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Biomedical subjects

H E Kulin

Publications and source records attributed to H E Kulin.

At least 55 records · Page 3Linked to original sources
PubMed1982

Responsiveness of gonadotropin secretion to infusion of an opiate-receptor antagonist in hypogonadotropic individuals.

We tested the hypothesis that suppressive effects of endogenous opiate substances are involved in certain hypogonadotropic states. For this purpose, we studied gonadotropin secretion in idiopathic hypopituitarism (five children), constitutionally delayed adolescence (five boys), and Kallmann's syndrome (three men). Endogenous opiate pathways were antagonized by the iv infusion of naloxone hydrochloride at a dose previously shown to elicit a prompt and significant increase in serum levels of LH in normal men. Under these conditions, naloxone did not increase serially sampled serum concentrations or mean urinary levels of LH: or FSH in eight patients with idiopathic hypopituitarism or Kallmann's syndrome. Gonadotropin concentrations in four of five patients with constitutional delay of adolescence also were unaffected. In one boy with clinical and biochemical indices of late pubertal development, naloxone elicited a significant increase in LH levels in blood and urine, similar to the pattern observed in normal men. In contrast to results in experimental animals, naloxone did not suppress serum PRL concentration significantly in any subject. These observations suggest that: 1) endogenous opiate mechanisms are unlikely to constitute a principal factor in maintaining hypogonadotropism in idiopathic hypopituitarism, delayed adolescence, or Kallmann's syndrome, at least acutely; 2) endogenous opiate mechanisms also cannot be implicated in the acute regulation or PRL secretion in children; and 3) the capability of adult men, but not early pubertal boys, to respond with increased gonadotropin secretion during inhibition of opiate receptors suggests that maturation of the opiate-related neuroendocrine system occurs during the course of sexual development in the human.

Adolescent↗
PubMed1981

The effect of growth hormone on the Leydig cell response to chorionic gonadotrophin in boys with hypopituitarism.

Eleven boys with growth hormone (hGH) deficiency received human chorionic gonadotrophin (hCG) stimulation tests for the assessment of Leydig cell function before, during, and after 1 year of treatment with somatotrophin. Two patients entered puberty during the course of the study protocol. Analysis of the data in nine prepubertal boys revealed an augmentation of testosterone (T) responses to hCG in the presence of hGH. In six of these individuals in whom dihydrotestosterone (DHT) was determined, a similar augmentation in responsiveness of this steroid was found in the presence of hGH. Three prepubertal boys exhibited poor T responses to the basal hCG test with only partial improvement following hGH. In man growth hormone may be an important permissive factor in Leydig cell activity during periods of changing testicular function such as occur in utero or during puberty.

Adolescent↗
PubMed1981

Frequency of transient hypothyroxinaemia in low birthweight infants. Potential pitfall for neonatal screening programmes.

Thyroid function was studied in 54 low birthweight infants during a 3-week period. Each infant was placed in one of three groups. Group 1 (n = 21), infants who were well and appropriately grown fro gestational age; group 2 (n = 23), infants who were appropriately grown but who had hyaline membrane disease; group 3 (n = 10), infants who were small-for-gestational-age. In group 1, 5 (24%) infants had at least one serum thyroxine value less than 3.0 micrograms/100 ml (39 nmol/l). There were 8 (35%) infants in group 2 who had similarly low serum thyroxine values as did 5 (50%) of the 10 infants in group 3. Serum thyrotropin levels and serum binding of the thyroid hormones, as measured by a T3-charcoal uptake test, were normal in all infants. In all instances but 2, serum thyroxine values were at least 4.0 micrograms/100 ml (51 nmol/l) by the end of the 3-week period. There is thus a high incidence of transient 'hypothyroxinaemia' in low birthweight infants, particularly if such infants have hyaline membrane disease or are small-for-gestational-age. These findings must be considered when interpreting results of screening programmes for congenital hypothyroidism and they lend further support to the use of a combination of serum thyroxine and thyrotropin determinations for optimum screening of such infants.

