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Biomedical subjects

Z Dickerman

Publications and source records attributed to Z Dickerman.

At least 37 records · Page 2Linked to original sources
PubMed1984

Intraadrenal steroid concentrations in man: zonal differences and developmental changes.

Adrenal gland samples from 34 individuals 0-68 yr of age were dissected into four layers of equal thickness parallel to the capsule and the zonal boundaries of the cortex, and were analyzed by RIA for their concentrations of 17OH-progesterone, 11-desoxycortisol, cortisol, progesterone, corticosterone, aldosterone, 17OH-pregnenolone, dehydroepiandrosterone, androstenedione, and testosterone, with DNA content to correct for variations in sample size. Intraadrenal steroid concentrations were 10-1000 times higher than reported serum levels, and varied significantly with age, adrenal weight, and cortical thickness. The concentrations of cortisol,11-desoxycortisol, corticosterone, androstenedione, and testosterone increased with age. Levels of 17OH-pregnenolone, dehydroepiandrosterone, and 17OH-progesterone decreased during infancy in parallel with involution of the adrenal, and then rose again in late childhood and puberty. The concentrations of all steroids, except aldosterone, increased significantly from the outer to the inner layers of cortex. Comparisons of product-substrate ratios suggested that changes in adrenal androgen secretion are induced by shifts in the relative activities of key branch-point steroidogenic enzymes, notably 3 beta-hydroxysteroid dehydrogenase-isomerase and 17,20-desmolase. Since intraadrenal steroid concentrations are in the range of the Michaelis-Menten constant (Km) for these enzymes (10(-6) M) and can be shown in vitro at this concentration to influence relative enzyme activities, these data support the hypothesis that zonal and developmental changes in adrenal androgen secretion relative to that of cortisol are induced by changes in the steroidal micro-environment which in turn are imposed by adrenal growth and the centripetal blood flow through the gland.

17-Hydroxysteroid Dehydrogenases↗
PubMed1983

Human chorionic gonadotropin (hCG) treatment in cryptorchidism.

One hundred twenty-eight prepubertal boys, ages 1-12 years, were referred to our institute because of uni- or bilateral cryptorchidism. Patients with mobile (retractile) testes were not included in the study. They were treated with human chorionic gonadotrophin (hCG, Pregnyl-Teva) twice weekly for five consecutive weeks by the following doses; 1-4 years (n = 53) - 250 U X 10; 4-7 years (n = 51) - 500 U X 10; 7-12 years (n = 24) - 1000 U X 10;i.m. Plasma testosterone (T) levels were measured before and once weekly during the treatment period. A good clinical response (a complete descent of the testes into the scrotum) was obtained in 32 (25%), a partial response (a distal movement of the testes towards the scrotum) - in 41 (32%) of the boys. The basal plasma T levels were within the normal range for prepuberty in all the patients (18 +/- 9 ng/dl) and a significant increase during hCG treatment was found in all (peak of 344 +/- 185 to 640 +/- 288 ng/dl). These values were not significantly different between the "responders", "partial responders". The result of these studies, indicate the use of hCG for the initial treatment of boys with cryptorchidism, the minimal effective dose being 500 U twice weekly for five consecutive weeks.

Aging↗
PubMed1983

Effect of chlorpromazine on hypothalamic-pituitary-gonadal function in 10 adolescent schizophrenic boys.

Low basal plasma testosterone levels with normal response to human chorionic gonadotropin (HCG) stimulation and mild hyperprolactinemia and blunted luteinizing hormone (LH) response to luteinizing-releasing hormone (LRH) stimulation were found in 10 adolescent schizophrenic boys who had been treated with chlorpromazine for more than 6 months. These findings may indicate a disturbance of the hypothalamic-pituitary-gonadal function in these patients, probably due to the prolonged administration of chlorpromazine. It remains to be established whether the decrease in basal testosterone secretion is caused directly by chlorpromazine or secondarily by the drug-induced hyperprolactinemia.

Adolescent↗
PubMed1982

Dynamics of basal pituitary gonadotropin secretion and responsiveness to LRH following estradiol benzoate in normal boys.

