN A) genes in general and the expression of messenger RNA (mRNA) encoding the subtypes IFN-alpha-2 and IFN-alpha-4 in blood and liver biopsy samples from patients with chronic hepatitis C or hepatitis non-A, non-B (HC/HNANB) infection entered into a trial of IFN-alpha-2a therapy. Peripheral blood mononuclear cells (PBMC) from healthy controls and HC/HNANB infected patients were studied for their capacity to produce transcripts encoding IFN-alpha after stimulation with Sendai virus. Expression at the level of mRNA for IFN A and the subtypes IFN A2 and A4 was detected in both controls and HC/HNANB infected patients PBMC and no significant difference was seen in expression of IFN A transcripts or level of total IFN-alpha secreted into culture supernatants between controls and patients. Interferon A, and specifically IFN A2 and IFN A4 transcripts were detected in a high proportion of liver biopsies from patients with HC/HNANB infection. The presence of IFN A mRNA (and specifically IFN A2 and IFN A4) showed no correlation to histological improvement nor response to therapy. The use of PCR to detect those IFN A genes that are not expressed, thereby identifying subtypes that may be lacking, could be the key to the choice of IFN-alpha subtypes that are used for effective therapy.
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PMID:Detection of interferon-alpha expression by PCR in patients with chronic hepatitis C and hepatitis non-A, non-B. 794 20

Chronic hepatitis D is a usually severe and progressive liver disease due to infection with the hepatitis delta virus, a unique RNA virus requiring the hepatitis B virus helper function to exert its pathogenic potential. Alpha IFN is at present the treatment of choice for chronic viral hepatitis, but the results obtained in chronic hepatitis D are far from being satisfactory. Available data show that IFN is more likely to be effective if administered to patients with a recent infection (lasting less than 1 year) at high doses (9-10 MU thrice in a week) and for a prolonged length of time (at least 12 months). The optimal timing of IFN treatment remains to be addressed: apart from the clearance of HBsAg and seroconversion to anti-HBs (an event often occurring months to years after completion of a successful IFN treatment) no other early biochemical or virological events can predict a sustained response. Better therapeutic options are therefore needed. Unfortunately, antiviral agents, such as Ribavirin, active against HDV in cell cultures, have failed to confirm their attitude in the clinical setting. In vitro and in vivo evidence points to HBV as a possible target for antiviral therapy in chronic hepatitis D, providing the rationale for trying new deoxynucleotide analogues also in this severe form of hepatitis.
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PMID:Interferon in HDV infection. 797 16

A 19-year-old male healthy hepatitis B virus (HBV) carrier developed fulminant hepatitis following allogenic bone marrow transplantation (BMT) from his brother, who was also a healthy HBV carrier, during the first complete remission of acute myelogenic leukemia (M1, FAB classification). Serum markers related to both HBV and hepatitis C virus (HCV) were elevated during active liver injury when a point mutation in the precore (pre-C) region occurred in the HBV. The patient received low-dose interferon alpha (IFN-alpha), while the dose of cyclosporin A was tapered; the patient eventually recovered from the liver injury. Fulminant hepatitis due to HBV and/or HCV following BMT is rare, and it is considered to have a very poor prognosis. The rationale for the use of low-dose IFN-alpha with cyclosporin A (CyA) is discussed.
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PMID:Fulminant hepatitis following bone marrow transplantation in hepatitis B virus carrier siblings. 800 May 16

Macrophages have been described to be important in determining the resistance of A/J mice or the susceptibility of BALB/c mice to the experimental infection with Mouse Hepatitis Virus 3 (MHV3). The interferon gamma (IFN gamma) activation of A/J and BALB/c mouse macrophages was shown to partially restrict the MHV3 replication only in macrophages from the resistant A/J mice. The activation by IFN gamma and/or infection with MHV3 showed that BALB/c mouse macrophages were capable of releasing tumor necrosis factor alpha (TNF alpha), interleukin 1 (IL-1) and anion superoxide (O2-), and A/J mouse macrophages were capable of releasing TNF alpha and IL-1 but not O2-. Comparable amounts of TNF alpha or IL-1 were released by IFN gamma-activated A/J or BALB/c mouse macrophages. Following MHV3 infection or IFN gamma activation and MHV3 infection, BALB/c mouse macrophages were always capable of releasing higher amounts of TNF alpha, IL-1 or O2- than A/J mouse macrophages, which correlated with their susceptibility to the virus infection. The data indicate that the anti-MHV3 effect induced by IFN gamma in A/J mouse macrophages is not related to the studied extrinsic activities of these cells.
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PMID:TNF alpha, IL-1 and O2- release by macrophages do not correlate with the anti-mouse hepatitis virus 3 effect induced by interferon gamma. 800 17

In a long-term study (27 months) of patients affected by C-virus active hepatitis we have evaluated the effect of decreasing the dose of interferon by 50% and by 75% with respect to the initial efficacious dose (6 MU tiw). Sixty patients received recombinant interferon alpha-2b(r-IFN- alpha-2b) 6 MU tiw for two months followed by 3 MU for seven months (Group A), and 60 patients received r-IFN alpha-2b 6 MU tiw for two months followed by 1.5 MU for seven months (Group B). Three patients in group B failed to return to follow-up and were not considered in subsequent evaluations. Side effects such as to cause suspension of treatment occurred only during the first two months of the study at 6 MU of interferon (3 patients in group A and 6 in group B). During the two months at 6 MU, transaminase values returned to normal in 94 patients (80%). At the end of follow-up, 49 of these patients (42% of the 117 patients examined; or 48.3% in group A and 35.1% in group B) had normal transaminase levels. In no case did the anti-HCV test become negative. On a reduced dose of interferon, relapses occurred more frequently in group B (21.4%) than in group A (9.6%), but the difference was not significant. No difference between responders and non-responders, including relapsing patients, was observed in relation to gender, age, presence of cirrhosis, presence of B-virus antibodies and initial levels of serum transaminase.
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PMID:Long-term follow-up evaluation in HCV chronic hepatitis treated with alpha-2b interferon. A comparison of two protocols. 802 1

The patient was a 25-year-old male doctor, who had pricked his finger with a needle contaminated with blood from a 69-year-old male patient with liver cirrhosis (HCV-Ab positive, genotype II). He was informed from the blood bank that his blood was positive for anti-HCV and his GPT being 148 IU/l on the 65th day after exposure. He was admitted on February 16, 1993 and received a liver biopsy, which was consistent with acute viral hepatitis. His genotype was the same (type II) with the donor patient. IFN-alpha-2b of total doses of 656 Megaunits resolved the hepatitis completely and the HCV-RNA became negative as early as two weeks after starting IFN therapy. Liver biopsy after IFN therapy showed convalescence of acute hepatitis. The progression of acute hepatitis C to chronicity could be prevented by interferon therapy even in unfortunate cases of HCV transmission by needlestick. In conclusion, accidental needlestick should be followed for at least six months, and serum GPT and second-generation anti-HCV ELISA tests are recommended for all infected personnel.
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PMID:[A case of needlestick-induced acute type C hepatitis]. 805 46


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