Cases reported "Hepatitis A"

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1/120. Fetal meconium peritonitis after maternal hepatitis A.

    hepatitis a virus has rarely been implicated in congenital infections. After maternal hepatitis A at 13 weeks' gestation, ultrasonographic examinations revealed fetal ascites (20 weeks) and meconium peritonitis (33 weeks). After delivery, a perforated distal ileum was resected. Elevated levels of hepatitis A immunoglobulin g persisted in the infant 6 months after delivery.
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2/120. Acute pancreatitis associated with viral hepatitis: a report of six cases with review of literature.

    association of hepatitis viruses with acute pancreatitis in the setting of nonfulminant viral hepatitis is rare. We report six cases of nonfulminant viral hepatitis complicated by acute pancreatitis, including the first documented case of hepatitis e virus (HEV) associated acute pancreatitis. The other five patients had acute viral hepatitis caused by hepatitis A infection. Besides features of viral hepatitis, the presence of typical abdominal pain, high serum amylase, and ultrasound or CT scan features suggested the diagnosis of acute pancreatitis. This complication generally developed in the initial phase of the hepatitic illness. All of the patients had mild to moderate pancreatitis that recovered uneventfully with conservative treatment.
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3/120. Autoimmune hepatitis in a genetically susceptible patient: is it triggered by acute viral hepatitis A?

    The pathogenic mechanisms for autoimmune hepatitis (AIH) are not completely known. Susceptibility to AIH is associated with the human leukocyte antigens (HLA) class II: DR3 and DR4. Nevertheless, AIH does not have a strong genetic predisposition, suggesting that other factors are involved. Perhaps the strongest evidence of a viral cause for AIH exists for hepatitis c virus. AIH has been reported to develop rarely after acute infection with hepatitis a virus. We report on a 55-year-old woman in whom AIH developed during the convalescence period of serologically proven acute viral hepatitis type A. HLA class II DRB1*0401, which was reported to be associated with AIH with a moderate coarse and late appearance in life, was found in this patient. Steroid therapy was followed by a complete clinical remission. Our case supports the possibility that acute hepatitis A may trigger the development of AIH in a genetically susceptible subject.
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4/120. Hepatitis A outbreak in an institution.

    In February 1996, four serologically confirmed cases of hepatitis a virus (HAV) occurred in one household. Investigation showed that the source was a family member with sub-clinical HAV who attended a Unit for learning Disabilities. Reports of two further cases in the institution followed and control measures were instigated. Contacts were unwilling to accept human normal immunoglobulin (HNIG). Following salivary antibody and serological testing, hepatitis A vaccine was offered to the non-immune. An investigation found that sub-clinical infection was significantly associated with being less than 5 years old (RR = 6.07, p < 0.005) and being in one particular classroom (RR = 6.21, p < 0.0005). None of the staff in the institution became infected. In all, 31 cases of hepatitis A (18 clinical and 13 subclinical cases) occurred. This paper (a) describes an outbreak of hepatitis A (b) refers to the use of a salivary antibody test (assay performance to be published elsewhere) (c) identifies factors associated with the acquisition of HAV and (d) endeavours to assess the effectiveness of the vaccine to contain the outbreak.
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5/120. Photo-accentuated eruption and vascular deposits of immunoglobulin a associated with hepatitis a virus infection.

    skin rash associated with hepatitis a virus infection has rarely been reported. We describe a patient with hepatitis a virus infection who presented a rubelliform rash markedly accentuated in sun-exposed areas; direct immunofluorescence studies of the lesion revealed immunoglobulin (Ig) A deposition on the endothelial cells in the upper dermis. Oral rechallenge tests of the previously administered drugs failed to reproduce the eruption. The preferential setting of immune complexes containing IgA at sites of sun exposure and sunlight as a triggering factor might have been responsible for the development of the eruption in this patient. Eruptions associated with hepatitis A virus infections may be more frequent than commonly thought. Because of difficulty to exclude the possibility of drug eruptions, these cases might have been overlooked. In patients with such a disorder, a careful clinical workup such as IgM antibodies for hepatitis a virus at diagnosis and during follow-up is especially recommended.
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6/120. Persisting hiv-1 replication triggered by acute hepatitis a virus infection.

    We report the case of two patients in whom acute hepatitis A was associated with a marked and prolonged increase in human immunodeficiency virus type 1 (hiv-1) viral load. Although in one patient the rise in hiv-1 rna might also have been related to the interruption of antiretroviral therapy, we also observed a similar pattern in the other patient who had a stable undetectable plasma viraemia prior to acute hepatitis and never received treatment with anti-retrovirals. Our observation supports the hypothesis that immune activation that is induced by acute hepatitis a virus (HAV) infection may trigger hiv-1 replication. This highlights the importance of maintaining antiretroviral therapy throughout the acute phase of hepatitis A and of preventing HAV infection through active immunization.
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7/120. Fulminant hepatitis A in patients with chronic liver disease.

    Fulminant hepatitis is a rare complication of acute hepatitis a virus (HAV) infection. We report three cases of fulminant hepatic failure with death due to HAV infection in patients with pre-existing chronic liver disease. Data from the literature also indicate a high case fatality rate during HAV superinfection in patients with chronic hepatitis b, particularly those with cirrhosis, and in patients with alcoholic cirrhosis. In patients with chronic hepatitis c, results are conflicting with some reports indicating a high fatality rate of HAV superinfection and others not, irrespective of the presence or absence of cirrhosis. Based on our observations and this review of the literature, we suggest that patients with chronic liver disease should be vaccinated against hepatitis A.
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8/120. Acute renal failure complicating nonfulminant hepatitis a in HLA-B27 positive patient.

    Here we report the case of a previously healthy 32-year-old HLA B27 positive male who developed completely reversible acute oliguric renal failure in the course of nonfulminant hepatitis A infection. This is a rare complication of uncertain etiology. B27 positive individuals are prone to a number of immune system derangements including overreacting in interactions with some microbiologic agents. We made our consideration on the basis of some experimental models and the presumed pathogenesis of reactive arthritis in these individuals. As a result here we postulate a hepatitis a virus-triggered, immune mediated mechanism of renal injury restricted to genetically susceptible (i.e. B27 positive) individuals. In regard to this hypothesis we warrant additional HLA-profiles and future similar cases for further confirms and conclusions.
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9/120. Familial cluster of fulminant hepatitis A infection.

    hepatitis a virus is a common cause of a self-limited liver disease. Fulminant hepatitis is a rare complication of acute hepatitis A infection. We report a small epidemic of three consecutive fulminant hepatitis A infections in three previously healthy siblings. This is the first report of a cluster of fulminant hepatitis A.
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10/120. Allogenic bone marrow transplantation with a donor presenting with an acute hepatitis A.

    We report the unique occurrence of an allogenic bone marrow transplantation performed as the donor was suffering from an acute hepatitis A. The bone marrow was contaminated at the time of collection, as demonstrated by hepatitis a virus (HAV) rna detected by RT-PCR. hepatitis a virus infection in such a situation could have resulted in a severe liver disease in the recipient. However, although we could demonstrate that the recipient had been infected, he did not develop a symptomatic hepatitis A but only minor disturbances of liver function tests between days 35 and 55. Both the postponement of the transplantation and the use of intravenous polyvalent immunoglobulins have probably played a key role in decreasing the viral load and allowing a rapid clearance of the virus. A possible role of the grafted immune system might also be envisaged, as suggested by the de novo synthesis of IgM in the recipient.
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