Aging↗
PubMed1981

A model for validation of radioimmunoassay kit reagents: measurement of follitropin and lutropin in blood and urine.

We measured lutropin and follitropin in blood and urine with radioimmunoassay kits from Diagnostic Products Corporation and compared the results with those obtained by use of reagents from the National Institutes of Health (NIH) and the World Health Organization (WHO). The urine standard (second IRP-HMG) from WHO, the blood standard (LER-907) from NIH, and the commercial standards all effected similar displacement of trace material when the commercial gonadotropin kit reagents were used. Highly significant correlations were achieved for these hormones in blood or urine on comparing commercial and NIH/WHO reagents. Serial dilutions of urine samples produced similar relative potencies with the commercial reagents. Conversion factors are presented to relate results for LER-907, second IRP, or commercial standards. Commercially available reagents can provide a practical and reliable means of gonadotropin radioimmunoassay in blood or urine.

Evaluation Studies as Topic↗
PubMed1980

Inborn error in the terminal step of aldosterone biosynthesis. Corticosterone methyl oxidase tpe II deficiency in a North American pedigree.

Profound salt wasting developed in a male infant who had marked reductions in serum and urinary aldosterone concentrations despite striking hyperreninemia. Coincident elevations in plasma and urinary levels of specific 18-hydroxysteroids localized the defect to corticosterone methyl oxidase Type II, the adrenal enzyme responsible for the final step of aldosterone synthesis. Salt replacement but not hydrocortisone ameliorated the clinical and metabolic abnormalities. Evaluation of 33 other family members disclosed the biochemical disorder in six other subjects who were affected in an autosomal-recessive pattern with variably severe clinical manifestations and abnormal ratios of 18-hydroxycorticosterone (or its metabolites) to aldosterone. This inborn error in aldosterone biosynthesis must be distinguished from other heritable, salt-losing defects in adrenal steroidogenesis.

18-Hydroxycorticosterone↗
PubMed1980

The maturation of ovulatory potential in man.

The maturation of the potential for ovulation in man is reviewed in the light of recent data quantitating gonadotropins and gonadal steroids in the prepubertal child. The primary limitations of the hypothalamic-pituitary-gonadal axis are seen as related to feedback control mechanisms. Based on preliminary data obtained in patients with gonadal dysgenesis, a hypothesis which links positive and negative feedback maturation is proposed. The development of full reproductive potential in man is clearly a process which extends over a decade or more.

Adolescent↗
PubMed1979

Urinary follicle-stimulating hormone during pregnancy: relationship to sex of fetus.

FSH excretion was determined by RIA in 111 urine samples from 23 pregnant women. The use of acetone extraction allowed a 20-fold concentration of urine and the accurate quantitation of hormone levels. Between 10 weeks of gestation and term, FSH secretion was consistently low, with a mean excretion of 18 mIU/h; this amount compares to levels found in other states of marked hCG excess (e.g. choriocarcinoma) and is considerably less than the FSH excretion by prepubertal children. Maternal levels of urinary FSH did not differ with sex, suggesting a primary maternal pituitary origin for pregnancy FSH.

Female↗
PubMed1977

Hypothalamic hamartoma: a source of luteinizing-hormone-releasing factor in precocious puberty.

The presence of a hypothalamic hamartoma and precocious puberty in a 19-month-old boy provided an opportunity to study their relation. Excised tissue had the ultrastructural characteristics of an independent neuroendocrine unit -- i.e., neurons containing neurosecretory granules and blood vessels with fenestrated endothelium and double basement membranes. Immunofluorescence studies using specific antibody to luteinizing-hormone-releasing factor showed antigenicity to the factor in the hamartoma. The testicular-hypothalamic-pituitary axis was tested. Clomiphene unresponsiveness suggested a lack of maturation of central-nervous-system events characteristic of normal puberty. The negative feedback system between gonad and brain was intact but partially resistant to steroid suppression. These studies suggest that hypothalamic hamartomas may cause precocious puberty by autonomous production and release of luteinizing-hormone-releasing factor into vessels that communicate with the pituitary portal blood system.

