PubMed Health⌕ Search

Biomedical subjects

E Kattner

Publications and source records attributed to E Kattner.

32 records · Page 2Linked to original sources
PubMed1990

[Prenatal development and postnatal morbidity of newborn infants of HIV positive mothers].

Does the maternal HIV-infection itself influence fetal development and neonatal morbidity or are adverse effects related to maternal opiate and nicotine abuse? 17 neonates of HIV-positive women (7 drug users) and 37 controls (17 healthy and 21 opiate exposed newborns) were examined prospectively. A discriminant analysis showed that opiate and nicotine abuse during pregnancy were associated with fetal growth retardation and neonatal morbidity, while HIV-infection of the mother did not influence these parameters. Symptoms of an HIV-embryopathy were not seen.

Birth Weight↗
PubMed1989

Hereditary progressive muscular dystrophies: serum myoglobin pattern in patients with different types of muscular dystrophies.

Serum myoglobin (Mb) levels and creatine kinase (CK) activity were investigated in patients with different types of progressive muscular dystrophy and controls. The Mb levels were determined by radioimmunoassay and found to be significantly elevated in all patients under resting conditions. There was no correlation between Mb levels and CK activity. Physical exercise was followed by an increase in Mb levels and CK activity in patients and a minor variation in controls. Isoelectric focusing, electroblotting and application of a specific Mb antibody (rabbit anti-human Mb) make it possible to recognize marked differences between the Mb bands of patients and controls. All patients with progressive muscular dystrophy had an additional fourth Mb band (isoelectric point pH 6.3) in contrast to controls with three Mb bands.

Creatine Kinase↗
PubMed1988

Myoglobinuria in hereditary progressive muscular dystrophies.

Myoglobin (Mb) levels in pooled urine samples were investigated and compared in patients with different types of hereditary progressive muscular dystrophies (MD). The samples were taken before and after physical exercise. The Mb levels in the patients were significantly higher than in controls under both resting and exercise conditions. The formation of separate clusters of Mb values enabled us to distinguish patients with different types of MD according to the clinical diagnosis. Urine protein detection with SDS-acrylamide electrophoresis showed an abnormal pattern in patients compared to healthy controls.

Adolescent↗
PubMed1988

Biochemical changes in hereditary progressive muscular dystrophies. Defect of protein synthesis in fibroblasts, muscle tissues and blood cells.

80S ribosomes and ribosomal subunits were isolated from fibroblasts, muscle tissues and blood cells of patients with different muscular dystrophies (MD) as well as of controls and were used for in vitro measurement of ribosomal protein synthesis (RPS) in a poly(U)-directed polyphenylalanine synthesis system. The activity of ribosomes from the patients showed a disease-dependent decrease compared to normal controls. Examination of hybrid 80S ribosomes consisting of 40S and 60S subunits of patients and the corresponding control cells revealed that the loss of RPS activity was related to one or both of the ribosomal subunits depending on the type of MD.

Blood Cells↗
PubMed1987

Altered ribosomal protein synthesis in congenital non-progressive myopathy.

Ribosomes isolated from fibroblasts, muscle tissues, and blood cells of a patient with congenital non-progressive myopathy were used for in vitro measurement of protein synthesis in a heterologous poly(U)-directed polyphenylalanine synthesis system. The activity of ribosomes obtained from the patient was 35% lower than that in normal controls.

Adult↗
PubMed1985

[Transient unilateral oculomotor paralysis].

A three-year-old girl was admitted to the hospital one day after the acute onset of drooping of the left eyelid, associated with oculomotor external ophthalmoplegia. General neurological and physical examination was unremarkable. Results of serological tests as well as the clinical course of the disease (spontaneous recovery) show that the unilateral oculomotor neuropathy was most likely due to a self-limited enteroviral infection. The virus could not be cultured in the CSF. Echovirus type 11 as well as Coxsackie B4 virus might have caused the disease. During treatment with prednisone for 3 weeks in decreasing doses the girl recovered, by the seventh day she was able to raise her eyelid. 3 1/2 months later she had no evidence of residual ptosis and full range of ocular movements.

Acute Disease↗
PubMed1983

The genetic significance of accessory bisatellited marker chromosomes.

Ten new cases of accessory bisatellited marker chromosomes examined in different laboratories are reported. As a basis for genetic counseling in the context of prenatal diagnosis a cytogenetic categorization of such marker chromosomes is proposed and an estimation of the genetic risk associated with each category is carried out. The results are as follows: There is no increased risk for offspring with abnormal phenotype born to a healthy carrier of an accessory bisatellited marker chromosome with either a single or two closely adjacent C-bands (Category AI or AII). The unbiased sample of cases with de novo accessory bisatellited marker chromosomes of categories AI and AII is too small to allow a satisfactory estimation of the actual risk that, in case of such a prenatal finding, the foetus may not show a normal phenotype as a consequence of the marker chromosome. There is, however, evidence that this risk may be lower than 10%. Accessory bisatellited marker chromosomes showing a discrete pattern of G- and R-bands situated between two distant C-bands (Category AIII) usually indicate a chromosomal imbalance giving rise to an abnormal phenotype. Mosaic carriers of such dicentric marker chromosomes may, however, present a normal phenotype.

