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O Butenandt

Publications and source records attributed to O Butenandt.

At least 37 records · Page 2Linked to original sources
PubMed1996

Growth hormone treatment of short children born small for gestational age: metanalysis of four independent, randomized, controlled, multicentre studies.

A minority of children born small for gestational age (SGA) fail to achieve sufficient catch-up growth during infancy and remain short throughout childhood, apparently without being growth hormone (GH) deficient. The effect of GH administration was evaluated over 2 years in short prepubertal children born SGA. The children (n = 244), who were taking part in four independent multicentre studies, had been randomly allocated to groups receiving either no treatment or GH treatment at a daily dose of 0.1, 0.2 or 0.3 IU/kg (0.033, 0.067 or 0.1 mg/kg) s.c. At birth, their mean length SD score (SDS) was -3.6 and their mean weight SDS -2.6; at the start of the study, mean age was 5.2 years, bone age 3.8 years, height SDS -3.3, height SDS adjusted for parental height -2.4, weight SDS -4.7 and body mass index (BMI) SDS -1.4. The untreated children had a low-normal growth velocity and poor weight gain. Although bone maturation progressed more slowly than chronological age, final height prognosis tended to decrease, according to height SDS for bone age, GH treatment induced a dose-dependent effect on growth, up to a near doubling of height velocity and weight gain; BMI SDS was not altered. Bone maturation was also accelerated differentially; however, final height prognosis increased in all GH treatment groups. The more pronounced growth responses were observed in younger children with a lower height and weight SDS. In conclusion, GH administration is a promising therapy for normalizing short stature and low weight after insufficient catch-up growth in children born SGA. Long-term strategies incorporating GH therapy now remain to be established.

Age Determination by Skeleton↗
PubMed1996

Spontaneous growth in idiopathic short stature. European Study Group.

Documenting the spontaneous growth pattern of children with idiopathic short stature (ISS) should be helpful in evaluating the effects of growth promoting treatments. Growth curves for children with ISS were constructed, based on 229 untreated children (145 boys and 84 girls) from nine European countries. The children were subdivided according to target range and onset of puberty, and the growth of these subgroups was evaluated from standard deviation scores (SDS). At birth, children with ISS were already shorter than normal (means; boys -0.8 SDS, girls -1.3 SDS). Height slowly decreased from -1.7 SDS at the age of 2 years to -2.7 SDS at the age of 16 years in boys and 13 years in girls. Final height was -1.5 SDS in boys and -1.6 SDS in girls (mean (SD): boys 164.8 (6.1) cm, girls 152.7 (5.3) cm)), which was 5-6 cm below their target height. The onset of puberty was delayed (boys 13.8 (1.3) years, girls 12.9 (1.1) years). Subclassification resulted in similar growth curves. These specific growth data may be more suitable for evaluating the effects of growth promoting treatments than population based references.

Adolescent↗
PubMed1996

Measurement of spontaneous, 12-hour sleep-associated GH secretion in prepubertal children with short stature: clinical relevance and practicability?

We have asked whether or not sleep-associated 12-hour GH profiles were a clinically relevant and practicable tool to identify short children with low spontaneous GH secretion. In 67 prepubertal patients (19 girls and 48 boys, mean age 9.34 years, range 1.99-14.5) sleep-associated 12-hour GH profiles were obtained by drawing peripheral venous blood every 30 min over a 12-hour night period. The diagnosis of GH deficiency (GHD, n = 26), constitutional delay of puberty and growth (CDPG, n = 19), familial short stature (FSS, n = 8), GH neurosecretory dysfunction (GHND, n = 5), and constitutional delay of puberty and growth plus familial short stature (CDPGFSS, n = 9) was made by clinical parameters (SDS height range:-0.69 to -5.59, SDS growth velocity:-4.6 to -2.4) and provocative testing of GH secretion. Integrated GH secretion (area above baseline = AOB, area above zero line = AOOL), peak frequency, area under the peaks, peak amplitude length, peak amplitude height, maximal peak values, and median peak values were calculated using the PULSAR program. Significant differences of GH secretion between patient groups in regard to mean values for area over baseline, area over zero line, amplitude height, maximal peak values, and median peak values of secretion were found. However, there was a large interindividual variation of integrated GH secretion within each patient group and, most importantly, a large overlap between the different patient groups. We conclude that the assessment of pulsatile GH secretion during sleep, even if it can contribute to distinguish between different groups of short children, is not helpful to distinguish between different causes of short stature in an individual child. We suggest that measurement of sleep-associated spontaneous GH secretion needs to be restricted to research facilities.

Adolescent↗
PubMed1995

Final height and predicted height in boys with untreated constitutional growth delay.

