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Biomedical subjects

H Frisch

Publications and source records attributed to H Frisch.

At least 91 records · Page 5Linked to original sources
PubMed1989

Melatonin secretion in Turner's syndrome: lack of effect of oestrogen administration.

Melatonin secretion was investigated in 13 girls with Turner's syndrome before and after long-term oestrogen administration. Oestrogen treatment resulted in an increase in the serum levels of the hormone and a decrease in blood progesterone concentration. No change, however, was observed in the melatonin secretion pattern (in terms of peak values, time of peak level and total melatonin secretion) after oestrogen therapy. A distinct circadian rhythm in serum melatonin was evident in all subjects with peak occurring around 0200 h and concentration similar to those of normal subjects.

Adolescent↗
PubMed1989

Effect of recombinant human growth hormone on urinary 15N-nitrogen balance in girls with Turner syndrome as compared to children with growth hormone deficiency.

15N-nitrogen balances before and on human growth hormone (hGH) were studied in 13 girls with Turner syndrome (TS) aged 4.4-16 (median 13.2) years (45,X0 or equivalent, no X0/XX mosaicism, no estrogen replacement). The results were compared with those reported from 9 patients with growth hormone deficiency (GHD). The TS patients received subcutaneous hGH doses of 2 x 3 (group A, n = 6), 3 x 2 (group B, n = 3), or 2 x 6 (group C, n = 4) IU/m2 on consecutive days. The mean 15N dose given to the patients of groups A and C was higher (13.6 mg/kg) than that given to those of group B (2.7 mg/kg). The lower hGH doses in the first two groups induced small positive mean 15N balance changes (+0.6 +/- 0.6 mg/kg 15N, group A; +0.03 mg/kg, group B). The higher hGH dose in group C caused a more marked mean balance change (+3.0 mg/kg 15N) comparable to that in GHD patients (+3.2 mg/kg). Individual variation of response, however, was larger in patients with TS than in those with GHD. With low and high hGH doses, there were responders and nonresponders. It is concluded from this pilot study in a small number of cases that 15N balance studies might be potentially useful to choose the appropriate hGH dose for long-term treatment in TS patients.

Adolescent↗
PubMed1989

Influence of estrogen administration on growth hormone response to GHRH and L-Dopa in patients with Turner's syndrome.

The modulating effect of estrogen on GH secretion was studied in 22 patients with Turner's syndrome. Estrogen administration (0.5 microgram/kg ethinylestradiol) for a period of 4 weeks resulted in a significant increase in basal GH concentrations (2.6 vs 4.8 micrograms/l, P less than 0.01). The L-Dopa-stimulated GH concentrations were also significantly increased (P less than 0.01), whereas no effect of estrogen substitution on GH responses to GHRH (1-44) and Sm-C levels was seen. Our findings demonstrate a priming effect of estrogen on GH secretion in patients with Turner's syndrome. These patients generally lack the puberty-associated rise in GH secretion, which might be due to ovarian failure and the concomitant estrogen deficiency.

Adolescent↗
PubMed1988

Isolated growth hormone deficiency after severe head trauma.

In a 12-yr-old boy growth arrest occurred after severe head trauma. Evaluation of pituitary endocrine function revealed isolated growth hormone (GH) deficiency. Lack of GH response to GH-releasing factor indicated that the responsible lesion was most likely to be localized in the pituitary gland. GH substitution resulted in biochemical (somatomedin increase) and clinical (catch up growth) response.

Adolescent↗
PubMed1988

Incidence of childhood diabetes mellitus in Austria 1979-1984.

The mean annual incidence of childhood diabetes mellitus in Austria was 7.22 cases per 100,000 with a year to year variation of 6.09-8.67 per 100,000. A seasonal variation of onset, with peaks in autumn and winter and with lower rates in summer in children older than 4 years, could be observed. The peak incidence in girls occurred at 11-12 years and preceded the highest incidence in boys by 1-2 years. Both sexes showed a small peak around 6 years of age. The male to female ratio was 1.2/1. Compared to epidemiologic studies in north-western Europe the incidence of childhood diabetes in Austria is low, however higher than in France or Italy.