Brain Neoplasms↗
PubMed1977

Timed urinary gonadotropin measurements in normal infants, children, and adults, and in patients with disorders of sexual maturation.

Timed urine collections-mostly over a three-hour period-were obtained from 58 newborn, 68 prepubertal children, 27 adolescents, and 51 adults. For comparison, similar samples were collected from 69 patients with presumptive abnormalities of sexual maturation. Follicle-stimulating hormone and luteinizing hormone were extracted by acetone precipitation and measured by radioimmunossay. Adult nem and women excreted approximately 11 times as much FSH and 33 times as much LH as perpubertal children. Elevated and/or diminished excretory values of gonadotropins were associated with appropriate diagnoses of abnormal pubertal advance or delay. Timed urinary FSH and LH measurements can provide a simple, sensitive, and accurate test of gonadotropin function in children.

Adolescent↗
PubMed1977

Radiological quiz. Familial hyperphosphatasemia.

Hyperphosphatasemia is a genetic disorder of intramembranous bone formation which is radiographically similar to Paget's disease. The authors report a case of hyperphosphatasemia complicated by salt-losing congenital adrenal hyperplasia in a Puerto Rican child. Recognition of this condition is important because of the promising results with calcitonin therapy.

Adrenocortical Hyperfunction↗
PubMed1977

Usefulness of urinary gonadotropin measurements to assess luteinizing hormone releasing factor (LRF) responsiveness in hypogonadotropic states.

Multiple blood sampling techniques and short-term, timed urine collections were employed before and after luteinizing hormone releasing factor (LRF) administration to 51 individuals on 58 occasions. Correlation of blood and urine per cent responses to LRF were significant for LH (P less than .05) and FSH (P less than .001), indicating that urine measurements provide an adequate means of assessing response to LRF. In 7 patients with basal blood gonadotropin levels below assay sensitivity, urine measurements provided the only means of accurately determining a response to LRF. Per cent response to LRF was negatively correlated with basal LH levels in the urine (P less than .02) but not in the blood. A significant negative correlation between basal levels and per cent response was demonstrated for FSH in blood and urine (P less than .01). Accurate measurement of basal gonadotropins and the expression of LRF responses as per cent increments aided in distinguishing between patients with hypothalamic and pituitary diseases. A marked response to LRF in the presence of very low basal LH levels was found in patients with hypothalamic disorders, a finding revealed only by using urine determinations. Low per cent responses to LRF were seen primarily in patients with pituitary disease, a situation most clearly delineated by blood FSH measurements.

Adolescent↗
PubMed1976

Gonadotropin and testosterone measurements after estrogen administration to adult men, prepubertal and pubertal boys, and men with hypogonadotropism: evidence for maturation of positive feedback in the male.

Nineteen male subjects were fiven five daily injections of 17beta-estradiol and circulating levels of estradiol (E2), testerone (T), and gonadotropins were determined by radioimmunoassay before, during, and after the steroid course. Peak levels of E2 attained during the 5 days of treatment ranged from 173-577 pg/ml. Four of seven normal adult men and one castrate man demonstrated suppression of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) with a subsequent rise in LH (positive feedback) while E2 levels remained elevated. A rise in T was associated with the LH increment in the four normal men. Nine pre-, early, or midpubertal boys and two men with hypogonadotropic hypogonadism displayed only gonadotropin suppression after E2 administration. The difference in LH response to estrogen (i.e., positive feedback) between the adult men with normal or elevated gonadotropin levels as compared with the endocrinologically normal boys is significant (P less than 0.01).

Adolescent↗
PubMed1976

Circadian rhythms in gonadotropin excretion in prepubertal and pubertal children.

Timed urinary collections were obtained during sleep and waking hours from 27 prepubertal children ranging in age from 2-12 years and from 13 subjects in various stages of puberty, 12-18 years old. The urine samples were extracted with acetone and introduced into FSH and LH radioimmunoassays. Results of the study indicate a significant nocturnal augmentation of LH secretion in pubertal subjects, confirming existing reports using blood sampling techniques. Increased LH and FSH excretion during sleep was also found in prepubertal children.

Adolescent↗