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PubMed1989

[Etiology of toxic erythema in newborn infants and its effects on the health status of young children].

A total of 68 neonates with toxic erythema (TE) were examined for risk factors of its origin depending on the intensity of the clinical manifestations of erythema. It has been established that sensitizing factors (aggravated allergological anamnesis, food, allergens, late toxicosis of pregnancy) and high content of estrogen hormones in the newborn are implicated in the genesis of the generalized TE pattern. The study of the catamnesis of 84 children of the first three years of life with a history of TE of the newborn revealed that the children appeared highly susceptible to respiratory diseases and showed early formation of the allergic manifestations. It is recommended that neonates with marked TE should be attributed to the second health group and be administered the treatment and prophylactic measures beginning from the stay at the maternity home.

Age Factors↗
PubMed1994

Pathological studies on the placenta from pre-term and term maternal toxicosis.

Fifty one placentae with maternal pre-term and term toxicosis were studied pathologically. In the severe pre-term maternal toxicosis, the placenta reveals hyperplasia of syncytial cytotrophoblasts(S-cells) with knots, fibrin deposit at their surface, fibrinoid degeneration of the stroma, in addition to marked interstitial fibrosis of chorionic villi. The basement membrane is thick and cytotrophoblasts(C-cells) are scattered beneath it. Decidual arteries are hyalinized, but a few decidual arteries are thick and almost obstructed in their lumina. On the other hand, the placenta of maternal term toxicosis show chorionic villi with few C-cells under the thin S-cell lining. Their basement membrane is thin with well developed vasculosyncytial membrane. Decidual arteries are more hyalinized and widened. These pathological changes seen in term maternal toxicosis are the severer than those of placental aging.

Eclampsia↗
PubMed1996

Endemic Tyrolean infantile cirrhosis: an ecogenetic disorder.

BACKGROUND: 138 infants and young children died from an endemic infantile liver cirrhosis in a circumscribed rural area of western Austria between 1900 and 1974. Frequency of the disease peaked between 1930 and 1960. It has disappeared from this area since 1974. METHODS: Clinical and genetic data on the patients was gathered; pedigrees analysed and ethnographic studies and interviews were undertaken. FINDINGS: The disease, which was clinically and pathologically indistinguishable from Indian childhood cirrhosis and hepatic copper toxicosis, was transmitted by autosomal recessive inheritance. Cow's milk, contaminated with copper from untinned copper or brass vessels, may have contributed to the development of copper toxicosis. Replacement of untinned copper cooking utensils by modern industrial vessels has eradicated the disease. INTERPRETATION: Our findings strongly suggest that the endemic Tyrolean childhood cirrhosis-and by analogy non-Wilsonian hepatic copper toxicosis occurring elsewhere-is an ecogenetic disorder requiring the involvement of both genetic and environmental factors for the disease to become manifest.

Animals↗
PubMed1970

[Further development of children of mothers following pregnancy toxicoses].

Three hundred and sixty-four children born by mothers with gestational toxicoses were repeatedly reexamined at intervals of from four months to more than four years. While the somatic development of these children was normal, neuropsychic disorders were found in 7.7% of them. Children with a pathological neonatal period are more susceptible than children with a physiological neonatal period. The proportion of children with neurological lesions was found to increase with increasing severity of toxicosis.

Brain Damage, Chronic↗
PubMed1975

[Sulphated glycosaminoglycans as virus inhibitors. 2nd communication: Inhibitory effect of glycosaminoglycanpolysulphates on yellow fever virus 17 D in animal experiments (author's transl)].

Glycosaminoglycanpolysulfates (GAGPS) have virus inhibiting properties demonstrable by means of tissue culture in the plaque method. In brain preparations of children who had died of a hyperpyretic toxicosis, cell necroses were found corresponding to the picture of tissue culture plaques. The question arose from these observations whether this inhibiting effect of GAGPS can perhaps also be demonstrated in vivo. In animal experiments, cell necroses corresponding to those of the infant brain could be observed during the course of a 17 D yellow fever encephalitis in mice. The Luitpoldt-Werk Munich placed to our disposal 13 different GAGPS for tests. Each of these substances was tested in 210 mice (fig. 1). Virus dilutions (LD 50/ml) were mixed to the same volume with the indicated concentrations of substance directly before vaccination. The differing LD 50 doses is due to the fact that each ampoule contains a different content of virus.) The toxicity of all substances is practically zero (table 2a, 2b). The effect of the inhibiting substances was evaluated at first by means of a deviation of the rate between alive and dead animals (table 1). The statistical significance of the effect of some substances was that high so that an inhibition of the virus replication has obviously to be considered. The significance for L1 and L4 - they are chemically very similar - is higher than 0.001 (table 4). The virus inhibiting effect of the substances was controlled by histopathology. 31 brains of mice were dissected and histologically evaluated; the lesions of the brains were examined and recorded (table 3). The effect of the substances was measured by absence or diminution of the lesions. The most effective substance was L1 as far as its concentration was higher than the critical limit of 625 gamma/ml.

Animals↗
PubMed1991

[Medium-weight molecules in the determination of the level of endogeneous intoxication in newborn babies].

Criteria for the diagnosis of the syndrome of endogenous intoxication were specified in neonates in a critical condition because of pathology of the early neonatal period. It has been established that early diagnosis of toxicosis is promoted by the determination of the pool of medium-weight molecules, the growth of which precedes the clinical picture manifestation. The totality of the indicators of the content of medium-weight molecules and the leukocytic index of intoxication determine the type of toxicosis (infectious, hypoxic, traumatic), predict its course and outcome, being an alternative in the choice of methods for body detoxifying.

Humans↗