Adolescent↗
PubMed1988

Effect of a recombinant human growth hormone preparation on the urinary 15nitrogen balance in growth-hormone-deficient children.

In 10 patients with idiopathic growth hormone (GH) deficiency (9 boys and 1 girl, aged 7.5-14.5 years, mean 12.1 +/- 2.2 years), urinary 15N-balance studies were performed before and on recombinant hGH (2 x 3 IU/m2 of body surface area subcutaneously on consecutive days). Before and on the 2nd day of recombinant hGH, 99% 15N-labeled ammonium chloride (0.05 g/kg, divided in 3 doses per day, corresponding to 389 +/- 30 mg/m2 of 15N) was administered and 24 h urine was collected. In urine, total nitrogen and the percentage of 15N were measured. From the ingested and excreted quantity, a urinary 15N balance was calculated. Mean 15N percentage from total N was 3.3 +/- 0.5. In 9 patients, basal 15N balance was +79 +/- 15 mg/m2 or +2.9 +/- 0.4 mg/kg. On recombinant hGH, it was +166 +/- 16 mg/m2 or +6.1 +/- 0.6 mg/kg (p less than 0.001). The recombinant hGH-induced positive 15N balance change was +87 +/- 17 mg/m2 or +3.2 +/- 0.6 mg/kg. 1 patient with a higher basal 15N balance (+196 mg/m2, +7.1 mg/kg) had no positive 15N balance change due to latent hypothalamic hypothyroidism. In previous similar studies with pituitary hGH the change of 15N balance was +80 +/- 27 mg/m2 or +2.8 +/- 1.1 mg/kg. It is concluded that the acute nitrogen-retaining effect of recombinant hGH is at least equal to that of pituitary hGH.

Adolescent↗
PubMed1988

Alterations in nocturnal serum melatonin levels in humans with growth and aging.

The available data on potential alterations in serum melatonin (MLT) levels during a human lifetime are fragmentary and inconsistent. We, therefore, measured day- and nighttime serum MLT concentrations in 367 subjects (210 males and 157 females), aged 3 days to 90 yr. Blood samples were collected between 0730 and 1000 h and between 2300 and 0100 h. Serum MLT levels were measured by RIA. The mean nighttime serum MLT concentration was low during the first 6 months of life, i.e. 27.3 +/- 5.4 (+/- SE) pg/mL (0.12 +/- 0.02 nmol/L). It then increased to a peak value at 1-3 yr of age [329.5 +/- 42.0 pg/mL; (1.43 +/- 0.18 nmol/L)], and it was considerably lower [62.5 +/- 9.0 pg/mL; (0.27 +/- 0.04 nmol/L)] in individuals aged 15-20 yr. During the following decades serum MLT declined moderately until old age (70-90 yr of age), i.e. 29.2 +/- 6.1 pg/mL (0.13 +/- 0.03 nmol/L). This biphasic MLT decline follows 2 exponential functions with different slopes (from age 1-20 yr: r = -0.56; P less than 0.001; y = 278.7 X e -0.09x; from age 20-90 yr: r = -0.44; P less than 0.001; y = 84.8 X e -0.017x). The decrease in nocturnal serum MLT in children and adolescents (1-20 yr) correlated with the increase in body weight (r = -0.54; P less than 0.001) and body surface area (r = -0.71; P less than 0.001). At a later age (20-90 yr) there was no correlation among these variables. Daytime serum MLT levels were low and no age-related alterations were found. This study revealed major age-related alterations in nocturnal serum MLT levels. The negative correlation between serum MLT and body weight in childhood and adolescence is evidence that expansion of body size is responsible for the huge MLT decrease during that period. The moderate decline at older ages must derive from other factors.

Adolescent↗
PubMed1988

[Age-related changes in stimulation and secretory rhythm of serum gonadotropins in children with Ullrich-Turner syndrome].

