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Biomedical subjects

A Pertzelan

Publications and source records attributed to A Pertzelan.

At least 19 recordsLinked to original sources
PubMed1992

Growth hormone therapy in normal short children induces a transitory decrease in plasma growth hormone releasing hormone levels and in human growth hormone responsiveness to exogenous growth hormone releasing hormone.

A three-month study of the effect of growth hormone (hGH) therapy (0.1 U/kg/day sc) on plasma levels of GH releasing hormone (GHRH), somatostatin and insulin-like growth factor I (IGF-I) and on the hGH responsiveness to exogenous GHRH was carried out in 32 prepubertal short-stature children with normal GH secretion. Blood samples were collected prior to initiation of therapy, and at 5, 30 and 90 days of onset of therapy, as well as 2 and 90 days after termination of therapy. The nonconventional hGH therapy induced an increase in serum IGF-I levels which lasted as long as therapy was continued. Plasma GHRH levels showed an early transitory decrease after five days of therapy, whereas plasma somatostatin levels were unaltered. A slight suppression in hGH responsiveness to exogenous GHRH was found at 2 but not at 90 days after termination of hGH therapy. It is concluded that nonconventional hGH treatment does not cause permanent changes in physiological hGH secretion.

Adolescent↗
PubMed1992

Growth hormone and insulin-like growth factor regulate insulin-like growth factor-binding protein-1 in Laron type dwarfism, growth hormone deficiency and constitutional short stature.

Insulin-like growth factors (IGFs) mediate the effects of growth hormone (GH), and the insulin-like growth factor-binding proteins (IGFBPs) modulate the actions of IGFs in tissues. We studied the circulating levels of IGFBP-1 in 6 children and 9 adults with Laron type dwarfism (LTD), in 11 children and 21 adults with growth hormone deficiency (GHD), and in 8 children with constitutional short stature. Compared with the situation in healthy children, the basal serum IGFBP-1 concentration was 5.4-fold higher in LTD children, 4.1-fold higher in GHD children, and 3.8-fold higher in children with short stature (p < 0.02 vs controls in all groups). In adult patients with multiple pituitary hormone deficiency (MPHD), the IGFBP-1 concentration was 2-fold elevated, but it was normal in adult LTD patients. Intravenous (N = 10) or subcutaneous (N = 9) administration of IGF-I (75 micrograms.kg-1 and 150 micrograms.kg-1, respectively) in LTD children resulted in a rapid 50-60% fall in serum insulin (p < 0.02), a decline in blood glucose and a concomitant 40-60% rise of IGFBP-1 levels (p < 0.05). Treatment for seven days with IGF-I (150 micrograms.kg-1 x d-1) resulted in a decrease by 34% and 44% of serum IGFBP-1 level in two out of three children with LTD. After prolonged GH therapy, the IGFBP-1 level fell in GHD children by 29% (p < 0.05), in GHD adults by 52% (p < 0.02) and in children with constitutional short stature by 17% (p < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Congenital hereditary hypothyroidism--prenatal diagnosis and treatment.

Intrauterine diagnosis of congenital hypothyroidism was established on the basis of TSH concentration in amniotic fluid in the 22nd week of gestation for the offspring of a couple both known to have an iodide organification defect. Prenatal treatment consisted of intramniotic injections of 500 mcg Na-1-thyroxine, which was administered from the first amniocentesis until one week before delivery. Following delivery, the diagnosis was confirmed by the elevated level of TSH, 60.5 uU/ml, and a gradual decrease of fT4 to 0.8 ng/ml. Regular substitution therapy was commenced on the third day of life. The normal shape and location of the thyroid gland was demonstrated by Technetium scintiscan. At 18 months the infant revealed no significant deviation from normalcy in growth or mental capacity. This experience indicates that testing of amniotic fluid for TSH in the 22nd week of gestation can be diagnostic for congenital primary hypothyroidism. Furthermore, it is suggested that the treatment approach described is warranted in all cases in which there is a high risk of congenital primary hypothyroidism.

