[Odontometric study on the correlation between tooth and body size].
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Adult↗
Biomedical subjects
O Butenandt
Publications and source records attributed to O Butenandt.
[Estimate of prospective body height of patients with Ullrich-Turner syndrome].
The prospective final height was assessed in girls with Ullrich-Turner syndrome and compared with the final height attained, using different methods of evaluation for the prospective final height. The Bayley-Pinneau method gave the best results, which were further improved by correction of the data by using our own measurements.
Adolescent↗
Regulation of GH binding to specific cellular receptors in vitro--a new model of growth regulation in vivo.
A new theory on the complex growth hormone (GH) mediated promotion of tissue growth has been developed on the basis of in vitro studies of growth hormone receptors on human peripheral mononuclear cells (PMC). It is hypothesized that GH acts through its tissue receptors and regulates its own receptors through two different pathways: first GH directly downregulates GH binding, second a partially GH-dependent serum factor (the so-called SM-B) enhances GH binding. Some experimental evidence for this hypothesis is presented using a new method to investigate GH receptors in circulating human blood cells: The effect of trypsin, antitrypsin, growth hormone, somatomedin-B (SM-B) and anti-SM-B-antiserum on GH binding to PMC was studied. Trypsinization of cells leads to a decrease both of specific binding and of binding affinity (affinity constant after 60 minutes of trypsinization 0.5 X 10(6) M-1 versus 1.5 X 10(6) M-1 in untreated control cells). Exposure of PMC to antitrypsin activities was followed by an increase of binding affinity and specific binding (affinity constants with 10 KIU 1.9 X 10(6) M-1, with 100 KIU 2.4 X 10(6) M-1, with 1000 KIU 3.6 X 10(6) M-1). This antitrypsin effect exceeds the binding values expected after blocking trypsin activities possibly being present in the incubation medium. In a subset of experiments the partially GH-dependent serum factor SM-B was used as the antitrypsin moiety and was shown to increase specific GH binding to PMC in a similar manner as did antitrypsin (with 1000 ng SM-B affinity constant 12.0 X 10(6) M-1, specific binding 9.7%).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
The effects of cyproterone acetate on statural growth in children with precocious puberty.
Forty-four patients (42 f, 2 m) with precocious puberty (31 idiopathic, 1 familial, 7 cerebral, 5 McCune-Albright) were treated with cyproterone acetate for periods of 1-8.75 years in different (P less than 0.05) daily dosages of 117 +/- 6.1 mg/m2 per day (mean +/- SEM, group A, N = 20) and 60.8 +/- 2.42 mg/m2 per day (group B, N = 24). Thirty-three girls had experienced menarche before therapy at a mean age of 4.89 +/- 0.42 years. Treatment was started at a chronologic age of 5.45 +/- 0.33 years in the girls and 5.74 +/- 1.34 years in the boys. At the time of evaluation, 31 of our patients had reached final height. With respect to the effects of treatment on statural growth, the Standard Deviation Scores were retrospectively determined for height, weight, and growth velocity. The initial Bayley-Pinneau height predictions were compared with final height and target height, and the skeletal maturation was studied. There were no significant differences between those parameters in the patients of group A and B or between treated and untreated subjects as far as final height and target height were concerned. It is concluded that cyproterone acetate administered orally at daily doses from 50-150 mg/m2 does not improve statural growth of patients with precocious puberty.
Body Height↗
[Growth hormone secretion following administration of growth hormone releasing hormone in constitutional short stature and idiopathic growth hormone deficiency].
A stimulation test using 1 microgram growth-hormone-releasing factor (GRF 1-29 X NH2)/kg bodyweight was performed in children with familial short stature and in children with constitutional delay of growth and development. The GH secretion induced by this means was not different in these groups, but there was a difference in the response between normal children and children with idiopathic growth hormone deficiency (GHD). GH secretion after GRF administration was significantly lower in the GHD group than in the other groups. However, 6 of 24 patients with GHD responded to the test with a normal increase in GH (greater than 10 ng/ml), and 11 with an intermediate response (2-10 ng/ml). Thus, the test does not differentiate individual patients with defective growth hormone secretion from normal short children.
Adolescent↗
[Therapy of pituitary dwarfism with recombinant human growth hormone. A multicenter study].
