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Biomedical subjects

D Rating

Publications and source records attributed to D Rating.

At least 73 records · Page 4Linked to original sources
PubMed1985

Neonatal behaviour disturbances in infants of epileptic women treated during pregnancy.

Infants exposed in utero to antiepileptic drugs showed significantly more behaviour disturbances such as sedation (p less than 0.05) and hyperexcitability (p less than 0.01) than infants of a control group. The presence of these clinical symptoms and the time of their appearance did not seem to be dependent on the type of maternal medication, nor on the drug serum concentration in cord blood nor on the rate of drug disappearance from the infant's plasma.

Akathisia, Drug-Induced↗
PubMed1985

[Erythema migrans disease. 3 case examples with neurologic complications].

The erythema-migrans-disease is closely related to Lyme-disease as described in the USA, and represents a tickborne spirochetosis with highest incidence during summer and autumn. Besides nonspecific general symptoms in its earlier stages, it is characterized by a distinctive erythema migrans; later, additional neurological, cardiac and/or arthritic symptoms may develope. Its typical neurologic complication, the lymphocytic meningoradiculitis Garin-Bujadoux-Bannwarth, was observed in three children whose clinical features illustrate the great variability of symptoms of Erythema-migrans-disease. Serological tests for specific spirochete antibodies are valuable aids in differential diagnosis, especially for cases with late complications if a tick bite is not remembered, or as is not uncommon, the typical skin lesion has not occurred, or has not been noted. Antibiotic therapy with penicillin or tetracycline is a successful treatment of the earlier stages of the disease and can prevent, or at least ameliorate, subsequent complications.

Adolescent↗
PubMed1984

Measurement of fatty acid oxidation in premature newborn infants with the 13C-triolein breath test.

The 13C-triolein breath test is a method giving evidence of extent and rate of fatty acid oxidation in newborn infants on parenteral nutrition. The test has the special advantage of being non-invasive. Triolein labeled with the stable carbon isotope 13C and emulsified in soybean-oil is used as a tracer. 10 mg of 13C triolein per kg body weight are administered intravenously. The 13CO2 resulting from the fatty acid oxidation is analysed in expired breath by ratio-mass-spectrometry. The calculated 13C elimination is representative of the rate of fatty acid oxidation during the examination period. First studies on 15 premature infants have shown that an average of 27.0 +/- 1.8% of the dose administered is oxidized within 4 h. The present results suggest that the oxidation rate may be related to the maturity of the prematurely born infants.

Journal Article↗
PubMed1984

Succinic semialdehyde dehydrogenase deficiency.

A coupled assay using [14C]4-aminobutyric acid and a direct assay using [14C]succinic semialdehyde have been designed to assay te activity of succinic semialdehyde dehydrogenase in a patient with 4-hydroxybutyric aciduria and family members. In the coupled assay less than 3% of control succinic semialdehyde dehydrogenase activity was found in lysates of lymphocytes isolated from whole blood of the patient. In the direct assay there was no detectable activity of the enzyme in lysates of isolated lymphocytes or cultured lymphoblasts. Results indicated the parents to be heterozygous carriers carriers of the abnormal gene, consistent with an autosomal recessive inheritance.

Adult↗
PubMed1983

Succinic semialdehyde dehydrogenase deficiency: an inborn error of gamma-aminobutyric acid metabolism.

Gamma-hydroxybutyric aciduria is a disorder of gamma-aminobutyric acid metabolism in which a compound of known neuropharmacologic activity accumulates. We have studied two patients in whom high levels of gamma-hydroxybutyric acid were found in blood, urine and cerebrospinal fluid. A coupled assay has been developed which estimates succinic semialdehyde dehydrogenase activity in isolated human lymphocytes. The mean activity of succinic semialdehyde dehydrogenase in a control and the four parents and two healthy siblings of these patients was 8.8 +/- 1.9 pmol . min-1 . mg-1 protein. In the patients the activities were 0.8 and 1.1 pmol . min-1 . mg-1 protein, approximately 9-13% of control. In the presence of saturating amounts of NAD+, lymphocyte sonicates, derived from the patients accumulated a significant amount of 14C-succinic semialdehyde from 14C-gamma aminobutyric acid, whereas none could be detected in controls. The data suggest a deficiency of succinic semialdehyde dehydrogenase in these patients, the first documented defect of the metabolism of gamma-aminobutyric acid in man.

4-Aminobutyrate Transaminase↗
PubMed1983

[Anti-epileptic agents during pregnancy. A prospective study on the course of pregnancy, malformations and child development].

In a prospective controlled study 70 children of females with epilepsy and on anticonvulsant medication during pregnancy were investigated. It was shown that epileptic females had stillbirths more frequently than expected. After delivery particularly children on phenobarbitone are sedated. Due to weak suckling this may lead to inadequate food intake. Withdrawal symptoms manifest in affected children as hyperexcitability lasting for weeks. Children of epileptic women on medication are generally smaller, of lower weight and have smaller heads than children from all control groups. Ingestion of more than one anticonvulsant leads to an even more pronounced reduction of infantile body measurements below the expected mean value. Small malformations are observed more frequently after intrauterine exposition to anticonvulsants than in the control groups. Ingestion of more than one anticonvulsant leads to an increase of the number of small malformations in the child than after single drug therapy. Children of epileptic parents are affected more frequently by large malformations than children of nonepileptic parents.

