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  • Electronic Resource  (2)
  • Colour Doppler  (1)
  • humoural and cellular markers  (1)
  • 1
    ISSN: 1432-0428
    Keywords: Secondary drug failure ; C-peptide ; anti-Beta-cell autoimmunity ; humoural and cellular markers ; HLA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In some cases patients with Type 2 (non-insulin-dependent) diabetes mellitus fail to respond to treatment with oral hypoglycaemic agents. These patients may respond in the same way as Type 1 (insulin-dependent) diabetic patients. Cellular immune aggression (defined as the capacity of peripheral mononuclear cells to inhibit stimulated insulin secretion by dispersed rat islet cells), insulin autoantibodies, C-peptide response and HLA antigens were determined in 31 Type 2 diabetic patients with secondary failure to oral hypoglycaemic agents and in 22 control subjects. Nine (29.03%) of the 31 Type 2 diabetic patients showed positive cellular immune aggression (2 SD below control group) and 22 (70.97%) presented no cellular immune aggression. There was a relationship between positive cellular immune aggression and each of the following parameters: age, body mass index and microangiopathy. No correlation was found between positive cellular immune aggression and glycaemia, HbA1, blood lipids or atherosclerosis. Patients with positive cellular immune aggression showed a significantly lower glucagon-stimulated C-peptide response vs those with no cellular immune aggression. Within a sub-group of patients who had never been treated with insulin, insulin autoantibodies were present in four of six patients with positive cellular immune aggression. DR2 antigen was found with decreased frequency in patients whereas no DR3/DR4 heterozygotes were observed. Our data support the hypothesis that a group of Type 2 diabetic patients with secondary failure to oral hypoglycaemic agents presented autoimmunity towards pancreatic Beta cells.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1076
    Keywords: Keywords Portal vein thrombosis ; Umbilical catheterization ; Exchange transfusion ; Neonatal intensive care ; Colour Doppler
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aetiopathology of extrahepatic portal vein obstruction is unknown. In retrospective studies, umbilical vein cannulation and sepsis have been alleged to cause portal thrombosis. This prospective study was undertaken to detect whether thrombosis and consequent obstruction of the splenoportal venous system develops after umbilical vein catheterization for exchange transfusion in newborns using Doppler ultrasound. Forty children (M = 24; F = 16) who had undergone exchange transfusion for hyperbilirubinaemia were studied at school age. Maximal duration of the venous umbilical cannulation was 120 min and sepsis did not occur. Clinical, biological and sonographic examinations were normal, except in 3 children. In 2 the left branch of portal vein could not be identified (normal variant). Conclusion Our results show that, in these children, umbilical vein catheterization did not lead to development of portal vein thrombosis. However, when other risk factors such as umbilical infection, traumatic catheterization are associated, children should be screened for obstruction of the portal vein.
    Type of Medium: Electronic Resource
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