During the period from 1982 to 1985, biosynthetic growth hormone (methionyl-hGH) was administered to 55 children with pituitary growth deficiency, 49 with idiopathic, six with other forms of the disorder. Preparations with a relatively high content of Escherichia coli polypeptides (ECP) were given to 32 children (group I), those with a markedly reduced ECP content to 12 (group II), while 11 children received almost ECP-free preparations (group III). The treatment achieved an intensive rise of growth acceleration in all three groups. At the same time, somatomedin C, biological somatomedin activity and alkaline phosphatase rose steeply, reaching a maximum after six months and remaining at high concentrations even thereafter. High antibody titres against ECP and hGH (with high binding capacity) were demonstrated in group I children, significantly lower titres with little binding capacity in those of group II, while most of those in group III had no measurable antibodies. Even in high concentrations the antibodies did not have any inhibiting effect on growth. No positive correlation between antibody titre and growth velocity was demonstrable. An exception was a boy with an allergy in group I, who had a maximal antibody titre and, at the same time, a high serum concentration of IgE. He had marked delay in growth which, however, quickly became normal on administration of extractive hGH.
Bacterial Proteins↗
[Therapy of endocrine diseases in childhood and adolescence. 5: Primary hypogonadism].
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Adolescent↗
Lymphocyte subsets and natural-killer activity in growth hormone deficiency.
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Child↗
Single and repeated testing of growth hormone secretory capacity in hypopituitarism using growth hormone releasing factor.
38 patients with proven growth hormone deficiency (GHD) and 19 children with familial short stature received an iv GRF-bolus injection of 1 microgram/kg body weight. Whereas in all control children plasma growth hormone rose significantly (mean of maximal values 36 ng/ml), only 7 out of 38 patients with GHD reached peak values of 8 ng/ml or more. GRF-priming by 1 microgram GRF/kg BW given once daily s.c. for 5 days in 19 patients improved the response of the pituitary gland in 11. Thus, following the first GRF test, only 21% of patients demonstrated function of the pituitary gland whereas 45% did so when all test results are combined. To evaluate the pituitary function in patients with GHD correctly, GRF tests following a GRF priming period seems to be necessary to reactivate atrophic somatotropic cells of the pituitary gland.
Adolescent↗
[Congenital hypothyroidism--a diagnosis made by abdominal x-ray?].
Meteorism in a newborn may be a symptom of different diseases including hypothyroidism. It is caused by a disturbed peristalsis of the gut. Since in rare cases - as demonstrated in one infant - obligatory screening for hypothyroidism may be missed, meteorism should be considered a serious symptom and should lead to the right diagnosis before too much time is lost.
Congenital Hypothyroidism↗
[Progress beside setbacks in pediatrics].
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Child Development↗
Specific growth hormone receptors on human peripheral mononuclear cells: reexpression, identification, and characterization.
Although specific GH receptors have been demonstrated in various tissues of a number of species, the presence of GH receptors on human peripheral mononuclear cells (PMC) is controversial. Binding of human GH (hGH) to its receptor as the hypothesized initial step of hormone action was consequently studied using mononuclear cells from peripheral venous blood of normal subjects. Specific binding of [125I]hGH was rapid, reversible, and time and temperature dependent. Specific GH binding to PMC was maximal after 8-24 h of preincubation. Binding of hormone was maximal at 37 C after incubation of cells for 2 h. Dissociation of GH was maximal at 37 C after the addition of 6 M NaCl. A linear relationship between specific GH binding and cell number was found. Saturation of GH binding to 10(6) PMC was obtained with 25 ng iodinated hormones. Half-maximal inhibition of GH binding occurred at 12-25 ng unlabeled hGH/tube. Hypothalamic and pituitary hormones as well as insulin did not interfere with specific hGH binding to PMC. Scatchard analysis of [125I]hGH binding to PMC revealed a receptor with a mean affinity constant of 1.5 +/- 0.2 (+/- SD) X 10(9)/M-1 (n = 72) and a maximal binding capacity of 7.1 +/- 2.0 X 10(-11) M/10(6) cells. The concentrations of calcium, sodium, and magnesium ions in the incubation medium strongly influenced GH binding, whereas pH or potassium concentration did not. As interassay variation of the binding assay was low (14% for total binding; 6% for specific hGH binding), this direct approach to study tissue receptors for hGH in a human in vitro test was reproducible and should encourage the investigation of receptor regulation as well as the study of binding in human disease.