Abnormalities, Drug-Induced↗
PubMed1983

Low CSF GABA concentration in children with febrile convulsions, untreated epilepsy, and meningitis.

In 14 children with epilepsy, 51 with febrile convulsions and 22 with meningitis gamma-aminobutyric acid (GABA) concentrations in lumbar CSF were determined. While the mean for CSF GABA concentrations for all epileptic children was unchanged [144 (range: 73-285) pmol/ml; controls: 148 (range: 90-243) pmol/ml] extraordinarily high GABA levels were found in the CSF of two children on valproate (525 and 557 pmol/ml) and remarkably low GABA concentrations in hitherto untreated epileptic children [109 (range: 67-176) pmol/ml]. Children with febrile convulsions [103 (range: 63-170) pmol/ml] and acute meningitis [105 (range: 65-171) pmol/ml] had significantly decreased CSF GABA concentrations (P less than 0.001 and P less than 0.02 compared with controls). The data indicate that valproate intake increases dramatically the GABA concentrations in the CSF of epileptic children. Furthermore, the study supports the concept that low GABAergic activity within the CNS may be one cause for an increased seizure frequency.

Adolescent↗
PubMed1983

Change of seizure frequency in pregnant epileptic women.

The effect of pregnancy on seizure frequency was monitored prospectively in 136 pregnancies of 122 epileptic women. Pregnancy did not influence the seizure frequency in 68 pregnancies (50%). In 50 pregnancies (37%) the number of seizures increased during pregnancy or puerperium. The seizure frequency decreased in 18 pregnancies (13%). In 34 out of 50 pregnancies (68%) the increase was associated with non-compliance with the drug regimen or sleep deprivation. In seven out of 18 pregnancies (39%) improvement was related to correction of non-compliance or sleep deprivation during the pregestational nine months. Insufficiently low plasma concentrations of antiepileptic drugs were found in 47% of the women with uncontrolled epilepsy during pregnancy. The course of epilepsy during pregnancy is primarily influenced by non-compliance, sleep deprivation during pregnancy, and inadequate therapy before and during pregnancy. With good medical attention pregnancy itself seems to have only a minimal influence on the course of epilepsy.

Adult↗
PubMed1983

Enzyme induction in neonates after fetal exposure to antiepileptic drugs.

The 13C-AP breath test is shown to be a convenient, noninvasive method to monitor velocity and capacity of P450-dependent AP N-demethylation in infancy and childhood. According to 13C-AP breath tests, neonates have a very low capacity to eliminate 13CO2, which is only 15 to 21% of the activity in adults. During the first year of life AP N-demethylation increases to reach its maximum at about 2 years; afterwards a slight decrease occurs. In 25 neonates exposed prenatally to different antiepileptic drugs 13C-AP breath test was efficiently used to prove that cytochrome AP N-demethylation was considerably stimulated. After primidone/phenobarbitone, especially in combination with phenytoin, 13C elimination reaches and even surpasses the range for older children. Valproate exposure during fetal life is not consistently followed by a significant increase in AP N-demethylation. The enzyme induction demonstrated by 13C-AP breath test was often accompanied by accelerated metabolic clearance and shortened half-life times of transplacentally acquired antiepileptic drugs. There was good agreement between 13C-AP breath tests and pharmacokinetic data for primidone/phenobarbitone but not for phenytoin. In contrast, in the case of phenytoin exposure during pregnancy the pharmacokinetic parameters and the 13C breath test data will transport very different informations about enzyme induction in these neonates.

Aminopyrine↗
PubMed1983

Carbamazepine and carbamazepine-10,11- epoxide during pregnancy and postnatal period in epileptic mother and their nursed infants: pharmacokinetics and clinical effects.

A total of 11 epileptic mothers treated with carbamazepine (CBZ) as well as their 12 newborns were included in this study. Maternal CBZ concentrations remained rather constant during pregnancy and slightly increased after parturition. Carbamazepine-10, 11-epoxide ( CBZE ) levels were less predictable and either increased or decreased during pregnancy. Fetal/maternal serum concentration ratios at birth were 0.78 +/- 0.14 (n = 5) for CBZ and 0.75 +/- 0.09 (n = 5) for CBZE . Neonatal half-lives were 28 +/- 11 hours (n = 4) for CBZ and 20 and 24 hours (n = 2) for CBZE . maternal milk/serum concentration ratios of CBZ and CBZE were 0.39 +/- 0.22 (N = 11) and 0.49 +/- 0.28 (n = 6), respectively. The steady-state CBZ serum levels of nursed infants were about 1.0 micrograms/ml in all cases but one, where a maximum concentration of 4.7 micrograms/ml was reached. One of the infants had major malformations. Minor anomalies were less frequent in the CBZ group, compared to the whole group of infants exposed to anticonvulsive drugs other than CBZ and as frequent as in a matched pair control group of unexposed neonates. Neonatal somatic data were found to be below the corresponding values of neonates exposed to antiepileptic drugs other than CBZ.

Abnormalities, Drug-Induced↗