[High-dose gamma globulin for children with thrombopenic purpura].
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Child, Preschool↗
Biomedical subjects
G Hattevig
Publications and source records attributed to G Hattevig.
Clinical symptoms and IgE responses to common food proteins in atopic and healthy children.
The appearance of symptoms suggestive of allergy through the first 4 years of life was studied prospectively in eighty-six healthy newborn babies. Blood samples were obtained at birth, at 3, 8, 25 and 48 months of age and analyzed for levels of total serum IgE and for IgE antibodies to some common foods. The occurrence of IgE antibodies was related to atopic manifestations and to a detailed history of infant feeding and family history of allergy. All infants with elevated cord blood IgE (more than 1.3 kU/l) developed manifestations of atopy. Specific IgE antibodies against egg, cow's milk and soy were demonstrated at 3, 8, 25 and 48 months in nine, twenty-three, six and two children respectively. Egg was a more potent sensitizing agent than cow's milk, IgE antibodies to egg being present in thirty-one samples, to cow's milk in eleven and to soy in five samples. Nine infants developed IgE antibodies to eggs or cow's milk before the introduction of these nutrients into the food. The IgE antibody levels were generally low in healthy non-atopic children and did, with one exception, not reach RAST class 1. In contrast, the levels of IgE antibodies to egg or cow's milk were higher in eleven blood samples from atopic children. We conclude that transient low IgE antibody responses to food proteins appear relatively often even in healthy infants. High concentrations of IgE antibodies however are almost exclusively seen in infants with atopic disease. Sensitization may appear early in infancy sometimes even before the offending food has been introduced into the diet.
Age Factors↗
Dextran-reactive antibodies in children. Appearance during the first 4 years of life and relation to E. coli infections in the urinary tract.
The appearance of dextran-reactive antibodies (DRA) was investigated in 88 children with sampling of serum at birth (n = 87), at 3 months of age (n = 87), at 8 months (n = 88), at 2 years (n = 86) and at 4 1/2 years of age (n = 87). Serum DRA appeared at 3 months of age and a peak level exceeding the levels in adults was noted at 8 months of age. At 4 1/2 years the titres were close to those in adults. Investigation of DRA in 8 children with acute pyelonephritis and in 8 children with asymptomatic bacteriuria caused by E. coli did not indicate that the appearance of DRA was a consequence of Gram-negative infections. The practical conclusion drawn is that if therapy with i.v. dextran is considered for infants or children, they should undergo preventive therapy with hapten dextran similar to the procedure recommended for adults.
Anaphylaxis↗
Congenital permanent diabetes mellitus and celiac disease.
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Celiac Disease↗
Dextran-reactive antibodies in healthy infants and toddlers--relation to type of feeding.
The appearance of dextran-reactive antibodies (DRA) during the first 2 years of life was studied in 88 healthy newborn babies in an effort to provide information about the origin of DRA in normal persons. The results were related to type of feeding, immunizations and to blood group of infants and their mothers. No DRA were detected in cord sera by passive hemagglutination. At 3 months of age 42% had DRA, at 8 months 95% and at 27 months 84%. The latter figure corresponds to previous reports of DRA in healthy adults. Peak titers were also seen at 8 months (mean 2 log titers at 3, 8 and 27 months; 2.1, 6.2 and 4.9, respectively). Breast-feeding influenced the time of appearance of DRA and the magnitude of the titers. Babies breast-fed at 3 months more often were DRA negative than those that had received cow's milk-based formula at that time (p less than 0.005). However, in those breast-fed babies that were DRA positive the titers were higher than in the formula-fed infants (p less than 0.001). Other types of feeding e.g. juices did not influence the DRA levels. The appearance of DRA could not be explained by polyclonal stimulation of antibody production since changes of DRA titers in 11 tested patients could not be clearly related to similar changes of levels of antibodies to an unrelated hapten, trinitrophenyl. The study demonstrates that DRA appear during the first year of life, and that the appearance is influenced by exogenous factors. The most likely source of the antigen stimulation is the gastrointestinal flora which is altered by introduction of cow's milk into the diet.
Age Factors↗
Screening of Rh-antibodies in Rh-negative female infants with Rh-positive mothers.
The sera of 96 consecutive Rh-negative female infants born to Rh-positive mothers were examined at birth, and sera from 88 of these infants were examined for the presence of Rh-antibodies at the ages of about three and eight months. A two-stage papain test and an AutoAnalyzer method were used for antibody screening and identification. Weak anti-D antibodies were found by the papain and AutoAnalyzer techniques in two cord sera, In neither case could the antibodies be demonstrated in samples taken on later occasions. Weak anti-D antibodies were found by the AutoAnalyzer technique but not by the manual methods in the sera of two other infants at the age of eight months. These antibodies could still be demonstrated by the same technique in samples taken about one month later. Though far from conclusively, the results support the "grandmother theory", but because of the low incidence of sensitization and uncertain nature of the anti-D antibodies demonstrable only by the AutoAnalyzer technique, anti-D prophylaxis is not recommended for newborn Rh-negative female infants with Rh-positive mothers.
Antibody Formation↗
Borderline galactosemia.
A family with combined heterozygosity for "classical" galactosemia (deficiency of uridyl-transferase) and for galactokinase deficiency is reported. The proband, who had this genetic combination was detected as newborn in the ordinary screening for galactosemia. A lactose tolerance test at the age of three months proved normal and he has no symptoms or signs on ordinary diet. The mother of the proband was not only heterozygote for "classical" galactosemia and galactokinase deficiency but also for the Durarte variant. She had a substantial urine excretion of galactose and high serum galactose after an oral lactose load. She had no clinical symptoms or signs. Patients with combined heterozygosity for galactosemia may develop cataracts and should be followed by clinical examinations.
Adult↗