In 22 girls with Ullrich-Turner-Syndrome (UTS) aged 1.3 to 17.6 years basal and LHRH-stimulated gonadotropin (Gn)-concentrations as well as spontaneous variations of Gn-secretions were measured in order to recognize age dependent changes. Basal Gn-concentrations were elevated in the 1-year old girl, showed normal values in patients whose bone age was less than 11 years and were elevated again in the group with a bone age greater than 11 years. Stimulated LH and FSH concentrations were significantly elevated in all age-groups when compared with the values of age-matched controls. Minimal and maximal Gn-concentrations during spontaneous secretion were low in patients with a bone age less than 11 years, whereas a distinct elevation could be noted in the 1-year old child and in the elder group when compared with age-matched controls. According to these findings the typical age-dependent change of Gn-secretory dynamics could also be demonstrated in children with UTS albeit on an elevated level. A bone age of 11 to 11.5 years, when serum concentrations of Gn rise in healthy girls followed by onset of puberty seems to be the biological indicator for changes of the hypothalamo-hypopituitary level also in girls with Ullrich-Turner-Syndrome.

Adolescent↗
PubMed1987

[Basic-bolus therapy of diabetic children and adolescents using Novo Pens].

A multiple injection regimen using a pen-injector (Novo Pen) was applied to 34 diabetic adolescents (age: 15.4 +/- 2.4 years). During the observation-period of 6 months HbA1c fell significantly from 8.98 +/- 0.31 to 7.82 +/- 0.25 rel%. At the end of the study all patients wanted to continue this regimen considering the advantage of improved life quality compensating for the inconvenience of multiple injections.

Adolescent↗
PubMed1987

P450XXI (steroid 21-hydroxylase) gene deletions are not found in family studies of congenital adrenal hyperplasia.

Congenital adrenal hyperplasia (CAH) is a common genetic disorder due to defective 21-hydroxylation of steroid hormones. The human P450XXIA2 gene encodes cytochrome P450c21 [steroid 21-monooxygenase (steroid 21-hydroxylase), EC 1.14.99.10], which mediates 21-hydroxylation. The P450XXIA2 gene may be distinguished from the duplicated P450XXIA1 pseudogene by cleavage with the restriction endonuclease Taq I, with the XXIA2 gene characterized by a 3.7-kilobase (kb) fragment and the XXIA1 pseudogene characterized by a 3.2-kb fragment. Restriction endonuclease mapping by several laboratories has suggested that deletion of the P450XXIA2 gene occurs in about 25% of patients with CAH, as their genomic DNA lacks detectable 3.7-kb Taq I fragments. We have cloned human P450c21 cDNA and used it to study genomic DNA prepared from 51 persons in 10 families, each of which includes 2 or more persons with CAH. After Taq I digestion, apparent deletions are seen in 7 of the 20 alleles of the probands; using EcoRI, apparent deletions are seen in 9 of the 20 alleles. However, the apparently deleted alleles seen with Taq I do not coincide with those seen with EcoRI. Furthermore, studies with Bgl II, EcoRI, Kpn I, and Xba I yield normal patterns with at least two enzymes in all cases. Since all probands yielded normal patterns with at least two of the five enzymes used, we conclude that the P450XXIA2 gene "deletions" widely reported in CAH patients probably represent gene conversions, unequal crossovers, or polymorphisms rather than simple gene deletions.

Adrenal Hyperplasia, Congenital↗
PubMed1987

Growth hormone blocking antibodies in a patient with deletion of the GH-N gene.

We present another patient with the rare disorder of isolated GH deficiency (IGHD) type 1A. The diagnosis was confirmed by the clinical course, serology and genetic structure. Analysis of the post GH treatment serum of this patient with several thoroughly characterized monoclonal antibodies against GH established the presence of polyclonal, high titre and high avidity IgG-class antibodies against GH. These had the ability to neutralize GH as they could inhibit the binding of radiolabelled GH to GH-receptors on IM9 lymphoblastoid cells. DNA restriction mapping indicated a deletion of the GH-N gene and a family DNA pattern that was consistent with the proposed autosomal recessive aetiology of this disorder. These findings explain the inability of this patient to synthesize GH and his total immunological intolerance to GH replacement therapy.

