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Biomedical subjects

M S Scotta

Publications and source records attributed to M S Scotta.

At least 37 records · Page 2Linked to original sources
PubMed1985

[Role of children with chronic hepatitis in the intrafamilial spread of hepatitis B virus infection].

In order to evaluate the intrafamilial spread of hepatitis B virus (HBV) infection we studied the serological markers of HBV in 101 relatives of 35 children with chronic hepatitis B. Sixty per cent of relatives had markers of infection and 25% showed persistent HBs antigenemia. The high prevalence of HBeAg versus anti-HBe in chronically infected relatives suggests a close temporal relationship of the infection between adults and children. These results support the hypothesis that the child is the main carrier of HBV infection in his family.

Adolescent↗
PubMed1984

[Chronic HB virus hepatitis in children. A study of 29 cases].

Clinical, biochemical and histological features of chronic hepatitis type B were studied in 29 children aged 8 months to 13 years. On entry into the study, all were known to have had hepatitis B surface antigen (HBsAg) with elevated serum transaminase levels for at least six months. A possible source of infection was found in 15 children. When they entered the study, all patients were anicteric and all but one asymptomatic. Hepatomegaly was detected in 15 patients and was associated with splenomegaly in two. Hypergammaglobulinemia was present in 4 children. Serological evaluation of hepatitis B virus markers showed evidence of complete viral replication (HBeAg positivity) in 24 cases and incomplete replication (anti-HBeAg positivity) in 5. Liver histology showed chronic persistent hepatitis (CPH) in 18 children, and chronic aggressive hepatitis (CAH) in 10 (3 moderately active and 7 with major signs of aggressivity ) associated with cirrhosis in 5. One patient had only minimal histological changes. Evaluation of clinical, biochemical and virological parameters did not strictly parallel the histological diagnosis in terms of "activity" of the disease. Follow-up for a mean period of 13 months showed good clinical tolerance to the disease in both CPH and CAH patients. Only 2 children with CAH were given corticosteroids and/or azathioprine for a short period. During follow-up no children with active disease developed liver insufficiency or evidence of portal hypertension. No significant difference in the percentage of children who had seroconversion to antiHBe was found between CPH and CAH groups. Only one child with CAH became HBsAg negative.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗
PubMed1984

Hepatitis B virus infection and Schönlein-Henoch purpura.

Sch onlein -Henoch purpura developed in two children in association with hepatitis B virus (HBV) infection. The first child, an 8-year-old boy, first had a clinical picture of Sch onlein -Henoch purpura and then was found to have HBV-related chronic persistent hepatitis. In the second child, a 6-year-old girl, characteristic skin lesions, arthralgia, and proteinuria developed during acute hepatitis B. Immunofluorescence demonstrated IgA deposition in the renal glomeruli of the first patient. We suggest that evidence of HBV infection should be sought in patients with Sch onlein -Henoch purpura.

Acute Disease↗
PubMed1983

Defective neutrophil motility in children with chronic liver disease.

Neutrophil motility was assessed in 31 children with chronic liver disease to estimate the eventual increased susceptibility of these patients to bacterial infections. Twelve children had chronic hepatitis (seven with chronic persistent hepatitis and five with chronic active hepatitis), which was mostly related to hepatitis B virus (HBV) infection. Nineteen children had chronic intrahepatic or extrahepatic cholestasis. A total of six serious bacterial infections occurred in four of the 31 patients during the study. Twenty of the 31 children had a persistent defect of neutrophil chemotaxis. This defect was found in four types of childhood chronic liver disease: HBV-related chronic hepatitis and idiopathic intrahepatic cholestasis of infancy, in which the defect did not seem to predispose significantly to bacterial infection, and in Byler's disease and biliary atresia, in which this neutrophil defect was associated with an increased frequency of severe infections.

Adolescent↗
PubMed1983

Membranous glomerulopathy and chronic small-intestinal enteropathy associated with autoantibodies directed against renal tubular basement membrane and the cytoplasm of intestinal epithelial cells.

A child with an immune-mediated disease is described, who presented two very rare clinical manifestations, a membranous glomerulopathy with circulating anti-renal tubular basement membrane antibody and a small-intestinal enteropathy with circulating antibody directed against the cytoplasm of intestinal epithelial cells. Steroid treatment was followed by complete resolution of the renal but not the intestinal manifestations.

Autoantibodies↗
PubMed1982

Cell-mediated immunity in children with chronic cholestasis.

Cell-mediated immune response was evaluated in 14 children with long-lasting intra- or extrahepatic cholestasis. Cell-mediated immunity was clearly depressed in children with intrahepatic cholestasis while children with extrahepatic biliary obstruction had a more modest and variable degree of impairment. This finding may be related to the longer duration of cholestasis and the higher total bile acid level in the intrahepatic compared to the extrahepatic group. In particular, in children with Byler disease, long-lasting, severe intrahepatic cholestasis was associated with depressed cell-mediated immunity and recurrent severe infections.

Adolescent↗
PubMed1982

IgA-containing plasma cells in the intestinal mucosa of children with selective IgA deficiency.

In 8 children with selective IgA deficiency (serum IgA less than 5 mg/dl, secretory IgA less than 0.5 mg/dl in unstimulated saliva) immunofluorescent staining of intestinal biopsy specimens revealed the presence of IgA-containing plasma cells. This finding supports the hypothesis that in the intestinal mucosa of patients with IgA deficiency B lymphocytes undergo "sterile" differentiation into IgA-containing plasma cells probably incapable of secreting the IgA synthesized.

B-Lymphocytes↗
PubMed1981

Goodpasture's syndrome in a child: natural history and effect of treatment.

An 8-year-old girl with microhematuria of recent onset developed a picture of pulmonary hemosiderosis in the space of 2 months. Some months later while pulmonary involvement was improving severe extracapillary glomerulonephritis developed. Circulating anti-glomerular basement membrane antibody was detected and linear deposition of IgG along glomerular basement membrane was observed. A diagnosis of Goodpasture's syndrome was made and treatment was started with prednisone, cyclophosphamide and periodic plasmapheresis with complete progressive disappearance of circulating anti-glomerular basement membrane antibody. After suspension of plasmapheresis despite immunosuppressive therapy and lack of evidence for circulating anti-glomerular basement membrane antibody, the child went into terminal renal failure. The natural history of the disease in this case and the results of treatment are discussed. To our knowledge this is the first case of Goodpasture's syndrome reported in childhood with demonstration of the presence of anti-glomerular basement membrane antibody.

Anti-Glomerular Basement Membrane Disease↗