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 determine whether natural human interferon administered under the usual therapeutic dosing scheme would inhibit the hepatic drug metabolism, we performed an antipyrine test in eight patients with chronic B or non-A, non-B hepatitis before and after a subchronic interferon therapy (6 megaunits/day for 17 +/- 4 days, mean +/- SD). Six patients received interferon-beta and 2 received interferon-alpha. To circumvent a possible influence of interferon-induced fever on the hepatic drug metabolism, the antipyrine test during the interferon therapy was performed at least 14 days after the interferon-induced fever disappeared. The kinetic parameters of antipyrine were obtained from seven saliva samples over 32 hours postdose. There were no significant differences in any kinetic parameters of antipyrine observed before and during the interferon therapy. With the sample size of the study, there was only a 20% chance (i.e., beta-power = 0.8 at alpha = 0.05) that we might have missed a 17% reduction in antipyrine clearance by the interferon therapy (type II error). On the other hand, the subchronic interferon therapy lowered serum aminotransferases and DNA polymerase activity significantly (P less than .05) compared with the respective baseline values. Our results suggest that the subchronic therapeutic dosing scheme of interferon as conducted in the present study does not cause the inhibitory effect on the oxidative drug metabolism to a statistically significant or clinically relevant degree in patients with chronic hepatitis, while it improves their liver function. Further studies are required for determining if different types of interferons administered under the different dosing schemes would alter the hepatic drug metabolism and the inhibitory effect would be time-dependent.
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PMID:Effects of subchronic treatment with natural human interferons on antipyrine clearance and liver function in patients with chronic hepatitis. 211 64

Several strains of human fibroblast were identified as good producers of human interferon-beta (HuIFN-beta), among DIP-2 cell was one of the best. We have developed an improved microcarrier culture system for both the mass culture of such cells and the large scale HuIFN-beta production. A routine pilot plant, and successively a large plant, have been accomplished for preparation, purification and preclinical or clinical trials of HuIFN-beta. The purified and lyophilized HuIFN-beta was assayed for its safety for clinical use under the regulation of the National Institute of Health of Japan. Using this HuIFN- preparation, the clinical trials on various viral diseases and malignant tumors were started from the middle of 1979. More recently, the Ministry of Health and Welfare approved this HuIFN-beta as a new drug against melanoma, glioblastoma and chronic active B type hepatitis.
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PMID:Development of a new type of drug by using cell technology; preparation of human interferon-beta from human diploid fibroblast cultures. 324 61

We report here on two patients with kidney allografts who had hepatitis and duodenal ulcer caused by cytomegalovirus. In one case, hepatosplenomegaly and jaundice appeared after high fever lasting for ten days. Laboratory examinations showed liver dysfunction and lymphocytosis with atypical forms. Virological studies revealed cytomegalovirus infection and we successfully treated the patient with human interferon-beta. In the other case, duodenal bleeding followed by interstitial pneumonia occurred at the 54th day after transplantation. Bleeding from the small duodenal ulcer did not stop in spite of conservative and endoscopic therapies, and gastrectomy was performed. Histologically many epithelial cells with intranuclear inclusions were found around the ulcer. Virological studies showed elevation of antibody titres to cytomegalovirus which was isolated from the urine and oropharyngeal secrete. After gastrectomy and treatment with ganciclovir, the general condition improved and graft function was maintained. Our experience with these cases suggests that aggressive diagnostic investigations for cytomegalovirus infection are essential in patients with organ allografts who present liver and gastrointestinal lesions.
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PMID:Cytomegalovirus-associated hepatitis and duodenal ulcer in kidney allograft recipients. 761 76