Amniotic Fluid↗
PubMed1979

XY gonadal dysgenesis associated with hGH and gonadotrophin deficiencies.

A girl of remarkably short stature, referred for investigation with the diagnosis of gonadal dysgenesis and the finding of a male karyotype, proved to be deficient in growth hormone and gonadotrophin secretion, and was treated with growth and sex hormones. It was concluded that this case demonstrates an apparently casual coincidence of pituitary insufficiency with XY gonadal dysgenesis, evidently the first to be reported.

Adolescent↗
PubMed1979

Linear growth in hypopituitary patients treated with hGH after age fifteen.

Two groups of hHG deficient adolescents (isolated growth hormone deficiency: 11 patients and multiple pituitary hormone deficiency: 20 patients) receiving hGH therapy were analyzed for their linear growth response. It was found that even at a chronological age of 15 years or more, growth can be markedly enhanced, depending upon the bone age and pubertal stage in the IGHD patients and upon optimal balance between hGH and sex hormones in the MPHD patients.

Adolescent↗
PubMed1979

Effect of triiodothyronine administration on the plasma TSH and prolactin responses to TRH in patients with hypothalamic-pituitary insufficiency.

A study was carried out in 10 patients with multiple pituitary hormone deficiencies to determine the response of thyroid-stimulating hormone (TSH) and prolactin (PRL) to thyrotropin-releasing hormone (TRH) and their suppressibility by treatment with triiodothyronine (T3) given at a dose of 60 microgram/day for 1 week. In 3 patients the basal tsh values were normal and in 7 patients, 2 of whom had not received regular thyroid replacement therapy, they were elevated. The response of TSH to TRH was normal in 6 patients and exaggerated in 4 (of these, 1 patient had not received previous substitution therapy and 2 had received only irregular treatment). The basal and stimulated levels of TSH were markedly suppressed by the treatment with T3. The basal PRL levels were normal in 7 and slightly elevated in 3 patients. The response of PRL to TRH stimulation was exaggerated in 2, normal in 6 and absent in 2 patients. The basal PRL levels were not suppressible by T3 treatment but in 4 patients this treatment reduced the PRL response to TRH stimulation. From these findings the following conclusions are drawn: (1) T3 suppresses TSH at the pituitary level, and (2) the hyperreactivity of TSH to TRH and the low set point of suppressibility are probably due to a lack of TRH in the type of patients studied.

Adolescent↗
PubMed1978

Gonadotrophin release in untreated congenital virilising adrenal hyperplasia.

A 9.9-year-old boy and a 9.8-year-old girl with virilising congenital adrenal hyperplasia were subjected to an IV LH-RH (luteinising hormone-releasing hormone) test (so microgram/m2 before initition of therapy with corticosteroids. The pattern of response of LH and follicle-stimulating hormone to LH-RH was found to correspond to the stage of their precocious sexual development and advanced bone age, but not to their chronological age. This finding has implications with regard to the mechanism controlling gonadotrophin secretion at puberty.

Adrenocortical Hyperfunction↗
PubMed1977

The combined effect of growth hormone and methandrostenolone on the linear growth of patients with multiple pituitary hormone deficiencies.

Six patients with multiple pituitary hormone deficiencies (MPHD) were initially treated with separate courses of methandrostenolone and growth hormone and later with the two drugs combined. During the basal period the mean growth velocity was 2.8 cm/year. Methandrostenolone alone, 0.02-0.05 mg/kg/day given to four of the patients led to an acceleration of the growth velocity to a mean of 5.0 cm/year, while growth hormone 6 mg/week alone accelerated the growth rate to a mean of 6.0 cm/year. Combined therapy led to a striking increase in the mean growth rate to 9.3 cm/year. The shortcoming of the combined growth hormone-androgen therapy was the fast acceleration in skeletal maturation even after short-term administration.

Adolescent↗
PubMed1977

Prolactin secretion in girls with isolated gonadotrophin deficiency.

