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)

A patient with primary herpes simplex virus (HSV) type 2 genital infection had dissemination in the 37th week of her first pregnancy. This was manifested by severe hepatitis, pancreatitis, and genital lesions. Temporary improvement followed the delivery of a healthy infant by cesarean section. Encephalitis became evident on the third postpartum day, and recovery was complicated by profound bradycardia, possibly due to viral myocarditis. Vidarabine was administered for seven days, and the patient survived with only mild neurologic sequellae. To our knowledge, this the fourth reported case of disseminated herpesvirus infection in pregnancy and the first due to HSV type 2. Pregnancy must be considered as a possible predisposing factor in dissemination of primary HSV infection.
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PMID:Disseminated herpesvirus infection. Association with primary genital herpes in pregnancy. 17 38

77 patients with chronic active or persistent hepatitis of type B proved by liver biopsy were divided into two groups. 39 cases were treated with Ara-A. dauricine and polysaccharide of pore umbellate as group I. 38 cases were treated with Ara-A, radix isatidis and radix salviae mitiorrhize as group II. By the end of 3 months in the course, the effective rates of ALT and AST were 68.6% and 68.4% in group I, 34.4% and 34.8% in group II. The rates of HBeAg from positive to negative were 35.9% and 39.5% in group I and II respectively. Follow up to 3 months after cessation of therapy, ALT level was normal in 55.6% of group I and 60% of group II: HBeAg was negative in 42.9% of group I and in 50% of group II. Follow up to 9 months after cessation of the treatment, ALT was normal in 56.3% of group I and in 62.5% of group II, HBeAg was negative in 37.5% of group I and in 60% of group II. These results show that dauricine and polysaccharide of pore umbellate did not strengthen the antiviral effect of Ara-A.
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PMID:[Therapeutic effect of combined treatment with Ara-A dauricine and Chinese herbs in chronic hepatitis B infection]. 179 48

Adenine arabinoside (ARA-A) and its monophosphate (ARA-AMP) are potent inhibitors of hepatitis B virus, but they have not been shown to beneficially alter the natural history of chronic type B hepatitis. Analysis of responders to ARA-AMP therapy has shown that responses can be temporary and that truly long-term beneficial responses are rare. Most long-term responses occur in patients with marked elevations in serum aminotransferase activities and severe chronic active hepatitis. This group of patients, however, may also be the most likely to have a spontaneous improvement in chronic hepatitis. Analyses from England suggest that male homosexual patients have a lower response rate to ARA-AMP than heterosexual patients. This difference has not been shown in studies from the United States. The effect of HTLV-III infection on the course and outcome of hepatitis B virus infection and on clinical responses to antiviral therapy needs further evaluation. In view of the side-effects of ARA-AMP and its marginal efficacy, it is unlikely to play a role as a single agent in the therapy of this important chronic liver disease. However, the use of ARA-AMP after a short course of immunosuppressive therapy is an approach to therapy that deserves future investigation in prospective controlled trials.
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PMID:Therapy of chronic type B hepatitis with adenine arabinoside and adenine arabinoside monophosphate. 243 79

Vidarabine (ara A) produces severe dose-dependent side-effects. To examine whether its monophosphate ester (ara-AMP) can be effective in the treatment of chronic hepatitis B when given in reduced dosage as a conjugate with lactosaminated human serum albumin (L-HSA), which selectively enters hepatocytes, five patients with chronic type B hepatitis (HBsAg/HBV-DNA positive for at least 2 years) were treated with the conjugate. The daily dose of conjugate given (35 mg/kg) contains 1.5 mg ara-AMP, whereas the usual daily dose of free ara-AMP is 5-10 mg/kg. In three patients HBV-DNA fell to undetectable levels and remained negative in two; in one of them anti-HBe developed. In the other two patients HBV-DNA decreased but was detectable during treatment--one received three cycles of therapy, and became HBV-DNA negative and anti-HBe positive 45 days after the end of treatment; the other remained HBeAg/HBV-DNA positive. No adverse effects were observed, and biochemical variables (including aminotransferases) remained unchanged or decreased with viraemia. No antibodies (IgM and IgG classes) that bound the conjugate were detected. Thus L-HSA-ara-AMP inhibits HBV replication as well as free ara-AMP but at a third to a sixth of the dose.
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PMID:Inhibition of hepatitis B virus replication by vidarabine monophosphate conjugated with lactosaminated serum albumin. 245 4

Interferon-gamma (IFN-gamma) was induced from a human peripheral mononuclear fraction by incubation with a streptococcal preparation stabilized with penicillin G (OK432). This IFN-gamma-producing activity was significantly reduced in patients with chronic hepatitis and hepatocellular carcinoma. In patients with liver cirrhosis it was also reduced but not significantly. Serum hepatitis B virus DNA and skin tests for the purified protein derivative of tuberculin, phytohemagglutinin-P and a polysaccharide fraction prepared from streptococcus pyogenes Su strain were determined to have no significant relation to this IFN-gamma-producing activity. Although the addition of interleukin 2 (IL-2) to the culture medium enhanced the IFN-gamma-producing activity, there was no difference in this enhancement between normal control and chronic hepatitis. Therefore reduction of the IFN-gamma-producing activity observed in chronic hepatitis seems to be caused by a decreased number of IFN-gamma-producing activity cells or hypofunction of these cells or both. Since HBeAg became negative in patients whose IFN-gamma-producing activity was increased by the administration of the immunopotentiator OK432 or IFN-beta, the IFN-producing system in the patients with B type hepatitis may contribute to the elimination of HBV. Adenine arabinoside suppressed IFN-gamma-producing activity both in vivo and in vitro.
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PMID:In vitro interferon producing activity of peripheral mononuclear cells in patients with chronic liver disease. 303 38

