Cases reported "Hepatitis, Viral, Human"

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1/15. Neonatal syncytial giant cell hepatitis with paramyxoviral-like inclusions.

    Syncytial giant cell hepatitis in the neonatal period has been associated with many different etiologic agents and may present initially as cholestasis. Infectious causes are most common and include: (1 ) generalized bacterial sepsis, (2) viral agents, (3) toxoplasmosis, (4) syphilis, (5) listeriosis, and (6) tuberculosis. Viral hepatitis may be due to cytomegalovirus, rubella virus, herpes simplex, HHV-6, varicella, coxsackievirus, echovirus, reovirus 3, parvovirus B19, hiv, enteroviruses, paramyxovirus, and hepatitis A, B, or C (rare). Giant cell hepatitis may result in fulminant liver failure with massive hepatocyte necrosis and severe liver dysfunction leading to death, resolution with severely compromised liver function, or liver transplantation. The authors report a 6-week-old male who had an unremarkable perinatal period, became jaundiced after developing diarrhea, and subsequently developed liver dysfunction with massively increased liver enzymes and a coagulopathy. Open wedge and core liver biopsies were performed to determine if the patient should be listed for liver transplantation. Giant cell hepatitis with a significant mixed lymphocytic and neutrophilic infiltrate was present on both the wedge and core biopsies. The residual 60% of hepatocytes had ballooning degeneration and many possessed pyknotic nuclei. The hepatocytes were arranged in a pseudoacinar pattern. Electron microscopy showed paramyxoviral-like inclusions in the giant cells, characterized as large inclusions with fine filamentous, beaded substructures (18-20 nm). paramyxoviridae are nonsegmented, negative-sense, single-stranded rna viruses. This family is divided into the paramyxovirinae subfamily containing respirovirus (sendai virus, parainfluenza virus type 3), rubulavirus (mumps, parainfluenza virus type 2), and morbillivirus genera (measles); and pneumovirinae subfamily (pneumovirus genus [respiratory syncytial virus]). Supportive care to determine if hepatic function resolves following the viral episode, liver transplantation with fulminant liver failure, and ongoing evaluation in those who recover to assess chronic liver disease are necessary. Ultrastructural evaluation may unmask the etiologic agent for hepatitis and direct therapy.
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ranking = 1
keywords = varicella
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2/15. Varicella infection in a renal transplant recipient associated with abdominal pain, hepatitis, and glomerulonephritis.

    A 36-year-old renal transplant patient developed 9 years after a successful transplantation a fatal secondary varicella infection. The disseminated varicella infection was associated with hepatitis with liver necrosis, disseminated intravascular coagulation and fibrinolysis and glomerulonephritis. To our knowledge this is the first description of glomerulonephritis associated with varicella infection in a renal transplanted patient. The autopsy showed morphologically a mesangial glomerulonephritis with minor proliferative activity and extensive deposits by electronmicroscopy, mainly in the mesangium. The ongoing immunosuppression may have modified the mesangial cell response to the deposition of immune complexes.
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ranking = 3
keywords = varicella
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3/15. Fulminant hepatitis due to varicella zoster virus in a girl with acute lymphoblastic leukemia in remission: report of a case and review.

    The authors describe a 4-year-old girl with acute lymphoblastic leukemia in remission who developed fulminant hepatic failure due to varicella-zoster virus (VZV). Diagnosing VZV visceral infection in immunocompromised patients is often difficult due to atypical clinical presentation with few or no skin lesions and severe abdominal or back pain. Prompt initiation of empirical treatment with acyclovir and VZV immunoglobulin pending results of the serum polymerase chain reaction for VZV is warranted in this clinical setting.
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ranking = 5
keywords = varicella
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4/15. A novel mutation of varicella-zoster virus associated to fatal hepatitis.

    BACKGROUND: Lethal varicella in immunocompetent hosts is rare and its pathogenesis is largely unknown. The discovery of glycoprotein E (gE) mutants showing attributes consistent with increased virulence in vitro and in animal models, provided a possible molecular mechanism underlying a more aggressive virus infection. However, these mutants have never been associated with unusually severe clinical cases. OBJECTIVES: To varicella-zoster virus (VZV) mutations that correlate with increased virulence. RESULTS: We report a case of fatal hepatitis caused by a VZV bearing a novel mutation on the 3B3 monoclonal antibody epitope of gE in an immunocompetent host. CONCLUSIONS: This report describes a mutant VZV responsible for an aggressive clinical course in an immunocompetent host. Linking these severe clinical presentations of VZV infection to virus mutations might provide insights into the underlying pathogenic mechanisms.
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ranking = 6
keywords = varicella
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5/15. Fulminant varicella hepatitis in a human immunodeficiency virus infected patient: case report and review of the literature.

