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O Butenandt

Publications and source records attributed to O Butenandt.

At least 19 recordsLinked to original sources
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↗
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↗
PubMed1979

[Maldescensus testis, therapy and prognosis].

Since histologic changes are found in undescended testes after the second year of life, treatment is necessary. Often therapy with human choriongonadotrophin is successful, otherwise operative treamtnet is indicated. Infertility at a high rate is found in boys treated for maldescence of the testicles in later childhood. Therapy before the age of two years improves the prognosis.

Child↗
PubMed1979

Rheumatoid arthritis and growth retardation in children: treatment with human growth hormone.

Twenty patients with rheumatoid arthritis or Still's disease associated with growth failure were treated with human growth hormone, 7.5 to 17 U/m2 body surface per week. Five patients did not respond with better growth. In the remainder the mean growth rate increased from 1.9 cm/year (range: 0 to 3.3) to 6.2 cm/year (range: 3.6 to 12) over 5 to 7 months. Twelve patients treated for longer periods increased their mean growth rate from 2.6 cm/year (range: 0.7 to 5.7) to 6.3 cm/year (range: 2.4 to 9.7) and continued to grow during a second year of treatment. Growth velocity decreased in 6 patients when the hGH therapy was discontinued. The causes for this improvement in growth are possibly multifactorial: the growth rate is depressed by the severity of the disease and high-dose glucocorticoid therapy. Increases of growth rate occurred during improvements in the disease, reduction of steroid medication, as a result of therapy with human growth hormone, and because of puberty in some patients. Human growth hormone seemed to improve the underlying condition of four of the patients but had no influence on the disease in the remaining children.

Adolescent↗
PubMed1979

Comparison of two tests for heterozygosity in congenital adrenal hyperplasia (CAH).

The increase of plasma cortisol (F), androstenedione (A), 17 alpha-hydroxy-progesterone (17-OH-P) and testosterone (T) was measured after iv administration of ACTH in heterozygotes for CAH and in controls under two different conditions: Test 1: ACTH stimulation was performed without any particular preparation. Test 2: 1.5 mg of dexamethasone (dex.) was given the evening before the ACTH stimulation. Plasma F, A, 17-OH-P and T were measured by specific radioimmunoassays (RIA). Following ACTH stimulation, the increase of 17-OH-P was significantly higher in CAH-heterozygotes than in controls in both tests (P less than 0.0005). Heterozygotes were characterized by a 17-OH-P increase after ACTH stimulation exceeding the + 2 SD limit of the 17-OH-P increase found in controls. The detection of female heterozygotes was considerably improved by the administration of dex. before testing (test 2). In males, however, a better identification of heterozygotes was obtained without previous administration of dex. (test 1). By these tests, 100% of female (test 2) and 79% of male (test 1) CAH heterozygotes could be correctly identified. There were no significant differences in the levels of F, A and T between heterozygotes and controls except for decreased T levels in test 1 (2P less than 0.01) in most male heterozygotes after ACTH stimulation.

Adrenal Cortex Function Tests↗
PubMed1978

[Diagnostic means to exclude deficient secretion of growth hormone in paediatric practice (author's transl)].

Growth hormone serum levels were measured radioimmunologically in 365 children with stunted growth before and after 10 minutes of stair-climbing, and in 134 children before and after 10 minutes of physical stress produced by means of a bicycle ergometer. Only 20% of the children had a growth hormone level of more than 5 ng/ml before initiation of the study. After climbing the stairs, the hormone level rose in 160 children to more than 5 ng/ml (max. 41.1 ng/ml). Growth hormone deficiency could thus be definitively eliminated as the cause of retarded growth in only 46% of the patients. In 16 (of 22) children of normal size, in 34 (of 49) chilkren with arrested growth who had a corresponding familial background, and in 33 (of 57) children with constitutionally conditioned retarded development, the growth hormone content after exercise on an rose to more than 5 ng/ml. Hence, a total of 65% of the children showed a satisfactory increase of the growth hormone. It follows from this that the ergometer exercise test is more suitable that the stair-climbing test to exclude hormone deficiency as the cause of stunted growth, and can, therefore, be recommended for use in paediatric practice as a supplementary examination method besides clinical findings, case history and determination of the growth rate.

Child↗
PubMed1977

Adult height of patients treated in childhood for undescended testes.

101 patients successfully treated for undescended testes with human chorionic gonadotrophin (HCG) or with HCG followed by surgery reached normal adult heights. Deviations from normal growth in individual patients did not appear to be related either to their earlier undescended testes or to the successful therapy, but rather to their genetic background. Therefore, apart from patients with chromosomal abnormalities and other primary causes for maldescent of the testes, boys with undescended testes show a normal distribution for height and do not represent a different population with regard to growth.

Adolescent↗
PubMed1977

Plasma volume estimation in severely ill infants and children using a simplified Evans blue method.

Plasma volume was measured using Evans blue dye and 125iodinated human serum albumin (RIHSA) simultaneously in order to evaluate the accuracy of a simplified Evans blue method recommended by Nielsen and Nielsen (1962). 9 studies were performed in 8 newborn infants weighing 1.07 to 2.85 kg and 16 studies in 14 patients aged 6 months to 14 years suffering from severe circulatory disturbances. In 20 studies, plasma volumes measured by Evans blue and by RIHSA agreed within +/-5%, and in all the studies within +/-10%. The Evans blue method yielded higher plasma volumes than the RIHSA method in 19 instances. The mean difference (paired t-test) was only significant in newborn infants (+4.0+/-3.6%; P less than 0.05). The disappearance rates of Evans blue exceeded that of RIHSA in 16 studies, but this was only significant in the patients older than 6 months (+2.3+/-4.2%/h; P less than 0.05).

Adolescent↗