Abortion, Spontaneous↗
PubMed1981

Acetylation of procainamide and isoniazid by a rat liver-N-acetyl-transferase.

The genetic variation of the enzyme isoniazid-N-acetyltransferase has been studied in man and other species. Homogenates of liver samples of adult LEW rats also acetylate procainamide. The kinetic properties of isoniazid and procainamide acetylation are similar and are consistent with a ping-pong Bi-Bi mechanism. The experimental data support the hypothesis that one acetyltransferase catalyses both procainamide and isoniazid. Furthermore, a simple spectrophotometric assay to determine procainamide acetylation is presented.

Acetylation↗
PubMed1980

Sulfadimidine and isoniazid loading in man and laboratory rats. Pharmacokinetic and pharmacogenetic results on drug acetylation.

Drug acetylation polymorphism is of clinical importance in slow and rapid acetylators. There are therapeutic and toxic consequences of interindividual drug acetylation of, e.g. isoniazid, procainamide and various sulfonamides. For comparing pharmacokinetic and pharmacogenetic data it is necessary to establish a useful model in experimental animals: 1. We determined the half-lives of isoniazid and sulfadimidine in man and rats using a simple loading test and we compared these data with those of in vitro acetylation. In man the half-lives of both substances correlate very well and correspond to acetylation values in vitro. 2. There is no sufficiently good correlation of sulfadimidine concentration in blood and saliva. Furthermore we found no strict correlation between drug concentration in venous and capillary blood. This should be should be considered in pharmacogenetic research. 3. The sulfadimidine half-lives in male Sprague-Dawley and Wistar rat are similar. Both half-lives and acetylation rates in vivo are normally distributed. Sulfadimidine half-lives and the rate of acetylation in vitro do not correlate. Compared with human values the investigated rats are rapid acetylators. Young rats reach their total acetylation capacity in vivo 65 days post partum. 4. Many organs of the rat acetylate sulfadimidine (kidney, lung, intestinal mucosa) with the exception of the spleen. 5. Excess substrate inhibits acetylation of sulfadimidine in vitro. Results of further inhibition studies suggest two or more N-acetyltransferases. 6. Isoniazid inhibits the sulfadimidine acetylation in rat liver homogenates and vice versa. To sum up all data, Sprague-Dawley and Wistar rats seem to be a useful model for human sulfadimidine metabolism pharmacokinetic and, in part, pharmacogenetic studies. Furthermore drug analysis in human saliva can be helpful in pharmacogenetic and pharmacokinetic research in the future.

Acetylation↗
PubMedDate not supplied

[Heart failure caused by myocardial hypertrophy in diabetic fetopathy].

Diabetic fetopathy is still a common clinical problem correlated with a high morbidity of the neonate. These children are often macrosome, suffer from respiratory distress syndrome due to delayed lung maturity, acidosis, hypoglycaemia, electrolyte-imbalances and polycythaemia. We describe a male neonate with diabetic fetopathy as a result of gestational diabetes of the mother. In addition to the symptoms described above, our patient clinically presented with severe hypertrophy of the right ventricle associated with intrauterine heart failure. The boy was born with serious prenatal asphyxia which made initial neonatal intensive care treatment necessary. The hypertrophic cardiomyopathy normalized within 6 weeks after birth without further treatment. Different causes of a hypertrophic cardiomyopathy (infections, metabolic disorders, neurologic affections, syndromes) could be ruled out, so that the diabetic fetopathy was the most probable cause for the condition. If we are looking at the heart only, this case-report suggests a good prognosis of septumhypertrophy as well as right ventricular hypertrophy in patients with diabetic fetopathy. The case also elucidates that not only the diabetes type I can entail serious fetal damage but also gestational diabetes can. Therefore, in suspect mothers screening for gestational diabetes should be expanded to oral glucose tolerance testing.

Adult↗
PubMedDate not supplied

[Pre- and postnatal diagnosis and treatment of hydrops fetalis--an interdisciplinary problem].

Hydrops fetalis (HF) is diagnosed prenatally in one out of 600 pregnancies, thirty percent of these fetuses will die in utero. Post partum, one out of approximately 25,000 newborn infants is affected. With the introduction of Rhesus immunoprophylaxis only fifty percent of the cases with HF are caused by Rhesus hemolytic disease. There is a large variety of non-immunological reasons such as cardiac defects (hypoplastic left healt syndrome, atrio-ventricular canal), arrhythmias, cytomegalovirus- or parvovirus infection (9% HF), twin-to-twin transfusion syndrome (15-30% HF) or chromosomal abnormalities (28-45% HF). However, in one third of the non immunological cases of HF the etiology remains unclear. Early diagnosis by ultrasound scan faces both the obstetrician and the neonatologist with the problem of differential diagnosis as well as therapeutic options, respectively. Various diagnostic procedures such as fetal echocardiography, karyotyping, molecular genetic techniques and sophisticated serological testings will help to classify the etiology and to determine the pre- and postnatal management. Nevertheless, neonatal mortality still varies between 50 and 95%.

Diagnosis, Differential↗