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Biomedical subjects

O Butenandt

Publications and source records attributed to O Butenandt.

At least 73 records · Page 4Linked to original sources
PubMed1983

[Therapy of endocrine diseases in childhood and adolescence. 2. Connatal athyreosis. 3. Diabetes insipidus neurohormonalis].

Congenital athyreosis may be due to different though mostly unknown factors. It should be diagnosed by TSH-screening. Immediate therapy consists of supplementation of thyroxin. The dose should be adjusted to the child's needs controlled by normal growth and bone age advance, normalization of TSH and thyroxin levels in serum. The goal must be to reach normal intelligence. Therapy should be continued during the entire life. Absence of adiuretin is the cause for diabetes insipidus neurohormonalis due to genetic disorders, tumor or infection of the hypothalamo-pituitary system. The disorder is best treated with synthetic desamino-8-vasopressin (minirin, alternatively with an oily suspension of pitressin). Diabetes insipidus renalis and psychogenic polydipsia should be ruled out before this therapy is started.

Adolescent↗
PubMed1983

[Therapy of endocrine diseases in childhood and adolescence. 1. Goiter in childhood].

Euthyroid or hypothyroid goitre in childhood is due to hyperstimulation by TSH in iodine deficiency or inborn errors of thyroid hormone synthesis. Hyperthyroid goitre results from presence of LATS. Hashimoto's strumitis may be hypo- or hyperthyroid. Therapy consists of iodine, thyroxine in hypothyroid goitres or in thyrostatic suppression in hyperthyroid goitres. Whereas hypothyroidism requests lifelong therapy, hyperthyroidism requires therapy for 1 to 2 years if successful. Otherwise, operative procedures are necessary.

Adolescent↗
PubMed1983

Modulation of lymphoproliferation by human growth hormone.

This study was designed to investigate the capacity of human growth hormone (hGH) to induce proliferation of human peripheral blood lymphocytes (PBL) and its effect on lectin-induced lymphoproliferation, as measured by [3H]-thymidine (3H-TdR) incorporation into lymphocyte DNA. We observed that hGH itself induced lymphoproliferation. Maximal responses were reached with 50 ng/ml after 4 days and 25 ng/ml after 7 days. Anti-hGH-antiserum completely blocked the stimulatory capacity of hGH. Further evidence for the specificity of the effect was obtained by the finding that no other hormone present in the hGH preparation produced any effect on lymphocyte cultures. In contrast to its stimulatory capacity, hGH reduced the proliferative response of PBL to phytohaemagglutinin (PHA). This effect was also neutralized by anti-hgH-antiserum. These results show a direct stimulatory effect of hGH on PBL and a regulatory effect of the hormone on lectin-induced lymphoproliferation.

Cell Division↗
PubMed1983

[Plasma prolactin levels and pubertal gynecomastia].

Twenty-three boys with pubertal gynecomastia had higher mean levels of prolactin than boys of similar development but without gynecomastia (10.1 vs. 6.2 ng/ml). In girls of comparable pubertal staging prolactin level was 12.3 ng/ml. In boys no hyperprolactinemia was found, not even after stimulation with TRH, prolactin levels were not elevated in two boys with secreting mammary glands. Therapy with bromocriptine stopped the secretion. During therapy, prolactin levels could not be raised by stimulation. The results contradict the hypothesis that prolactin is involved in the development of gynecomastia.

Adolescent↗
PubMed1983

[A method of modernized milk formula preparation in children's hospitals].

Nurses on the ward prepare the milk formula just before feeding by the nurse on the ward. Bottles and nipples are cleaned mechanically by dishwashers using alkaline cleaner for bottles, or a mild-alkaline cleaner (WA 725 S) and an antiseptic (Septo DA) for nipples. The nipples are sealed into plastic bags immediately after cleaning using sterile equipment. No further sterilisation is necessary as frequent bacterial culturing has shown. This procedure is safe, easy, and saves cost and time.

Animals↗
PubMed1982

[Growth check-ups as part of preventive medical examinations].

Failure to thrive as well as increased growth velocity may have different causes. Specific diagnostic evaluation has to be performed as soon as a delineation of the growth rate is observed. Examples are hypopituitarism, hypothyroidism, celiac disease in depressed growth or congenital adrenal hypoplasia or pubertas praecox in enhanced growth.

Child, Preschool↗
PubMed1981

[Ichthyosis vulgaris, growth retardation, hair dysplasia, tooth abnormalities, immunologic deficiencies, psychomotor retardation and resorption disorders. Case report of 2 siblings].