The prognosis of fulminant hepatitis due to non-A, non-B virus infection and acute reactivation of hepatitis B virus in HB carriers is generally poor, and the treatment of choice in Western countries is recognized as liver transplantation. In countries such as Japan where liver transplantation is not readily available, however, these intractable types of fulminant hepatitis have to be treated medically. Based on the assumption that persistent replication of causal viruses and enhanced host immune responses, especially cellular immunity, to eradicate the viruses are the key mechanism in progressive liver cell destruction and the poor prognosis, we attempted a combination treatment with interferon and cyclosporin A for these types of fulminant viral hepatitis. Subjects in the present study consisted of 1 patient with acute severe hepatitis without coma and 13 patients with coma (13 with fulminant hepatic failure) due to non-A, non-B virus and acute reactivation of hepatitis B virus. The patients were given interferon-beta, 300 x 10(4) U daily, and cyclosporin A, at an initial dose of 3 mg/kg, with tapering. Fourteen patients with coma received artificial liver support that we devised. The patient with acute severe hepatitis survived, showing histologically remarkable liver regeneration. Eight of the 14 patients with hepatic coma, all of whom were indications for liver transplantation according to the criteria of the King's College group, survived. Decreased transaminase level, increased liver volume, and histological liver regeneration were observed in all the survivors. The combination of interferon and cyclosporin A is worth attempting in fulminant hepatitis caused by non-A, non-B virus and acute reactivation of hepatitis B virus in HB carriers.
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PMID:Interferon and cyclosporin A in the treatment of fulminant viral hepatitis. 771 17

An ex vivo antiviral assay was established which uses hepatocytes from mice given recombinant mouse interferon-beta (rmIFN-beta). Assay results were compared with results obtained with a 2',5'-oligoadenylate synthetase (2-5AS) assay. rmIFN-beta was intraperitoneally administered to C3H mice and the antiviral state of their liver parenchymal cells was evaluated in an in vitro cytopathic effect assay. In this assay, cells are infected with vesicular stomatitis virus (VSV) and surviving cells are determined colorimetrically. The antiviral state was measured as the resistance of hepatocytes to VSV infection with increasing doses of rmIFN-beta. The antiviral state correlated well with the dose-dependent increase in hepatic 2-5AS activity. This good correlation suggests that induction of 2-5AS mediates the antiviral action of interferon in liver tissue. This ex vivo assay could be a useful tool for estimating the ability of hepatocytes to resist hepatitis virus infection.
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PMID:An ex vivo assay for estimating the antiviral state of hepatocytes. 773 17

We reported a case of reversible posterior leukoencephalopathy syndrome (RPLS) that occurred during cyclosporin A (CyA) therapy for fulminant hepatitis. A 22-year-old man was given an intravenous drip of interferon-beta, metylprednisolone sodium succinate and CyA, and also received plasma exchange and hemodiafiltration. On the 7th day of the intravenous CyA therapy, in which its dose had been increased from 60 mg/day to 84 mg/day, he became somnolent and had headache, double vision, hallucination and then a generalized tonic-clonic seizure. The blood CyA concentration increased to a level as high as 455 ng/ml. Brain computed tomography (CT) scan without contrast medium revealed symmetric low-density areas in the bilateral occipital white matter and partly in the cortex. T2-weighted magnetic resonance imaging (MRI) showed an increased signal intensity, and single-photon emission CT using 99 mTc showed a hypoperfusion of cerebral blood flow in those areas. After CyA administration was changed to 100 mg/day orally to decrease its uptake in the blood, his consciousness and vision recovered within 4 weeks. Then abnormalities in MRI findings completely disappeared. On the basis of the clinical course and time-sequential change of serum CyA level in this patient, he was diagnosed as having RPLS caused by CyA therapy. Recently, the number of cases of RPLS has increased in the Western countries. However, there are few reports of RPLS after CyA therapy in Japan. From this case, we emphasize that careful following up the patient's neurological findings during CyA therapy is very important and that a cranial MRI is an essential tool for the diagnosis of RPLS.
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PMID:[Reversible posterior leukoencephalopathy in a patient receiving cyclosporin therapy]. 1039 Oct 82