We report on 49 boys with constitutional growth delay (CGD) who were initially seen in our clinic at a mean chronological age of 13.3 years (range, 7.3-16.4) and a bone age of 11.1 years (range, 6.0-13.5). All were below the 5th height percentile for chronological age. A positive family history with delayed growth and puberty in one or both parents could be elicited in 75%. All 49 patients were re-examined at a mean age of 22.9 years (range, 20.4-31.2). Measured final height was 171.3 cm (range, 161.2-181.7), which was slightly, but significantly lower than mean target height of 173.0 cm. Final height expressed as standard deviation score (SDS) of a male adult population standard was -1.0 (range, -2.4 to 5), also significantly lower than initial height SDS related to bone age (SDSBA) of -0.5 (range, -1.6 to 2). If related to target height (Tanner), final height was found to correlate positively with the initial bone age deficit and the initial height SDSBA. Observed final height was also compared with the predicted adult height by the methods of Bayley-Pinneau (BP), Tanner-Whitehouse Mark II (TW II) and Roche-Wainer-Thissen. Regression equations between all three prediction methods and final height showed an excellent correlation (P < 0.0001). However, only by the BP method was predicted height very close to and no different from measured final height (paired t-test). Despite this, final height in 16 of 49 patients (32.6%) differed by more than 5.0 cm from BP predicted height.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

[Growth hormones today].

Human growth hormone (hGH) stimulates the growth rate in children with GH deficiency, but also in children secreting GH, when given in higher doses. Concomitantly, there is an anabolic effect on the protein metabolism and an anticatabolic effect by increasing the content of free fatty acids. Growth hormone may be helpful in management of patients with subfertility or hypogalacty. The hormone increases the amount of muscles and decreases the fat of skin in adults with GHD. Biosynthetic products should be used since pituitary hGH could transmit diseases from the organ donors. No oncogenic properties have been confirmed. Only hGH is effective in man, since there is a marked species specificity.

Adult↗
PubMed1992

[Growth hormone therapy in childhood. Certain indications].

The diagnosis of growth hormone deficiency is established on the basis of auxological and endocrinological studies. Without treatment, the final stature will be reduced; by way of treatment, administration of biosynthetic human growth hormone is required. Total and partial growth hormone deficiency can be distinguished, as also neurosecretory dysfunction of growth hormone secretion. Growth hormone can also be successfully administered to girls with the Ullrich-Turner syndrome, but the doses required are somewhat higher than in the case of growth hormone deficiency. Other forms of reduced stature might possibly benefit from growth hormone treatment, but the results of ongoing studies on this point must first be obtained.

Achondroplasia↗
PubMed1992

Therapy of growth hormone deficiency.

Treatment with human growth hormone in growth hormone deficient patients will improve growth rate significantly, initially demonstrating catch-up growth and later bringing forth a normal growth rate. During childhood, a dose of 0.3-0.6 units/kg body weight per week (or 14 units/m2 body surface area per week) is recommended, but during puberty the dose should be increased by 50-100%. The goal of therapy is the attainment of a normal final height, which in the past has often not been fulfilled. This was partly due to the inadequate supply of growth hormone. Since recombinant human growth hormone is now available in unlimited amounts, all patients can be treated continuously. The shorter the child is at time of presenting for therapy, the lower final height will be. It is mandatory to start therapy as early as possible. Concomitant hormonal deficiencies must be corrected by adequate therapy. Despite the fact that growth hormone is diabetogenic, supplementary therapy will not induce diabetes mellitus. Subtle changes in the immune system can be detected but no clinical correlates, such as increased susceptibility to infection, exist. Induction of leukaemia has been suspected as a possible side-effect of human growth hormone treatment but so far there is insufficient evidence to prove that growth hormone is oncogenic.

Growth Disorders↗
PubMed1992

Prevalence of autoantibodies to endocrine organs in girls with Ullrich-Turner syndrome aged 5-14 years.

Endocrine function tests and a broad panel of autoantibodies to endocrine organs were assessed in 77 patients aged 5-14 years with Ullrich-Turner syndrome (UTS), who were included in the German UTS Multicenter Study. None of these patients had abnormal pituitary, thyroid or adrenocortical function, as assessed by the adequate hormone tests. Antibodies to thyroid microsomes were found in 3 of the 77 (3.9%), antibodies to thyroglobulin in 0/77, antibodies to adrenocortical cells in 1/77 (1.3%), gastric parietal cell antibodies in 2/77 (2.6%), and anterior pituitary cell antibodies in 3/77 (3.9%) probands. These prevalences were not significantly higher than those obtained in 154 age- and sex-matched normal control children when 2 control subjects were assigned to each patient with UTS. Our data do not show an increase in serological signs of endocrine autoimmunity in young patients with UTS suggesting that a putative association of these syndromes does not exist from birth and is not usually present in childhood. However, we cannot exclude the possibility that UTS is associated with factors that render these patients more susceptible to endocrine autoimmunity later in life.

Adolescent↗
PubMed1991

[Glucocorticoid therapy in childhood].

In children, too, treatment with glucocorticoids may occasionally be necessary. On the one hand, replacement treatment in children with the adrenogenital syndrome, on the other pharmacotherapy in a number of diseases may be required. The latter include the genuine nephrotic syndrome, autoimmunological diseases, hypsarrhythmia, and, in the field of neonatology and neonatological intensive care, the treatment of the respiratory distress syndrome and bronchopulmonary dysplasia. Side effects of pharmacotherapy include suppression of the adrenal cortical function and growth disorders, together with truncal obesity, formation of striae of distension or osteoporosis.