Two siblings (4 and 10 years old) with ichthyosis vulgaris, growth and mental retardation, hair dysplasia, teeth abnormalities, recurrent infections and malabsorption are presented. The elder sister of the children as well as the rest of the family are unremarkable. The complex of symptoms does not fit into one of the known Ichthyosis syndromes. Microscopically the dystrophic hairs show changes in diameters, nodules, lack of the medulla, rough cuticle and splits vertical to the axis, sometimes resembling trichorrhexis nodosa. In the scanning electron-microscope there is a clear difference to Netherton's syndrome. The plasma concentrations of the vitamines A, B12 as well as of beta-carotines are low in spite of normal nutrition. During parenteral therapy with vitamin A and B12 symptoms ameliorate slightly.

Abnormalities, Multiple↗
PubMed1980

[Etiology of congenital hypothyroidism].

Iodine deficiency, intrathyroidal defects of thyroxine synthesis and morphological defects of the thyroid gland are the causes for connatal hypothyroidism of various degrees. Morphological defects include the most severe forms of cretinism due to aplasia of the gland as well as various more milder forms following application of iodine or antithyroidal drugs to the mother or TSH deficiency of the newborn. Due to general TSH-screening programs, more will be learned about the still not fully understandable etiology of connatal hypothyroidism.

Congenital Hypothyroidism↗
PubMed1980

[The Ullrich-Turner syndrome].

The etiology of the Ullrich-Turner's syndrome is a chromosomal anomality, the karyotyp 45 XO being the most common one. This results in stunted growth, a number of deformities as pterygium colli or cubita valga, and primary amenorrhea due to gonadal dysgenesis. Treatment consists of anabolic steroids for improvement of growth and substitution of estrogens at a later age. Final height probably will rarely exceed 150 cm. Usually, patients are infertile.

Anabolic Agents↗
PubMed1980

Growth hormone deficiency and growth hormone therapy in Ullrich-Turner-syndrome.

In a girl with Ullrich-Turner-Syndrome (gonadal dysgenesis 45, XO) and growth hormone deficiency, 10 U of human growth hormone/m2 body surface area/week increased the growth rate from 2.0 to 4.1 cm/year. Doses of up to 36 U/m2/week did not improve the growth rate in 4 girls with Ullrich-Turner-Syndrome who had normal plasma growth hormone concentration and increation. We conclude that growth hormone therapy is unsuccessful in dwarfism in Ullrich-Turner-Syndrome and should be reserved for patients with proven growth hormone deficiency.

Age Determination by Skeleton↗
PubMed1980

17-ketosteroid reductase deficiency -- plasma steroids and incubation studies with testicular tissue.

The patient, diagnosed as a case of testicular feminisation in infancy, was examined at the age of 15 years because of severe symptoms of virilising puberty with poor breast development. Plasma steroid analyses revealed a 10-fold elevated androstenedione concentration (A: 1562 ng/100 ml). Testosterone (T: 266 ng/100 ml) was in the male pubertal range. Thus the A/T-ratio was far above normal. The oestrone/oestradiol ratio was also elevated (Oe1/Oe2: 10.2/2.2 ng/100 ml). A, T, Oe1 and Oe2 could not be suppressed by dexamethasone, but reacted promptly to fluoxymesterone (A: 781 ng/100 ml). hCG caused a further increase of the A/T-radio (2220/246 ng/100 ml); ACTH did not alter the A-concentration. These findings together with simular investigations after gonadectomy suggest that the failure to convert A to T and Oe1 to Oe2 is essentially located in the testes. In vitro incubations of testicular tissue showed reduced 17-ketosteroid reductase activity in tissue slices and in the subcellular fractions microsomes and cytosole. This form of male pseudohermaphroditism can easily be detected already in infancy, if steroid analyses and stimulation tests are performed. In case of female sex assignment patients should be submitted to early orchidectomy in order to avoid virilisation in puberty.

17-Hydroxysteroid Dehydrogenases↗
PubMed1980

Treatment of anorchia with oral testosterone undecanoate: pharmacodynamics and clinical effectiveness.

The pharmacodynamics of plasma testosterone (T) and androstenedione (A) levels were studied in ten hypogonadal boys after oral administration of testosterone undecanoate (TU). Plasma T and A levels were measured by specific radioimmunoassays. Six hours after a single dose of 120 mg TU, there was a significant increase (P < 0.005) in plasma T and A with a median T peak level of 940 ng/100 ml. Furthermore, twelve agonadal boys treated with a mean dose of 60 mg TU/day were examined over a period of 18-24 months. During this therapy, plasma T and A levels were significantly higher than before (P < 0.005), whereas plasma levels of LH and FSH did not decrease significantly. With the exception of one anorchic boy, all patients showed signs of sexual maturation, such as growth of pubic and axillary hair, and steady development of bone age during oral TU treatment.

Administration, Oral↗