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  • 1
    ISSN: 1432-1076
    Keywords: HIV infection ; Acquired immunodeficiency syndrome ; AIDS-related complex ; Thalassaemia major ; Transfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the incidence, clinical and immunological characteristic of human immuno-deficiency virus (HIV) infection in a group of multi-transfused patients with thalassaemia major who were exposed to transfusion-associated HIV infection. Seropositivity to HIV by Western blot and immunofluorescence analysis was detected in 26 out of 590 patients. At a follow up 21–40 months later, none of these seropositive patients had developed acquired immuno-deficiency syndrome (AIDS), and six manifested the AIDS related complex (ARC). ARC was unusually mild and consisted of moderate laterocervical and submandibular lymph node enlargement associated with hypergammaglobulinaemia and a reduced CD4/CD8 ratio resulting from the decreased number of CD4 lymphocytes. These findings suggest that multi-transfused patients with thalassaemia major are relatively resistant to the development of severe manifestations of HIV infection, presumably because their immune status is relatively better preserved than that of other infected population. Longer follow up is, however, necessary to determine whether the incidence of AIDS will be lower in this population or whether overt AIDS merely takes longer to develop.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1076
    Keywords: Key words Hyperbilirubinemia ; Neonatal jaundice ; Glucose-6-phosphate dehydrogenase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The pathogenesis of neonatal hyperbilirubinemia has not yet been completely defined in normal and glucose-6-phosphate-dehydrogenase (G6PD)-deficient newborns. The recent identification of a variant promoter in the gene encoding for the bilirubin uridine-diphosphoglucuronosyl-transferase (UGT-1 A) associated with Gilbert's syndrome, allowed us to explore whether the presence of this variant promoter is a risk factor for the development of neonatal hyperbilirubinemia in normal newborns and in association with G6PD deficiency. We found that the variant (TA)7/(TA)7 promoter shows no statistically significant difference in normal or G6PD-deficient newborns developing severe hyperbilirubinemia and in control subjects from the same population. This finding indicates that the variant promoter of UGT-1 A does not contribute to the development of hyperbilirubinemia in the newborn.
    Type of Medium: Electronic Resource
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