Primary varicella-zoster virus infection (chickenpox) in immunocompromised children is frequently associated with visceral dissemination and attendant high mortality. Eight children with malignant neoplasms and chickenpox with visceral involvement (seven with hepatitis, three with pneumonitis, two with encephalitis, and two with coagulopathy) were initially treated with intravenously (IV) administered vidarabine but demonstrated progressive visceral involvement. After three days of vidarabine treatment (two days for two patients), seven had rising serum SGPT levels, all eight had pneumonitis, seven had deteriorating mental status and/or seizure activity, and six had worsening coagulopathy. Vidarabine was replaced by IV administered acyclovir, with subsequent improvement in all but the most severely ill patient who died. Seven of eight patients recovered completely; no side effects of acyclovir were observed. This clinical experience suggests that acyclovir may be more effective than vidarabine in disseminated varicella infection; however, controlled clinical trials will be necessary to establish this.
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PMID:Acyclovir treatment of disseminated varicella in childhood malignant neoplasms. 385 82

A considerable amount of information has accumulated during the past 10 years in the search for antiviral agents. Ribavirin and inosiplex are 2 interesting developments to come out of this search. Ribavirin, a synthetic nucleoside, has an unusually wide spectrum of antiviral activity, especially when tested in vitro. A large number of RNA and DNA viruses are sensitive, especially herpes viruses, poxvirus, influenza, parainfluenza, reovirus, togavirus, and RNA tumour viruses. The in vivo antiviral spectrum of activity is much narrower, with activity against herpes virus, influenza, parainfluenza, measles and adenoviruses. However, controlled clinical trials have not been uniformly successful in treating influenza, hepatitis, herpes simplex and herpes zoster. Inosiplex has been shown to have antiviral activity in vivo against influenza, herpes simplex, rhinovirus and vaccinia virus infections. However, antiviral activity has not been consistently demonstrated, and this observation led to further studies which revealed its immunomodulating effects. The accumulated evidence has indicated that inosiplex is more a prohost agent rather than an antiviral drug. Immune functions which are depressed during viral infection can be restored to normal by inosiplex therapy. At present, neither ribavirin nor inosiplex alone has been shown to be uniformly successful in the treatment of human viral diseases. Nevertheless, their potential place in chemotherapy should not be neglected, although further data are needed to determine what this place will be. Whether combining them with other antiviral agents such as interferon, acyclovir, Ara-A, and so on, would produce a potentiation of action and improved antiviral chemotherapy, will be an interesting area for further study.
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PMID:Ribavirin and inosiplex: a review of their present status in viral diseases. 616 18

The current status of therapy for chronic HBsAg positive hepatitis is reviewed. Corticosteroid therapy usually has little, if any, benefit; in fact, in addition to its customary side-effects, it may enhance viral replication. Corticosteroids are indicated only in the rare case of life-threatening HBsAg-positive severe chronic active hepatitis with immune features. Clinical studies on antiviral treatment are continuing. Today interferon, ARA-A, and acyclovir appear the most promising agents under investigation. Patients with HBeAg-positive chronic hepatitis should be referred to centers evaluating antiviral treatment, particularly in the case of progressive liver dysfunction, relapsing activity or psychological imbalance because of contagious blood. There are at present few prospects of eradicating hepatitis B virus in patients with HBsAg, antiHBe positive cirrhosis, who remain at risk of developing hepatocellular carcinoma. With the exception of the above-mentioned categories, patients with chronic HBsAg-positive hepatitis should be encouraged to pursue as normal a life as possible. To define the natural history of the disease more precisely, they should be followed carefully after being adequately informed about their disease and the proper preventive measures.
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PMID:Treatment of chronic hepatitis type virus B. 619 73

We present a case of fetal liver failure caused by the activation of lamivudine-resistant hepatitis B virus (HBV) nine months after lamivudine treatment. A 57-year old man visited our hospital for the treatment of decompensated chronic hepatitis B. Lamivudine was started in December 2001. Subsequently, serum HBV was negative for HBV DNA with seroconversion from HBeAg to anti-HBe and improvement of liver function. However, HBV DNA and HBeAg were again detected in September 2002. He was complicated by breakthrough hepatitis and admitted to our hospital in November for severely impaired liver function. Vidarabine treatment was started and serum HBV DNA and alanine aminotransferase (ALT) decreased transiently. However, after the start of alpha-interferon treatment, HBV DNA level increased and liver function deteriorated. He died 1 mo after admission. An analysis of amino acid sequences in the polymerase region revealed that rtM204I/V with rtL80I/V occurred at the time of viral breakthrough. After the start of antiviral treatment, rtL180M was detected in addition to rtM204I/V and rtL80I/V, and became predominant in the terminal stage of the disease. HBV clone with a high replication capacity may be produced by antiviral treatment leading to the worsening of liver function. Antiviral therapy for patients with breakthrough hepatitis in advanced liver disease should be carefully performed.
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PMID:Fatal liver failure caused by reactivation of lamivudine-resistant hepatitis B virus: a case report. 1735 33