Plasma prolactin, basal levels and the response to an i.v. injection of TRH (100 microgram/m2) was determined in five girls with isolated gonadotrophin deficiency of hypothalamic origin before and after at least 3 months cyclic replacement therapy with conjugated oestrogens (1.25 mg/day). The basal plasma prolactin levels were similar during both tests, however, during oestrogen therapy the mean peak response to TRH almost doubled and the sum of all the values obtained (basal, +15, +30 and +60 min) was significantly higher. It is of note that even upon prolonged oestrogen deprivation the releasable prolactin response to TRH was adequate.

Adolescent↗
PubMed1976

Comparative HGH response to i.v. glucagon and i.v. arginine stimulation tests in children and adolescents.

Thirty-seven children and adolescents of several diagnostic entitites (constitutional growth retardation, diabetes mellitus and pituitary insufficiency) were tested with an i.v. bolus injection of glucagon for plasma human growth hormone (HGH) response. Most of the subjects were also tested for the same purpose by the arginine stimulation test, and the data were compared. It was found that i.v. glucagon is a potent stimulus of human growth hormone release. The HGH is released in two peaks, the first one occuring within 30 min, most probably by a direct effect. The second peak occurs after 120 min, most probably as a secondary effect caused by the drop in blood glucose after its initial rise, which is induced by glucagon. The peak concentrations of HGH induced by glucagon, were very similar to those provoked by i.v. arginine in the same subjects.

Adolescent↗
PubMed1976

Cyproterone acetate in treatment of precocious puberty.

Twenty-nine children (23 girls, 6 boys) with precocious puberty were treated with cyproterone acetate for various periods of time ranging from 6 months to 3 years 4 months. They received an oral dose ranging from 70-150 mg/m2 per day, or an intramuscular depot injection once a fortnight or once a month at a dose ranging from 107-230 mg/m2. Both forms of therapy were found to suppress the signs of sexual maturation, but the oral form proved to be superior. Only the younger patients with a bone age under 11 years showed a beneficial effect upon linear growth and bone maturation. No side effects were noted, but additional advantageous effects upon behaviour and sociability were. It is concluded that at present cyproterone acetate by mouth is the drug of choice in the treatment of precocious puberty. The treatment should be initiated as early as possible to attain maximum benefit.

Administration, Oral↗
PubMed1976

Correlation between plasma growth hormone and insulin and blood glucose concentrations in premature infants.

Plasma growth hormone, insulin and blood glucose levels were measured longitudinally during the first 60 days of life in 21 premature infants (8 males and 13 females) born between the 6th and 8th month of gestation. When these variables were related to age it was found that insulin and glucose, which are lower than in the prepubertal children and adults, rise simultaneously. Whereas growth hormone, which is higher than in older prepubertal children, decreases during the first 2 weeks of life. The decrease in growth hormone continues during the first 2 months of life, in contrast to the increases in insulin and glucose which do not persist in as long a period.

Blood Glucose↗
PubMed1976

Intermittent treatment with human growth hormone (GH) in isolated GH deficiency and in multiple pituitary hormone deficiencies.

The results of intermittent GH treatment of 3-7 1/2 years duration in seven patients with isolated GH deficiency (IGHD) and five patients with multiple pituitary hormone deficiencies (MPHD) are presented. This therapeutic schedule was found to be comparably effective to those using a continuous-administration schedule. In contradistinction to the findings obtained with the latter, there was no progressive decline in growth velocity. The patients with IGHD were found to respond better than the patients with MPHD both in the first course as well as in consequent courses. In the intervals between courses, the growth velocity was less than in the pretreatment period in both groups. It is concluded that optimal results can be obtained by instituting an initial course of continuous treatment of 1 year's duration for the IGHD patients and of 2 years' duration for the MPHD patients, followed by an intermittent therapeutic schedule. This regime not only leads to the same growth achievement obtained with long-term continuous administration of GH but allows conservation of supplies of this very scarce hormone.

Adolescent↗