Cases reported "Hepatitis A"

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1/5. lassa virus hepatitis. Observations on a fatal case from the 1972 sierra leone epidemic.

    During a recent outbreak of lassa fever in Sierre Leone, a 20-year-old woman developed an acute febrile disease with tonsillar exudates and hemorrhagic manifestations. lassa virus was isolated in cell cultures from pharyngeal secretions and pleural fluid and was identified by complement fixation. Typical arenavirus particles were observed in these infected cell cultures. In a liver biopsy specimen, diffuse hepatocellular damage and focal necroses were evident, with a spectrum of liver cell change, ranging from slight vacuolizaiton to frank lysis. Virus was frequently observed in nearby extracellular spaces and was clearly associated with hepatocytes rather than sinusoidal cells. The demonstration for the first time of lassa virus particules in human tissue provides direct evidence that the virus is responsible for the observed pathologic changes.
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2/5. Fulminant herpes simplex hepatitis in an adult: report of a case in renal transplant recipient.

    A case of disseminated herpes simplex infection is reported in a 31-year-old renal transplant recipient. The patient presented with a unique clinical syndrome: high fever, severe sore throat with buccal and pharyngeal ulcerations, fulminant hepatitis, thrombocytopenia, and leukopenia. The patient died from hepatic failure, disseminated intravascular coagulopathy, and upper gastrointestinal bleeding. The diagnosis was made by positive herpes simplex virus culture from the throat, and was confirmed at autopsy by typical Cowdry's type A intranuclear inclusions in hepatocytes with positive herpes simplex virus culture from the liver. review of the literature reveals that other reported cases have had very similar clinical findings, making disseminated herpes simplex infection with fulminant hepatitis a recognizable syndrome.
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3/5. Aplastic anemia associated with type A viral hepatitis--possible role of t-lymphocytes.

    Posthepatitic aplastic anemia (PHAA) is rather uncommon. Most reported cases have developed after non-A, non-B or B type hepatitis. The only case of PHAA occurring after hepatitis A reported so far, was described by Smith et al., who diagnosed it by the long-term elevation of IgG-class antibody in response to hepatitis a virus. Recently, the detection of IgM-class antibody specific against hepatitis a virus (IgM anti-HAV) has been commonly employed for precise diagnosis of hepatitis A. The case reported here is the first case of PHAA occurring after hepatitis A to be diagnosed by radioimmunoassay of IgM anti-HAV. Furthermore, evidence is presented suggesting that the PHAA may have been an immune-related response. Addition of the patient's peripheral t-lymphocytes to cultures of her own bone marrow cells resulted in a reduction in the number of colony-forming units in culture (CFU-C).
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4/5. Reiter's syndrome following shigella flexneri 2a: a sequel to traveler's diarrhea. Report of a case with hepatitis.

    shigella flexneri 2a was isolated from a patient with Reiter's syndrome (RS) following a family outbreak of traveler's diarrhea. Among 3 members at risk, only the patient was positive for HLA-B27. Data from 3 similar families support the hypothesis that susceptibility to RS is genetically transmitted. It is urged that every effort be made to culture and subtype Shigella and other enteric pathogens in RS following diarrhea. Concurrently, the patient had hepatitis, interpreted as a parallel enteric infection.
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5/5. Suppression of mixed lymphocyte reactivity by cellular and humoral factors in aplastic anemia--both before and after bone marrow transplantation.

    A patient with infectious hepatitis who developed severe aplastic anemia received a bone marrow transplant from her HLA-identical, mixed lymphocyte culture (MLC)-negative sister. It was found that pretreatment of normal lymphocytes with the immunoglobulin fraction of the patient's serum resulted in marked inhibition of their proliferative response to mitogens, as well as their ability to serve as stimulators and responders in MLC. The patient's lymphocytes, unlike those of her HLA-identical sister were unable to stimulate and respond in MLC and markedly suppressed mixed lymphocyte reactivity between two unrelated healthy individuals. Donor-type lymphocytes obtained from the patient after engraftment were also unable to respond or stimulate in MLC. It is suggested that the suppression of lymphocyte responses was mediated by an immunoglobulin present in the patient's serum.
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