The influence of a single intramuscular injection of estradiol benzoate (E2B), 2.5-15 micrograms/kg, on the basal estradiol, LH and FSH and their response to LRH stimulation (50 micrograms/m2, i.v.) performed 20 h after E2B injection, was studied in 52 normal boys aged 6-16 9/12 years. The minimal effective dose of E2B was found to be 10 micrograms/kg. This same dose of E2B which increased plasma estradiol level from 15 +/- 8 to 22 +/- 15 pg/ml (mean +/- SD) at 20 h after the intramuscular injection, suppressed basal plasma LH and FSH and their response to LRH in the prepubertal (n = 12), early-pubertal (n = 12) and late-pubertal (n = 8) boys. It is suggested that the maturation of the hypothalamo-pituitary axis in boys during puberty is under the influence of endogenous estradiol.

Adolescent↗
PubMed1982

Dynamics of basal pituitary gonadotropin secretion and responsiveness to LRH following estradiol benzoate in normal girls.

The influence of a single intramuscular injection of estradiol benzoate (E2B), 2.5-15 micrograms/kg, on the basal plasma estradiol, LH and FSH and their response to LRH stimulation (50 micrograms/m2, i.v.) performed 20 h after E2B injection, was studied in 50 normal girls aged 6-17 years. It was found that the minimal dose of E2B which caused a significant change in the basal and/or LRH stimulated LH and FSH levels was 10 micrograms/kg. This dose increased plasma estradiol level by 10-35 pg/ml, i.e. still within the normal range for the appropriate pubertal stage of the subjects. The same dose of E2B significantly suppressed the basal FSH level in most of the prepubertal (n = 8), early-pubertal (n = 9) and late-pubertal (n = 14) girls and the FSH response to LRH in most prepubertal girls. The basal LH was suppressed in most pre- and early-pubertal girls, but increased significantly in 50% of the late-pubertal girls. The LH response to LRH was significantly increased in most of the girls at all pubertal stages. It is suggested that endogenous estradiol is an important mediator in the maturation of the hypothalamo-pituitary axis in girls from mid-puberty onwards, and that the low physiological level of estradiol present in adolescence is sufficient to induce a gradual increase in pituitary sensitivity to LRH and a positive hypothalamo-pituitary feedback.

Adolescent↗
PubMed1981

Long-term effect of D-Trp6-luteinizing hormone-releasing hormone on testicular size and luteinizing hormone, follicle-stimulating hormone, and testosterone levels in hypothalamic hypogonadotropic males.

Six men, ages 18 to 34 years, with hypothalamic hypogonadotropism were treated with D-Trp6-luteinizing hormone-releasing hormone (10 micrograms intramuscularly on alternate days) for a period of 6 months. They underwent an intravenous luteinizing hormone-releasing hormone (LH-RH) test (50 micrograms/sq m) before and after 1, 3, and 6 months of treatment. During the first 3 months of therapy, the mean (+/- standard deviation) testicular volume increased from 3.5 +/- 1.0 ml to 6.0 +/- 2.0 ml, but decreased to 5.0 +/- 1.0 ml after 6 months. A significant increase in the plasma LH response to LH-RH over pretreatment levels was noted after 1 month (10.2 +/- 4.2 mIU/ml versus 1.6 +/- 1.0 mIU/ml, P less than 0.001) and 3 months (3.0 +/- 1.6 mIU/ml, P less than 0.01) with a subsequent decline to pretreatment levels after 6 months of treatment. The follicle-stimulating hormone response to LH-RH was not significant. It is concluded that D-Trp6-LH-RH induced an initial stimulation in these patients but, probably because of the excessively high dose used, a paradoxical inhibitory response was obtained after 3 months of therapy.

Adolescent↗
PubMed1981

Rise in plasma growth hormone in response to exogenous LRH in Klinefelter's syndrome.