Adult↗
Effect of enzyme and enzyme inhibitors on specific binding of hGH to human peripheral lymphocytes.
A recently described method to investigate growth hormone (GH) receptors on circulating human blood cells has been used to study the effect of a trypsin preparation and antitrypsin moieties on hormone binding to lymphocytes. Trypsinization with one defined dose of trypsin (10 ng/ml) led to a considerable decrease both of specific binding and of binding affinity (affinity constant after 60 min trypsinization 0.5 X 10(9) vs 1.5 X 10(9) M-1 in untreated control cells). Exposure of peripheral blood lymphocytes (PBL) to antitrypsin activities was followed by a steady increase of affinity and specific binding (affinity constant: with 10 KIU anti-trypsin 1.9 X 10(9) M-1, with 100 KIU 2.4 X 10(9) M-1, with 1000 KIU 3.6 X 10(9) M-1). This antitrypsin effect exceeds the binding values expected after blocking trypsin activities in the incubation medium. In a subset of experiments somatomedin-B (SM-B) was used as the antitrypsin moiety and was shown to increase specific GH binding to PBL in a similar manner as did antitrypsin (with 1000 ng SM-B affinity constant (Ka) 12.0 X 10(9) M-1, specific binding 9.7% of total radioactivity). It is concluded that enzymatic factors and their inhibitors including partially GH dependent moieties like SM-B modulate specific GH binding to human peripheral lymphocytes in vitro.
Adult↗
[Psychosocial dwarfism].
A 4 year old girl with psychosocial dwarfism showed hepatomegaly, abdominal distension and behavioral disturbances. Laboratory tests revealed a reversible elevation of serum liver enzymes and a reversible partial growth hormone deficiency. The child's family was characterised by severe social problems and all signs of a depriving and child abusing environment. All pathologic findings were reversed by removing the child from her depriving family background. This case demonstrates that psychosocial dwarfism represents an aspect of child abuse (battered child syndrome).
Body Height↗
[Therapy of endocrine diseases in childhood and adolescence. 4: Hypophyseal dwarfism].
A deficiency in growth hormone depresses growth and leads to dwarfism. The cause of hypopituitarism may be the destruction of the hypothalamus by a tumor infection or trauma. Birth trauma is often the underlying cause. Genetic forms or cerebral defects have also been described. Growth hormone may be completely lacking or partially reduced. Neurohormonal dysfunction is of particular interest. Administration, either intramuscular or subcutaneously, of human growth hormone leads initially to "catch-up" growth and to subsequent normal growth. Early treatment should be instituted if normal adult height is to be achieved.
Adolescent↗
[Therapy of hypogonadotropic hypogonadism. Indications for the pulsatile administration of gonadotropin-releasing hormone].
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Adolescent↗
[Growth hormone secretion and plasma renin activity in children following administration of clonidine].
Growth hormone and plasma renin activity were measured following oral clonidine. 50 out of 61 (82%) children without pituitary dysfunction receiving 75 micrograms Clonidine per sqm bodysurface area reached maximal levels of more than 6 ng GH/ml, and only 44 (72%) of more than 8 ng/ml. Following 25 micrograms Clonidine only 50% of children without pituitary dysfunction reached GH-levels of more than 6 ng/ml, and only 40% of more than 8 ng/ml. In 72% of children the growth hormone level determined in a single specimen taken 60 min after they fell asleep was higher than 6 ng/ml. Only 2 out of 33 children without pituitary dysfunction did not present sufficient amounts of growth hormone following clonidine or sleep to exclude growth hormone deficiency to screen for growth hormone deficiency. It is recommended to use 75 micrograms of Clonidine/m2 as a provocative test, and additionally to determine growth hormone after onset of sleep. Plasma renin activity prior to clonidine was 3.13 ng/ml/h, and 2.03 ng/ml/h 30 min after drugintake. Systolic blood pressure decreased from 118 mm Hg initially to 104 mm Hg (mean) within 30 min after clonidine was given orally.
Adolescent↗