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Biomedical subjects

E Kontor

Publications and source records attributed to E Kontor.

At least 19 recordsLinked to original sources
PubMed1998

[Aortopexy as a surgical treatment method in infantile congenital tracheo-chondrohypoplasia and tracheomalacia].

Congenital tracheal chondrohypoplasia and tracheomalacia have come to present a significant challenge in recent paediatric surgery. Authors shortly describe their pathology, pathophysiology, symptoms, diagnostic evaluation and outline the most frequency surgical procedures for them. The first three aortopexies in the authors' departments are described in this paper, with particular attention paid to the clinical problems of congenital tracheal chondrohypoplasia and tracheomalacia and the role of this method in surgical treatment, respectively. Aortopexy is quick, easy to carry out and atraumatic for the growing trachea. Authors want to draw attention to the fact that not every form of congenital tracheal chondrohypoplasia and tracheomalacia may be treated by conservative therapy, and that surgical treatment is recommended not only for life threatening forms, but for other severe forms as well.

Abnormalities, Multiple↗
PubMed1997

[Androgen-producing adrenocortical adenoma in childhood. Pitfalls of differential diagnosis].

A two-year-old girl presented with clitoromegaly and an abdominal mass. Diagnostic procedures including sonography, computerized tomography, scintigraphy and measurement of catecholamines in urine excluded neuroblastoma, but suspected Wilms-tumor. Before completing the steroid measurements therapy was initiated according to Wilms-tumor (preoperative cytostatic therapy followed by surgical removal of the tumor). Morphology of the tumor, the serum and urinary steroid profile proved a benign adrenocortical adenoma producing mainly delta 5-steroids including the weak androgen, dehydroepiandrosterone.

Adenoma↗
PubMed1996

[17 beta-hydroxysteroid dehydrogenase defect: female phenotype with 46,XY karyotype].

Deficiency of the 17 beta-hydroxysteroid dehydrogenase (17b-HSD-d) causes female external genital phenotype in spite of 46,XY karyotype and presence of testes due to disorder in biosynthesis of testosterone. However, marked somatic and genital virilization occurs during puberty. Clinical and laboratory investigation of three cases are presented with typical elevation of the precursor steroid androstenedione, and decrease of product steroid testosterone. All the three patients were reared as girls. During puberty orchidectomy was performed in two cases and vaginoplasty in one case. Estrogen replacement therapy contributed to development of female secondary sex characteristics.

17-Hydroxysteroid Dehydrogenases↗
PubMed1990

Characteristics of cholinergic neuroeffector transmission of ganglionic and aganglionic colon in Hirschsprung's disease.

Differences in the release and content of acetylcholine and the alpha 2 adrenoceptor mediated interaction between noradrenergic and cholinergic neurons were investigated by neurochemical and pharmacological methods in aganglionic and ganglionic segments of isolated human colon taken from children suffering from Hirschsprung's disease. Both at rest and during transmural stimulation the release of acetylcholine was significantly higher in the spastic (aganglionic) segment than in the proximal dilated bowel. Significant differences were found in the tissue concentration of acetylcholine between ganglionic and aganglionic specimens. The pattern of response to transmural stimulation was also different in the spastic and dilated bowel. Transmural stimulation induced relaxation and contraction in ganglionic specimens but only contractions in aganglionic specimens. The sensitivity of the smooth muscle in the aganglionic portion to exogenous acetylcholine and to field stimulation was found to be higher than in the ganglionic portion. While noradrenaline added to the organ bath reduced the stimulation-evoked release of acetylcholine from spastic segments, via an alpha 2 adrenoceptor mediated process, yohimbine did not enhance the release. It is suggested that in Hirschsprung's disease the increased acetylcholine release, the enhanced sensitivity of smooth muscle cells to acetylcholine, and the lack of alpha 2 adrenoceptor mediated noradrenergic modulation of acetylcholine release from cholinergic interneurons might be responsible for the spasm of aganglionic segments.

Acetylcholine↗