Antibodies↗
PubMed1987

Increase of serum lipids and serum lipoproteins in girls under therapy with estrogen and norethisteron for height reduction.

The effect of a combined treatment with ethinyl estradiol and norethisteron for height reduction on serum lipids and lipoproteins was investigated in 23 excessively tall girls (greater than 97th percentile). Serum cholesterol, triglycerides, HDL-C and LDL-C were determined before and 3, 6, 9 and 12 months after the onset and 3 to 12 months after cessation of therapy. Treatment with ethinyl estradiol and norethisteron resulted in significant (p less than 0.01) mean increases in serum cholesterol, triglycerides, HDL-C, and LDL-C of 20.6%, 95.5%, 23.6%, and 22.2% above pretreatment values, respectively. This increase occurred during the first 3 months of therapy and thereafter no further significant change was observed. After cessation of therapy elevated levels returned to pretreatment levels within 3 to 12 months in all but two patients. The results obtained suggest an influence of ethinyl estradiol and norethisteron on serum lipids and lipoproteins. Whether these reversible changes of serum lipids and lipoproteins are associated with an increased risk for developing atherosclerosis has to be evaluated in long term investigations.

Adolescent↗
PubMed1987

A pharmacological dose of melatonin increases PRL levels in males without altering those of GH, LH, FSH, TSH, testosterone or cortisol.

Since reports on the influence of melatonin (aMT) on the human endocrine system are scant and inconsistent, the effect of an acute, pharmacological dose of aMT on various hormone levels in healthy males was examined in 3 different experiments. Experiment I: 80 or 240 mg of crystalline aMT were administered per os to 8 volunteers. Before, during and after this treatment, serum levels of aMT, PRL, LH, FSH and testosterone were examined. Although aMT increased at least 1,500-fold over basal levels, only PRL was significantly and consistently elevated after aMT treatment, whereas serum levels of the other hormones were not altered. Experiment II: in 2 subjects, the pulsatile secretion pattern of LH was monitored for 6 h before and 6 h after aMT administration (240 mg p.o.). Neither the amplitude nor the frequency of LH pulses was influenced by the pineal hormone. Experiment III: in 14 volunteers, serum PRL, GH, TSH and cortisol concentrations were examined, once after oral administration of 240 mg aMT and once after placebo. Serum PRL levels were significantly higher after aMT than after placebo; GH showed a slight but not significant trend towards elevation after aMT, whereas other hormones were not altered. An acute pharmacological dose of aMT causes isolated elevation of serum PRL levels and may slightly increase GH. Hormones of the pituitary gonadal axis as well as TSH and cortisol are not altered by aMT.

Adult↗
PubMed1987

[Gonadotropin secretion in children with galactosemia].

Basal and stimulated gonadotropin levels were evaluated in 8 children with galactosemia (2 boys, 6 girls). 5 girls demonstrated increased gonadotropin concentrations being in accordance with hypergonadotropic hypogonadism. It appears, that galactose and its metabolites-either dietary or by self-intoxication-exerts a toxic effect on the ovarian parenchyma, whereas the testis seems to be resistant to the damaging agent.

Adolescent↗
PubMed1986

[Basal gonadotropin level and gonadotropin response to stimulation in patients with anorexia nervosa].

Serum gonadotropin (GN) levels were examined before and after stimulation with luteinizing-hormone-releasing-hormone (LHRH) (100 micrograms/m2 body surface) in 25 female patients with anorexia nervosa (AN) and in 19 healthy young women. 12 patients were reexamined after clinical improvement. Basal GN levels and the luteinizing hormone (LH) response to stimulation were significantly lower in patients than in controls, whereas the response of follicle-stimulating hormone (FSH) to LHRH was normal. The GN response in patients was weight dependent, displaying an inverse correlation to the weight loss. After clinical improvement the GN response was significantly higher than in the acute stage of the disease. The data demonstrate that the activity of the hypothalamic-hypophyseal-gonadal (H-H-G) axis, evaluated on the basis of the GN response to LHRH, depends on the body weight of the patient. Hence, the alteration in activity of the H-H-G axis seems to be a consequence, and not the cause of AN.

Adolescent↗