    We report the case of a 35-y-old hiv-infected female, who presented fulminant varicella hepatitis and recovered under medical treatment. Varicella zoster virus is an uncommon cause of acute liver disease which occurs mainly in immunocompromised patients. acyclovir is the cornerstone of the treatment.
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ranking = 5
keywords = varicella
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6/15. Severe herpes simplex virus hepatitis following autologous bone marrow transplantation: successful treatment with high dose intravenous acyclovir.

    A 17-year-old male patient with T-cell type lymphoblastic lymphoma in complete remission underwent high dose chemotherapy (busulfan 16 mg/kg and cyclophosphamide 120 mg/kg) followed by autologous bone marrow transplantation (ABMT). The patient had been taking oral acyclovir (200 mg x 5) daily from seven days prior to the ABMT (day -7). On day 24, he complained of epigastralgia and general malaise, and the next day his GOT and GPT rose to 570 U/l and 397 U/l, respectively. Although he had no mucocutaneous lesions, hepatitis caused by a herpes virus was suspected, and high dose intravenous acyclovir (10 mg/kg x 3/day) was immediately started. His GOT, GPT and total bilirubin reached peaks of 2,870 U/l on day 26, 1,830 U/l on day 27 and 10.3 mg/dl on day 39, respectively, and rapidly improved thereafter. Serological analyses on IgG antibody titers to herpes simplex virus type 1 using an enzyme-linked immunosorbent assay revealed specific increases (454-fold before transplantation to 3,830-fold on day 46). Antiviral antibody titers to cytomegalovirus, varicella-zoster virus and Epstein-Barr virus showed no significant changes. The serologic markers of hepatitis b virus, hepatitis a virus and hepatitis c virus were all negative. The results indicate the patient's severe icteric hepatitis to have been caused by a reactivation of herpes simplex virus type 1 due to immunosuppression after high dose chemotherapy with ABMT. It is suggested that prompt commencement of high dose intravenous acyclovir is required to treat severe herpes simplex virus hepatitis affecting immunocompromised patients.
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ranking = 1
keywords = varicella
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7/15. Fatal varicella in a healthy girl.

    A fatal case of chickenpox in a healthy 6-year-old girl is reported. She presented with hemorrhagic bullae from thrombocytopenia and then progressed rapidly to disseminated infection involving many systems causing myocarditis, pneumonitis and hepatitis. A peculiar blood picture with marked leukocytosis (leukemoid reaction) is revised and discussed.
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ranking = 4
keywords = varicella
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8/15. Adult respiratory distress syndrome secondary to varicella infection in a young adult.

    A case is described of chickenpox in a young non-immunosuppressed adult, resulting in adult respiratory distress syndrome and hepatitis, which was successfully managed with artificial ventilation and vidarabine.
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ranking = 4
keywords = varicella
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9/15. Varicella-zoster virus infections in children infected with human immunodeficiency virus.

    Primary varicella-zoster (VZ) infection in eight children with perinatally acquired human immunodeficiency virus infection tended to be severe, prolonged, complicated by bacterial infections and in one case fatal. Depletion of CD4-lymphocytes was associated with chronic and recurrent VZ infection. In some patients convalescent VZ antibody titers were low and did not correlate with recurrence of VZ lesions. Administration of acyclovir appeared to be beneficial in suppressing VZ in human immunodeficiency virus-infected children with primary or recurrent VZ infection.
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ranking = 1
keywords = varicella
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10/15. Pancreatic islet-cell damage in children with fatal viral infections.

    The pancreases from 250 children with fatal infections caused by at least fourteen different viruses were examined for lesions in the islets of langerhans. Viral cytopathology was found in 4 of 7 cases of Coxsackievirus B infection, 20 of 45 cases of cytomegalovirus infection, 2 of 14 cases of varicella-zoster infection, and 2 of 45 cases of congenital rubella. Destruction of beta cells and acute and chronic inflammatory infiltrates were found in islets from cases with Coxsackievirus B infections. Characteristic inclusion bodies were observed in islets from cases with cytomegalovirus and varicella-zoster infections. This survey provides further evidence that some viruses can infect and damage human beta cells.
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ranking = 2
keywords = varicella
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