Addison Disease↗
PubMed1990

[Alcohol embryopathy. Review and case example].

Fetal alcohol syndrome is a disorder that occurs in children of alcoholic mothers and is characterized by typical craniofacial dysmorphia and retardation of mental and physical growth. Semiquantitative evaluation of the most common symptoms permits clinical classification into three stages. Although numerous hypotheses have been suggested, the pathogenetic mechanism is not yet well understood. Prevention through medical advice and counselling still remains the most successful form of therapy. A case of fetal alcohol syndrome caused by excessive maternal drinking accompanied by high nicotine consumption during pregnancy is reported.

Adult↗
PubMed1990

[Nocturnal growth hormone secretion in children with constitutional and acquired developmental delay].

We investigated the spontaneous secretion of GH during sleep (20.00 to 8.00) in 76 children with short statute. No difference could be found between a group of 12 children with familiar short stature or a group of 28 children with familial delay of growth and development: mean GH level 5.88:5.71 maxima 26.9:25.4 ng/ml, and integrated concentration of GH 2360:2617 ng x min/ml. 14 children with severe growth hormone deficiency proven by 2 stimulation tests, secreted significantly lower amounts of GH (mean 0.83 ng/ml, maximum 2.9 ng/ml, integrated concentration 371 ng x min/ml). 22 children with nonfamilial delay of growth and development presented values being lower than the first two groups, but higher than the group of GH deficiency patients (mean 3.07 ng/ml, maximum 13.8 ng/ml, integrated concentration 1429 ng x min/ml). Since in these children the anamnesis revealed events like breech delivery, shock or commotio cerebri as the history of patients with GH deficiency does, these events apparently cause the defective GH secretion in nonfamilial delay of growth and development.

Adolescent↗
PubMed1989

[Therapy of endocrine diseases in childhood and adolescence. 6: Endocrinologic emergencies in pediatrics].

Endocrinological emergencies in childhood include tetany - also in the form of epileptiform seizures - and Addisonian crisis. Acute tetany is treated by the administration of calcium, with subsequent calcitriol given as an adjunct. An Addisonian crisis or similar salt-loss crisis in the adrenogenital syndrome requires the administration of salt-containing solutions, replacement of gluco- and mineralocorticoids and the balancing of the acid-base household.

Addison Disease↗
PubMed1989

Comparison of growth hormone releasing hormone therapy and growth hormone therapy in growth hormone deficiency.

Seven children with growth hormone deficiency of hypothalamic origin responded to an i.v. bolus of growth hormone releasing hormone (GHRH) (1-29)-NH2 with a mean serum increase of 10.7 ng/ml growth hormone (GH) (range 2.5-29.3 ng/ml). Continuous s.c. administration of GHRH of 4-6 micrograms/kg twice daily for at least 6 months did not improve the growth rate in five of the patients. One patient increased his growth rate from 1.9 to 3.8 cm/year and another from 3.5 to 8.2 cm/year; however, the growth rate of the latter patient then decreased to 5.4 cm/year. When treatment was changed to recombinant human growth hormone (rhGH) in a dose of 2 U/m2 daily, given s.c. at bedtime, the growth rate improved in all patients to a mean of 8.5 cm/year (range: 6.2 to 14.6). Presently GHRH cannot be recommended for the routine therapy of children with growth hormone deficiency since a single daily dose of rhGH produced catch-up growth which GHRH therapy did not.

Child↗
PubMed1989

Diagnostic value of growth hormone-releasing hormone tests in short children.

The growth hormone-releasing hormone (GHRH) test was applied to more than 230 children. Twenty-five out of 61 patients with proven growth hormone (GH) deficiency responded to GHRH with a GH increase of greater than 10 ng/ml. In most of the patients with idiopathic GH deficiency, a priming procedure using daily injections of GHRH improved the secretory response to GHRH. Nearly all children with familial shortness of stature showed a prompt increase in GH levels, with a mean peak level of 34.9 ng/ml (range 0.5-144 ng/ml). A second test was performed in five children with familial short stature because of failure to respond to the first test. Children with constitutional delay of growth and development did not differ in their GH response from patients with familial shortness of stature. Ten girls with Ullrich-Turner's syndrome responded with a mean increase of 22 ng/ml GH (range 10.1-34.0 ng/ml). Therapy with glucocorticoids, as well as endogenous hypersecretion of cortisol, suppressed the responsiveness of the pituitary gland to GHRH. Suppression was also observed following a single dose of dexamethasone during the steroid-suppression test in eight obese children. Low responsiveness of the pituitary gland was also seen in patients with thalassaemia and transfusion-induced haemosiderosis. It is concluded that it is not possible to detect GH deficiency with a single GHRH test. A full endocrinological evaluation is necessary to prove the diagnosis.

Adolescent↗