The significance of the route for administration of murine recombinant interferon-beta (IFN-beta) for inducing its therapeutic effects has been studied. BALB/c mice were daily injected intravenously, intramuscularly or subcutaneously with 1.5x10(3), 1. 5x10(4), or 1.5x10(5) IU of IFN-beta, from one day before to 8th day after mouse hepatitis virus (MHV-2) challenge. All mice received IFN-beta survived significantly longer than those without IFN. In the liver of those IFN-treated mice, viral growth and the histopathological damages were extremely alleviated. These results suggest that, irrespective of the differences in the route of administration, IFN-beta markedly suppressed viral activity when its administration was started prior to viral infection. For clinical use, however, further studies are needed on the optimal route for administration if IFN-beta is given after viral infection.
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PMID:Protective effects of murine recombinant interferon-beta administered by intravenous, intramuscular or subcutaneous route on mouse hepatitis virus infection. 1099 1

In patients with hepatitis C virus infection interferon-beta therapy is most effective when administered by the intravenous route. However we would like to present a patient with multiple sclerosis and chronic hepatitis C virus infection who obtained dual benefit from intramuscular interferon-beta therapy. Intramuscular interferon-beta 1a (Avonex) 6 million U/week was started for prevention of attacks in a 32-year-old woman with multiple sclerosis. She had acquired hepatitis C virus infection from blood transfusion during a Caesarean section. Although serum transaminases were within normal limits anti-hepatitis C virus test by ELISA and hepatitis C virus RNA by polymerase chain reaction were positive. Liver biopsy revealed chronic persistent hepatitis. Considering the use of interferon-beta 1a for multiple sclerosis prophylaxis and the stage of hepatitis the patient was not offered any additional treatment. Repeat liver biopsy performed after one year showed the absence of previous findings. The patient has also cleared the hepatitis-C virus RNA.
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PMID:Dual benefit from intramuscular interferon-beta treatment in a patient with multiple sclerosis and chronic hepatitis-C virus infection. 1239 66

Autoimmune hepatitis (AIH) is usually a chronic portal-based hepatitis with prominent plasma cells. Although necroinflammatory activity throughout the lobule is described, centrilobular necrosis (CN) is only rarely the predominant pattern of injury. Recognition of the possibility of AIH in zone 3 hepatitis will lead to prompt steroid therapy and may avert cirrhosis. We report the clinicopathologic features of 6 cases of AIH with CN. The 3 females and 3 males averaged 48 years of age (range 32-66 years). Four patients had a history of autoimmune disorders. All had elevated transaminases and negative serology for viral hepatitis B and C. One had a history of ethanol use. One patient was taking interferon-beta and 1 patient was taking atorvastatin, but none of the patients was taking medication with a temporal relationship to suggest a drug hypersensitivity hepatitis. All patients had positive antinuclear antibody, anti-smooth muscle antibody, or both, although 1 patient was negative for autoantibodies at initial laboratory testing. Four biopsies showed confluent zone 3 necrosis, whereas two biopsies showed spotty CN. Portal inflammation was relatively mild in all cases. Plasma cells were few to numerous in both zone 3 and portal tracts in four biopsies; they were absent in 2 cases. All patients responded to steroid therapy. Two patients relapsed, and rebiopsy in 1 of them showed CN, bridging necrosis, and an increase in the degree of portal-based hepatitis. Another patient was not treated initially; a second biopsy 35 months after presenting revealed periportal hepatitis as well as CN. The histologic spectrum of AIH should be expanded to include zone 3 hepatitis. As with classic AIH, most patients with CN demonstrate serologic and clinical evidence of autoimmunity. Subsequent biopsies in patients with a centrilobular pattern may show evolution to portal-based hepatitis characteristic of AIH but may also show persistence of the zone 3 hepatitis. Unlike other causes of zone 3 hepatitis, AIH is steroid responsive; therefore, timely diagnosis is important.
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PMID:Autoimmune hepatitis with centrilobular necrosis. 1508 66

Post marketing studies of Interferon-beta (IFN beta) therapy in multiple sclerosis (MS) have demonstrated surprisingly high rates of hepatotoxicity. Grade 3 hepatotoxicity (AST and ALT > 5 to 20 upper limit normal) or higher has been observed in as many as 1.4% of MS patients on IFN beta. We report three cases of IFN beta induced hepatitis in MS and discuss the pathology findings and possible mechanisms of drug-induced liver injury.
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PMID:Drug induced liver injury secondary to interferon-beta (IFN-beta) in multiple sclerosis. 1653 69


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