In a group of sixteen patients with Klinefelter's syndrome (KS) aged from 2 years 8 months to 31 years, a study was made of the plasma growth hormone (hGH) response to LRH (50 micrograms/m2 i.v.; n=16), TRH (200 micrograms i.v.; n=14) and insulin-induced hypoglycaemia (0.1 u R.I,/kg i.v.; n=6). There was a rise in hGH following LRH from a level below 5 ng/ml during fasting to a level above 8 ng/ml (P less than 0.001) in nine (56.3%) of the sixteen patients tested; a similar response was found in only one of a control group of fifteen boys matched for age. TRH stimulation led to a rise in hGH in one of the fourteen KS patients tested, with none in the control group. Insulin-induced hypoglycaemia elicited a normal response of hGH in the six KS patients tested, from 1.8 +/- 0.7 to 16.5 +/- 3.7 ng/ml, (M +/- SD, P less than 0.001). Basal prolactin (PRL) levels were normal in the KS patients (9.4 +/- 4.1 ng/ml, M +/- SD) but the response to TRH stimulation was significantly higher (63.3 +/- 40 ng/ml; P less than 0.01) than that of the control group (30 +/- 15 ng/ml). Plasma gonadotrophin levels and the response to LRH stimulation were increased in all of the KS patients except those below the age of 13. Plasma TSH levels and the response to TRH stimulation as well as the levels of serum thyroxine were found to be normal in all the KS patients tested. The abnormal rise of hGH following LRH stimulation and of PRL following TRH stimulation suggests a disturbance in the neuroendocrine regulation mechanisms of these hormones in KS.

Adolescent↗
PubMed1981

Addison's disease associated with precocious sexual development in a boy.

An eleven-year-old boy was diagnosed to have Addison's disease with an ACTH level of over 4500 pg/ml after a short episode of fever and dehydration. From the age of 6 years his skin and buccal mucosa had been hyperpigmented but there were no other subjective complaints. The clinical examination also revealed signs of advanced puberty for his age (3rd--4th stage according to Tanner's criteria), with advanced bone age (13 years). The elevated levels of plasma testosterone and gonadotropins and their response to LH-RH stimulation were appropriate for his clinical stage of puberty and supported the diagnosis of true precocious puberty. It is proposed that the concomitant appearance of Addison's disease and precocious puberty is due to a "drift" phenomenon of LH-RH and/or gonadotropins following the prolonged elevation of ACTH secretion.

Addison Disease↗
PubMed1981

Abnormal growth hormone response to LRH and TRH in adolescent schizophrenic boys.

The authors studied the effect of LRH and TRH on HGH in 10 adolescent schizophrenic boys and 9 age-matched normal boys. Before antipsychotic treatment, LRH and TRH induced a marked rise in hGH in 8 of 10 patients and 4 of 6 patients, respectively. No effect on HGH was observed in the normal controls. After 3 months of treatment with chlorpromazine, thioridazine, or haloperidol, LRH failed to induce a rise in HGH in 5 of the 6 patients tested, but TRH induced a significant rise in HGH in 3 of 4 patients tested. The authors postulate that these results indicate a dysfunction in the mechanism regulating HGH secretion in schizophrenia.

Adolescent↗
PubMed1980

Follow-up of boys with unilateral compensatory testicular hypertrophy.

Of a total of 148 boys with unilateral compensatory testiculary hypertrophy (CTH) diagnosed at our clinic, 30 were followed for many years throughout puberty. These boys underwent the pubertal stages fo pubic hair development in a normal manner, including penile growth. The basal plasma levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) of the boys with CTH showed a wider range than those of normal boys. Even in prepuberty the mean basal plasma FSH levels were significantly higher than those of normal boys, as was the peak FSH response to intravenous LH-releasing hormone. In puberty stage 4 the mean plasma LH levels were also higher than normal. Plasma testosterone levels were within the normal range in pubertal stages 1 to 4, but in stage 5 the mean basal level and response to stimulation with human chorionic gonadotropin were significantly lower than normal. Among seven spermatograms performed, five showed oligospermia and two showed azoospermia. It is concluded that compensatory hypertrophy of one testis does not seem able to prevent testicular insufficiency in adulthood.

Adolescent↗
PubMed1980

Evaluation of the renin-aldosterone system during hypo- and hyperglycemia in children and adolescents.

The effect of hypo- and hyperglycemia on the renin-aldosterone system was studied in 10 endocrinologically normal children. Insulin-induced hypoglycemia caused an elevation of plasma renin activity (PRA) up to 371 +/- 23% (mean +/- SEM) over the basal level (p less than 0.001) and of the plasma aldosterone level up to 243 +/- 7% (mean +/- SEM) over the basal values (p less than 0.001). Hyperglycemia caused an elevation of PRA up to 135 +/- 40% (mean +/- SEM) over the basal values (p less than 0.05) and a reduction in the plasma aldosterone level to 53 +/- 12% (mean +/- SEM, p less than 0.01). It is suggested that the widely used diagnostic procedures, the insulin tolerance and oral glucose tolerance tests, be also applied for the investigation of the renin-aldosterone system.

Adolescent↗